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Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e
>
Chapter 25. Approach to the Patient inShock
FIGURE 25-1.Ronny M. Otero; H. Bryant Nguyen; Emanuel P.
Rivers
EpidemiologyThe exact number of cases of shock that present to
the ED in the U.S. is difficult to ascertain due to the
insensitivity of clinical parameters, current definitions, and lack
of a central
database repository. Previous estimates propose that
approximately 1 million cases of shock are seen in the ED each year
in the U.S.1 These estimates are largely based upon theassumption
that hypotension, defined as a systolic blood pressure
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PaO2 Arterial oxygen pressure
PAOP Pulmonary artery occlusion (wedge) pressure
SaO2 Arterial oxygen saturation
ScvO2 Central venous oxygen saturation
SmvO2 Mixed venous oxygen saturation (pulmonary artery)
SIRS Systemic inflammatory response syndrome
SVR Systemic vascular resistance
VO2 Systemic oxygen consumption
Table 25-2 Oxygen Transport and Utilization Components
Arterial oxygen content CaO2= 0.0031 PaO2+ 1.38 Hb SaO2
CaO2 is the amount of O2 within 100 mL blood. Oxygen is
contained within blood in two forms: dissolved in plasma and
chemically combined withhemoglobin. Assuming 15 grams hemoglobin
per 100 mL blood and an oxygen saturation of 97%, the
representative normal value of CaO2 is 20.1 mL/100mL blood
(vol%).
Central venous/mixed venous oxygen saturation ScvO2 or SmvO2
SmvO2 reflects physiologic efforts to meet tissue O2 demands.
Normal SmvO2 is 65% to 75%. When the SmvO2 falls below 50%, the
bodys limits tocompensate have been reached and O2 availability for
tissue metabolism will be compromised, leading to lactic
acidosis.
Central venous/mixed venous oxygen content CmvO2 = 0.0031 PmvO2
+ 1.38 Hb SmvO2
CmvO2 is the amount of oxygen content returning to the heart.
Normal CmvO2 is 15 mL/100 mL blood (vol%).
Systemic oxygen extraction ratio (OER) OER = C(a-v)O2/ CaO2
The amount of O2 taken out of the blood by the tissues is the
systemic OER. It is described as a percentage. Normal OER is about
25%. Lactic acidproduction, an indicator of anaerobic metabolism,
usually accompanies an OER of >50%.
Oxygen delivery DO2= CO CaO2 10
DO2 is the amount of O2 delivered to the tissues per minute.
Assuming a normal cardiac output of 5 L/min and a CaO2 of 20.1
(vol%), a normal value for O2delivery would be 1000 mL O2 per
minute.
Oxygen consumption VO2 = CO Hb 1.38 (SaO2 SmvO2) 10
The amount of O2 consumed by tissues each minute is equal to the
difference in O2 delivered to tissues and the O2 returning from
tissues. The normal valueis about 250 mL O2 per minute. Note that
this formula ignores the small contribution from dissolved
oxygen.
Oxygen affinity
Shifts in the oxyhemoglobin dissociation curve affect the
release of O2 in the peripheral circulation. Increased pH,
decreased temperature, decreased carbondioxide concentration
(PCO2), and decreases in 2,3-diphosphoglycerate levels all result
in a shift of the oxyhemoglobin curve to the left. Thus, for
anyparticular value of PaO2, the O2 saturation will be higher. This
increased affinity of hemoglobin for O2 makes O2 loading easier,
but release of O2 in theperipheral tissues is impaired. The reverse
is true with a decreased pH, increased temperature, increased PCO2,
and increased 2,3-diphosphoglycerate:there is a shift of the
oxyhemoglobin dissociation curve to the right resulting in a
decreased affinity of hemoglobin for O2.
Note: See Table 25-1 for abbreviation definitions.
When compensatory mechanisms fail to correct the imbalance
between tissue supply and demand, anaerobic metabolism occurs,
resulting in the formation of lactic acid. Lactic acid israpidly
buffered, resulting in the formation of measured lactate. Normal
lactate levels are 0.5 to 1.5 mmol/L. An elevated lactate level is
often associated with decreased SmvO2. Mostcases of lactic acidosis
are a result of inadequate oxygen delivery, but lactic acidosis
occasionally can develop from an excessively high oxygen demand;
for example, in statusepilepticus. In other cases, lactic acidosis
occurs because tissue oxygen utilization is impaired. Examples of
impaired tissue oxygen utilization include septic shock or
thepostresuscitation phase of cardiac arrest, in which a normal
SmvO2 and an elevated lactate may be encountered. Elevated lactate
is a marker of impaired oxygen delivery and/orutilization and
correlates with short-term prognosis of critically ill patients in
the ED. SmvO2 can also be used as a measure of the balance between
tissue oxygen supply and demand.SmvO2 is obtained from the
pulmonary artery catheter, but similar information can be from
central venous oxygen saturation (ScvO2). ScvO2 correlates well
with SmvO2, and ScvO2 is
easier to obtain in the ED setting.10
Shock provokes a myriad of autonomic responses, many of which
serve to maintain perfusion pressure to vital organs. Stimulation
of the carotid baroreceptor stretch reflex activatesthe sympathetic
nervous system leading to (1) arteriolar vasoconstriction,
resulting in redistribution of blood flow from the skin, skeletal
muscle, kidneys, and splanchnic viscera; (2) anincrease in heart
rate and contractility that increases CO; (3) constriction of
venous capacitance vessels, which augments venous return; (4)
release of the vasoactive hormonesepinephrine, norepinephrine,
dopamine, and cortisol to increase arteriolar and venous tone; and
(5) release of antidiuretic hormone and activation of the
renin-angiotensin axis toenhance water and sodium conservation to
maintain intravascular volume.
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These compensatory mechanisms attempt to maintain DO2 to the
most critical organsthe heart and brainbut blood flow to other
organs such as the kidneys and GI tract may becompromised.
The cellular response to decreased DO2 is adenosine triphosphate
depletion, leading to ion-pump dysfunction, influx of sodium,
efflux of potassium, and reduction in membrane restingpotential. As
shock progresses, lysosomal enzymes are released into the cells
with subsequent hydrolysis of membranes, deoxyribonucleic acid,
ribonucleic acid, and phosphateesters. As the cascade of shock
continues, the loss of cellular integrity and the breakdown in
cellular homeostasis result in cellular death. These pathologic
events give rise to themetabolic features of hemoconcentration,
hyperkalemia, hyponatremia, prerenal azotemia, hyper- or
hypoglycemia, and lactic acidosis.
In the early phases of septic shock, these physiologic changes
produce a clinical syndrome called the systemic inflammatory
response syndrome or SIRS (Table 25-3).
Table 25-3 Clinical Feature of Systemic Inflammatory Response
Syndrome (SIRS)54
Two or more of the following features are required to make a
diagnosis of SIRS:
Temperature >38C (100.4F) or 90 beats/min
Respiratory rate >20 breaths/min
White blood cell count >12.0 109/L, 10% immature forms or
bands
Reproduced with permission from American College of Chest
Physicians/Society of Critical Care Medicine consensus
conference: definitions for sepsis and organ failure and
guidelines for the use of innovative therapies in sepsis. Crit
Care
Med 20: 864, 1992.
As SIRS progresses, shock ensues, followed by multi-organ
dysfunction syndrome manifested by myocardial depression, adult
respiratory distress syndrome, disseminatedintravascular
coagulation, hepatic failure, or renal failure. The fulminant
progression from SIRS to multi-organ dysfunction syndrome is
determined by the balance ofanti-inflammatory and proinflammatory
mediators or cytokines that are released from endothelial cell
disruption11 (Figure 25-1).
FIGURE 25-1.
The pathophysiology of shock, systemic inflammatory response
syndrome (SIRS), and multi-organ dysfunction syndrome (MODS).
Clinical Features
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History and Comorbidities
Often, the presence of shock and the underlying cause will be
quite apparentsuch as acute myocardial infarction, anaphylaxis, or
hemorrhage. Some patients may be in shock withfew symptoms other
than generalized weakness, lethargy, or altered mental status.
Symptoms that suggest volume depletion include bleeding, vomiting,
diarrhea, excessive urination,insensible losses because of fever,
or orthostatic light-headedness. Ask about a history of
cardiovascular disease, episodes of chest pain, or symptoms of
congestive heart failure.Underlying neurologic disease can render
patients more susceptible to complications from hypovolemia.
Consider the possibility of an anaphylactic reaction to a new
medication orcardiovascular depression from a drug. Some
medications can cause volume depletion (e.g., diuretics) and others
depress myocardial contractility (e.g., -blockers and
calciumchannel blockers).
Physical Examination
Shock is usually, but not always, associated with systemic
arterial hypotensionsystolic blood pressure 1.0) indicates an
impaired left ventricular function(as a result of blood loss and/or
cardiac depression) and carries a high mortality rate.13
Central nervoussystem
Acute delirium or brain failure, restlessness, disorientation,
confusion, and coma secondary to decrease in cerebral perfusion
pressure(mean arterial pressure intracranial pressure). Patients
with chronic hypertension may be symptomatic at normal blood
pressures.
Skin Pallor, pale, dusky, clammy, cyanosis, sweating, altered
temperature, and decreased capillary refill.
CardiovascularNeck vein distention or flattening, tachycardia,
and arrhythmias. An S3 may result from high-output states.
Decreased coronaryperfusion pressures can lead to ischemia,
decreased ventricular compliance, increased left ventricular
diastolic pressure, andpulmonary edema.
Respiratory Tachypnea, increased minute ventilation, increased
dead space, bronchospasm, hypocapnia with progression to
respiratory failure,and adult respiratory distress syndrome.
Splanchnic organs Ileus, GI bleeding, pancreatitis, acalculous
cholecystitis, and mesenteric ischemia can occur from low flow
states.
Renal Reduced glomerular filtration rate, renal blood flow
redistributes from the renal cortex toward the renal medulla
leading to oliguria.Paradoxical polyuria can occur in sepsis, which
may be confused with adequate hydration status.
Metabolic Respiratory alkalosis is the first acid-base
abnormality. As shock progresses, metabolic acidosis occurs.
Hyperglycemia,hypoglycemia, and hyperkalemia.
Diagnosis
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Clinical Criteria
The result of shock is global tissue hypoperfusion and is
associated with a decreased venous oxygen content and metabolic
acidosis (lactic acidosis). Shock is classified into fourcategories
by etiology (Table 25-5). Clinically, shock usually presents with
signs and symptoms of hypovolemia, but as the shock state persists
or progresses to irreversible end-organdamage, other
pathophysiologic mechanisms become operative.15
Table 25-5 Classification of Shock
Type Comment
Hypovolemic Caused by inadequate circulating volume
Cardiogenic Caused by inadequate cardiac pump function
Obstructive Caused by extra cardiac obstruction to blood
flow
Distributive Metabolic derangements that impair cellular
respiration such as cyanide toxicity, sepsis.
Laboratory Evaluation
The clinical presentation and the presumptive etiology of shock
dictate the use of ancillary studies. A battery of standard
hematologic, coagulation, and biochemical tests usuallyprovides an
assessment of the patients general physiologic condition and
occasionally detects an abnormality that requires specific
treatment (Table 25-6). A wide range of laboratoryabnormalities may
be encountered in shock, but most abnormal values merely point to
the particular organ system that is either contributing to, or
being affected by, the shock state.No single laboratory value is
sensitive or specific for shock.
Table 25-6 Ancillary Studies in Shock
Basic evaluation
Complete blood count: white blood cell count and differential,
hemoglobin and hematocrit, platelet count
Electrolytes, glucose, calcium, magnesium, phosphorus
Blood urea nitrogen, creatinine
Prothrombin time, partial thromboplastin time
Urinalysis
Chest radiograph
ECG
Moderate physiologic assessment
Arterial blood gas (measured oxygen saturation)
Serum lactate
Fibrinogen, fibrin split products, D-dimer
Hepatic function panel
Noninvasive hemodynamic assessment
End-tidal CO2
Noninvasive cardiac output measurement
Echocardiogram
Invasive hemodynamic assessment
Filling pressures: CVP, PAOP
Cardiac output
Central venous oxygen saturation ScvO2
Calculation of hemodynamic values: SVR, CO, DO2, VO2
As clinically indicated to define etiology or detect
complications
Blood, sputum, urine, and pelvic cultures
CT of head and sinuses
Lumbar puncture
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Culture suspicious wounds
Cortisol level
Pregnancy test
Acute abdominal series
Abdominal or pelvic US
Abdominal or pelvic CT
Note: See Table 25-1 for abbreviation definitions.
Imaging
Chest X-Ray
The portable anteroposterior-view chest roentgenogram (CXR) is
often used in the evaluation of unstable patients to avoid
transporting the patient during resuscitation. The CXR can
shed light on the etiology of shock and may aid in assessment of
volume status in the critically ill.16 However, the accuracy of
determining volume status is 70% compared withpulmonary artery
occlusion pressure >18 mm Hg. The likelihood ratio of CXR
determining volume status using objective vascular pedicle width
and cardiothoracic ratio is 3.1 [95% CI
(1.9% to 6.0%)].17
US
The use of ultrasonography in the assessment of patients with
suspected shock manifesting as symptomatic hypotension has been
advocated.18
US evaluation can help narrow diagnostic considerations.18 The
following are helpful in this assessment: subcostal cardiac view,
inferior vena cava view, parasternal long-axis cardiac
view, apical four-chamber cardiac view, right upper quadrant
abdominal view, pelvic view, and abdominal aorta view.18 Emergency
physician determination of left ventricular function
can be comparable to the assessment performed by a cardiologist
in hypotensive patients.19
Hemodynamic MonitoringHemodynamic monitoring helps assess the
severity of shock and the response to treatment. Monitoring
capabilities vary from institution to institution, but if possible
should includepulse oximetry, electrocardiographic monitoring,
continuous noninvasive but preferably intra-arterial blood pressure
monitoring, end-tidal CO2 monitoring, and central venous
pressure
(CVP) and ScvO2 monitoring.20 Average access time, number of
attempts, and mechanical complications are reduced when an
US-assisted approach to central access is
used.21Figure 25-1 outlines a systematic approach to the
evaluation of the patient in shock.
Treatment
Early Intervention
The benefit of timely ED intervention in nontraumatic critical
illness is significant. Comprehensive and timely ED care can
significantly decrease the predicted mortality of critically
ill
patients in as little as 6 hours of treatment.22,23 Application
of an algorithmic approach to optimize hemodynamic end points with
early goal-directed therapy in the ED reduces
mortality by 16% in patients with severe sepsis or septic
shock.23 Early goal-directed therapy has been validated in both
septic and nonseptic populations.24 The ABCDE tenets ofshock
resuscitation are establishing Airway, controlling the work of
Breathing, optimizing the Circulation, assuring adequate oxygen
Delivery, and achieving End points of resuscitation.
Establishing Airway
Airway control is best obtained through endotracheal intubation
for airway protection, positive pressure ventilation (oxygenation),
and pulmonary toilet. Sedatives used to facilitateintubation may
cause arterial vasodilatation, venodilation, and myocardial
suppression and result in hypotension. Positive pressure
ventilation reduces preload and CO. Thecombination of sedative
agents and positive pressure ventilation can lead to hemodynamic
collapse. Consider volume resuscitation or application of
vasoactive agents beforeintubation and positive pressure
ventilation.
Controlling the Work of Breathing
Control of breathing is required when tachypnea accompanies
shock. Respiratory muscles are significant consumers of oxygen
during shock and contribute to lactate production.Mechanical
ventilation and sedation allow for adequate oxygenation,
improvement of hypercapnia, and assisted, controlled, synchronized
ventilationall of which decrease the work ofbreathing and improve
survival. Arterial oxygen saturation should be restored to >93%
and ventilation controlled to maintain a PaCO2 of 35 to 40 mm Hg.
Normalizing pHabove 7.3 by hyperventilation is not beneficial.
Neuromuscular blocking agents should be considered to further
decrease respiratory muscle oxygen consumption and preserve DO2
tovital organs.
Optimizing the Circulation
Circulatory or hemodynamic stabilization begins with
intravascular access through large-bore peripheral venous lines.
The Trendelenburg position does not improve
cardiopulmonaryperformance compared with the supine position. It
may worsen pulmonary gas exchange and predispose to aspiration.
Passive leg raising above the level of the heart with the
patient
supine25 can be effective. If passive leg raising results in an
increase in blood pressure or CO, fluid resuscitation will be
helpful.25
Central venous access aids in assessing volume status (preload)
and monitoring ScvO2. It is the preferred route for the long-term
administration of vasopressor therapy and providesrapid access to
the heart if pacemaker placement is required.
Fluid resuscitation begins with isotonic crystalloid. The amount
and rate of infusion are determined by an estimate of the
hemodynamic abnormality. Most patients in shock have eitheran
absolute or relative volume deficit. The exception is the patient
in cardiogenic shock with pulmonary edema. Administer fluid
rapidly, in set quantities of 500 or 1000 mL normalsaline, and
reassess the patient after each bolus. Patients with a modest
degree of hypovolemia usually require an initial 20 mL/kg of
isotonic crystalloid. More fluids are needed forprofound volume
deficits.
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Vasopressor agents are used when there has been an inadequate
response to volume resuscitation or if there are contraindications
to volume infusion.26 Vasopressors are mosteffective when the
vascular space is full and least effective when the vascular space
is depleted. However, vasopressors may be necessary early in the
treatment of shock, beforevolume resuscitation is complete, to
prevent potentially lethal consequences of prolonged systemic
arterial hypotension. This is especially important in elderly
patients with significantcoronary and cerebrovascular disease.
Rapidly restoring the MAP (Formula 25-2) to 60 mm Hg or systolic
pressure to 90 mm Hg may avoid the coronary and cerebral
complicationsof decreased blood flow.
Formula 25-2
Diastolic blood pressure + [pulse pressure/3]
Mean arterial blood pressure (maintain 60 mm Hg or higher).
Vasopressor agents have variable effects on the -adrenergic,
-adrenergic, and dopaminergic receptors (Table 25-7). Although
vasopressors improve perfusion pressure in the largevessels, they
may decrease capillary blood flow in certain tissue beds,
especially the GI tract. Vasopressors will falsely elevate
intracardiac filling pressures (i.e., CVP). If multiplevasopressors
are used, they should be simplified as soon as the best therapeutic
agent is identified.
Table 25-7 Commonly Used Vasoactive Agents
Drug Dose (Mixture)* Action CardiacStimulation Vasoconstriction
VasodilationCardiacOutput
Side Effects andComments
Dopamine
0.525.0micrograms/kg/min(400milligrams/250 mL)
, , anddopaminergic
++ at 510micrograms/kg/min
++ at 10micrograms/kg/min
+ at 0.55.0micrograms/kg/min
Usuallyincreases
Tachydysrhythmias;increasesmyocardial O2consumption;
acerebral,mesenteric,coronary, and renalvasodilator at lowdoses
Norepinephrine212micrograms/min (4milligrams/250 mL)
Primarily 1,some 1
++ ++++ 0 Slightdecrease
Dose-related, reflexbradycardia; usefulwhen loss of venoustone
predominates;spares the coronarycirculation
Phenylephrine
100200micrograms/min,taper as drugtakes effect (10milligrams/250
mL)
Pure 0 ++++ 0 Decrease
Reflex bradycardia,headache,restlessness,excitability,
rarelyarrhythmias; idealfor patients in shockwith tachycardia
orsupraventriculararrhythmias
Ephedrine
5- to 25-milligramIV bolus; mayrepeat at 5- to10-min intervals
upto 150 mg in 24 h
and +++ ++ + Increases
Causes palpitations,hypertension,cardiac arrhythmias;an
indirect-actingcentral nervoussystem stimulant;limited
long-termvalue as therapy forshock
Vasopressin0.010.04units/min (200units/250 mL)
++++
Primarilyvasoconstriction;outcome data fromits use are
lacking;infusions of 0.04unit/min may lead
toadverse,vasoconstriction-mediated events
Epinephrine210micrograms/min (4milligrams/250 mL)
and ++++ at 0.030.15micrograms/kg/min++++ at
0.150.30micrograms/kg/min +++ Increases
Causestachydysrhythmia,leukocytosis;increasesmyocardial
oxygenconsumption
Dobutamine
2.020.0micrograms/kg/min(250milligrams/250 mL)
1, some 2and 1 inlargedosages
++++ + ++ Increase
Causestachydysrhythmia,occasional GIdistress, increases
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Drug Dose (Mixture)* Action CardiacStimulation Vasoconstriction
VasodilationCardiacOutput
Side Effects andComments
myocardial oxygenconsumption,hypotension involume
depletedpatient; has lessperipheralvasoconstrictionthan dopamine;
cancause fewerarrhythmias thanisoproterenol
Isoproterenol
0.010.05micrograms/kg/min(1 milligram/250mL)
1 and some2
++++ 0 ++++ Increases
Causestachydysrhythmia,facial flushing,hypotension
inhypovolemicpatients; increasesmyocardial oxygenconsumption;
neveruse alone in shock
Note: 0 = no effect; + = mild effect; ++ = moderate effect; +++
= marked effect; ++++ = very marked effect.
*Individual drugs may be diluted in 5%dextrose in water or
normal saline, and may be diluted in larger volumes or
concentrated into smaller volumes according to the fluid needs
of the individual patient.
Assuring Adequate Oxygen Delivery
Once blood pressure is stabilized through optimization of
preload and afterload, DO2 can be assessed and further manipulated.
Restore arterial oxygen saturation to physiologic 93%
to 95%. In shock state, transfusion of packed red blood cells
should be considered to maintain hemoglobin 10 grams/dL.26 If CO
can be assessed, it should be increased usingvolume infusion and
inotropic agents in incremental amounts until venous oxygen
saturation (SmvO2 or ScvO2) and lactate are normalized.
Control of VO2 is important in restoring the balance of oxygen
supply and demand to tissues. A hyperadrenergic state results from
the compensatory response to shock, physiologicstress, pain, and
anxiety. Shivering frequently results when a patient is unclothed
for examination and then left inadequately covered in a cold
resuscitation room. The combination ofthese variables increases
systemic oxygen consumption. Pain further suppresses myocardial
function, thus impairing DO2 and VO2. Providing analgesia, muscle
relaxation, warmcovering, anxiolytics, and even paralytic agents,
when appropriate, decreases this inappropriate VO2.
Tissue oxygen extraction assesses adequacy of the resuscitation
in meeting the oxygen needs of the tissues. Sequential examination
of lactate and SmvO2 or ScvO2 is a method to
assess adequacy of tissue oxygen extraction. Continuous
measurement of SmvO2 or ScvO2 through fiberoptic technology can be
used in the ED.10 A variety of technologic tools may
be used to assess tissue perfusion during resuscitation.2636 The
advantages and disadvantages of these measures are summarized in
Table 25-8.
Table 25-8 Tools for Hemodynamic Monitoring
Tool Comments
Invasive blood pressure monitoring
Intra-arterial pressure measurement is preferable because
vasoactive drugs may cause rapid swings in bloodpressure, and
multiple blood samplings will typically be required.
Radial artery pressure may underestimate central pressure in
hypotensive septic patients receiving high-dosevasopressor therapy
and may lead to excessive vasopressor administration.27
Pulse pressure variation and pulsecontour analysis of stroke
volumevariation
Measures of stroke volume variation using arterial pulse contour
analysis estimates cardiac output and candemonstrate fluid
responsiveness if cardiac output increases after volume loading
during positive pressureventilation.29
CVP
May not reliably reflect the left ventricular filling pressure
in clinical states that produce pulmonary hypertensionor compliance
changes in the right or left heart.
Common iliac venous pressure can approximate CVP.30
Static measures of fluid responsiveness
Central venous or right atrial pressure, wedge, or pulmonary
artery occlusion pressure, right ventricularend-diastolic volume
index, left ventricular end-diastolic area, global end-diastolic
volume, and intrathoracic bloodvolume.
One of the disadvantages of this diagnostic approach in unstable
patients is that it is definitive in only 50% ofsuch
patients.20,28
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Tool Comments
Central and mixed venous oximetry(ScvO2 and SmvO2)
ScvO2 closely approximates mixed venous O2 saturation (SmvO2)
and can be monitored continuously usinginfrared oximetry.
Enables the clinician to detect clinically unrecognized global
hypoperfusion in the treatment of myocardialinfarction, general
medical shock, trauma, hemorrhage, septic, hypovolemic, end-stage
heart failure, cardiogenicshock during and after cardiopulmonary
arrest.10
Systemic arterial-venous CO2 difference
Increased arterial-mixed venous carbon dioxide gradients or
(a-v)CO2 are seen in acute circulatory failure, andinversely
correlate with the cardiac index.
Central venous and pulmonary artery CO2 values can be
interchanged to determine cardiac index.31
Gastric tonometry and sublingualcapnography
Serial measurements of gastric and sublingual mucosal blood flow
are based on hydrogen ion diffusion and CO2elimination.
Inadequate visceral perfusion as evidenced by persistently low
intramucosal pH or increased sublingual CO2concentration after
resuscitation is associated with subsequent organ dysfunction and
death.32,33
Pulmonary artery catheterization
Can measure left-sided heart filling, pulmonary artery occlusion
pressure, cardiac output, and mixed venousoxygen saturation.
Enables calculation of hemodynamic and oxygen transport
variables.
Special catheters can measure right ventricular end-diastolic
volume index calculated from right ventricularejection
fraction.
US and echocardiography
Intracardiac, vena caval diameters, left ventricular
end-diastolic area after a fluid challenge or passive leg
raisingmay be used to assess volume status.
Controlled-compression sonography measures venous pressure in
peripheral veins and allows reliable indirectassessment of CVP.
US can also be used to assist in line placement.19,21
Noninvasive cardiac outputCardiac output can be measured by
pulse pressure variation, pulse contour analysis, transesophageal
Doppler(esophageal Doppler monitor), thoracic cutaneous
bioimpedance, lithium dilution, or
transpulmonarythermodilution.34
NIRS
Patients with severe sepsis have lower StO2; StO2 recovery
slope, tissue hemoglobin index, and total tissuehemoglobin increase
on venous occlusion.
Patients with severe sepsis had longer StO2 recovery times and
lower NIRS-derived local oxygen consumption
values versus healthy volunteers.35
Orthogonal polarization spectral
Disordered microcirculatory flow is associated with systemic
inflammation, acute organ dysfunction, andincreased mortality.
New technologies that directly image microcirculatory blood flow
will help define the role of microcirculatorydysfunction in oxygen
transport and circulatory support in severe sepsis.36
Abbreviations: CVP = central venous pressure; NIRS =
near-infrared spectroscopy; StO2 = tissue oxygen saturation.
End Points of Resuscitation
The goal of resuscitation is to maximize survival and minimize
morbidity using objective hemodynamic and physiologic values to
guide therapy. No therapeutic end point is universally
effective, and only a few have been tested in prospective
trials, with mixed results.37 Hypotension at ED presentation is
associated with poor outcomes.38 Noninvasive parameters,such as
blood pressure, heart rate, and urine output, may underestimate the
degree of remaining hypoperfusion and oxygen debt, so use of
additional physiologic end points may be
informative (Table 25-8).37,39,40 A goal-directed approach of
urine output >0.5 mL/kg/h, CVP 8 to12 mm Hg, MAP 65 to 90 mm Hg,
and ScvO2 >70% during ED resuscitation
of septic shock significantly decreases mortality.23
Troubleshooting a Persistently Hypotensive Patient
Table 25-9 lists important issues to consider if hypotension and
shock persist.
Table 25-9 Troubleshooting Persistent Shock or Hypotension
Equipment and monitoring
Is the patient appropriately monitored?20
Has the early use of vasopressors falsely elevated the central
venous pressure and masked persistent hypovolemia?
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Is there an equipment malfunction, such as dampening of the
arterial line or disconnection from the transducer?
Is the IV tubing into which the vasopressors are running
connected appropriately?
Are the vasopressor infusion pumps working?
Are the vasopressors mixed adequately and in the correct
dose?
Patient assessment
Do mentation and clinical appearance match the degree of
hypotension?
Is the patient adequately volume resuscitated?
Does the patient have a pneumothorax after placement of central
venous access?
Has the patient been adequately assessed for an occult
penetrating injury (a bullet hole or stab wound)?
Is there hidden bleeding from a ruptured spleen, large vessel
aneurysm, or ectopic pregnancy?
Does the patient have adrenal insufficiency? The incidence of
adrenal dysfunction can be as high as 30% in this subset of
patients.55
Is the patient allergic to the medication just given or taken
before arrival?
Is there cardiac tamponade in the dialysis patient or cancer
patient?
Is there associated acute myocardial infarction, aortic
dissection, or pulmonary embolus?
Controversies of Treatment
Fluid Therapy
Rapid restoration of fluid deficits modulates inflammation and
decreases the need for subsequent vasopressor therapy, steroid
administration, and invasive monitoring (pulmonary
artery catheterization and arterial line placement) if the
condition progresses to shock.26,30 Although there is general
agreement that volume therapy is an integral component of
earlyresuscitation, there is a lack of consensus for the type of
fluid, standards of volume assessment, and end points. Table 25-10
compares the most commonly used fluid therapies.
Table 25-10 Fluid Therapy
Fluid Comments
Crystalloids
NSSlightly hyperosmolar solution containing 154 mEq/L of both
sodium and chloride.
Risk of inducing hyperchloremic metabolic acidosis when given in
large amounts due to relatively high chloride concentration.42
LR
Lactate can accept a proton and subsequently be metabolized to
CO2 and water by liver, leading to release of CO2 in the lungs
andexcretion of water by the kidneys. LR results in a buffering of
the acidemia that is advantageous over NS.
Risk of inducing hyperkalemia in patients with renal
insufficiency or renal failure due to small potassium content (very
small amount).
D-isomer of LR causes immune activation and induction of
cellular injury. Replacement of the lactate with ethyl pyruvate
or-hydroxybutyrate or using only the L-isomer of lactate in Ringers
solution decreases this adverse effect.42,43
Colloids
Albumin
Derived from human plasma.
Available in varying strengths from 4% to 25%.
The Saline versus Albumin Fluid Evaluation (SAFE) study compared
fluid resuscitation with albumin or saline on mortality and found
similar28-day mortalities and secondary outcomes in each arm.
However, a subset analysis of septic patients resuscitated with
albumin showed adecrease in mortality, although statistically it
was insignificant. There was an increase in mortality in trauma
patients complicated by headinjury.44
Hydroxyethylstarch
Hydroxyethyl starch should be avoided in sepsis.4547
Synthetic colloid derived from hydrolyzed amylopectin.
Many harmful effects: renal impairment at recommended doses and
impairing long-term survival at high doses,45 coagulopathy
andbleeding complications from reduced Factor VIII and von
Willebrand factor levels, impaired platelet function.
DextranArtificial colloids/glucose polymers synthesized by
Leuconostoc mesenteroides bacteria grown in sucrose media.
Used to lower blood viscosity.
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Fluid Comments
Can cause renal dysfunction, anaphylactoid reactions.
Gelatin
Produced from bovine collagen.
Small molecular weight limits effectiveness of plasma volume
expansion.
Less expensive than other plasma volume expanders.41,42,46
Can cause renal impairment, allergic reactions.
Not currently available in the U.S.
Abbreviations: LR = lactated Ringers solution; NS =normal
saline.
Colloids are high-molecular-weight solutions that increase
plasma oncotic pressure. Colloids can be classified as either
natural (albumin) or artificial (starches, dextrans, and
gelatins).Due to their higher molecular weight, colloids stay in
the intravascular space significantly longer than crystalloids. The
intravascular half-life of albumin is 16 hours versus 30 to 60
minutes for normal saline and lactated Ringers solution.4144
Resuscitation with crystalloids requires two to four times more
volume than colloids.41 The outcome advantage
between crystalloid and colloids continues to remain unresolved
in sepsis.4148
The issue of liberal versus conservative fluid resuscitation in
the face of lung injury is also unsettled.4951 The Fluids and
Catheters Treatment Trial demonstrated no difference in60-day
mortality between the two strategies but did reveal significantly
improved lung and central nervous system function and a decreased
need for sedation, mechanical ventilation,
and intensive care unit care in patients who received
conservative fluid resuscitation.52 Other trials comparing early
liberal fluid resuscitation strategy with more conservative
strategies
failed to demonstrate an increased need for mechanical
ventilation.49
Bicarbonate Use in Shock
Bicarbonate administration shifts the oxygen-hemoglobin
dissociation curve to the left, impairs tissue unloading of
hemoglobin-bound oxygen, and may worsen intracellular
acidosis.There is no evidence that bicarbonate administration
reverses myocardial depression or improves sensitivity to
endogenous catecholamines.
Many clinicians remain uncomfortable withholding bicarbonate if
metabolic acidosis is severe. A compromise position is to partially
correct the metabolic acidosis over time, asillustrated in Formula
25-3. Correct only to arterial pH 7.25.
Formula 25-3
1. Calculate the bicarbonate deficit.
[(normal HCO3 the patients HCO3) 0.5 body weight (kg)]
2. Slowly infuse one half of the calculated deficit.
3. Infuse the remainder over 6 to 8 hours.
4. Stop bicarbonate when arterial pH = 7.25.
1.
Slow and partial correction of metabolic acidosis with HCO3.
Disposition and Transition to the Intensive Care UnitDocument
and communicate all steps of ED resuscitation to the critical-care
team. Even when resuscitation is systematic and thoughtful,
miscommunication can undo the benefits ofinitial ED treatment.
Ideally, verbally communicate and document a system-oriented
problem list with an assessment and plan, including all procedures
and complications, before
transfer. For prolonged or boarded ED stays, provide
appropriately timed notations regarding patient status, diagnostic
and therapeutic interventions, and sentinel events.22
PrognosisSome clinical variables are associated with poor
outcome, such as severity of shock, temporal duration, underlying
cause, preexisting vital organ dysfunction, and reversibility.
Direct
noninvasive measurement of VO2 is predictive of outcome in
patients who developed cardiogenic shock secondary to myocardial
infarction and after cardiac arrest.10 Persistent
elevated lactate levels are prognostic in trauma, septic shock,
and after cardiac arrest.12 Base deficit is also correlated with
the development of multisystem organ failure in trauma.36
Outcome predictions using physiologic scoring systems in the ED
are still being studied.53
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Useful Web Resources
Critical Care Medicine Tutorials (SHOCK)http://ccmtutorials.com,
http://ccmtutorials.com/cvs/index.htmCritical Care
Archiveshttp://ccforum.com
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Your IP address is 132.248.9.8
The pathophysiology of shock, systemic inflammatory response
syndrome (SIRS), and multi-organ dysfunction syndrome (MODS).
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