Principles and Practice of Critical Carefacweb.northseattle.edu/cduren/North Seattle AT Program 2011-2012...identify the key principles underpinning assessment and ... as correct interpretation

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Principles and Practice of Critical Care

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Learning objectivesAfter reading this chapter, you should be able to:

■ describe the reasons for the assessment and monitoring of critically ill patients

■ identify the key principles underpinning assessment and monitoring

■ explore reasons for haemodynamic monitoring

■ understand the physiological bases for different types of monitoring

INTRODUCTIONThe critical care environment is one that is ‘specifically staffed and equipped for the continuous monitoring, observation and care of individuals with a critical illness’.1 The physiological response of critically ill patients to disease or other stressors such as trauma will in most cases determine the outcome of that episode of illness. Monitoring of physiological data provides baseline details from which future assessments can be made, and facilitates the response to various medical and nursing interventions. A vast amount of data is generated by an unstable patient in an intensive care unit each day—estimated to be as great as 2000 items in 1987, and presumably much higher in today’s technological environment.2 It is vital therefore that nurses understand the principles related to assessment, monitoring, and diagnostic information obtained from various sources, as correct interpretation of the data generated is important in providing timely and effective interventions while minimising any potential errors.

When considering the data generated from monitoring and diagnostic devices, it is important that trends be carefully assessed, rather than relying on one-off results. Trends reveal

patterns among individual and grouped variables and should therefore be regularly reviewed to reveal the response to therapy. Although the focus of this chapter is on physiological data, the importance of the assessment and monitoring of subjective responses of patients and other psychosocial issues is acknowledged (see Chapter 8).

Critical care nursing includes assessment and monitoring of all relevant systems—respiratory, cardiovascular, gastrointestinal, neuromuscular and urinary. Consequently, nurses require an in-depth understanding of anatomy, physiology, pathophysiology and pharmacology to undertake the ongoing assessment and to achieve early recognition of complications and the related interventions. Underpinning all of these are the principles of delivery of optimal and culturally competent care, relief of distress, compassion and support, dignity, information, and the care and support of relatives and caregivers.3

The monitoring and diagnostics specifically addressed in this chapter include those related to the haemodynamic, respiratory and neurological systems of the body.

CHAPTER 7

Assessment, Monitoring and DiagnosticsBridie Kent Bruce Dowd

■ explore the nursing roles in relation to evidence-based practice and monitoring.

Key wordshaemodynamic monitoring

oxygen delivery

oxygen consumption

neurological assessment

diagnostic imaging

ventilation monitoring

110 SECTION 2 ■ Principles and practice of critical care

RELATED PHYSIOLOGYThe wellbeing of a patient is dependent on the normal supply of oxygen and nutrients to the tissues and vital organs. The monitoring of normal anatomy and physiology in order to understand the pathophysiology related to patients’ problems is therefore an essential part of critical care nursing. The interrelated nature of the body’s systems must be appreciated, as dysfunction in one system will result in anomalies or alterations in others. Take, for example, the delivery of oxygen to the tissues. The cardiovascular and respiratory systems work harmoniously to ensure that the tissues receive oxygen to maintain homeostasis. However, other systems also have vital parts to play in this process: the brain and other aspects of respiratory control, the kidneys for the production of buffers, the metabolic systems for production and removal of other elements, all interact to ensure that normal functions are maintained. The following section will revisit essential physiology; if further detail is required, please refer to a comprehensive anatomy and physiology text.4

Principles of oxygen delivery and oxygen consumption The delivery of oxygen (DO2) to the tissue and vital organs is governed by three important components: 1. cardiac output (stroke volume × heart rate)2. haemoglobin3. oxygen saturation. A balance between DO2 and oxygen consumption (VO2) is required. The amount of oxygen that tissues need or demand is determined by the level of metabolic activity of the tissues, which varies throughout the body. If VO2 exceeds DO2, deficits occur and a physiological effect will be observed. The tissues generally extract oxygen in direct proportion to blood flow. However, at a certain level of oxygen delivery, a plateau of oxygen consumption is achieved; it is therefore important that for patients who have sepsis, for example, there is enhanced blood flow, as supply dependency is more likely in these patients.5

Oxygen extraction is the percentage of oxygen that is extracted and utilised by the tissues. At rest, normally just 25% of the total oxygen delivered to the tissue is extracted, although this amount does vary throughout the body, with some tissue beds taking more and others taking less. Venous oxygen content is the amount of oxygen contained in the venous blood as it returns to the lungs (CvO2). It is determined by the haemoglobin concentration and the oxygen saturation of the haemoglobin in venous blood (SvO2). SvO2 is determined by the amount of oxygen delivered to the tissues in the arterial blood, as well as the amount of oxygen extracted and utilised by the tissues. Normally, the oxygen saturation of venous blood is 60%–75%, with values below this indicating that more oxygen than normal is being extracted by the tissues. This can be due to a reduction in oxygen delivery to the tissues, or to an increase in the tissues’ consumption of oxygen. Common causes of decreased oxygen delivery are decreased cardiac output, low haemoglobin levels, and

hypoxia. Tissue oxygen demands can be increased by the increased effort of breathing, pyrexia, sepsis, shivering, agitation/restlessness, and increased physical activity.6

Oxygen transportAssessment of the lungs’ ability to adequately oxygenate arterial blood is a vital part of critical care. Respiratory monitoring ensures that oxygenation and all other aspects of the respiratory system are assessed either continuously or intermittently. Assessment of oxygenation is performed by examining arterial oxygen saturation (SaO2) and arterial oxygen tension (PaO2), usually via arterial blood gas analysis, which will be described later in this chapter. Caples and Hubmayr provide an informative summary of the respiratory monitoring tools used in ICUs.7

Oxygen and carbon dioxide use the process of diffusion to move around the body. This enables molecules to move from areas of high concentration to those where the concentration of molecules is much lower, and is reliant on the amount of driving pressure, or the pressure gradient. Where the driving pressure is high, more diffusion of gases takes place. Oxygen and carbon dioxide concen tration differences in the lungs and surrounding blood vessels drive the gases across the alveolar membrane; in the alveoli, oxygen is highly concentrated and the pressure generated pushes oxygen molecules into the pulmonary capillaries. Conversely, the same process pushes carbon dioxide from the highly concentrated pulmonary capillaries into the alveoli, where concentrations are low. Other determinants of the rate of diffusion include the thickness of the alveolar membrane, the amount of surface area of the membrane available for gas transfer, and the inherent solubility of the gas.6 Further information on respiratory pathophysiology is contained in Chapter 11. Oxygen is transported around the body in two ways: in plasma (3%), and attached to haemoglobin (97%). There are a number of determinants of tissue oxygen supply, including haemoglobin level; oxygen saturation of haemoglobin; oxygen dissociation; and perfusion pressure.6

HAEMOGLOBINHaemoglobin (Hb) contains iron (haem) and polypeptide proteins called globin. The molecules are relative large when compared with other blood cells, and consequently, haemoglobin is not normally found in interstitial fluid or urine. There are approximately 900 g of circulating haemoglobin, carried in the red bllod cells, in a 70 kg adult, and new red blood cells are constantly synthesised while others are destroyed; the erythrocyte (red blood cell) has a life of approximately 120 days. Old cells are metabolised by macrophages and this process releases iron, which is used for further haemoglobin synthesis in the liver, while waste products are excreted in bile.6

One gram of haemoglobin can carry 1.34 mL oxygen, and the level of saturation within the total circulating haemoglobin can be measured clinically, commonly by pulse oximetry. As noted previously, a large reserve of oxygen is available if required, without the need for any increase in respiratory or cardiac workload. The amount of oxygen

CHAPTER 7 ■ Assessment, monitoring and diagnostics 111

bound to haemoglobin in comparison with the amount of oxygen the haemoglobin can carry is commonly reported as SaO2. If the SaO2 is 90%, this means that 90% of the haemoglobin attachments for oxygen have oxygen bound to them.

OXYGEN–HAEMOGLOBIN DISSOCIATION CURVE The affinity of haemoglobin for oxygen can be portrayed by the oxygen–haemoglobin dissociation curve (see Figure 7.1). The transfer of oxygen across the capillary membranes is determined by pressure differences on either side of the membranes. In the upper part of the curve, relatively large changes in the PaO2 cause only small changes in haemoglobin saturation. Therefore, if the PaO2 drops from 100 to 60 mmHg (8–14 kPa), the saturation of haemoglobin changes only 7% (from the normal 97% to 90%). The lower portion of the oxygen–haemoglobin dissociation curve, however, indicates that as haemoglobin is further desaturated, larger amounts of oxygen are released for tissue use to ensure that an adequate oxygen supply to peripheral tissues is maintained, even when oxygen delivery is reduced.6

The affinity of haemoglobin for oxygen varies in certain circumstances and so a number of factors cause shifts to occur in the oxygen–haemoglobin dissociation curve, resulting in changes to the affinity between oxygen and haemoglobin.

CARBON DIOXIDE TRANSPORTCarbon dioxide (CO2) is also carried in the blood and plays a vital part in maintenance of normal respiratory and haemostatic functioning. CO2 is produced at a rate of 200 mL/min by metabolism and with only minor differentials in the normal concentrations of CO2 in arterial (48 mL/dL) and venous (52 mL/dL) blood. The greater solubility of CO2 when compared with oxygen results in rapid diffusion across the capillary membranes, and therefore the gas can be easily removed for excretion. CO2, a byproduct of cellular respiration, is carried in the blood in three ways: plasma (approx 1%); haemoglobin (approx 25%); and as bicarbonate (approx 74%). When dissolved, CO2 forms bicarbonate ion (HCO3

-), carbonic acid (H2CO3) and carbonate ion (CO3

2-), concentrations of which affect the acid–base balance in the body.8 In common with other acids, carbonic acid partially dissociates when in solution, to form CO2 and water or bicarbonate and hydrogen ion:

CO2 + H2O ↔ H2CO3 ↔ HCO3 + H+

The strength of the dissociation is defined by the Henderson-Hasselbach equation which describes the relationship between bicarbonate, CO2 and pH, and helps to explain why an increase in dissolved CO2 causes an increase in the acidity of the plasma, while an increase in bicarbonate causes the pH to rise (i.e. the acidity falls):

Oxy

gen

satu

ratio

n, p

erce

nt

10

20

30

40

50

60

70

80

90

100

0 10 20 30

A

LeftRight

Common factors shifting curve to the right↓ pH↑ PCO2↑ Temperature↑ 2, 3-DPG (hyperthyroidism, anaemia, chronic hypoxaemia)

1.2.3.4.

Common factors shifting curve to the left↑ pH↓ PCO2↓ Temperature↓ 2, 3-DPG (hypothyroidism, bank blood)Carboxyhaemoglobin

1.2.3.4.5.

B C

40 50

PaO2, mmHg

P50

60 70 80 90 100

FIGURE 7.1 Oxygen–haemoglobin dissociation curve29 (published with permission)


pH = 6.1 + log (HCO3) (CO2)

(6.1 = the dissociation constant in plasma)6

Determinants of cardiac outputCardiac performance is altered by numerous homeostatic mechanisms. Cardiac output is regulated in response to stress or disease, and changes in any of the factors that determine cardiac output will result in changes to cardiac output (see Figure 7.2). Cardiac output is the product of heart rate and stoke volume; alteration in either of these will increase or decrease cardiac output, as will alteration in preload, afterload or contractility. In the healthy individual, the most immediate change in cardiac output is seen when heart rate rises. However, in the critically ill, the ability to raise the heart rate in response to changing circumstances is limited, and a rising heart rate may have negative effects on homeostasis, due to decreased diastolic filling and increased myocardial oxygen demand.

Preload is the load imposed by the initial fibre length of the cardiac muscle before contraction (i.e. at the end of diastole).9 The primary determinant of preload is the amount of blood

filling the ventricle during diastole, and as indicated in Figure 7.2, it is important in determining stroke volume. Preload influences the contractility of the ventricles (the strength of contraction) because of the relationship between myocardial fibre length and stretch (the Frank-Starling rule—the greater the volume, the more stretch and force in the contraction; see Figure 10.8, Chapter 10). However, a threshold is reached when fibres become overstretched, and force of contraction and resultant stroke volume will fall.

Preload reduces as a result of large-volume loss (e.g. haemorrhage), venous dilation (e.g. due to hyperthermia or drugs), tachycardias (e.g. rapid atrial fibrillation or supraventricular tachycardias), raised intrathoracic pressures (a complication of IPPV), and raised intracardiac pressures (e.g. cardiac tamponade). Some drugs such as vasodilators can cause a decrease in venous tone and a resulting decrease in preload.10,11 Preload increases with fluid overload, hypothermia or other causes of venous constriction, and ventricular failure. Body position will affect preload, through its effect on venous return.

The volume of blood filling the ventricles is also affected by atrial contraction: a reduction in atrial contraction ability, as can occur during atrial fibrillation, will result in

Contractility

Stroke volume

Cardiac output

Oxygen utilisation(oxygen

consumption, VO2)

Deoxygenated venous return

Preload Afterload

Ventricular chamber pressure

Ventricular chamber dimension/wall thickness

Heart rate

Mean arterial pressure

Oxygen delivery (D02)

Arterial oxygencontent

Systemic vascularresistance

FIGURE 7.2 Determinants of cardiac function and oxygen delivery183 (published with permission)


a reduction in ventricular volume, and a corresponding fall in stroke volume and cardiac output.

Preload of the left side of the heart, assessed at the end of filling of the left ventricle from the left atrium using the PCWP, is assumed for clinical purposes to reflect left ventricular end-diastolic volume (LVEDV). Due to the non-linear relationship between volume and pressure,12,13 caution must, however, be taken when interpreting these values, as rises in left ventricular end-diastolic pressure (LVEDP) may indicate pathology other than increased preload, such as ischaemia.9 Preload of the right side of the heart is indirectly assessed at the end of filling of the right ventricle from the right atrium through central venous pressure (CVP) monitoring.

Afterload is the load imposed on the muscle during contraction, and translates to systolic myocardial wall tension. It is measured during systole, and is inversely related to stroke volume and therefore cardiac output, but it is not synonymous with systemic vascular resistance (SVR), as this is just one factor determining left ventricular afterload. Factors that increase afterload include:• increased ventricular radius;14 • raised intracavity pressure; • increased aortic impedance; • negative intrathoracic pressure; and• increased SVR. As afterload rises, the speed of muscle fibre shortening and external work performed falls, which can cause a decrease in cardiac output in critically ill patients. Afterload of the right side of the heart is assessed during the ejection of blood from the right ventricle into the pulmonary artery. This volume is indirectly assessed by calculating pulmonary vascular resistance. Ventricular afterload can be altered to clinically affect cardiac performance. Reducing afterload will increase the stroke volume and cardiac output, while also reducing myocardial oxygen demand. However, reductions in afterload are associated with lower blood pressure, and this limits the extent to which afterload can be manipulated.

Contractility is the force of ventricular ejection, or the inherent ability of the ventricle to perform external work, independent of afterload or preload. It is difficult to measure clinically. It is increased by catecholamines, calcium, relief of ischaemia, and digoxin. It is decreased by hypoxia, ischaemia, and certain drugs such as thiopentone, β-adrenergic blockers, calcium channel blockers or sedatives. Such changes affect cardiac performance, with increases in contractility causing increased stroke volume and cardiac output. Increasing contractility will increase myocardial oxygen demand, which could have a detrimental effect on patients with limited myocardial perfusion.

Stroke volume is the amount of blood ejected from each ventricle with each heartbeat. For an adult, the volume is normally 50–100 mL/beat, and equal amounts are ejected from the right and left ventricle. Further discussion of related cardiovascular physiology and pathophysiological states is provided in Chapters 10 and 19.

Intracranial physiologyNeurological compromise affects many critically ill patients. Problems such as raised intracranial pressure complicate a

variety of conditions, such as meningitis, hepatic failure and pre-eclampsia, while other patients may experience transient neurological impairment arising from the treatments given during the care episode, such as sensory derangement, and deep sedation. Consequently, knowledge of the related physiology will assist with the assessment and monitoring of these patients.

The brain can be divided into three anatomical areas: the cerebrum, the brainstem, and the cerebellum. Intracranial volume is 1.7 L in total, consisting of blood (150 mL), cerebrospinal fluid (150 mL) and brain tissue (1400 mL). This is encased by the rigid structure of the skull. The brain contains four ventricles that are filled with cerebrospinal fluid, and are connected to each other and to the central canal of the spinal cord. The two lateral ventricles are large, c-shaped chambers located deep in each cerebral hemisphere, and are separated anteriorly by a thin membrane, the septum pellucidum.15 Each of these ventricles connects to the smaller, narrow third ventricle via the intraventricular foramen. The third ventricle connects with the fourth ventricle via the cerebral aqueduct, which runs through the midbrain. This fourth ventricle forms the connection with the spinal cord, and has three openings in its walls: the paired lateral apertures in the side walls, and the median aperture in the roof. These apertures connect the ventricles with the subarachnoid space.15

Intracranial contents are non-compressible, so if one part increases in volume, it will negatively affect the others. Pressure exerted by the contents is normally 0–15 mmHg, but this pressure is not constant throughout the intracranial area. There is limited capacity for compensation if there is an increase in the intracranial volume; blood or cerebrospinal fluid may be temporarily displaced into the spinal cord space (this may occur naturally during sneezing, coughing or straining), but if this exceeds the compliance threshold, then intracranial pressure will rise (see Figure 7.3).16,17

Tissue injury occurs if pressures of 20–30 mmHg are sustained, and cerebral autoregulation ceases when ICP rises above 40 mmHg. Sustained pressure over 60 mmHg is usually fatal, as it results in ischaemic damage to the brain tissue, a vicious cycle of intracranial hypertension and further tissue damage (see Figure 7.4). Further discussion of related physiology and clinical neurological states is provided in Chapter 12.

Compensation

Volume

Exhaustion50

40

30

20

10

0

Pre

ssu

re (

mm

Hg

)

FIGURE 7.3 Intracranial pressure–volume curve185 (published with permission)


PHYSICAL ASSESSMENT Advanced clinical assessment skills are essential for critical care nurses, as it is important that data are collected that can be used to identify the immediate and future needs of the patient and their family members, thereby facilitating the development of a comprehensive plan of care. Assessment should use a systematic approach. Initial assessment will include the history, functional capability of the patient, and current physiological status to provide a baseline against which to compare subsequent assessments. For the critically ill patient, assessments need to occur continuously to evaluate the response to interventions and to determine the extent to which goals have been achieved. There are two levels of assessment: the brief initial assessment, when the patient arrives in the critical care unit (the primary survey); and a secondary comprehensive assessment, which generates more detailed information and will take more time to complete.

There are four main assessment techniques used in undertaking the primary and secondary surveys. These are inspection (also referred to as observation), palpation, percussion, and auscultation:18 • Inspection is a visual examination of body regions

that is much more than just looking. It needs to be undertaken in a systematic, deliberate and focused manner, comparing what is seen with what is already known.

• Palpation is examination of the body using touch, rather than eyesight. It should be both light and deep to reveal information about tenderness, painful areas, areas of rigidity and muscular spasm, swellings, masses, pulsations, as well as areas of moisture, temperature differentials and crepitus.

• Percussion is a technique that uses finger tapping to elicit different sounds that will reveal details about the underlying area. Direct percussion is the direct tapping of the body with one or two fingers to obtain sound.

More commonly, however, percussion is performed indirectly; the middle finger of the non-dominant hand is placed against the patient’s body and the tip of the middle finger of the dominant hand strikes against the distal phalanx to elicit sound. Percussion is commonly used to assess lung fields or the abdomen.

• Auscultation is listening to sounds, usually via a stethoscope to block out surrounding sounds. The diaphragm of the stethoscope is sensitive to high-pitched sounds, while the bell is better for detecting low-pitched sounds. Auscultation is used to evaluate sounds emanating from the heart, lungs, abdomen and vascular systems.

Wherever possible, no parts of the body should be left out of the primary or secondary survey, but inevitably the condition of critically ill patients will determine the appropriateness of the assessment, and some parts may have to be delayed until the patient’s condition has stabilised.

Primary survey In essence, assessment begins when a nurse first learns of an impending admission. A pre-arrival assessment is often based on limited information obtained from the clinician caring for the patient in locations such as the ward, emergency department or operating theatre. Sufficient detail must be provided to ensure that the receiving nurse can prepare the bed area with the necessary equipment, monitoring and supplies. Many critical care units have their own pre-admission checks, and nurses should refer to these for local guidance.

As soon as the patient arrives in the critical care unit, a rapid primary survey to elicit evidence of any airway obstruction, respiratory failure, circulatory failure or neurological dysfunction is conducted, using the ABCDE guide:19 • Airway assessment—any evidence of obstruction;

failure of airway patency/protection; and check position of artificial airway (if present).

• Breathing assessment—check whether the breathing is artificial or spontaneous; any evidence of increased respiratory effort (check rate and pattern of respirations); any evidence of abnormal breath sounds indicative of pneumothorax, asthma, heart failure?

• Circulation assessment—ECG rhythm, rate; blood pressure; peripheral pulses and refill; presence of bleeding.

• Disability assessment—altered level of consciousness; evidence of fitting; hypoglycaemia; any localising signs in pupils, limbs or cranial nerves?

• Environment/exposure assessment—evidence of rash; abnormal temperature.

It may also be useful to include the following:20

• Presenting problem—primary affected body system; associated symptoms.

• Drugs and diagnostic tests—drugs administered prior to admission; current medications; review of available diagnostic results.

• Equipment—patency of drainage systems and vascular devices (IV infusions/cannulae); appropriate

FIGURE 7.4 Intracranial hypertension/tissue damage cycle185 (published with permission)

Raisedintercranial

pressure

Capillaryvasodilation

Reduced cerebralblood flow

Plasmaextravasation

Tissuehypoxia

Intracellularoedema

Metabolicacidosis

Cell membrane(Na+/K+ pump)

damage

Increased vascularpermeability

Hypercapnia


functioning and labelling of infusion devices, and other equipment connected to the patient.

• Allergies—note whether any are known.

Comprehensive assessmentOnce the initial checks have been completed, the secondary, comprehensive assessment to provide a complete picture of the patient’s condition is undertaken. Details should be elicited from family members if the patient is unable to provide them. In addition, each body system should be assessed using a top-to-toe approach, to ensure that nothing is missed. Collaboration with other members of the healthcare team is important in this process, as the relevant information should be obtained without subjecting the patient to unnecessary examinations. The nervous, cardiovascular, respiratory, renal, gastrointestinal, endocrine, haematological, immune and integumentary systems all require examination to determine whether there are any existing problems, or whether problems identified are new. Information about past health history, social history, family history, psychosocial issues and spirituality must also be obtained.

Assessment is an ongoing process, and therefore all subsequent assessments will be used to establish trends, determine response to treatments and identify new problems that may arise. In general, the stability of the patient will determine the frequency of these ongoing assessments, which will range from every few minutes for the extremely unstable patient to every couple of hours for those patients who are stable and requiring less intensive care. It is important that the patient be reassessed whenever new nurses take over the patient’s care, at shift change for example; before and after new therapy or interventions; before and after any movements out of or within the unit; and whenever any deterioration in physical or mental status is observed. Chuley et al provide a useful template for ongoing assessment (see further reading).20

HEART RATE AND RHYTHM MONITORING Heart rate and rhythm are determined by a conduction system that is highly specialised. Stimulation of cardiac nerve fibres produces an action potential that is responsible for initiating depolarisation of cardiac muscle fibres, which have a resting membrane potential of -80 mV. Individual fibres are separated by membranes but depolarisation spreads rapidly because of the presence of gap junctions. There are five key phases to the cardiac action potential:21

0. depolarisation1. early rapid repolarisation2. plateau phase3. final rapid repolarisation4. resting membrane phase.

The contractile response begins just after the start of depolarisation and lasts about 1.5 times as long as the depolarisation and repolarisation (see Figure 7.5).

The action potential is created by ion exchange triggered by an intracellular and extracellular fluid transmembrane imbalance. There are three ions involved: sodium, potassium, and calcium. Normally, extracellular fluid contains approximately 140 mmol/L sodium and 4.0 mmol/L potassium. In intracellular fluid these concentrations are reversed. At rest, cell membranes are more permeable to potassium and consequently, potassium moves slowly and passively from intracellular to extracellular fluid. However, when the cell is excited, rapid ion movement caused by sodium flowing into the cell alters the charge from -90 mV to +30 mV. There follows a brief influx of calcium via the fast channel and then more via the slower channel to create a plateau, the time of which determines stroke volume due to its influence on the contractile strength of muscle fibres. The third phase occurs when the potassium channel opens, allowing potassium to leave the cell, to restore the negative

ACTIONPOTENTIAL

ECG

QRS

Phase 0

Mechanical

contraction

�20 mV

�90 mV

Phase 1

Phase 2

Phase 3

Phase 4

Depolarisation Repolarisation

T

�90 mV

FIGURE 7.5 Action potential29 (published with permission)


charge, causing rapid repolarisation. The final resting phase occurs when slow potassium leakage allows the cell to increase its negative charge to ensure that it is more negative than surrounding fluid, before the next depolarisation occurs and the cycle repeats.22

Cardiac muscle is generally slow to respond to stimuli and has relatively low ATPase activity. Its fibres are dependent on oxidative metabolism and require a continuous supply of oxygen. The length of fibres and the strength of contraction are determined by the degree of diastolic filling in the heart. The force of contraction is enhanced by catecholamines.23

The electrical activity of the heart can be detected on the body surface because body fluids are good conductors; the fluctuations in potential that represent the algebraic sum of the action potential of myocardial fibres can be recorded on an electrocardiogram. In the case of the critically ill patient, there are two main forms of cardiac monitoring, both of which are used to generate essential data: continuous cardiac monitoring, and the 12-lead ECG.

Continuous cardiac monitoringInternationally, a minimum standard for an ICU is availability of facilities for cardiovascular monitoring.24 Continuous cardiac monitoring allows for rapid assessment and constant evaluation with, when required, the instantaneous production of paper recordings for more detailed assessment or documentation into patient records. In addition, practice standards for electrocardiographic monitoring in hospital settings have been established.25

It is now common practice for five leads to be used for continuous cardiac monitoring,26 as this allows a choice of seven views. The five electrodes are placed as follows:27

• right and left arm electrodes—placed on each shoulder;

• right and left leg electrodes—placed on the hips or level with the lowest ribs on the chest;

• V-lead views can be monitored—for V1 place the electrode at the 4th intercostal space, right of the sternum; for V6 place the electrode at the 5th intercostal space, left midaxillary line.

The monitoring lead of choice is determined by the patient’s clinical situation.27 Generally, two views are better than one; therefore, one of the channels on the bedside monitor should display a V lead, preferably V1, and the other display leads II or III for optimal detection of dysrhythmias. When the primary purpose of monitoring is to detect ischaemic changes leads III and V3 usually present the optimal combination.25

The skin must be carefully prepared before electrodes are attached, as contact is required with the body surface and poor contact will lead to inaccurate or unreadable recordings, causing interference or noise. Patients who are

sweaty need particular attention, and it may be necessary to shave the areas where the electrodes are to be placed in very hairy people.

Heart rate can be obtained from other sources, such as a pulse oximeter or a defibrillator, which will also display rhythm.

12-Lead ECG The Dutch physiologist Einthoven was one of the first to represent heart electrical conduction as two charged electrodes, one positive and one negative.28 The body can be likened to a triangle, with the heart at its centre, and this has been called Einthoven’s triangle. Cardiac electrical activity can be captured by placing electrodes on both arms and on the left leg. When these electrodes are connected to a common terminal with an indifferent electrode that stays near zero, an electrical potential is obtained. Depolarisation moving towards an active electrode produces positive deflection.

The 12-lead ECG consists of six limb leads and six chest leads. The limb leads examine electrical activity along a vertical plane. The standard bipolar limb leads (I, II, III) record differences in potential between two limbs (see Figure 7.6):29

I = right arm–left arm (positive); II = right arm–left leg (positive);III = left arm–left leg (positive).

The three augmented unipolar limb leads (aVR, aVL, aVF) record activity between one limb and the other two limbs to increase the size of the potentials.

The six unipolar chest leads (praecordial leads) are designated V1–6 and examine electrical activity along a horizontal plane from the right ventricle, septum, left ventricle and the left atrium. They are positioned in the following way (see Figure 7.7):

Practice tip Monitors are not substitutes for the observation of patients, but they do provide information that should be evaluated in context with other data and the whole person.

FIGURE 7.6 Einthoven triangle formed by standard limb leads29 (published with permission)

RALA

LL

IIIII

I

aVF

aVR aV L

� �

�

�

�

��

�


V1 = 4th intercostal space, to the right of the patient’s sternum;

V2 = 4th intercostal space, to the left of the patient’s sternum;

V3 = equidistant between V2 and V4;V4 = 5th intercostal space on the midclavicular line;V5 = 5th intercostal space, anterior axillary line;V6 = 5th intercostal space on the midaxilla line.

Depolarisation is initiated in the sino-atrial (SA) node and spreads rapidly through the atria, then converges on the atrio-ventricular (AV) node; atrial depolarisation normally takes 0.1 second.

There is a short delay at the AV node (0.1 sec) before excitation spreads to the ventricles. This delay is shortened by sympathetic activity and lengthened by vagal stimulation. Ventricular depolarisation takes 0.08–0.1 sec, and the last parts of the heart to be depolarised are the posteriobasal portion of the left ventricle, the pulmonary conus and the upper septum.21

Amplitude (voltage) in the ECG is measured by a series of horizontal lines on the ECG (see Figure 7.8a). Each line is 1 mm apart and represents 0.1 mV. Amplitude reflects the wave’s electrical force and has no relation to the muscle strength of ventricular contraction.21

Duration of activity within the ECG is measured by a series of vertical lines also 1 mm apart (see Figure 7.8a). The time interval between each line is 0.04 sec. Every 5th line is printed in bold, producing large squares. Each represents 0.5 mV (vertically) and 0.2 sec (horizontally).

KEY COMPONENTS OF THE ECGKey components of the cardiac electrical activity are termed PQRST (see Figure 7.8b):• The P wave represents electrical activity caused by

spread of impulses from the SA node across the atria and appears upright in lead II. Inverted P waves indicate atrial depolarisation from a site other than the SA node. P wave = 0.08 sec.

• The P-R interval reflects the total time taken for the

Angle of Louis

Anteriorview

V2

V5V4V6

V3

V1

R L

FIGURE 7.7 Position of chest leads29 (published with permission)

10 mm

3 sec

0.04 sec

5 mm

1 mm

0.20 sec

0.20 sec

FIGURE 7.8a ECG graph paper29 (published with permission)


atrial impulse to travel through the atria and AV node. It is measured from the start of the P wave to the beginning of the QRS complex, but is lengthened by AV block or some drugs. P-R interval = 0.12–0.2 sec.

• The QRS complex is measured from the start of the Q wave to the end of the S wave and represents the time taken for ventricular depolarisation. Anything longer than 0.12 sec is abnormal and may indicate conduction disorders such as bundle branch block. The deflections seen in relation to this complex will vary in size, depending on the lead being viewed. However, small QRS complexes occur when the heart is insulated, as in the presence of a pericardial effusion. Conversely, an exaggerated QRS complex is suggestive of ventricular hypertrophy. A ‘pathological’ Q wave (>0.04 sec plus >25% of R wave height) indicates a previous myocardial infarction.

• The Q-T interval is the time taken from ventricular stimulation to recovery. It is measured from the beginning of the QRS to the end of the T wave. Normally, this ranges from 0.35 to 0.45 sec, but shortens as heart rate increases. It should be less than 50% of the preceding cycle length.

• The T wave reflects repolarisation of the ventricles. A peaked T wave indicates hyperkalaemia, myocardial infarction (MI) or ischaemia, while a flattened T wave usually indicates hypokalaemia. An inverted T wave occurs following an MI, or ventricular hypertrophy. T wave = 0.16 sec.

• The ST segment is measured from the J point (junction of the S wave and ST segment) to the start of the T wave. It is usually isoelectric in nature, and elevation or depression indicates some abnormality in the onset of recovery of the ventricular muscle, usually due to myocardial injury.

• The U wave is a small positive wave sometimes seen following the T wave. Its cause is still unknown but

it is exaggerated in hyperkalaemia. Inverted U waves may be seen and often associated with coronary heart disease (CHD), and these may appear transiently during exercise testing.30

ECG INTERPRETATIONInterpretation of a 12-lead ECG is an experiential skill, requiring consistent exposure and practice. Some steps to aid interpretation are noted below.• Heart rate:

— This can be calculated from the ECG. Count the R waves on a 6 sec strip and multiply by 10 to calculate the rate (the top of the ECG paper is usually marked at 3 sec intervals).

— Use an ECG ruler if one is available.• Rhythm (regularity):

— To assess regularity, mark the R waves on a plain piece of paper, and if you move the paper either way, the marks should not be interrupted.

— The R-R interval should not differ by more than 0.12 sec.

• Atrial activity: — Observe for the presence or absence of P waves. — Check regularity and shape. — Is the P wave positive? — Do P waves precede every QRS complex? — What is the duration of the P wave?

• AV node activity: — What is the duration of the P-R interval?

• Ventricular activity: — Measure the QRS interval.— Q wave (if present) = less than 0.04 sec.

• General notable aspects of ECG: — Observe whether the isoelectric line is present

between the S and T waves.— Examine the T wave to see whether it is positive,

and less than 0.16 sec.

PRinterval

Q S

QRS STsegment

QT interval

P

R

Atrialsystole

Ventricularsystole

Atrialdepolarisation

Ventriculardepolarisation

Ventriculardepolarisation

T

FIGURE 7.8b Normal ECG29 (published with permission)


— Examine the duration of the Q-T interval. — Observe for any extra complexes and note their

rate and shape, and whether they have the same or different morphology.

HAEMODYNAMIC MONITORINGHaemodynamic monitoring is performed to provide the clinician with a greater understanding of the pathophysiology of the problem being treated than would be possible with clinical assessment alone. Knowledge of the evidence that underpins the technology and the processes for interpretation is therefore essential to facilitate optimal usage and evidence-based decisions.31

This section explores the principles related to haemodynamic monitoring and the different types of monitoring available, and introduces the most recent and appropriate evidence related to haemodynamic monitoring. The reasons for haemodynamic monitoring are generally threefold: 1. to establish a precise health-related diagnosis;2. to determine appropriate therapy; and3. to monitor the response to that therapy. Haemodynamic monitoring can be non-invasive or invasive, and may be required on a continuous or intermittent basis depending on the needs of the patient.32 In both cases, signals are processed from a variety of physiological variables, and these are then clinically interpreted within the individual patient’s context.

Non-invasive monitoring does not require any device to be inserted into the body and therefore does not breach the skin. Directly measured non-invasive variables include body temperature, heart rate, blood pressure, respiratory rate and urine output, while other processed forms can be generated by the ECG, arterial and venous Dopplers, transcutaneous pulse oximetry (using an external probe on a digit such as the finger or on the ear), and expired carbon monoxide monitors.

Invasive monitoring requires the vascular system to be cannulated and pressure or flow within the circulation interpreted. Invasive haemodynamic monitoring technology includes: • systemic arterial pressure monitoring;• central venous pressure;• pulmonary artery pressure; and• cardiac output (thermodilution). Invasive monitoring has also facilitated greater use of blood component analyses, such as arterial and venous blood gases.

The invasive nature of this monitoring allows the transducing of pressures that are sensed at the distal ends of the catheters, and the continuous display and monitoring of the corresponding waveforms. The extent of monitoring should reflect how much information is required to optimise the patient’s condition, and how precisely the data are to be recorded. As Pinsky argues, a great deal of information is

generated by this form of monitoring, and yet little of this is actually used clinically.33 Consequently, monitors are not substitutes for careful examination and do not replace the clinician. The accuracy of the values obtained and a nurse’s ability to interpret the data and choose an appropriate intervention directly affect the patient’s condition and outcome.34

Principles of haemodynamic monitoringA number of key principles need to be understood in relation to invasive haemodynamic monitoring of critically ill patients. These include haemodynamic accuracy, the ability to trend data, and the maintenance of minimum standards. These are reviewed below.

HAEMODYNAMIC ACCURACYAccuracy of the value obtained from haemodynamic monitoring is essential, as it directly affects the patient’s condition.35,36 Electronic equipment for this purpose has four components (see Figure 7.9): 1. an invasive catheter attached to high-pressure tubing;2. a transducer to detect physiological activity;3. a flush system; and 4. a recording device, incorporating an amplifier to

increase the size of the signal, to display information. High-pressure (non-distensible) tubing reduces distortion of the signal produced between the intravascular device and the transducer; the pressure is then converted into electrical energy (a waveform). Fluid (0.9% sodium chloride) is routinely used to maintain line patency using a continuous pressure system; the pressure of the flush system fluid bag should be maintained at 300 mmHg, which delivers a continual flow of 3 mL/h.37

Accuracy is dependent on levelling the transducer to the appropriate level (and altering this level with changes in patient position as appropriate), then zeroing the transducer in the pressure monitoring system to atmospheric pressure as well as evaluating the response of the system by fast-flush wave testing. The transducer must be levelled to the reference point of the phlebostatic axis, at the intersection of the 4th intercostal space and the midthoracic anterior-posterior diameter (not the midaxillary line).36 Error in measurement can occur if the transducer is placed above or below the phlebostatic axis.35,36 Measurements taken when the patient is in the lateral position are not considered as accurate as those taken when the patient is lying supine or semirecumbent up to an angle of approximately 45°.38–40

Zeroing the transducing system to atmospheric pressure is achieved by turning the 3-way stopcock nearest to the transducer open to the air, and closing it to the patient and the flush system. The monitor should display zero (0

Practice tip The transducer must be relevelled when the patient’s position has been changed, and the height checked prior to data recording. Too high, and an erroneously low reading will be given; too low, and a falsely high reading will be produced.


mmHg), as this equates to current atmospheric pressure (760 mmHg at sea level). With the improved quality of transducers, repeated zeroing is not necessary, as once zeroed, the drift from the baseline is minimal.41 Some critical care units, however, continue to recalibrate transducer(s) at the beginning of each clinical shift.

Fast-flush square wave testing, or dynamic response measurement,41 is a way of checking the dynamic response of the monitor to signals from the blood vessel. It is also a check on the accuracy of the subsequent haemodynamic pressure values. The fast-flush device within the system,

when triggered and released, exposes the transducer to the amount of pressure in the flush solution bag (usually 300 mmHg). The pressure waveform on the monitor will show a rapid rise in pressure, which then squares off before the pressure drops back to the baseline (see Figure 7.10a).

Interpretation of the square wave testing is essential; the clinician must observe the speed with which the wave returns to the baseline as well as the pattern produced. One to three rapid oscillations should occur immediately after the square wave, before the monitored waveform resumes. The distance between these rapid oscillations should not exceed 1 mm or

Normal saline andpressure bag

Bedside monitor

Macrodripchamber

Fluid-filledtubingfor flush

Electricalcable

High-pressuretubing

Phlebostaticaxis

Electricalconnection

Manualflush

Disposabletransducer

3-waystopcock(air reference)

Patient with invasive catheter

Rollerclamp

45°

30°

0°

Invasivecatheter

FIGURE 7.9 Haemodynamic monitoring system29 (published with permission)


0.04 sec.41 Absence, or a reduction, of these rapid oscillations, or a ‘square wave’ with rounded corners, indicates that the pressure monitoring system is overdamped, in other words its responsiveness to monitored pressures and waveforms is reduced (see Figure 7.10b). An underdamped monitoring system will produce more rapid oscillations after the square wave than usual.

DATA TRENDS The ability to trend data via a monitor or a clinical information system (as discussed in Chapter 3) is essential for critical care practice. Current monitoring systems used in Australia and New Zealand can retain data for a period of time, produce trend graphs, and link to other devices to allow review of data from locations other than the immediate bedside.

HAEMODYNAMIC MONITORING STANDARDSThere are stated minimum standards for critical care units in Australia and New Zealand.24,42 The standards require that patient monitoring include circulation, respiration and oxygenation, with the following essential equipment available for every patient: an ECG that facilitates continual cardiac monitoring; a mechanical ventilator, pulse oxymeter; and other equipment available where necessary to measure intra-arterial and pulmonary pressures, cardiac output, inspiratory pressure and airway flow, intracranial pressures and expired carbon dioxide.24

Blood pressure monitoringIndirect and direct means of monitoring blood pressure are widely used in critical care units. These are outlined in more detail below.

NON-INVASIVE BLOOD PRESSURE MONITORING Non-invasive blood pressure (NIBP) monitoring requires the use of a manual or electronic sphygmomanometer. Oscillation in the pressure generated by alterations in arterial flow is captured either through auscultation or automatic sensing. On auscultation, a number of Korotkoff sounds can be heard as the cuff pressure is released:43

• a sharp thud that is heard when the patient’s systolic pressure is reached;

• a soft tapping, intermittent in nature;• a loud tapping, intermittent in nature;• a low, muffled noise that is continuous in nature and

is heard when the diastolic pressure is reached; as the cuff pressure diminishes further, the sound disappears.

For critically ill patients, this method of blood pressure monitoring has limitations but is better than nothing when invasive methods cannot be utilised.44 It is a less accurate alternative, as results vary with the size of cuff used, equipment malfunction, and incorrect placement of the sphygmomanometer (this must be placed at heart level). In addition, the pressures generated by the inflating cuff, particularly those generated by automatic machines, can be high and become uncomfortable. It is therefore important that skin integrity be checked regularly to prevent ischaemia and that the frequency of automated inflations be minimised.44

Invasive intra-arterial pressure monitoringArterial pressure recording is indicated when precise and continuous monitoring is required, such as in periods of instability of cardiac output and blood pressure.45 A cannula is commonally placed in the radial artery, although other sites can be accessed, including the brachial, femoral, dorsalis pedis and axillary arteries. Arterial cannulation is performed aseptically, and it is important that collateral circulation, patient comfort and risk of infection be assessed before cannulation is attempted. The radial artery is the most common site, as the ulnar artery provides additional supply to extremities if the radial artery becomes compromised.

Complications of arterial pressure monitoring include: • infection;• arterial thrombosis;• distal ischaemia;• air embolism;• accidental disconnection (the sites cannulated should

be visible); and• accidental drug administration through the cannula;

all arterial lines and connections should be clearly identified as such (e.g. marked with red stickers or have red bungs).

Pressure in blood vessels has three components: dynamic blood pressure, hydrostatic pressure, and static pressure. The blood pressure is the same at all sites along a vertical level

FIGURE 7.10a Normal dynamic response test

FIGURE 7.10b Over-damped dynamic response test


but when the vertical level is varied, pressure will change. Consequently, referencing is required to correct for changes in hydrostatic pressure in vessels above and below the heart; if not, the blood pressure will appear to rise when this is not really the case. It is important to zero the monitoring system at the left atrial level (phlebostatic axis, see above).36

Arterial waveform. A steep upstroke (corresponding to ventricular systole) is followed by brief, sustained pressure (anacrotic shoulder). At the end of systole, pressure falls in the aorta and left ventricle, causing a downward deflection (see Figure 7.11). The systolic pressure corresponds to the peak of the waveform. The arterial pressure waveform changes its contours when recorded at different sites, becoming more sharp in distal locations.

Disease has an effect on waveforms: for example, atherosclerosis causes an increase in systolic waveform, as well as a decrease in the size of the diastolic wave and dicrotic notch due to changes in elasticity. Cardiomyopathy causes reduced stroke volume and mean arterial pressure, and there is a late secondary systolic peak seen on the waveform.

Direct pressure versus cuff pressure. At times the accuracy of the direct arterial pressure reading may be checked by comparing the reading against that generated by a non-invasive device using an inflating cuff. However, there is no basis for comparing these values, because direct values are a measure of the actual pressure within the artery whereas those from the cuff depend on flow-induced oscillations in the arterial wall.46 Pressure does not equal flow, as resistance does not remain constant. In addition, radial arterial pressure is normally higher than that obtained by brachial non-invasive pressure monitoring because the smaller vessel size exerts greater resistance to flow, and therefore generates a high pressure reading.36,46

Invasive cardiovascular monitoringFor many critically ill patients, haemodynamic instability is a potentially life-threatening condition that necessitates urgent action. Accurate assessment of the patient’s intracardiac status is therefore essential. A number of values can be calculated, and Tables 7.1 and 7.2 list the measurements commonly made.

PRELOADAs noted earlier, preload is the filling pressure in the ventricles at the end of diastole. Preload in the right ventricle is generally measured as CVP, although this may be an unreliable predictor because CVP is affected by intrathoracic pressure, vascular tone and obstruction.47,48 Left ventricular preload can be measured as the pulmonary capillary wedge pressure (PCWP), but again, due to unreliability, this parameter provides an estimate rather than a true reflection of volume.48,49 In view of this, other modalities are now being explored, including right ventricular end-diastolic volume evaluation via fast-response pulmonary artery catheters, left ventricular end-diastolic area measured by echocardiography, and intrathoracic blood volume measured by transpulmonary thermodilution.50

Central venous pressure (CVP) monitoring. Central venous catheters are inserted to facilitate the monitoring of central venous pressure, as well as facilitating the administration of large amounts of IV fluid or blood; providing long-term access for fluids, drugs, specimen collection; and/or parenteral feeding. Monitoring CVP has been used for many years to evaluate circulating blood volume, albeit with little scientific support.51 However, it is a common monitoring practice and continues to be used; consequently, clinicians need to be aware of possible limitations to this form of measurement and interpret the data accordingly.33,47,52 CVP monitoring can produce erroneous results: a low CVP does not always mean low volume and it may reflect other pathology, including peripheral dilation due to sepsis. Hypovolaemic patients may have normal CVP due to sympathetic nervous system activity increasing vascular tone.

Systole

Diastole

Time

Dicrotic notch

120

110

100

90

80

Pre

ssu

re (

mm

Hg

)

FIGURE 7.11 Arterial pressure waveform184 (published with permission)

TABLE 7.1 Haemodynamic pressures

Parameter Resting values

Central venous pressure 0 to +8 mmHg (mean)

Right ventricular pressure +15 to +30 mmHg systolic0 to +8 mmHg diastolic

Pulmonary artery wedge pressure

+5 to +15 mmHg (mean)

Left atrial pressure +4 to +12 mmHg (mean)

Left ventricular pressure 90 to 140 mmHg systolic+4 to +12 mmHg diastolic

Aortic pressure 90 to 140 mmHg systolic60 to 90 mmHg diastolic 70 to 105 mmHg (mean)

Practice tip CVP measures should be taken at the end of the expiratory phase. Don't forget that this point on the waveform will differ according to the type of ventilation the patient is receiving. Failure to be consistent with this measurement may lead to significant fluid status errors. Always have the waveform on appropriate scales and freeze the waveform, using the cursor to identify and obtain the end-expiratory reading.


Central venous catheters used for haemodynamic monitoring are classed as short-term percutaneous (non-tunnelled) devices. Short-term percutaneous catheters are inserted through the skin, directly into a central vein, and usually remain in situ for only a few days or for a maximum of 2–3 weeks.47,52 They are easily removed and changed, and are manufactured as single- or multi-lumen types. However, they can be easily dislodged, are thrombogenic due to their material, and are associated with a high risk of infection.47,53

A number of locations can be used for central venous access; the two commonest sites in critically ill patients are the

subclavian and the internal jugular vein approaches. Other less common sites are the antecubital fossa (generally avoided but may be used when the patient cannot be positioned supine), the femoral vein (associated with high infection risk), and the external jugular vein (although the high incidence of anomalous anatomy and the severe angle with the subclavian vein make this an unpopular choice).53

Internal jugular cannulation has a high success rate for insertion; however, complications related to insertion via this route include carotid artery puncture and laceration of local neck structures arising from needle probing.53,54 There are a number of key structures adjacent to the vein, including the

TABLE 7.2 Normal haemodynamic values13,159

Parameter Description Normal values

Stroke volume (SV) Volume of blood ejected from left ventricle/beatSV = CO/HR

50–100 mL/beat

Stroke volume index (SVI) Volume of blood ejected/beat indexed to BSA 25–45 mL/beat

Cardiac output (CO) Volume of blood ejected from left ventricle/minCO = HR × SV

4–8 L/min

Cardiac index (CI) A derived value reflecting the volume of blood ejected from left ventricle/min indexed to BSA

CI = CO/BSA

2.5–4.2 L/min/m2 (normal assumes an average weight of 70 kg)

Flow time corrected (FTc) Systolic flow time corrected for heart rate 330–360 msec

Systemic vascular resistance (SVR)

Resistance left heart pumps againstSVR = [(MAP – RAP) × 79.9]/CO

900–1300 dynes/sec/cm-5

Systemic vascular resistance index (SVRI)

Resistance left heart pumps against indexed to body surface area

SVRI = [(MAP – RAP) × 79.9]/CI

1700–2400 dynes/sec/cm5/m2

Pulmonary vascular resistance (PVR)

Resistance right heart pumps againstPVR = [(mPAP – LVEDP) × 79.9]/CO

20–120 dynes/sec/cm-5

Pulmonary vascular resistance index (PVRI)

Resistance right heart pumps against indexed to body surface area

PVRI = [(mPAP – LVEDP) × 79.9]/CI

255–285 dynes/sec/cm5/m2

Mixed venous saturation (SvO2)

Shows the balance between arterial O2 supply and oxygen

demand at the tissue level 70%

Left ventricular stroke work index (LVSWI)

Amount of work performed by LV with each heartbeat(MAP – LVEDP) × SVI × 0.0136

50–62 g-m/m2

Right ventricular stroke work index (RVSWI)

Amount of work performed by RV with each heartbeat(mPAP – RAP) × SVI × 0.0136

7.9–9.7 g-m/m2

Right ventricular end-systolic volume (RVESV)

The volume of blood remaining in the ventricle at the end of the ejection phase of the heartbeat

50–100 mL/beat

Right ventricular end-systolic volume index (RVESVI)

30–60 mL/m2

Right ventricular end-diastolic volume (RVEDV)

The amount of blood in the ventricle immediately before a cardiac contraction begins

100–160 mL/beat

Right ventricular end-diastolic volume index (RVEDVI)

60–100 mL/m2

BSA = Body surface area


vagus nerve (located posteriorly to the internal jugular vein); the sympathetic trunk (located behind the vagus nerve); and the phrenic nerve (located laterally to the internal jugular).55 Damage can also occur to the sympathetic chain, which leads to Horner’s syndrome (constricted pupil, ptosis, and absence of sweat gland activity on that side of the face). Central venous catheters inserted in the internal jugular vein pose a number of nursing challenges, particularly in relation to beard growth; diaphoresis; and poor control of oral secretions, which can cause fixation problems and the need for repeated dressing changes.

The subclavian approach is used often, perhaps because of a reported lower risk of catheter-related bloodstream infection.55–57 Coagulopathy is a significant contraindication for this approach, as puncture of the subclavian artery is a

known complication. There is also a risk of pneumothorax, which rises if the patient is receiving intermittent positive pressure ventilation (IPPV).56 Complications of any central venous access catheters include air embolism, pneumothorax, hydrothorax and haemorrhage.53

Pulmonary artery pressure (PAP) monitoring. Pulmonary artery pressure monitoring began in the 1970s, led by Drs Swan, Ganz and colleagues,58 and was subsequently adopted in ICUs worldwide. Pulmonary artery catherisation facilitates assessment of filling pressure of the left ventricle through the pulmonary artery wedge (occlusion) pressure (see Figure 7.12).54,59 By using a thermodilution pulmonary artery catheter (PAC), cardiac output and other haemodynamic measurements can also be calculated. PAP monitoring is

A

B

C

FIGURE 7.12 Pulmonary artery catheter29 (published with permission)


a diagnostic tool that can assist in determination of the nature of a haemodynamic problem and improve diagnostic accuracy.

The beneficial claims of PAP monitoring have, however, been questioned, with some proposing a moratorium.60,61 In response, two consensus conferences were held in the USA to make recommendations for future practice. These concluded that there was no basis for a moratorium on the use of PACs; instead, education and knowledge about the use of this technology must be standardised and monitored. Further research was indicated, particularly focusing on the use of PACs and ARDS, and congestive cardiac failure.62,63 More recently, an observational cohort study of 7310 patients found that PAC use was not associated with an overall higher mortality, although the authors concluded that severity of illness should be examined when considering the use of this measurement tool.64 A systematic review is currently underway through the Cochrane Collaboration to synthesise the available evidence relating to the effects of PACs on mortality and cost-of-care in adult intensive care patients.65 In the meantime, proponents for continuing clinical use of the PAC argue that it provides a physiological rationale for diagnosis and assists in the titration of therapies such as inotropes, which would otherwise be potentially dangerous.41,59,62

PAP monitoring is indicated for adults in severe hypovolaemic or cardiogenic shock, where there may be diagnostic uncertainty, or where the patient is unresponsive to initial therapy. The PAP is used to guide administration of fluid, inotropes and vasopressors. PAP monitoring may also be utilised in other cases of haemodynamic instability when diagnosis is unclear. It may be helpful when clinicians want

to differentiate hypovolaemic from cardiogenic shock or, in cases of pulmonary oedema, to differentiate cardiogenic from non-cardiogenic origins.66 It has been used to guide haemodynamic support in a number of disease states such as shock, and to assist in assessing the effects of fluid management therapy. 45,59

Complications do arise from PACs, as these catheters share all the complications of central lines and are additionally associated with a higher incidence of dysrhythmia (particularly due to cold bolus injectate, which irritates myocardium), valve damage, pulmonary vascular occlusion, emboli/infarction (reported incidence of 0.1%–5.6%) and, very rarely, knotting of the catheter.53

A number of measurements can be taken via the PAC, either by direct measurement, for example using pulmonary capillary wedge pressure (PCWP), which is an estimate of left ventricular preload (LVEDV) or through calculation of derived parameters, such as cardiac output (CO) and cardiac index (CI)45(see Table 7.2 for descriptors and normal values).

Pulmonary capillary wedge pressure (PCWP) monitor-ing. Pulmonary capillary wedge pressure, or pulmonary artery occlusion pressure (PAOP), is measured when the pulmonary artery catheter balloon is inflated with no more than 1–1.5 mL air. The inflated balloon isolates the distal measuring lumen from the pulmonary arterial pressures, and measures pressures in the capillaries of the pulmonary venous system, and indirectly the left atrial pressure. The PAP waveform looks similar to that of the arterial waveform, with the tracing showing a systolic peak, dicrotic notch and a diastolic dip (see Figure 7.13). When the balloon is

FIGURE 7.13 Pulmonary artery pressure and wedge waveforms29 (published with permission)

Right atrium Right ventricle Pulmonary artery Pulmonary artery wedge (PAOP)Pressure

30mm Hg

20mm Hg

10mm Hg

0mm Hg

Flow-directedcatheter


inflated, the waveform changes shape and becomes much flatter in appearance, providing a similar waveform to the CVP. There are two positive waves on the tracing: the first reflects atrial contraction, and the second reflects pressure changes from blood flow when the mitral valve closes and the ventricles contract.67 The PCWP should be read once the ‘wedge’ trace stops falling at the end-expiratory phase of the respiratory cycle (see Figure 7.13).

If balloon occlusion occurs with <1 mL air, then the balloon is wedged in a small capillary and consequently will not accurately reflect LA pressure. Conversely, if 1.5 mL air does not cause occlusion, the balloon may have burst (which can result in an air embolus) or it may be floating in a larger vessel. If balloon rupture is suspected, no further attempts to inflate the balloon should be made, and interventions to minimise the risk of air embolism should be initiated; the patient should be positioned to the left lateral with head-down tilt.68 Note: it is essential that the balloon be deflated as soon as the wedge has been recorded, as continued occlusion will cause distal pulmonary vasculature ischaemia and infarction.69

Left atrial pressure (LAP) monitoring. Left atrial pressure monitoring directly estimates left heart preload, but requires an open thorax to enable direct cannulation of the atrium. It is used only in the postoperative cardiac surgical setting, although such use is infrequent since the widespread use of PAC. Complications, recorded in a large retrospective study, occurred in just 0.2% of patients,70 although other modes of monitoring can also be used to achieve comprehensive left atrial assessment, such as Doppler echocardiography.71

AFTERLOAD As previously noted, afterload is the pressure that the ventricle produces to overcome the resistance to ejection generated in the systematic or pulmonary circulation by the arteries and arterioles. It is calculated by cardiac output studies: left heart afterload is reflected as systemic vascular resistance (SVR), and right heart afterload is reflected as pulmonary vascular resistance (PVR) (Table 7.2).

Systemic and pulmonary vascular resistance. Systemic vascular resistance is a measure of resistance or impediment of the systemic vascular bed to blood flow. An elevated SVR can be caused by vasoconstrictors, hypovolaemia or late septic shock. A lowered SVR can be caused by early septic shock, vasodilators, morphine, nitrates or hypercarbia. Afterload is a major determinant of blood pressure, and gross vasodilation causes peripheral pooling and hypotension, reducing SVR. The precise estimation of SVR enables safer use of therapies such as vasodilators (e.g. sodium nitroprusside) and vasoconstrictors (e.g. noradrenaline).11

Pulmonary vascular resistance is a measure of resistance or the impediment of the pulmonary vascular bed to blood flow. An elevated PVR (‘pulmonary hypertension’) is caused by pulmonary vascular disease, pulmonary embolism, pulmonary vasculitis or hypoxia. A lowered PVR is caused by medications such as calcium channel blockers, aminophylline or isoproterenol, or by the delivery of O2.10,11

CONTRACTILITY Contractility reflects the force of myocardial contraction, and is related to the extent of myocardial fibre stretch (preload see above) and wall tension (afterload, see above). It is important because it influences myocardial oxygen consumption.

Contractility of the left side of the heart is measured by calculating the left ventricular stroke work index (LVSWI), although the clinical use of this value is not widespread. Right ventricular stroke work index (RVSWI) can be similarly calculated. Contractility can decrease as a result of excessive preload or afterload, drugs such as negative inotropes, myocardial damage such as that occurring after MI, and changes in the cellular environment arising from acidosis, hypoxia or electrolyte imbalances. Increases in contractility arise from drugs such as positive inotropes.72

CARDIAC OUTPUTThe variety of cardiac output measurement techniques has grown over the past decade73 since the development of thermodilution pulmonary artery catheters, pulse-induced contour devices, and less invasive techniques such as Doppler. As many critically ill patients require ventilatory support, the associated rises in intrathoracic pressure, as well as changing ventricular compliance, make accurate haemodynamic assessment difficult with the older technologies. Therefore, volumetric measurements of preload, such as right ventricular end-systolic volume (RVESV), right ventricular end-diastolic volume (RVEDV) and index (RVESVI/RVEDVI) as well as measurements of right ventricular ejection fraction (RVEF) are now being used to more accurately determine cardiac output. The parameters RVEF, CO and/or CI, and stroke volume (SV) are generated using thermodilution technology, and from these the parameters of RVEDV/RVEDVI and RVESV/RVESVI can be calculated (see Table 7.2 for normal values).13 The availability of continuous modes of assessment has further improved a clinician’s ability to effectively treat these patients.13

Thermodilution cardiac output. Cardiac output (CO) and associated pressures such as global end-diastolic volume50 can be calculated using a thermodilution PA catheter. Intermittent measurements obtained every few hours produce a snapshot of the cardiovascular state over that time. By injecting a bolus of 5–10ml of crystalloid solution, and measuring the resulting temperature changes, an estimation of stroke volume is calculated. Cold injectate (run through ice) was initially recommended, but studies now support the use of room temperature injectate, providing there is a difference of 12º Celsius between injectate and blood temperature.74 Three readings are taken at the same part of the respiratory cycle (normally end expiration), and any measurements that differ by more than 10% should be disregarded (see Table 7.2 for normal values). Since the 1990s, the value of having continuous measurement of cardiac output has been recog-nised 59and this has led to the development of devices which permit the transference of pulses of thermal energy to pulmonary artery blood; the pulse-induced contour method.71

Pulse-induced contour cardiac output. Pulse-induced contour cardiac output (PiCCO) provides continuous assessment of


CO, and requires a central venous line and an arterial line with a thermistor (not a PAC).75A known volume of thermal indicator (usually room temperature saline) is injected into the central vein. The injectate disperses both volumetrically and thermally within the cardiac and pulmonary blood. When the thermal signal is detected by the arterial thermistor, the temperature difference is calculated and a dissipation curve generated.76 From these data, the cardiac output can be calculated. These continuous cardiac output measurements have been well researched over the past 10 years and appear to be equal in accuracy to intermittent injections required for the earlier catheters.73,77,78 The parameters measured by PiCCO75 include:• Pulse-induced contour cardiac output—derived normal

value for cardiac index 2.5–4.2 L/min/m2.• Global end-diastolic volume (GEDV)—the volume of

blood contained in the four chambers of the heart; assists in the calculation of intrathoracic blood volume. Derived normal value for global end-diastolic blood volume index 680–800 mL/m2.

• Intrathoracic blood volume (ITBV)—the volume of the four chambers of the heart plus the blood volume in the pulmonary vessels; more accurately reflects circulating blood volumes, particularly when a patient is artificially ventilated. Derived normal value for intrathoracic blood volume index 850–1000 mL/m2.

• Extravascular lung water (EVLW)—the amount of water content in the lungs; allows quantification of the degree of pulmonary oedema (not evident with X-ray or blood gases). Derived normal value for extravascular lung water index 3.0–7.0 mL/kg.

EVLW has been shown to be useful as a guide for fluid management in critically ill patients.74 An elevated EVLW may be an effective indicator of severity of illness, particularly

after acute lung injury or in ARDS, when EVLW is elevated due to alterations in hydrostatic pressures.79 Other patients at risk of high ELWV are those with left heart failure, severe pneumonia, and burns. There may be an association between a high EVLW and increased mortality, the need for mechanical ventilation and a higher risk of nosocomial infection.79 A decision tree outlining processes of care guided by information provided by PiCCO is provided in Figure 7.14.

PiCCO removes the impact of factors that can cause variability in the standard approach of cardiac output measurement, such as injectate volume and temperature, and timing of the injection within the respiratory cycle.80 The additional fluid volume injected with the standard technique is significant in some patients; with the continuous technology this is eliminated. A further advantage is that virtually real-time responses to treatment can be obtained, removing the time delay that was a potential problem with standard thermodilution techniques.71

An arterial catheter is widely used in critical care to enable frequent blood sampling and blood pressure monitoring, and is used to measure beat-by-beat cardiac output, obtained from the shape of the arterial pressure wave. The area under the systolic portion of the arterial pulse wave from the end of diastole to the end of the ejection phase is measured and combined with an individual calibration factor. The algorithm is capable of computing each single stroke volume after being calibrated by an initial transpulmonary thermodilution.

PiCCO preload indicators of intrathoracic blood volume (ITBV) and global end-diastolic volume (GEDV) are more sensitive and specific to cardiac preload than the standard cardiac filling pressures of CVP and PCWP, as well as right ventricular end-diastolic volume.50 One advantage of ITBV and GEDV is that they are not affected by mechanical

V+ = volume loading (! = cautiously) V- = volume contraction Cat = catecholamine / cardiovascular agents

*SVV only applicable in ventilated patients without cardiac arrhythmia

Without guarantee

1.

2.

Results

Therapy

Target

CI (l/min/m2)

GEDI (ml/m2)or ITBI (ml/m2)

ELWI (ml/kg)

GEDI (ml/m2)or ITBI (ml/m2)

Optimise SVV (%)*

GEF (%)or CFI (1/min)

ELWI (ml/kg)(slowly responding)

<700<850

<3.0 >3.0

>700>850

>700>850

700–800850–1000

>700>850

700–800850–1000

>700>850

700–800850–1000

700–800850–1000

<700<850

>700>850

<10

V+ V+!Cat

V+ V–V+!Cat CatV–

>10

≤10 ≤10 ≤10 ≤10

<10 >10 <10 >10 <10 >10

<10

>25>4.5

>25>4.5

>30>5.5

>30>5.5

<10 <10 <10 <10 <10 <10 <10

OK!

FIGURE 7.14 PiCCO decision tree (published with permission, Pulsion Medical Systems)


ventilation and therefore give correct information on the preload status under almost any condition. Extravascular lung water correlates moderately well with severity of ARDS, length of ventilation days, ICU stay and mortality,81 and appears to be of greater accuracy than the traditional assessment of lung oedema by chest X-ray. Disadvantages of PiCCO include its potential unreliability when heart rate, blood pressure and total vascular resistance change substantially.13,75

Oesophageal Doppler monitoring. Oesophageal Doppler monitoring, often referred to as transoesophageal echocardiography (TOE), also enables calculation of cardiac output82 from assessment of stroke volume and heart rate, but uses a less invasive technique than those outlined previously. Stroke volume is assessed by measuring the flow velocity and the area through which the forward flow travels. Flow velocity is the distance one red blood cell travels forward in one cardiac cycle, and the measurement provides a time velocity interval (TVI). The area of flow is calculated by measuring the cross-sectional area of the blood vessel or heart chamber at the site of the flow velocity management.83 TOE can be performed at the level of the pulmonary artery, mitral valve or aortic valve.

Doppler principles are that the movement of blood produces a waveform that reflects blood flow velocity, in this case in the descending thoracic aorta, by capturing the change in frequency of an ultrasound beam as it reflects off a moving object (see figure 7.15).32 This measurement is combined with an estimate of the aorta’s cross-sectional area for the stroke volume, cardiac output and cardiac index to be calculated, using the patient’s age, height and weight.84

Oesophageal Doppler monitoring provides an alternative for patients who would not benefit from PAC insertion,84

and can be used to provide continuous measurements under certain conditions: the estimate of cross-sectional area must be accurate; the ultrasound beam must be directed parallel to the flow of blood; and there should be minimal variation in movement of the beam between measurements. There is some debate at present among clinicians about the accuracy of TOE when compared with thermodilution technique for calculating cardiac output.85–87 However, Australian research purports that this technology has become and will continue to be an invaluable tool in critical care.82 This form of monitoring can be used perioperatively and in the critical care unit, on a wide variety of patients. It should not, however, be used in patients with aortic coarctation or dissection, oesophageal malignancy or perforation, severe bleeding problems, or with patients on an intra-aortic balloon pump.84

The Doppler probe that sits in the oesophagus is approximately the size of a nasogastric tube, is semirigid and is inserted using a similar technique.84 The patient is usually sedated but it has been used in awake patients.88 In such cases, however, the limitation is that the probe is more likely to require more frequent repositioning.83

The waveform that is displayed on the monitor is triangular in shape (see Figure 7.15) and captures the systolic portion of the cardiac cycle—an upstroke at the beginning of systole, the peak reflecting maximum systole, and the downward

slope of the ending of systole. The waveform captures real-time changes in blood flow and can therefore be seen as an indirect reflection of left ventricular function.84 Changes to haemodynamic status will be reflected in alterations in the triangular shape (see Figure 7.15).

Transthoracic bioimpedance. Transthoracic bioimpedance (impedance cardiography) is another form of non-invasive monitoring used to estimate cardiac output, and was first introduced by Kubicek in 1966.89 It measures the amount of electrical resistance generated by the thorax to high-frequency, very-low-magnitude currents. This measure is inversely proportional to the content of fluid in the thorax: if the amount of thoracic fluid increases, then transthoracic bioimpedance falls.32 Changes in cardiac output can be reflected as a change in overall bioimpedance. The technique requires six electrodes to be positioned on the patient: two in the upper thorax/neck area, and four in the lower thorax. These electrodes also monitor electrical signals from the heart.

Overall, transthoracic bioimpedance is determined by: (a) changes in tissue fluid volume; (b) volumetric changes in pulmonary and venous blood caused by respiration; and (c) volumetric changes in aortic blood flow produced by

a) Decreased preload

Fluids

b) Poor contractility

Inotropes

c) High afterload (high SVR)

Vasodilators

a) Increased preload

b) Increased contractility

c) Decreased afterload

FIGURE 7.15 Oesophageal Doppler waveforms83 (published with permission)


myocardial contractility. Accurate measurements of changes in aortic blood flow are dependent on the ability to measure the third determinant, while filtering out any interference produced by the first two determinants. Any changes to position or to electrode contact will cause alterations to the measurements obtained, and recordings should therefore be undertaken with the electrodes positioned in the same location as previous readings. Caution is required for patients with high levels of perspiration (which reduces electrode contact), atrial fibrillation (irregular R-R intervals makes estimation of the ventricular ejection time difficult), or pulmonary oedema, pleural effusions or chest wall oedema (which alter bioimpedance readings irrespective of any changes in cardiac output). The use of transthoracic bioimpedance in critically ill patients is variable, due in part to limitations of its usefulness in patients who have pulmonary oedema.90–93

RESPIRATORY MONITORING Respiratory insufficiency is one of the main reasons for admission to a critical care unit, as either a potential or actual problem, so comprehensive respiratory monitoring is essential.18 Critical care nurses need to utilise evidence in their practice to expand their roles and act on findings arising from accurate and comprehensive assessment. Patients with respiratory problems have a wide range of symptoms, some of which are not directly associated with the respiratory system. (Further information relating to respiratory diseases and other conditions that cause respiratory symptoms is provided in Chapter 11.) A thorough assessment, followed by accurate ongoing monitoring, enables early detection of condition changes and assessment of the impact of treatment. This section focuses on the main aspects of respiratory monitoring and the tools used, including arterial blood gas (ABG) analysis, capnography and pulse oximetry to assess the efficiency of the patient’s gas transfer mechanisms.18

Pulse oximetry Pulse oximetry is a non-invasive device that measures peripheral (capillary) saturation of haemoglobin by oxygen. The technology is now generally regarded as standard for critical care units24 and is recognised as being one of the major advances in clinical monitoring.94,95 It works by using select wavelengths of light and, as arterioles empty during diastole, differentiation of infrared light absorption by blood is recorded using a pulse oximeter probe.96 The signal emitted is measured over five pulses, causing a slight delay when monitoring. Two wavelengths of light are emitted, red and infrared, from a diode (positioned on one side of the probe) to a photodetector (positioned on the opposite side). Well-oxygenated blood absorbs light differently from deoxygenated blood, with the oximeter determining the amount of light absorbed by the vascular bed and calculating the saturation of oxygen in those capillaries (SpO2). SpO2 and heart rate are continuously displayed on the monitor as digital readings. Normal SpO2 is greater than 97%. The probes used to emit the infrared light source can be sited

on a finger, toe or ear. The probes used in pulse oximetry generate heat which, in extreme cases, may cause burns, especially in patients with poorly perfused peripheries. A frequent change of probe positions is required.97,98 Perfusion of the site also needs to be assessed, along with other visual observations of the probe site.

Pulse oximetry alone, however, does not provide all the information needed on ventilation status and acid–base balance. Therefore, arterial blood gases are also needed periodically to assess other parameters. Other limitations arise with oximetry monitoring:• Peripheral vasoconstriction results in poor perfusion,

causing poor flow and less accurate signals.99

• Cardiac dysrhythmias can impair perfusion and flow.• Shivering and other movements may give poor or

inaccurate readings.95

• The presence of high levels of bilirubin, dark skin and nail varnish may cause underestimation of SpO2, as light is absorbed in these circumstances.98

• External light can overestimate SpO2, especially fluorescent light and heat lamps; ear probes in particular may detect overhead lighting.

• Dyshaemoglobins such as carboxyhaemoglobin levels above 3% cause overreading, making SpO2 monitoring unreliable.7,100

• When hypercapnia is present (e.g. in patients with COPD), SpO2 monitoring alone is unreliable.97

Pulse oximetry is subject to low-level accuracy, and when the SpO2 is below 80% its use is unproven.7 It is therefore important that when SpO2 appears to be abnormal, the arterial blood is sampled and gases are checked.

Ventilation monitoringMechanical ventilation is a common intervention used in ICUs for patients with respiratory failure or who require respiratory support (see Chapter 11). The recent major advances in ventilation technology challenge all critical care clinicians.101,102 Many mechanical ventilators now offer integrated graphic displays, usually as waveforms that plot one of three parameters against time:103–105

• airway pressure vs time;• inspiratory and expiratory flow vs time; or• inspiratory and expiratory tidal volume vs time.Also available are data describing:• pressure vs volume loops; and• flow vs volume loops.Respiratory waveforms are normally displayed on the ventilator screen, and most systems provide the flexibility to adjust the vertical and horizontal axis, allowing the user to examine more closely particular sections and to fine-tune the ventilator settings. This can help in assessing patient–ventilator synchrony, assist in the setting of appropriate inspiratory/expiratory times, and determine the extent of increased airway resistance. Circuit leaks can also be identified through these data and the waveforms can be used to explain the different ventilation modes, utilising graphic analysis. Pressure vs volume loops may also be used to ascertain lung compliance, with lower inflection points guiding positive end-expiratory pressure (PEEP) application


and with upper inflection point providing a guide to lung overdistension.7,106

PRESSURESUnderstanding the various pressure displays is an important aspect of ICU nursing practice.103 For instance, in volume-cycled ventilation, peak inspiratory pressure does not always represent peak alveolar pressure, especially when there is increased inspiratory airways resistance. In such cases, pause or plateau pressure is more reflective of the pressure in the alveoli; this is when there is no influence of inspiratory flow on the pressure readings. In pressure control mode,107,108 the alveolar pressure cannot be inferred until inspiratory flow has fallen to the zero baseline, just prior to exhalation. Significant differences between peak inspiratory and end-inspiratory pressures require examination of the expiratory flow waveform to investigate the reasons for any increase in inspiratory resistance. Many valuable lung mechanics properties can be derived from knowing these simple values. Knowing these different pressures displayed by the waveforms allows the ventilator’s lung mechanics software packages to calculate many useful parameters, such as static lung compliance, inspiratory and expiratory airways resistances. These derived parameters may further guide therapeutic interventions.

WAVEFORMSEach of the ventilation waveforms requires careful analysis.103

A clinician can examine the airway pressure and the flow screens to assess whether the patient is triggering a breath, the level of the baseline pressure, the modality of ventilation, extent of patient synchronisation with the ventilator breath, and evidence of gas trapping.103 These are described further below.

Airway pressure vs time. The morphology of this waveform depends on which ventilation strategy is chosen (volume or pressure), and whether the patient is generating spontaneous breaths.109 Pressure–time waveforms110 reflect inspiratory and expiratory phases and can be used to facilitate calculation of inspiratory time, breathing rate, peak airway pressure, alveolar pressure (with co-analysis of the flow waveform) and PEEP (see Figure 7.16). With pressure–time waveforms, the vertical axis represents pressure and the horizontal represents time.

The resting value in expiration represents the PEEP setting or the baseline pressure. The breath then moves into the inspiratory phase, which is triggered either by time (ventilator set rate) or by the patient’s inspiratory effort. Patient effort can be sensed either by a pressure drop relative to PEEP (pressure triggering) or by direct patient inspiratory flow (flow triggering). This effort should be minimal and not cause the PEEP to drop by more than 2–3 cmH2O at the start of inspiration.103 The ventilator should respond quickly to this effort with a rapid rise in airway pressure. A slow rise, possibly only at the end of inspiration, implies that the patient is wanting more inspiratory flow and volume than the ventilator can, or has been programmed to, deliver; this is more common in volume-targeted ventilation modes than in pressure-targeted modes.103,108 In pressure-targeted modes (pressure control, pressure support) inspiratory flow is not set; the patient is allowed to take flow from the ventilator’s demand system, commonly up to 200 L/min.110

The airway pressure graphic represents what is occurring on the ventilator side of the endotracheal tube. Alveolar pressure will lag in time from what is seen on the ventilator

Pausephase

Flow-phase

Inspiration time Expiration time

Resistance Pressure (R V)

C

D E

F

B

A

Pressure (mbar)

Peak pressure

Plateau pressure

‘Resistance pressure’ (R V)

‘Compliance pressure’ (VT/C)

‘PEEP’

Time (s)

(V insp = const.)

GradientV/C

..

.

. .

FIGURE 7.16 Airway pressure vs time (published with permission, Dräger Medical)

Practice tip Clinicians should familiarise themselves with their unit’s ventilator graphic package. These are generally intuitive, and the manipulation of the various screens has no impact on actual ventilator settings. Confidence builds with basic familiarisation. This process in itself may constitute a good topic for a clinical workshop conducted in your ICU.


screen and, depending on airway resistance, may bear no resemblance to the pressures being displayed.110 For example, the presence of auto-PEEP (pressure inside the alveolus not routinely seen on the ventilator expiratory pressure waveform) may cause the patient to make inspiratory efforts, which the ventilator fails to detect, resulting in no breath being delivered. This increases the work of the breathing, which for some patients (e.g. those with severe asthma) may increase morbidity and mortality.111,112 Significant levels of auto-PEEP may also cause a reduction in cardiac output, as this pressure in the chest is impeding venous return. When any form of artificial ventilation is applied, expiratory time must be long enough to ensure that all the gas delivered is exhaled before the next breath is delivered. If this is achieved, auto-PEEP will be minimised.

Flow vs time. With flow–time waveforms, flow is plotted on the vertical axis, while time is on the horizontal.103 This waveform assists with detecting levels of auto-PEEP as well as the patient’s reponse to medications such as bronchodilators.111 Two components are displayed, inspiratory and expiratory flows (see Figure 7.17). The inspiratory waveform is generated from the inspiratory flow transducer commonly located inside the ventilator just prior to the inspiratory outlet port. The inspiratory flow waveform’s shape and peak value depends on a number of factors:• the ventilatory strategy chosen (i.e. volume vs

pressure);• the programmed inspiratory time; • the selected inspiratory flow waveform; and • the presence of spontaneous breathing.The inspiratory waveform is unique to the type of breath and will therefore be different for pressure, volume or spontaneous breathing.103 In volume modes of ventilation, the flow pattern is generally stable throughout the breath, thus reflecting the constant speed of gas delivery. This generates a square low waveform. Flow should start from the zero baseline, reach its peak and then, at the point at which exhalation commences, the value is read by the exhalation flow transducer (commonly located in the distal section of the expiratory limb, after the exhalation valve). In pressure modes, the flow is higher at the beginning of the breath than at the end, generating a tapering flow waveform as the lungs fill.103 Spontaneous breath waveforms have a similar shape to those of pressure modes, but they are generally more rounded.103

In the normal expiratory flow waveform, a sharp peak expiratory flow value, depicted below the zero baseline, is

Pressure

Time

Inspiration Expiration

Volume Volume-oriented

Time

Flow

Time

Pressure

Time

Volume

Time

Flow

Time

Flowphase

Pausephase

Flowphase

Pausephase

Pressure-oriented

FIGURE 7.17 Pressure, flow and volume vs time (published with permission, Dräger Medical)

Practice tip If there appears to be inconsistent triggering of the ventilator by the patient despite the patient breathing regularly, check the expiratory flow waveform. If this has failed to return to the zero baseline there may be gas trapping. Ventilation should be adapted to ensure that the patient expires all inspired tidal volume, e.g. by increasing expiratory time. Gas trapping may result in patient fatigue or cardiac embarrassment.


recorded, followed by the flow returning promptly to zero, prior to the next inspiratory effort. If this waveform fails to return to the baseline before the next breath, this indicates that not all of the previous volume has been exhaled, which leads to ‘gas trapping’.112 This can result in significant levels of ‘inadvertent’ or ‘auto-PEEP’, which has the potential to adversely affect a patient’s haemodynamics and prevent the patient from synchronising breaths with the ventilator.112 In such circumstances, the patient has to overcome the set trigger sensitivity, as well as the auto-PEEP value, and this can be distressing for some patients.

For some forms of intervention, such as bronchodilator therapy, the expiratory flow waveform provides information on therapeutic effect.111,112 In other circumstances, such as when a patient is suffering from acute asthma, the flow waveform indicates gas trapping (see Figure 7.18).111,112

The flow waveform can also be helpful when investigating internal faults within the ventilator and its circuitry. Normally the exhaled tidal volume should equal the inspired tidal volume. If this is not the case, a reason should be found for the discrepancy. If there is a leak in the ventilator circuitry (including the ETT cuff), gas trapping may be occurring. If, after all investigations, no reason for the leak can be found, consider whether the flow transducer may be out of calibration or damaged. Exhalation flow transducers are commonly part of the ventilator circuit, and care needs to be taken with their sterilisation, as this can result in transducers being out of calibration. Some ventilator manufacturers avoid this by placing a hydrophobic viral/bacterial filter before the exhalation flow transducer, thus protecting it from damage. If a viral/bacterial filter is used in the expiratory limb of the ventilator, regular checking of its resistance should be performed so as to avoid patient-triggering problems. Many modern ventilators have their triggering site located in the expiratory limb of the ventilator, possibly on the other side of an expiratory viral/bacterial filter.

Tidal volume vs time. In this graphic, the inspiratory and expiratory flow waveforms are mathematically integrated, yielding inspiratory tidal and expiratory tidal volume waveforms. This waveform (see Figure 7.19) starts from a baseline of the functional residual capacity (FRC) of the lung, then rises as inspiratory flow is delivered, to reach the inspiratory tidal volume. Once the inspiratory time has elapsed, the waveform falls back towards baseline as

exhalation occurs. It is usually the expiratory tidal volume waveform that is displayed on the ventilator monitor; however, some ventilators offer both inspiratory and expiratory tidal volume displays. Having both these volumes displayed can be useful, especially when you are trying to minimise a leak through a bronchopleural fistula. It is then possible to quantify the leak and have this recorded and trended in the patient’s record.

The tidal volume waveform is also useful in troubleshooting circuit leaks (see Figure 7.19); if it fails to return to its baseline, the clinician should look for a leak in the circuit–patient interface. However, an elevated baseline can also be caused by an incorrectly calibrated or damaged expiratory flow transducer. The tidal volume graphic may also be useful in detecting the presence of pulmonary leaks via intercostal catheters.113,114

Pressure vs volume loop. This graphic represents the dynamic compliance between the lungs and the ventilator circuit. The two parameters, airway pressure and tidal volume, are plotted against each other; the ascending limb of the loop represents inspiration and the descending limb represents expiration (see Figure 7.20).

As inspiratory pressure rises, there is initially little change in delivered tidal volume. However, as inspiratory pressure continues to rise, tidal volume suddenly increases as alveoli are recruited, causing a change in the slope of this inspiratory limb. This represents lung expansion with tidal volume recruitment. As the lung reaches its capacity, there is a flattening at the top of this pressure–volume

Volume

Pressure

Expiration

Inspiration

A

B

FIGURE 7.20 Pressure vs volume loop (published with permission, Dräger Medical)

Tid

al v

olum

e m

/sec

Time(sec)

0

Insp

irato

ry

Expiratory

Tid

al v

olum

e m

/sec

Time(sec)

0

Leakvolume

FIGURE 7.19 Tidal volume vs time, with and without leak

Flow Flow

Time

FIGURE 7.18 Expiratory flow curve in the case of increased expiratory resistance (published with permission, Dräger Medical)


loop, representing wasted and possibly injurious pressures. Expiration commences, as reflected in the expiratory limb of this loop. If pressure is allowed to return to zero the lung units will collapse, requiring further inflation on the next breath. Current ventilation strategies favour preventing the end-expiratory volume from going too low and the inspiratory volume going too high, with optimal operation within this region.115–118 The sudden change in volume on the lower portion of the inspiratory loop, representing lung recruitment, may be used as a reference point at which to set a patient’s PEEP, or slightly above this value, to avoid repeated alveolar stretch and possible alveolar damage.106,117

The expiratory part of the loop has been the subject of recent research, which suggests that this limb of the pressure–volume loop may offer more important clinical information than the inspiratory limb.117,119–121 The expiratory loop represents lung de-recruitment; the point at which this occurs may be a more accurate PEEP reference point. However, more evidence is needed to support this, and for the time being clinicians will continue to examine the loops for the inflection point on the inspiratory limb to help set optimal PEEP.122–124

The area between the loops represents the resistance to inspiration and expiration, known as hysteresis. The slope of the line drawn between the ‘no flow’ points of the loops represents the compliance of the lung/thorax; the flatter the line, the lower the compliance.125

END-TIDAL CARBON DIOXIDE MONITORINGEnd-tidal carbon dioxide levels can be monitored using capnography, which is defined as ‘the graphical and numerical representation of carbon dioxide concentration during the respiratory cycle’,126 and capnometry (the digital display of carbon dioxide measurement). Such technology is now widely available in the critical care environment.127 The first device was used in 1943 by Luft,123 and over the ensuing years this technology has become smaller, more accurate and affordable. With the reliability of capnometry to differentiate between endotracheal and oesophageal intubation, it has been proposed as standard practice for the confirmation of endotracheal tube placement in ICU.128,129

There are a number of methods to determine end-tidal CO2 tension (PETCO2),130,131 but the infrared determination appears most popular among monitoring manufacturers. Infrared rays have a wavelength >1.0 µm, and carbon dioxide is able to selectively absorb wavelengths of 4.3 µm. The end-tidal CO2 monitor compares the absorbed value to a known standard and the result is displayed in digital form (capnometry), or more commonly in graphic form.

There are two common methods of determining PETCO2 using infrared technology:132

1. Mainstream sampling. The PETCO2 housing and sensor head are in direct contact with the patient’s exhaled

gases (see Figure 7.21) and, as these are located in the airway, they respond quickly to changes in PETCO2. To prevent moisture from affecting the measurement,

Cuvette

Patient

CO2-sensor

FIGURE 7.21 Mainstream PETCO2 Ventilator setup (published with permission, Dräger Medical)


the sensor is usually heated; however, sputum may migrate over the sampling windows and interrupt measurement. These sensors/housings have over time become less bulky, reducing traction on the airway.

2. Sidestream sampling. The PETCO2 sensor is located in the main unit itself and a small pump, with a sampling tube attached to a T piece located in the breathing circuit, diverts sampled exhaled gases to the sensor. Special tubing that allows moisture to escape prior to the sensor should be used when using a sidestream system, as this ensures more consistent results. For accuracy, ideal sampling rates should be 50–200 mL/min.132,133

As with all monitoring modalities, a thorough understanding of this technique and its limitations is necessary.133 It is also essential that the system be calibrated appropriately before use. Potential sources of inaccuracy when using PETCO2 monitoring include:• Humidity. The presence of water in either system may

falsely elevate the reading, but using semipermeable tubing should minimise this. If the ventilator circuit produces a lot of water, attention should be directed to improving the efficiency of the humidifier–heater wire interface. It is preferable to run inspiratory and expiratory heater wires with full saturation of gases.

• Atmospheric pressure. Partial pressure does have an effect on the displayed value of CO2; many monitoring systems have a direct measurement of the presiding barometric pressure and include this value in the calculation of the displayed value of CO2. Periodic checks should be undertaken to determine that the machine-calculated value agrees with a known accurate independent monitor; a good source of these values is the local weather bureau/authority, and the hospital laboratories are another good source of barometric pressure readings. If a system requires a value to be input for barometric pressure, this will need checking on a regular basis. Reduced atmospheric pressure also adversely affects the pumping of gas through the sampling chamber, as well as appearing to trigger an ‘air-leak’ error in some machines.134 It appears that altitude levels above 3600 metres cause malfunctions to occur.134

• Nitrous oxide. The presence of this gas in the patient circuit can falsely elevate the PETCO2 reading, as the wavelength of N2O is close to that of CO2. Most current monitors allow compensation for the presence of this gas in the breathing circuit.

• Oxygen. At levels above 60% there is some collision with CO2, causing a falsely low PETCO2 reading.

Many monitors minimise this effect by adjusting for the presence of high oxygen levels above a certain percentage; however, the clinician may have to turn on this feature.

Relationship of PaCO2 to PETCO2. In normal human physiology the PaCO2 is 2–5 mmHg higher than PETCO2. A difference that exceeds this range indicates increases in alveolar dead space and subsequent ventilation (V) to perfusion (Q) mismatch. Research suggests that clinicians should not rely solely on PETCO2 for monitoring of carbon dioxide tension, due to the unreliability of current technology.126 Changes noted in PETCO2 should prompt ABG analysis, because the arterial/end-tidal carbon dioxide gradient is not constant.126

Capnogram interpretation. The capnogram represents the dynamic readings presented to the sensor in a graphic form, commonly PETCO2 versus time (see Figure 7.22). However, greater information about dead space (both anatomical and physiological) can be interpreted if PETCO2 is plotted against exhaled volume, using a flow sensor mounted between the endotracheal tube and the ventilator Y piece.

There are five phases (0–IV) possible on the capnogram:• 0—represents the inspiratory phase where fresh gas

enters the airway and lungs; this produces a rapid downstroke to a zero baseline from phase III (or IV if present).

• I—represents the start of expiration of CO2 free gas (dead space).

• II —normally has a steep rise, where there is a mixing of dead space gas (CO2 poor) and alveolar (CO2 rich) gas.

• III—a plateau pressure with a positive slope is reached as alveoli continue to expel CO2.

• IV—the closing volume at deep expiration results in a further rise in CO2. This phase is rarely seen except in patients who are pregnant or obese.130,131

Common abnormalities in PETCO2 waveforms. In normal subjects there is a balance between ventilation (excretion of CO2 from alveolus) and perfusion (delivery of CO2 to alveolus). This produces the normal gap seen between PaCO2 and PETCO2 of 2–5 mmHg. Where there is disturbance of

Practice tip During calibration of PETCO2 monitoring it is important to allow the system to warm up, to zero and reference the sensor head, as well as to calibrate the sensor housing outside the patient circuit away from any exhaled carbon dioxide. Failure to perform these calibrations appropriately will result in erroneous values and may influence clinical management.

PCO2

Time

0IVIIIIII

FIGURE 7.22 Typical capnograph waveform


the balance this normal relationship does not hold true (see Figure 7.23). There may be an increase of physiological dead space, for example with pulmonary embolism, PEEP or a fall in cardiac output. When this occurs the difference between PaCO2 and PETCO2 increases. This difference can be quantified by drawing an arterial blood gas and noting the PETCO2 value displayed on the bedside monitor at the same time; if the respiratory disease remains stable, this gap appears to remain constant.130,135

NEUROLOGICAL MONITORING The management of patients with head injuries and other cerebral disorders complicated by raised intracranial pressure has advanced significantly in recent years.17 Although primary damage to the brain tissue is usually irreversible, secondary damage arising from ischaemia and hypoxia can be treated. Assessment and ongoing monitoring of the neurological system, to ensure that complications are identified and treated early, remains key to the care of these patients, as it is important to minimise sustained damage to cerebral tissue. The importance of maintaining optimal cerebral perfusion pressure in patients with severe head injuries is now widely acknowledged, and intracranial pressure (ICP) assessment is a vitally important component of care.136 Raised ICP leads to a progressive fall in cerebral perfusion pressure and is the dominating cause of death in such patients. However, monitoring cerebral perfusion pressure and subsequent oxygenation at the bedside is challenging, and it is still unclear which method produces the most valid estimate of the balance between cerebral oxygen delivery and demand.137,138

A number of forms of monitoring are used in Australasian critical care units, including cerebral function monitoring, jugular venous bulb oximetry, near-infrared spectroscopy (NIRS), and intracranial pressure monitoring. However, all patients in whom a neurological problem is suspected will undergo initial assessment of level of consciousness, often using the Glasgow Coma Scale.

Glasgow Coma ScaleThe Glasgow Coma Scale (GCS) was originally devised in 1974 by Teasdale and Jennett139 to establish an objective, quantifiable measure to describe the prognosis of a patient with a brain injury. The GCS (see Table 7.3) requires a series of observations to be recorded that assess consciousness by measuring arousal, which depends on brainstem function; and cognition, or awareness, which depends on cerebral hemisphere function. In 2003, the UK National Institute for Clinical Excellence stipulated the use of the GCS for assessment and classification of all head-injured patients140,141 Head injuries can be classified into three categories according to GCS scores: minor, moderate, and severe (see Table 7.4).

The GCS includes scoring of separate subscales related to eye opening, verbal response and motor response. In

CO2 curve shapes

ETCO2

P

80

60

40

20

(mmHg)

10.08.06.04.02.0

(kPa)

4 8 12 s

CO2 curve shapes

ETCO2

80

60

40

20

(mmHg)

10.08.06.04.02.0

(kPa)

4 8 12 s

CO2 curve shapes

ETCO2

80

60

40

20

(mmHg)

10.08.06.04.02.0

(kPa)

4 8 12 s

t

Possible causesAccidental extubationComplete obstruction of the airwaysDisconnectionOesophageal intubation (drop after 1–2 tidal volumes)

Possible causesRespiratory depression caused by drugsMetabolic alkalosis (respiratory compensation)Insufficient minute ventilation

Possible causesAsthmaVentilatory maldistribution (asynchronous emptying)Asthmatic bronchitis

Possible causesCO2 rebreathing

Waveform

Waveform

Waveform

Waveform

FIGURE 7.23 PETCO2 waveforms (published with permission, Dräger Medical)


applying the GCS it is important to note that accuracy will be affected if the patient is receiving anaesthetic agents or sedation.

Monitoring consciousness is simple and non-invasive using this tool, which aids in the detection of those patients most at risk of developing raised intracranial pressure (see Chapter 12).

PUPILLARY ASSESSMENTPupillary responses, including pupil size and reaction to light, are important neurological observations. Normal pupils are round and equal in size, with an average size of 2–5 mm in diameter. The millimetre scale to estimate the size of each pupil should be indicated on the neurological observation chart. The shape of each pupil should also be noted.140,142

The immediate constriction of the pupil when light is shone into the eye is referred to as the direct light reflex. Withdrawal of the light should produce an immediate and brisk dilation of the pupil. Introduction of the light into one eye should cause a similar constriction to occur in the other pupil (consensual light reaction).140

Other points to consider when conducting pupillary observations include the following:140

• Pinpoint non-reactive pupils are associated with opiate overdose.

• Non-reactive pupils may also be caused by local damage.

• Atropine will cause dilated pupils.• One dilated or fixed pupil may be indicative of

an expanding or developing intracranial lesion, compressing the oculomotor nerve on the same side of the brain as the affected pupil.

• A sluggish pupil may be difficult to distinguish from a fixed pupil and may be an early focal sign of an expanding intracranial lesion and raised intracranial pressure. A sluggish response to light in a previously reacting pupil must be reported immediately.

LIMB MOVEMENTLocalised cerebral injury or damage may impair the movement of an individual limb or limbs. Increasing damage may be reflected in a deteriorating pattern of movement. Instructing the patient to move the limb laterally on the bed, lifting against gravity, or against your resistance, are techniques used to assess limb movement. The left and right side should be assessed separately and if the patient is unable to follow instructions, movement can be assessed in response to pain. The type of movement observed can be classified as:• normal power—movements are appropriate to the

normal muscle strength for that patient;• mild weakness—moves with difficulty against resistance and has difficulty fully lifting against gravity;• severe weakness—moves a limb laterally but has great

weakness against gravity and is unable to move against resistance.

Abnormal responses to stimulation may be noted that are indicative of tissue damage: • spastic flexion—the arm slowly bends at the elbow

and is very stiff;• extension—the limb straightens at the elbow or knee

joint.

The frequency of neurological observations is dependent on the patient’s condition and clinical judgment.

Although used worldwide, the value of the GCS has been challenged.143,144 Discrimination is poor when monitoring changes in levels of consciousness, and it may be unreliable in the middle-range scores. Individual ability to undertake the required components of the assessment can cause variations to occur: motor weakness is a subjective assessment, as is pupil size, as comprehensive guides are not available. The assessment of responses to painful stimuli has resulted in reports of unnecessary pressure being used, while for some patients who are deeply unconscious, insufficient pressure may be used to elicit a response. Additionally, the stimuli used may conflict with other requirements or interventions, such as the need for rest to minimise raised ICP.142

Cerebral function monitoringThe electroencephalogram has been used for many years to assess neurological function by recording electrical signals emitted from the brain, particularly those impulses from

TABLE 7.4 Head injury classification180,181

Severe head injury GCS score of 8 or less

Moderate head injury GCS score of 9–12

Minor head injury GCS score of 13–15

TABLE 7.3 Glasgow Coma Scale139,141

Response Score

Best eye response No eye opening 1

Open to pain 2

Open to verbal command

3

Open spontaneously 4

Best verbal response No verbal response 1

Incomprehensible sounds 2

Inappropriate words 3

Confused 4

Oriented 5

Best motor response No motor response 1

Extension to pain 2

Flexion to pain 3

Withdrawal from pain 4

Localising pain 5

Obeys commands 6


the surface of the brain that reflect the current awareness state (e.g. awake, asleep or sedated). Waves produced by the electrical impulses are displayed on a monitor and can then be interpreted by examining the frequency and morphology of each wave or series of waves. Some cerebral function monitors are used to assist in determining sedation levels or for analysing pattern changes in sedation, especially if different drugs have been used to induce sedation.145 Use of the EEG in critical care units has been variable, but the introduction of continuous EEG monitoring to assess and monitor a patient with brain injury or acute ischaemia enables prevention of further complications.146 In the USA and some other countries, EEG is considered useful for confirming suspected brain death and other brainstem injuries.147 (Brain death is discussed in more detail in Chapter 21.)

Intracranial pressure monitoring Invasive measures for monitoring intracranial pressure (ICP) are commonly used in patients with a severe head injury or after neurological surgery. The head injury management guidelines published by the Brain Trauma Foundation in 2000148,149 recommend intraventricular ICP measurement as the first-line approach to monitoring ICP. However, a Cochrane Systematic Review150 did not find sufficient data to reach a conclusion about the value of routine ICP monitoring in patients with acute coma, due to the small size of existing trials.

There are a few absolute contraindications to ICP monitoring—severe coagulopathy and other conditions that are associated with a high risk of intracranial haemorrhage that can occur when the monitoring catheter is inserted.151 Other conditions to be carefully considered before ICP monitoring devices are used include severe infection, severe haemodynamic instability, open scalp or skull wounds around the proposed insertion site, immunosuppression, and small ventricles (seen on CT or MRI).152

ICP measurements are used to estimate cerebral perfusion pressure (CPP). Mean CPP is calculated by subtracting the mean ICP from the mean arterial blood pressure153 and represents the blood pressure gradient across the brain. CPP is usually maintained between approximately 70 and 85 mmHg, although target levels for each patient will be individualised based on usual blood pressure levels and cerebral pathophysiology (see further reading, Vespa 2003). Reduced cerebral perfusion pressure (i.e. below 50 and 60 mmHg) results in inadequate cerebral blood flow and the potential for ischaemic changes. ICP monitoring devices can be inserted in epidural, subdural, subarachnoid, parenchymal or ventricular locations.154 Intraventricular monitoring is still considered to be the gold standard, although parenchymal catheterisation is now more common as it is generally faster and technically easier.154 Intraventricular catheters are usually inserted into the foramen of Munro (the duct joining the lateral and third ventricle that is in alignment with the middle of the ear).

This monitoring requires the use of a pressure transducer, three types of which are in use: external strain gauge, catheter-tip strain gauge, and catheter-tip fibreoptic technology.

External strain-gauge transducers connect to the intracranial space via fluid-filled lines, whereas catheter-tip transducers are inserted into the brain. External strain-gauge transducers are considered accurate and can be recalibrated, but they are susceptible to blockages, which increases inaccuracy. Catheter-tip transducers, of either strain-gauge or fibreoptic technology, have to be calibrated prior to insertion and cannot be recalibrated. However, these are generally easier to use because they do not require the patient’s head elevation to be static.152

The choice of catheter depends on unit policy and available equipment, the level of accuracy needed, anticipated duration of monitoring, and the infection risk to the patient. Intraventricular catheters with a burr hole have been the gold standard for several years now and are associated with low infection risks if the duration of placement is less than 72 hours. The infection risk is highest with fluid-filled monitoring devices, and so the preferred systems use closed circuits. Bolts measure subdural pressure, and, as they do not penetrate the ventricle, are associated with a lower risk of infection; however, the traces produced tend to be less reliable and clear.153

Fibreoptic catheters produce a pulse and trend waveform, and are considered more reliable than bolts in the short term. They have a catheter-tip transducer that must be calibrated by zeroing relative to atmospheric pressure. In general this is performed prior to insertion, as some catheter types do not allow in-vivo zeroing. A slight drift of ±2 mmHg is to be expected for the first day after insertion and then ±1 mmHg thereafter, although in reality the drift may be greater than this.155 The fibreoptic catheters usually have a drainage channel, which can be used to remove fluid and ease intracranial pressure. Once they are positioned, the catheter needs to be marked so that any migration can be readily observed.137

Equipment can be tested by applying jugular venous pressure momentarily, which will cause the ICP to rise quickly. For monitoring purposes systolic and diastolic pressures can be obtained, but normally mean values are recorded. Normal ICP ranges from 5 to 20 mmHg, although as stated earlier transient elevations of up to 40 mmHg can occur from everyday activities such as sneezing. Pressures that remain above 20–25 mmHg should be actively treated. These probes can also record tissue oxygen tension, the normal values of which range from 25 to 45 mmHg. Reductions in tissue oxygen tension have been reported to be associated with adverse events and poor outcome, but there is lack of agreement on the value of this measurement138 (see Chapter 12 for further discussion of clinical states and management).

PULSE WAVEFORMSInterpretation of waveforms that are generated by the cerebral monitoring devices is important in the clinical assessment of intracranial adaptive capacity (the ability of the brain to compensate for rises in intracranial volume without raising the ICP).156 Cardiac pulse waves are detected and transmitted as continuous waveforms on a cerebral monitoring system (see Figure 7.24). The cardiac waves reach the cranial circulation via the choroid plexus and resemble


the waveforms transmitted by arterial catheters, although the amplitude is lower.

There are three distinct peaks seen in the ICP waveform:154 • P1—the percussion wave, which is sharp and reflects

the cardiac pulse as the pressure is transmitted from the choroid plexus to the ventricle;

• P2—the tidal wave, which is more variable in nature and reflects cerebral compliance and increases in amplitude as compliance decreases; and

• P3—which is due to the closure of the aortic valve and is known as the dicrotic notch.

It is important that the waveform be continuously observed, as changes in mean pressure or in waveform shape usually require immediate attention. In acute states such as head injury and subarachnoid haemorrhage, the value of ICP depends greatly on the link between monitoring and therapy, so close inspection of the trend of the ICP and the details derived from the waveform is extremely important.153 Simple ongoing visual assessment of the ICP waveform for increased amplitude, elevated P2 and rounding of the waveform provides non-specific information suggestive of decreased intracranial adaptive capacity and altered intracranial dynamics.146,149

Inaccuracies in ICP readings can occur, and may be due to CSF leaks around the insertion site, obstruction of the intraventricular catheter or bolt, the difference in height between the bolt and the transducer (occurs in external strain-gauge transducers) and kinks in the tubing. In the strain-gauge transducer that connects to fluid-coupled systems, bubbles or air in the tubing will result in dampening of the waveform. Also interventions and environmental stimuli can cause an increase in the ICP, and thus particular events that do trigger a rise in ICP need to be minimised or prevented.157

Jugular bulb oximetry Jugular venous catheterisation is used in neurological units for the routine monitoring of a head-injured patient.157 It facilitates the assessment of jugular venous oxygenation (SjvO2), cerebral oxygen extraction (CEO2), and arteriovenous difference in oxygen (AVDO2). All of these variables indicate changes in cerebral metabolism and blood flow, and therefore the catheter generates continuous data that reflect the balance between supply and demand of cerebral oxygen.158 As this form of monitoring increases in popularity in ICUs, it is important that nurses and doctors understand the rationale for using such technology, the data generated and the care required.159

The catheter is inserted using the same sterile technique used for central venous catheters but in a retrograde (supine) direction in the jugular vein.160 Usually the right jugular vein is chosen, as it is slightly larger than the left and provides readings that are more representative of overall brain function.161 The catheter tip is advanced so that the tip sits in the bulb of the internal jugular vein. Correct positioning is confirmed by X-ray; the tip of the catheter should be located at the border of the first and second cervical spine and medial to the mastoid process.161,162

The normal requirement for cerebral oxygen delivery is consumption at 35%–40% of available oxygen, giving a normal SjvO2 of 60%–65%. Changes in SjvO2 reflect changes in cerebral metabolic rate and cerebral blood flow; however, as it is a global measure it does not detect regional ischaemia. A high SjvO2 is indicative of increased cerebral blood flow, reduced oxygen consumption, and hyperventilation. Low SjvO2 levels suggest that cerebral perfusion is reduced, with levels below 40% indicative of global cerebral ischaemia. However, caution must be used when interpreting values generated using this method, as high values might also imply an increase in arteriovenous shunting secondary to vasoconstriction or maldistribution of blood flow.138

As noted above, the major limitation of SjvO2 monitoring is that it is a global measure of cerebral oxygenation.163 As a result, smaller areas of ischaemia are not detected unless these are of sufficient magnitude to affect global brain saturation. It is possible therefore that regional ischaemia may be missed.158 This form of monitoring requires frequent recalibration to ensure accurate measurements. Catheter migration interferes with signal quality, and medical intervention is required to reposition the catheter. The position of the patient also affects signal quality, and ideally the patient should be nursed supine with a head elevation of 10°–15° and at least a neutral head alignment. It is important that measurement errors be excluded when abnormal readings are noted; algorithms have been developed to assist nurses when caring for patients with jugular bulb oximetry.159,161

NEAR-INFRARED SPECTROSCOPY Near-infrared spectroscopy (NIRS) is a non-invasive method of monitoring continuous trends of cerebral oxygenated and deoxygenated haemoglobin by utilising an infrared light beam transmitted through the skull. Normal saturations would be 70%. The clinical use of NIRS is constrained by potential sources of error, which include contamination of the

Percussion(arterial)

Tidal(rebound)

Dicrotic(venous)

P1

P1

P2

P3

P2

P3

FIGURE 7.24 Intracranial pressure monitoring: above, low-pressure wave, compliant cranium; below, high-pressure wave, non-compliant cranium184 (published with permission)


signal by the extracerebral circulation (such as in the scalp), extraneous light, and the presence of extravascular blood arising from subarachnoid or subdural haemorrhage.164

BEDSIDE/LABORATORY INVESTIGATIONSIn recent years, advances in technology have enabled more point-of-care testing to occur. However, there are still times when laboratory investigations are required. This section focuses on the key bedside and laboratory investigations required to manage critically ill patients.

Arterial blood gasesArterial blood gases (ABGs) are one of the most commonly performed laboratory tests in ICUs and other critical care areas, and ABG analysis is an important clinical skill. ABG measurements are essential for assessing oxygenation/gas exchange and ventilation and, accordingly, all ICUs are recommended to have a blood gas analyser as a minimum standard to facilitate assessment and monitoring of respiratory function.24 Despite this familiarity, interpretation of the blood gases can be difficult, and it is important that this is done with accuracy and speed. (Further details of the application or utilisation of this form of monitoring are provided in Chapter 11.)

ABGs are measured to determine the status of the acid–base balance and oxygenation, and include measurement of the PaO2, PaCO2, acidity (pH) and bicarbonate (HCO3

-). Blood for ABG analysis is sampled by arterial puncture or, more commonly in critically ill patients, from an arterial catheter in the radial or femoral artery. Both techniques are invasive and allow only intermittent analysis. Continuous blood gas monitoring is possible if a fibreoptic sensor or an oxygen electrode is inserted into the arterial catheter system. The advantage of the arterial catheter is that it facilitates ABG sampling without repeated arterial punctures. Normal values for ABGs are given in Table 7.5.

When assessing ABGs, a number of questions should be asked:165

• Does the PaO2 level show hypoxaemia?• Does the pH level fall on the acid or alkaline side of

7.4 (i.e. 6.9 ↔ acid ↔ 7.4 ↔ alkaline ↔ 7.9)?• Does the PaCO2 level show respiratory acidosis or

alkalosis?• Does the HCO3

- show metabolic acidosis or alkalosis?• Re-examine the pH: is it compensated or

uncompensated?— pH is abnormal, along with the abnormal PaCO2

and the HCO3– = uncompensated condition;

— pH is normal but the PaCO2 and the HCO3– are

abnormal = compensated condition (the body has had time to restore pH levels to normal).

The following points of interpretation should be noted. (More detailed information related to the pathophysiology can be found in Chapter 11.)

TABLE 7.5 Arterial blood gas normal values166

Blood gas measurements Description Normal value

Temperature (T) Default setting is 37°C. No consensus on analysis according to patient temperature. Consistency of greater importance.

37°C

Haemoglobin (Hb) Samples need to be fully mixed so should be constantly agitated until analysed.

Females 115–165 g/L

Males: 130–180 g/L

Acid–base status (pH) Overall acidity or alkalinity of blood. 7.36–7.44(36–44 nmol/L)

Carbon dioxide (PaCO2)

Partial pressure of arterial CO2. 4.5–6.0 kPa35–45 mmHg

Oxygen (PaO2) Partial pressure of arterial oxygen. 11–13.5 kPa80–100 mmHg(varies with age)

Bicarbonate (HCO3–) Standard bicarbonate is usually used to assess metabolic function; this is

calculated by removing the respiratory component from the HCO3– .

22–32 mmol/L

Base excess (BE) The number of molecules of acid or base that are needed to return 1 litre of blood to the normal pH (7.4): it measures acid–base balance. As with HCO3

–, standard BE is more useful for accurate assessment of metabolic components.

-3 to +3 mmol/L

Saturation (SaO2) Haemoglobin saturation by oxygen in arterial blood. >94%


• Lowered PaO2 is seen with hypoventilation, ventilation/perfusion mismatch, alveolar-capillary block and right-to-left shunts.

• Raised PaO2 may be seen with hyperventilation or oxygen therapy.

• Lowered PaCO2 (respiratory alkalosis) is usually a compensatory phenomenon in metabolic acidosis, but may be a primary abnormality; in both situations it is due to hyperventilation.

• Raised PaCO2 (respiratory acidosis) occurs in respiratory failure, but is also seen as a compensatory phenomenon, caused by hypoventilation, in metabolic alkalosis.

• Lowered pH indicates a net acidaemia and raised pH indicates a net alkalaemia. The acid–base balance component (be it metabolic or respiratory) is in the same direction as the pH and is the primary abnormality in acid–base imbalance.

• Base excess is decreased in metabolic acidosis and compensated respiratory alkalosis. It is increased in metabolic alkalosis or compensated respiratory acidosis.

• Alveolar-arterial PO2 difference is elevated in all causes of hypoxia except hypoventilation.166

Errors can be caused by sampling techniques. Commonly in Australasia, premixed, dry heparin syringes are the preferred choice, filled to 0.3–0.6 mL. One millilitre of arterial blood is collected anaerobically in a heparinised syringe and transported rapidly to the laboratory, or to the blood gas analyser in the ICU, in a capped syringe with the needle removed.166 Some blood gas syringes still contain liquid heparin, and are prone to producing dilutional inaccuracies if the excess heparin is not expelled once the internal surfaces of the syringe have been coated with the solution; only enough to fill the hub of the syringe should remain. Too much heparin can lower CO2 and HCO3

- readings. The syringes that contain dried heparin minimise this problem. Dilution can also occur from the saline in the flush solution of the arterial line, if too little is withdrawn prior to arterial blood sampling.

The amount of blood that needs to be withdrawn to minimise the risk of saline dilution varies, with published recommendations indicating that, in general, 2 mL fluid should suffice.167 However, a recent Australian study concluded that the blood discard volume should be twice the dead space to ensure clinically accurate arterial blood gas and electrolyte measurement, and to prevent unnecessary blood loss.168 Arterial blood exerts its own pressure, which is sufficient to allow the blood to fill the syringe to the required level; thus, negative pressure should be avoided, as this causes frothing. Any excess air will cause inaccurate readings and should be expelled before the syringe is capped with a hub; covering with a hub prevents further contamination with air. The sample must be analysed within 10 minutes if it is not packed in ice, or within 60 minutes if iced, as delays cause degradation of the sample. Degradation also occurs if the sample is shaken; it should be gently rolled between fingers to mix the sample with the heparin and prevent clotting.167

Other modes of assessment and monitoring are used in some ICUs that provide alternative or additional modes of data

collection and may become more widely used in the future. Transcutaneous and transconjunctival oxygen monitoring are being used in neonates but are proving to be of less value for ongoing monitoring of adult patients with hypotension or shock.7 Transcutaneous carbon dioxide monitoring is also less effective in critically ill adults, but there may be indication for its use in stable patients during weaning from artificial ventilation, or for the monitoring of CO2 during apnoea testing for brain death. Capnometry, particularly the measurement of end-tidal CO2, is being used to measure true alveolar carbon dioxide; but, as highlighted previously, its value is limited in general critically ill patients.126 New technologies are not yet proving superior to those existing diagnostic or monitoring modalities.7

Full blood count The full blood count (FBC) assesses the status of three major cells that are formed in the bone marrow: red blood cells (RBC), white blood cells (WBC), and platelets.

Although normal values have been given (see Appendix C), for critically ill patients changes will occur in certain conditions. For example, Hb is reduced in the presence of haemorrhage and also in acute fluid overload causing haemodilution. Haemoconcentration can occur during acute dehydration, which would show as a high Hb. Similar conditions will also affect the haematocrit. WBC levels will be elevated during episodes of infection, tissue damage and inflammation. When infections are severe, the full blood count will show a dramatic rise in the number of immature neutrophils. Platelets are easily lost during haemorrhage, and clotting deficiencies are noted when the count falls to below 20 × 109/L.166

BiochemistryDiagnostic tests provide information at cellular and biochemical levels that assist clinicians in determining abnormalities and diagnosing causality. (For parameters and normal values, see Appendix C.)

Cardiac enzymes For patients with suspected acute myocardial infarction, testing of the enzyme troponin T or I is now standard. Recent studies have also revealed that cardiac troponin levels are elevated in critically ill septic patients who do not have evidence of MI. Further, mortality rates are higher in troponin-positive patients than in those who are troponin-negative, suggesting that this may become an important enzyme to measure; however, more research is still required to refine the testing.169,170 But not all critically ill patients with elevated cardiac troponin levels should be treated as having myocardial infarction unless there is support from other data.171All injured cells release enzymes, and by measuring the levels of enzymes it is possible to determine which cells are damaged, thus aiding diagnosis. (For details of the tests that can be used to diagnose cardiac injury, and the management of patients requiring cardiovascular support, refer to Chapter 10.) See Table 7.6 for parameters and normal values.


Coagulation profiles Clotting studies are often undertaken when caring for critically ill patients, and they provide a great deal of information that helps clinicians diagnose and treat emerging problems. (See Appendix C for coagulation investigations and normal results.) Samples for these tests should not be taken from heparinised lines or using a heparinised syringe.

DIAGNOSTIC PROCEDURESData generated from many sources are used to determine the cause of illness, the severity of the illness episode, relevant co-morbidities, and the appropriateness of various interventions. Response to treatment also has to be evaluated to determine clinical progress. The diagnostic tests outlined above generate valuable information, but other modalities may be utilised in critical care units to provide additional data that will assist the diagnostic process.

X-RaysX-rays are widely used in critical care, and images are produced by directing short-wavelength X-rays at the body. Dense structures absorb these rays most and so appear as light areas on the image. Hollow air-containing organs and fat absorb fewer rays and so show up as dark areas. X-ray images are very useful for visualising hard, bony structures and revealing abnormal, dense structures in the lungs.172

CHEST X-RAY INTERPRETATION The chest X-ray (CXR) is one of the most commonly undertaken diagnostic procedures in ICUs. As most X-rays of patients in critical care are performed using portable equipment, the results are inferior to those taken using a fixed camera. Care must therefore be taken to minimise erroneous interpretations of subtle changes that have occurred due to overexposure or suboptimal technique. Chest X-rays can be taken looking at the chest via the posterior-anterior (PA) (see Figure 7.25) or anterior-posterior (AP) view.

Patients should ideally be positioned sitting or semierect for this procedure. Supine images can be taken but are less effective at revealing gravity-related abnormalities such as haemothorax. Lateral views of chest X-rays can also be taken to view lesions in the thorax (see Figure 7.26). Interpretation of the CXR in the critical care unit should follow a systematic process that is designed to identify common pathophysiological processes, as well as the location of catheters and other additional items (see Table 7.7). 172,173

Common abnormalities that can be detected by chest X-rays include:• Lobar collapse or atelectasis. The image will reveal all

or some of the following features: loss of lung volume, displacement of fissures and vascular markings, mediastinal and tracheal shift to the affected side, and diaphragmatic elevation or obscurity.

• Barotrauma. The commonest form is pneumothorax. Features to look for include a white, visible air–lung divide, mediastinal shift to the opposite side (seen in

TABLE 7.6 Cardiac enzymes—normal values159

Enzyme Description Normal value

Troponin T Detected within 4–6 hours of infarction, peaking in 10–24 hours.

not normally detected

Creatine kinase (CK) Levels of CK are raised in diseases affecting skeletal muscle. It can be used to detect carrier status for Duchenne muscular dystrophy, although not all carriers have increased levels.

CK-MB is the first of cardiac enzymes to rise, levels peaking in 24 hours but returning to normal within 2–3 days.

Adult female: 30–180 U/LAdult male: 60–220 U/L

CK-MB: 0–5% of total CK

Aspartate aminotransferase (AST)

Detection and monitoring of liver cell damage. No cardiac-specific isoenzymes; today rarely used because it is released after renal, cerebral and hepatic damage.

<40 U/L

Lactate dehydrogenase (LDH)

Of no value in the diagnosis of myocardial infarction. Occasionally useful in the assessment of patients with liver disease or malignancy (especially lymphoma, seminoma, hepatic metastases); anaemia when haemolysis or ineffective erythropoiesis suspected. Although it may be elevated in patients with skeletal muscle damage, it is not a useful in this situation. Post-AMI, cardiac-specific isoenzyme LDH1 peaks between 48 and 72 hours.

110–230 U/L

D-Dimer Presence indicates deep vein thrombosis, myocardial infarction, DIC

<0.25 ng/L

DIC = disseminated intravascular coagulation.


FIGURE 7.25 Chest X-ray, PA view (published with permission, University of Auckland Faculty of Medical and Health Sciences)

FIGURE 7.26 Chest X-ray, lateral view (published with permission, University of Auckland Faculty of Medical and Health Sciences)


TABLE 7.7 Guide to normal chest X-ray interpretation173

Technical issues • Check X-ray belongs to correct patient; note date and time of film.• Ensure you are viewing X-ray correctly (i.e. right and left markings correspond to thoracic

structures).• Determine whether X-ray was taken supine or erect, and whether PA or AP.• Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs & anterior aspects of

5th/6th ribs should be visible above diaphragm).• Note the penetration of the film: dark films are overpenetrated and may require a strong light to

view; white films are underpenetrated; good penetration will allow visualisation of the vertebrae behind the heart.

Bones • Check along each rib from vertebral origin, looking for fractures. • Ensure clavicles and scapulas are intact.

Mediastinum • Check for presence of trachea and identify carina (approximately level of 5th–6th vertebrae).• Check width of mediastinum: should not be more than 8 cm.

Apex • Ensure blood vessels are visible in both apices, particularly looking to rule out pneumothoraces that present as clear black shading on the X-ray. Erect X-rays are essential to facilitate visibility of pneumothoraces.

Hilum • Check for prominence of vessels in this region: it generally indicates vascular abnormalities such as pulmonary oedema or pulmonary hypertension, or congestive heart failure.

Heart • Cardiac silhouette should be not more than 50% of the diameter of the thorax, with 1/3 of heart shadow to the right of the vertebrae and 2/3 of shadow to the left of the vertebrae; this positioning helps to rule out a tension pneumothorax. It should be noted that, post-cardiac surgery, if the mediastinum is left open the heart may appear wider than this; also in AP films this may be the case due to the plate being further away from the heart.

Lung • Identify the lobes of the lungs and determine if infiltrate or collapse is present in one or more of them. Lobes are approximately located as follows: —left upper lobe occupies upper half of lung; —left lower lobe occupies lower half of lung; —right lower lobe occupies costophrenic portion of lung; —right middle lobe occupies cardiophrenic portion of lung;—right upper lobe occupies upper portion of lung.

• Also look for signs of pleural effusion, which appear as a collection of fluid in the lower, usually costophrenic, region in the erect X-ray, causing loss of visualisation of the costophrenic and/or cardiophrenic angles. In a supine X-ray pleural effusions may have a pale white appearance across the entire lung field.

Diaphragm • Check levels of diaphragm: right diaphragm will normally be 1–2 cm above the left diaphragm to accommodate the liver.

Catheters and lines

• Identify distal end of endotracheal tube and ensure above the carina (i.e. not in the right main bronchus).

• Trace nasogastric tube along length and ensure tip is in stomach, or below stomach if nasoenteric tube.

• Trace all central catheters and ensure distal tip in correct location. • Identify other lines (e.g. intercostal catheters, pacing wires) and note location.

PA = posterior-anterior; AP = anterior-posterior.

tension pneumothoraces), dark affected side with a lack of lung markings crossing the air–lung interface.

• Pleural effusion. Features include fluid meniscus, homogeneous white density, diaphragmatic and cardiac obscurity, no loss of hemithoracic volume, possible shift of the mediastinum away from the large effusion. These can be seen well when the image is taken with the patient in an upright position.

• Pulmonary oedema. This is a common abnormality

seen on X-ray, but difficult to determine if the origin is cardiac or non-cardiac.

• Pulmonary embolism. Although not the optimal diagnostic modality, there may be areas of infarction seen. However, these can be mistaken for collapse or consolidation.

Positioning of invasive catheters and other devices can be detected on a simple X-ray if these are made of a radio-opaque material.


UltrasoundUltrasound imaging (or sonography) uses high-frequency sound waves which, when probed on the body, reflect and scatter. Ultrasound waves are produced by a piezoelectric element, which acts as a transmitter and a receiver. Different body tissues produce different echoes, and therefore visual images of outlines of the body organs of interest can be constructed. A single hand-held device is used to emit the sound and pick up the echoes. This has many advantages over other diagnostic techniques because it is safe, portable, and can be easily moved over the body to scan from different body planes. However, it does have limitations, one being that sound waves have poor penetrating power and dissipate in air, so structures such as the lungs or those that are surrounded by bone do not produce good images. Ultrasound is therefore most helpful in diagnosing abnormalities with the liver and biliary tree, pancreas, renal tract, pelvic structures, and pleural, abdominal and pelvic fluid collections. Echocardiography ultrasound generates images in two ways: m-mode, which is a one-dimensional view of the heart; and two-dimensional devices that emit a beam which moves continually in an arc, thereby examining a pie-shaped slice of the heart.174

DOPPLERDoppler technology is a form of ultrasound that can detect and measure blood flow velocity. It can be used as a bedside diagnostic tool as well as a technique for continuous haemodynamic monitoring. The beam is directed at moving objects such as red blood cells, and the frequency of the reflected sound differs from that of the transmitted sound. The difference between the two is called the Doppler shift, and from this can be calculated the speed and direction of blood flow. Different modalities of Doppler are utilised: • Continuous-wave Doppler uses two transducers for

continuous transmission and receipt of sound. This can measure the velocity of all blood captured in the beam, including high-velocity blood flow.

• Pulsed-wave Doppler uses one transducer to transmit a burst of ultrasound and then receive the reflection for a specific period of time. It can be used only to receive sound from a target area, such as a specific area of the heart. It is commonly used for recording high-velocity flow, such as through a stenotic valve.

• Colour Doppler uses the same pulsed-wave technology but directs the beam onto many hundreds of tiny sample regions. The blood flow in each of these is analysed separately and displayed in colour. Blood flow towards the transducer is displayed in red, while

the away flow is blue. Data are displayed in real time and facilitate the detection of many problems, including

valvular regurgitation, turbulence and septal defects.175

Computerised tomographyComputerised tomography (CT) scanning techniques were introduced in the 1970s. A patient is slowly moved supinely through a doughnut-shaped machine and X-rays are emitted from a tube that surrounds the body of the scanner. These beams are directed onto a specific part of the body and

slice through to achieve a detailed cross-sectional picture of the consecutive body regions that have been scanned. CT images are produced with great clarity and revolutionised the diagnosing of the location and severity of head trauma and bleeds. A CT assists in evaluation of many problems affecting the brain, abdomen and skeletal systems. Ultrafast CT scanners are used in dynamic spatial reconstruction, which provides three-dimensional images of the body’s organs from any angle, as well as facilitating the review of movements and volume within the organ, at normal speed and at a specific moment in time.

Another computer-assisted diagnostic X-ray technique is digital subtraction angiography, which produces a detailed view of diseased blood vessels. This has been particularly useful in diagnosing blockages in the vessels that supply the heart wall and the brain. An image is taken before and after contrast medium is injected into the vessel and the computer subtracts one from the other, eliminating all the body structures that might be blocking the view of the vessel.

Magnetic resonance imaging Magnetic resonance imaging (MRI) uses radiofrequency waves and a strong magnetic field rather than X-rays to provide remarkably clear and detailed pictures of internal organs and tissues.176 The high-contrast images of soft tissue are clearer than those generated by X-ray or CT scans. MRI maps hydrogen molecules in the body by subjecting these to an extremely strong magnetic field, which causes the hydrogen molecules to spin. The energy released by this movement is translated into a visual image. MRI identifies differences in the water content of body tissues, which is useful in differentiating between the white and grey matter in the brain. Dense structures such as the skull and vertebral column do not appear in MRI images and so the technique can be used to obtain detailed images of the brain, tumours in various parts of the body, and degenerative diseases such as multiple sclerosis. The plaques produced by this disease are clearly visible using MRI but not in CT scans. MRI is also good at revealing metabolic reactions, particularly those that produce ATP molecules that are energy-rich.177

Newer variants of MRI have emerged. Magnetic resonance spectroscopy (MRS) is able to map other elements in the body to reveal information about the effect of disease on body chemistry.178 Other MRI developments have included functional MRI, which tracks blood flow into the brain in real time. This eliminates the need for the injection of tracer element, producing an alternative to positron emission tomography.

MRI does have limitations: one is that it cannot be used for patients who have implanted pacemakers, or loose dental fillings. The magnetic force can attract these items and dislodge them from the body.

Positron emission tomographyPositron emission tomography (PET) is a development in the field of nuclear medicine and, through the use of injected radioisotopes tagged with biological molecules (tracers), the scanner locates the high-energy gamma rays that are released


as the tracers get absorbed into the most active brain cells. Computers analyse these emissions and produce a colour picture of the brain’s biochemical activity.

SUMMARYA critical care nurse, in today’s changing and challenging healthcare environment, has to be adaptable and willing to

embrace new skills and knowledge. There is a wealth of data that nurses can use to assist them in making both simple and complex decisions related to the care of the critically ill patient, as reflected in the content of this chapter on assessment, monitoring and diagnostics. Nurses, however, must make full use of these data,179 and to achieve this they need to be able to quickly synthesise this information, consider all possible reasons for any changes found, and make decisions that are based on sound evidence wherever possible.

Clinical case studyHelen is a 23-year-old woman who has been admitted to the ICU with respiratory distress. Her respiratory rate is 38 breaths per minute, she is using her accessory muscles to breathe, and she appears exhausted. Oxygen therapy is commenced in the emergency department and continues to be delivered at 40% after her arrival in the ICU. Pulse oximetry reveals an SpO2 of 89% despite the additional oxygen therapy. Given the known inaccuracy at saturation levels of less than 90%,5 an arterial blood sample is obtained from the femoral artery and the results indicate uncompensated respiratory acidosis (pH 7.2, PaCO2 = 54 mmHg (7.2 kPa), HCO3

– = 20 mmol/L). A rapid assessment indicates that Helen has a pyrexia of 40°C, recorded via tympanic thermometer, and yet she appears cool peripherally, with poor capillary refill.

Cardiac monitoring is commenced and reveals a sinus tachycardia, rate 130 beats/min. Assessment of blood pressure using a non-invasive approach finds her to be hypotensive, at 80/55 mmHg. Intravenous access has been made in the emergency department but it is clear that central venous access is required. Before the central access can be obtained, the decision is taken to intubate Helen, because her current rate and pattern of breathing is unsustainable. It is anticipated that the commencement of artificial ventilation will reduce oxygen demand because the respiratory muscles will be rested.

DISCUSSIONIn view of Helen’s age and the preliminary diagnosis of septic shock, cardiac output measurements were warranted to facilitate more accurate assessment of haemodynamic status. Concern about the efficacy of pulmonary artery catheters, and the inaccuracy of central venous pressure

by itself to predict response to IV fluid, led to a PiCCO system being used to measure cardiac output. Therefore, a central line and a thermistor arterial catheter were inserted. The values obtained from this technique indicated that preload was low, reflected by a low ITBV (725 mL/m2). However, the EVLW was slightly elevated (8.5 mL/kg), due to increased capillary permeability. Cardiac output (9.1 L/min) and cardiac index (4.8 L/min/m2) were elevated, indicative of the hyperdynamic phase of sepsis.

The appropriate treatment was the administration of IV fluids to improve preload, in conjunction with inotropic therapy to improve the mean arterial pressure. Helen had a urinary catheter inserted, to enable accurate measurement of urine output in order to evaluate renal perfusion.

A comprehensive assessment of all systems, including biopsychological factors, was undertaken and a multidisciplinary plan of care formulated. Respiratory monitoring continued with the measurement of end-tidal CO2 tension (PETCO2) as, when combined with continuous oximetry, this can reduce the frequency of arterial blood gas sampling.126 Helen spent a period of 2 weeks in the ICU, during which time she required mechanical ventilatory support for 9 days. Renal impairment was minimal and therefore no renal support was required, as adequate cardiac output responded rapidly to positive inotropic and fluid therapy.

Hyperdynamic representation of septic shock is not unusual in younger patients. However, this response requires accurate haemodynamic monitoring because of the instability of the cardiovascular system, so the patient’s response to treatment must be carefully evaluated to achieve a favourable outcome wherever possible.

Research vignetteRickard CM, Couchman BA, Schmidt SJ, Dank A, Purdie DM. A discard volume of twice the deadspace ensures clinically accurate arterial blood gases and electrolytes and prevents unnecessary blood loss. Crit Care Med 2003; 31(6): 1654–8 (published with permission).

ABSTRACTObjective To determine the blood discard volume, as

a multiple of deadspace, that is required for accurate arterial blood gas and electrolyte testing from arterial catheters. Design Prospective, controlled, crossover trial. Setting An 18-bed ICU of a metropolitan teaching hospital. Patients A total of 84 critically ill patients with 20-gauge, radial arterial cannulae, pressure-monitoring transducer set, and stable oxygenation. Interventions System deadspace (priming volume from sampling port to catheter tip) was established. Patients had six 0.5 mL


arterial blood samples taken sequentially in random order using discard volumes of 1, 1.5, 2, 2.3 and 3.6 times the deadspace (experimental values) and 5.5 times the deadspace (control). Measurements and main results Samples were analysed for PaO2, SaO2, pH, PaCO2, HCO3

–, Na+, and K+. We performed repeated-measures analysis of variance with post-hoc linear contrasts and compared mean experimental and control values. The smallest discard volumes that provided measurements that were statistically equal to control were twice the deadspace (PaO2, P = 0.563; SaO2, P = 0.371) and 3.6 times the deadspace (pH, P = 0.107; PaCO2, P = 0.519; HCO3

–, P = 0.10). All discard volumes tested provided results that were statistically different from control for Na+ (P <0.003) and K+ (P <0.001). Conclusions Many results were statistically different from control, although the actual discrepancies were very small. At clinically relevant levels of measurement, there was minimal variation between values obtained after a discard volume of twice the deadspace and control values. The level of error was clinically acceptable and within, or close to, the precision limits of the blood gas analyser. Slight fluctuation in patient variables during sampling could also have contributed to the error. A blood discard volume of twice the deadspace is recommended for all variables. This will provide clinically accurate results and avoid the deleterious effects of unnecessary blood loss.

CRITIQUEThis study investigated an often raised question that has the potential to affect patient wellbeing, particularly those long-term critically ill patients who have many hundreds of blood analyses performed during their illness.

The principle of testing various multiples of the deadspace, rather than a predetermined absolute value, was particularly useful, as it ensures applicability of results to multiple brands of arterial lines. The authors identified 5.5 times the deadspace for the control specimens used in this study, although no evidence is provided as to why this multiple was selected. This is particularly important in the light of the result that Na+ and K+ samples drawn after 3.6 times the deadspace had been removed, remained statistically different from the control, and that measured values were still trending downwards (in the case of Na+) and upwards (in the case of K+) when all samples were considered.

A cohort of 84 clinically stable critically ill patients

was enrolled in the study. Determining clinically stable patients is difficult, although the following definition was provided: ‘the patient had neither required nor was anticipated to require any clinical intervention in the 30-min period before sampling or during the sampling period’.168 While it is difficult to predict what will happen during a future period, no emergency situation arose that required cessation of the sampling protocol, although no definition of what constituted an emergency situation was provided. It is not clear why a full year was required to enrol the patients in this study, given that the inclusion criteria do not appear particularly limiting and that the unit in which the work was conducted is a tertiary-level unit with 18 beds.

The procedure described for drawing and analysing the blood is well described and rigorous in its method. The samples appear to have been taken as rapidly as possible, although no indication of the time elapsed between the first and last sample has been provided. While this may affect the results obtained, the random order for each of the blood samples with each patient is likely to have been effective in preventing a systematic bias.

Results indicated that blood taken after removal of twice the deadspace was not statistically different from the control measurements for PaO2 and SaO2. The measures of pH, PaCO2 and HCO3– required 3.6 times the deadspace to be removed before measures were not statistically different from the controls, while Na+ and K+ levels remained statistically different from the controls after removal of 3.6 times the deadspace. Despite these statistical differences, the authors claim that above twice the deadspace, the differences identified were clinically negligible, and therefore suggest that removal of twice the deadspace is suitable to ensure accurate blood results. On perusal of mean results the differences in blood levels for each amount of discard volume were small (<1 mmHg for PaO2 and PaCO2; <1 mmol/L for HCO3–; 1.1 mmol/L Na+ and <0.2 mmol/L K+). However, there are no data indicating the degree of difference for each individual patient: this might have been considerable, and might account for the statistically significant differences on the repeated-measures analysis of variance that do take into account differences within each individual subject. Further examination of these differences is warranted before assuming that the small differences in mean measurements assure clinical accuracy.

Learning activitiesLearning activities 1–4 relate to the clinical case study.1. Why is levelling of the transducer so important?2. What are the key variables to note when

interpreting arterial blood gases?3. What are the key points to remember when

interpreting haemodynamic monitoring results in a patient receiving mechanical ventilation? Outline, and provide a rationale for, the other aspects of

assessment that should be undertaken in association with haemodynamic monitoring.

4. Describe the ventilation monitoring that should be in place when caring for a patient who has no specific respiratory disease but is experiencing a severe systemic disease such as sepsis. Outline the information you will gain from that monitoring, and how it will inform assessment and changes of ventilation support.


Online resources• Diagnostic Medlab. Diagnostic handbook: the

interpretation of laboratory tests. Available from: http://www.dml.co.nz/clin_handbook.asp

• Hammett RJH, Harris RD. Halting the growth in diagnostic testing. Med J Aust 2002; 177(3): 124–5 (accessed 07/03/05). Available from: http://www.mja.com.au/public/issues/177_03_050802/ham10334_fm.html

• Neurological Society of Australasia and Royal Australasian College of Surgeons (joint publication). The management of acute neurotrauma in rural and remote locations, 2nd edn, 2000. Available from: http:www.surgeons.org/Content/NavigationMenu/WhoWeAre/ReportsandPublications/guidelinesandpositionpapers/guidelines_end_posit.htm

• Webster NR, 2001. Monitoring the critically ill (accessed 30/12/2004). Available from: http://www.rcsed.ac.uk/journal/vol446/44_60010.htm 30/12/2004.

• Capnography: a comprehensive educational website, www.capnography.com

Further readingDutton RP, McCunn M. Traumatic brain injury. Current

Opinion in Critical Care 2003; 9: 503–9.Winkelman C. Effect of backrest position on intracranial and

cerebral perfusion pressures in traumatically brain-injured adults. American Journal of Critical Care 2000; 9(6): 373–80.

Winters AC, Munro N. Assessment of the mechanically ventilated patient: an advanced practice approach. AACN Clinical Issues: Advanced Practice in Acute and Critical Care 2004; 15(4): 525–33.

Vespa P. What is the optimal threshold for cerebral perfusion pressure following traumatic brain injury? Neurosurgical Focus 2003; 15(6): Article 4: http://www.aans.org/education/journal/neurosurgical/dec03/15-6-4.pdf

Monitoring and hemodynamics. Critical Care Nursing Clinics of North America vol 18(2): 145–272.

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Principles and Practice of Critical Carefacweb.northseattle.edu/cduren/North Seattle AT Program 2011-2012...identify the key principles underpinning assessment and ... as correct interpretation