CRITICAL CARE

BY Dr. M. MAHER KHAWATMI

ROUTINE MONITORING OF THE CRITICALLY ILL PATIENT1. ELECTROCARDIOGRAPHY

Continuous ECG monitoring is the most sensitive, safe, and cost-effective modality for detecting disturbances of cardiac rate, rhythm, and conduction.ST-segment monitoring is quite reliable for detection of myocardial ischemia and infarction. Leads II and V5 are most commonly used, as these two leads together can detect > 90% of ischemic events.Any disturbances detected on continuous ECG monitoring should prompt recording of a 12-lead ECG.

2 .RESPIRATORY MONITORING

PULSE OXIMETRY Pulse oximetry provides continuous assessment of the O2 saturation of arterial blood (SaO2).

A conventional cooximeter measures the attenuation of the different wavelengths to determine the relative concentration of oxygenated haemoglobin (O2Hb), deoxygenated hemoglobin (Hb), carboxyhemoglobin (CO Hb), and methhemoglobin (Met Hb).

For O2Hb, this is referred to as "fractional Hb-saturation", which = [O2Hb/(Hb+O2Hb+Met Hb+ CO Hb)] x 100.

If all haemoglobin molecules bonded with an oxygen molecule (O2), the total body of haemoglobin is said to be fully saturated (100% saturation). When haemoglobin unloads the oxygen molecule to tissue cells at capillary levels, the saturation progressively decreases and the normal venous saturation is about 75%. The normal saturation level is said to be between 87-97%.

The two wavelengths are chosen for the reason that deoxygenated haemoglobin (O2Hb) has a higher absorption at around 660 nm and at 910 nm oxygenated haemoglobin (Hb) has the higher absorption. The oxygenated haemoglobin allows red light to transmit through and absorbs more infrared light while the deoxygenated haemoglobin allows infrared to transmit

through and absorbs more red light.

Usually a finger is placed between the source (light emitting diodes, LEDs) and the receiver (photodiode) acting as a translucent site with good blood flow. Once these absorption levels are detected from the finger the ratio of absorption at different wavelengths can be obtained.

For O2Hb, this is referred to as "functional Hb-saturation", which = [O2Hb /(Hb+ O2Hb)] x l00.

Usually a finger is placed between the source (LEDs) and the receiver (photodiode) acting as a translucent site with good blood flow .

The oxygenated haemoglobin allows red light to transmit through and absorbs more infrared light while the deoxygenated haemoglobin allows

infrared to transmit through and absorbs more red light.

Probe malposition, motion, hypothermia, vasoconstriction, and hypotension may result in unreliable measurements.Nail polish, dark skin, and elevated serum lipids falsely lower SaO2 measurements, whereas elevated CO Hb and Met Hb(in carbon monoxide or cyanide poisoning) falsely raise the measurements.A leftward shift in the oxyhemoglobin dissociation curve (hypothermia, alkalosis, blood transfusion) results in a lower PaO2 for a given SaO2. Consequently, a large

drop in PaO2 may occur with no discernible change in SaO2 .

Oxygen-hemoglobin dissociation curveOxygen-hemoglobin dissociation curve..At low levels of OAt low levels of O22 tension, increases in PaO tension, increases in PaO22 translate into only small increases in SaO2. During mid-range translate into only small increases in SaO2. During mid-range OO2 2 tension, the relationship of PaO2 to SaO2tension, the relationship of PaO2 to SaO2 is nearly linear. The curve plateaus at higher Ois nearly linear. The curve plateaus at higher O22 tension, such tension, such

that continued increases in PaOthat continued increases in PaO22 result in very little increase in SaO result in very little increase in SaO22..

CAPNOGRAPHY

A rise in expired PCO2 (ETCO2) indicates a decrease in alveolar ventilation or an increase in CO2 production, as is seen with overfeeding, sepsis, fever, exercise, or acute increase in cardiac output.A fall in ETCO2 indicates either an increase in alveolar ventilation or an increase in dead space, as seen with massive pulmonary embolism, ET tube or main stem

bronchus obstruction, ventilator circuit leak, or a sudden drop in cardiac output .

3 .ARTERIAL PRESSURE MONITORING

Noninvasive Methods

Noninvasive blood pressure monitoring is sufficient for most surgical patients. With the auscultatory method gradual cuff deflation permits the artery to reopen and thus produce Korotkoff sounds. Alternatively, the oscillometric method relies on the principle of plethysmography, in which the pulsatile pressure changes in the underlying artery are sensed by the inflated cuff. Although practical and noninvasive, the indirect techniques can be inaccurate. Therefore, in cases of sustained hemodynamic instability, noninvasive blood pressure monitoring techniques should be abandoned in favor of invasive methods.

Invasive Methods

Direct blood pressure measurement is performed with an indwelling intra-arterial catheter (18- or 20-gauge) connected to fluid-filled tubing and a pressure-sensing transducer. The zero reference point for the transducer is at the level of the right atrium, which corresponds to the midaxillary line at the fourth intercostal space. The radial artery at the wrist is the most common site for insertion of an intra-arterial catheter. The advantages are that the radial artery is fairly superficial, it is of adequate diameter, and the area is easy to keep clean.The brachial artery should be avoided since thrombosis of it could yield

severe forearm and hand ischemia .

Allen’s test:

Using both hands, compress the patient’s radial and ulnar arteries. Raise the patient's hand over the head and have him clench the fist several times. This should result in a pale, cool hand. Let the patient relax and lower the hand, and then take the pressure off the ulnar artery; the hand should become pink immediately. If it become pink only when the radial artery is released, there in insufficient collateralization from the ulnar artery to permit cannulation of the radial artery.However, it is now generally believed that Allen’s test does not always predict

ischemic complications from radial artery cannulation .

Allen’s test

The most common complication associated with arterial cannulation is thrombosis. Other complications are infection, bleeding, and cerebral embolism. Although exceedingly rare, improper flushing of arterial lines has resulted in embolization of air, thrombi, and liquids to the cerebral circulation. In the case of the radial artery, retrograde flushing can lead to embolization of platelet aggregates or air through the vertebral artery to the brain stem. This can be avoided by employing small-volume, low pressure flushes and evacuating all air from the tubing and transducer assembly.

4 .CENTRAL VENOUS PRESSURE (CVP) MONITORING

The higher the CVP, the more end-diastolic right ventricular pressure will be, which leads to increased stroke volume (Starling's law).The CVP catheter must be placed in the SVC or the right atrium. Either fluid column manometric or electronic transducer systems can be used to measure CVP.In a patient with abnormal coagulation state, or who is profoundly thrombocytopenic, it may be safer to access the SVC by peripheral cutdown and placement of a "long line". Similarly, a patient with hyperinflated lungs or respiratory distress might not tolerate an inadvertent pneumothorax.

How do you place a CVP catheter?

Subclavian catheter The patient is placed in Trendelenburg position with a rolled towel under the interscapular space. The skin in the middle of infraclavicular space is infiltrated with lidocaine toward the suprasternal notch, using a 21-gauge "finder" needle, and maintaining suction. When the subclavian vein is entered, the "finder" needle is removed, a 16-18-gauge "access" needle is inserted to reenter the vein, and a catheter is passed through the "access" needle.

Seldinger technique is easier and safer. With the "finder needle in the vein, a guide wire is passed. Once the needle is removed, the catheter is passed over the wire. After catheter placement, obtain CXR to confirm catheter location and to rule out pneumothorax.

Internal jugular catheter With the patient in Trendelenburg position, infiltrate the skin at the lateral border of SCM muscle, just above the confluence of the sternal and clavicular components of the muscle.Direct the "finder" needle under the muscle toward the ipsilateral hip,

palpating the carotid artery so that not to puncture it .

5 .PULMONARY ARTERY PRESSURE MONITORING

What is a Swan-Ganz catheter?

Swan-Ganz catheter has at least 2 lumens with a 1.5 ml tip balloon. One lumen extends to the end (distal port); the second extends to 20 cm proximal to the end (proximal port). The catheter is in place when the distal port reflects the pulmonary artery pressure (PAP), and the proximal port reflects the right atrial pressure (i.e., CVP). Furthermore, the pulmonary artery wedge pressure (PAWP) is an accurate assessment of the mean left atrial pressure (i.e., left ventricular end-diastolic pressure).

Pulmonary arterial wedge pressure measured with a Swan-Ganz catheterPulmonary arterial wedge pressure measured with a Swan-Ganz catheter . .Because there are no valves between the pulmonary arteries and the left atrium, the pressure obtained Because there are no valves between the pulmonary arteries and the left atrium, the pressure obtained

with occlusion of proximal flow will be the same as the pressure in the left atrium. In the absence of mitral with occlusion of proximal flow will be the same as the pressure in the left atrium. In the absence of mitral valvular disease, left atrial pressure will be the same as left ventricular end-diastolic pressurevalvular disease, left atrial pressure will be the same as left ventricular end-diastolic pressure..

How do you place a Swan-Ganz catheter?

After placement of a 7-French introducer into a central vein, the catheter is passed through it to 20 cm. Then the balloon is inflated (catheter is "floated"). Once the balloon is inflated, feed the catheter so that it can follow blood flow. As the right ventricle (RV) is entered, stop and record pressure. Then, pass the catheter into the pulmonary artery (PA). At this point, a diastolic dicrotic notch is seen with an end-diastolic pressure higher than that seen in the RV. Then, pass the catheter until the systolic-diastolic curve changes into a straight line with rounded peaks associated with breathing (pulmonary artery wedge, or PAW, position).

Order CXR to confirm placement.

Pressure waveforms recorded during advancement of a pulmonary artery catheter through the right Pressure waveforms recorded during advancement of a pulmonary artery catheter through the right atrium (RA), right ventricle (RV), pulmonary artery (PA), and ultimately into the pulmonary artery wedge atrium (RA), right ventricle (RV), pulmonary artery (PA), and ultimately into the pulmonary artery wedge

(PAW) position(PAW) position . .

How is cardiac output (CO) measured and what is an oximetric Swan-Ganz catheter?

A thermodilution CO is measured by injecting a known amount of fluid at a known temperature (e.g., 100 ml at 120 C) into the proximal port of catheter. At the distal tip of catheter, a temperature-sensitive probe reads the change in temperature of the blood passing it. By electronically integrating this temperature-change over time, a computer reports the blood flow across the probe in liters per minute (i.e., CO).The oximetric Swan-Ganz catheter (Oximetrix, Inc.) has a fiberoptic monitor at its tip that continuously measures the

O2 saturation of mixed venous blood ( SvO2) .

Swan-Ganz Oximetery TD catheter (Edwards) enables monitoring of hemodynamic pressures, cardiac output, and continuous mixed venous oxygen saturation .

What is the importance of SvO2?

1. Blood O2 content (cO2) = O2 dissolved in blood + O2 combined with hemoglobin. Thus, cO2 = (0.003 x PO2) + (Hb x 1.38 x SaO2).0.003 x PO2 = only 1% and can be omitted.

2. A-V O2 difference = caO2 - cvO2 = (Hb x 1.38 x SaO2) - (Hb x 1.38 x SvO2) A-V O2 diff = Hb x 1.38 (SaO2 - SvO2)Example: Hb 15 g/100 ml, SaO2 = 96%, SvO2 = 75%A-V O2 diff = 15 x 1.38 (96% - 75%) = 20.7 x 0.21 =4.35 ccO2/100 ml blood, or 4.35 vol %

That is, every 100 ml of blood gives up 4.35 cc of O2.

3 .The Fick-principle: in steady-state situation, the body uses 125 cc of O2 /min/m2. Thus, by measuring the A-V O2 difference, one can determine the contribution of each 100 ml of blood that travel around the body to the total minute O2 consumption (VO2).

Example: in a man with BSA = 2m2, VO2 = 250 cc/min.If A-V O2 difference = 4.35 cc, one can conclude that every 100 ml of blood contributes to 4.35 cc of the VO2.Thus, 250/4.35 dl of blood (= 57.5 dl or 5.75 L) must travel around the body each

minute .

Therefore: CO = Vo2 / A-V o2 diff (dl/min) = Vo2 / [Hb x 1.38 ( Sao2 - Svo2)] 1/CO = [Hb X 1.38 ( Sao2 - Svo2)] / Vo2 Vo2/CO = Hb X 1.38 ( Sao2 - Svo2) Sao2 - Svo2 = Vo2 / (CO X Hb X 1.38)

Svo2 = Sao2 - [ Vo2 / (CO X Hb X 1.38) ] (CO is in dl/min)

A normal Svo2 of 75% indicates a balance between Do2 and Vo2, while a decreased Svo2 suggests a decreased Do2 (owing to decreased Sao2, increase in Vo2 , low CO, or

decreased Hb.

How can you evaluate shock?

1. Hypovolemic shock: CVP, PAP, PAWP, and CO are low; systemic vascular resistance (SVR) is high. SVR (Dynes/sec/cm-5 ) = [mean BP - CVP (mmHg)] X [80/CO (L/min)].

2. Cardiogenic shock: PAWP > 18 mmHg is characteristic of cardiogenic shock. Elevation CVP without elevated PAWP is characteristic of cor-pulmonale, right ventricular infarction, and pericardial tamponade.

3. Septic shock: PAWP is normal or low, CO is elevated, and very low SVR

(< 600 dyne/sec/cm-5).

ACUTE RESPIRATORY FAILUREThe alveolar-capillary surface of the lung is not working efficiently if the PaO2 is < 50 mmHg and PaCO2 is > 50 mmHg. This is the 50:50 rule. Furthermore, the patient who works hard to stay on the correct side of the 50:50 rule may soon run out of energy. What is ARDS?

ARDS is a diffuse capillary transudation of fluid into the lung interstitium that dissociates the normal concordance of alveolar ventilation (V) with lung perfusion (Q).Starling described the balance between hydrostatic pressure (Pc), which tends to push fluid out, and colloid oncotic pressure (COP), which sucks fluid in across

the capillary endothelial barrier (K) .

Thus: Fluid flux = K (Pc-COP)

Heart failure backs up (Pc), forcing fluid into the pulmonary interstitium.Malnutrition and liver failure decrease plasma proteins (i.e., COP), thus fluid is not sucked back out of the lung. Sepsis may break down the (K), thus permitting water and protein to leak into the lung.To make the diagnosis of ARDS, PAWP must be < 18 mmHg. If PAWP is > 18 mmHg, the diagnosis is pulmonary edema.

How can the pulmonary capillaries leak if COP exceeds PAWP?

The current concept invokes a septic expression of neutrophil CD-11 and CD-18 adhesion receptors, which stick to pulmonary vascular endothelial intercellular adhesion molecules (ICAM). Subsequent activation of neutrophils spews out proteases and toxic oxygen radicals, blowing big holes in the vascular lining. Water and plasma albumin leak through the holes.Resultant endovascular damage breaks down the capillary endothelial barrier (K), permitting lung leak-even at low hydrostatic pressure.

Characteristic Chest x-rayCharacteristic Chest x-ray and CT scanand CT scan in a patient with severe ARDS following multiple traumain a patient with severe ARDS following multiple trauma..

MECHANICAL VENTILATION

The goal is to of mechanical ventilation is to improve alveolar ventilation and oxygenation and to reduce the work of breathing.

Critical values in making decision for ventilation are:1. PaO2 < 60 mmHg with FIO2 > 0.6. 2. PaCO2 (acutely) > 50 mmHg with pH < 7.3. 3. Vital capacity < 10 ml/kg.4. Respiratory frequency > 30-40/min.

5. Negative inspiratory pressure < -25 cm H2O .

Spirometry. ERV, expiratory reserve volume; FRC, functional residual capacitySpirometry. ERV, expiratory reserve volume; FRC, functional residual capacity;;IC, inspiratory capacity; RV, residual volumeIC, inspiratory capacity; RV, residual volume ; ;

TLC, total lung capacity; VC, vital capacity; Vt, tidal volumeTLC, total lung capacity; VC, vital capacity; Vt, tidal volume . .

Modes of ventilation

Modes of ventilation can be divided into volume-limited and pressure-limited.The key to understanding the differences between these modes lies in the relationship of pressure (P) to volume (V), i.e. the pulmonary compliance (C), which equals the change in volume divided by the change in pressure (C = ΔV/ΔP). The goal of volume-limited modes is to deliver a set tidal volume at a set rate; air way pressures vary depending on compliance. In contrast, the goal of pressure-limited modes is to deliver a set airway pressure; tidal volume varies

depending on compliance .

1 .Volume-limited modes

Assist/control (A/C) ventilation delivers a preset tidal volume at a set rate. Patient initiates breaths and receives preset volume (assist); otherwise ventilator delivers preset breaths (control). Respiratory alkalosis from hyperventilation may develop in agitated patients.Synchronized intermittent mandatory ventilation (SIMV), like A/C ventilation, delivers a preset tidal volume at a set rate. SIMV differs from A/C, however, as the ventilator does not assist spontaneous respiratory efforts. To prevent "stacking" of mechanical breaths on top of spontaneous breaths, mechanical breaths are triggered by the patient's spontaneous breaths.

2 .Pressure-limited modes

Pressure-support ventilation (PS) delivers a preset inspiratory pressure but at no set rate. The tidal volumes are generated only when the patient is spontaneously breathing. As the inspiratory flow rate slows to 25% of peak flow rate, the ventilator allows exhalation. The disadvantages are that ventilation depends on patient's effort and that sudden increases in airway resistance (coughing, thick secretion, a kink in the ET tube, Valsalva maneuver) decrease the tidal volume.Pressure-control ventilation (PC) delivers a preset inspiratory pressure at a set rate. This mode is used in patients with low compliance to minimize barotrauma. The disadvantages are that tidal volume varies depending on compliance and that sudden increases in airway resistance decrease tidal volume. Therefore, patients must be heavily sedated.

MECHANICAL VENTILATION

Lung volume, airway pressure, and gas flow during commonly used modes of mechanical ventilation.The event that starts the gas flow is ( ) and the

event that stops the gas flow is (O) .The cessation of the gas flow is shown by the dotted

lines separating inspiration from expiration .Time and negative pressure (- P) may be responsible

for cycling or limiting gas flow.

SIMV = Synchronized Intermittent Mandatory Ventilation.

PSV = Pressure Support.PCV = Pressure Control Ventilation

Ventilation management

1. Choice of mode by considering advantages and disadvantages of each mode.

2. FIO2 should be adjusted to ensure SaO2 of 92%. The lowest FIO2 (≤ 0.40) is used to prevent pulmonary oxygen toxicity.

3. Tidal volumes should be significantly larger (7-12 ml/kg) than those of nonventilated individuals (4-7 ml/kg) for two reasons. First, the anatomic dead space is larger and, second, to ensure higher airway pressures to prevent atelactasis. However, in ARDS, low tidal volumes (6 mL/kg), to maintain plateau pressures at less than 30 cm H2O to minimize barotrauma but greater than 20 cm H2O to

minimize atelectasis, are associated with improved survival.

4. Ventilatory rate is chosen (typically 8-16/min) to provide adequate minute ventilation and optimal pH and PaCO2.

5. The normal inspiratory to expiratory ratio (I/E) is 1/2-1/3.Inverse ratio is used with severe, consolidating lung disease.

6. Positive end-expiratory pressure (PEEP) improves ventilation-perfusion matching by opening terminal airways and recruiting partially collapsed alveoli.5 cm H2O PEEP is considered physiologic. PEEP > 15 cm H2O increase the risk of barotrauma and pneumothorax.PEEP increases intrathoracic pressure and decreases CO. PEEP applied to the spontaneously ventilating patient without inspiratory

ventilatory support is called continuous positive airway pressure (CPAP).

7 .Sedation is often necessary to control anxiety, allow patient to rest, and synchronize breathing of the patient with the ventilator. Paralysis rarely is necessary but is useful in severe respiratory failure as it increases pulmonary compliance by decreasing the elastic recoil of the chest wall.

8. Prone positioning is one of several techniques that may have benefit in patients with severe ARDS. Patients are placed in a prone position for a scheduled period of time on a daily basis; theoretical benefits include recruitment of dorsal lung units, improved mechanics, decreased ventilation-perfusion mismatch, and increased secretion

drainage .

Weaning from Mechanical Ventilation

In general, hemodynamic instability or high work of breathing (e.g., minute ventilation >15 L/minute) are contraindications to weaning. Reduction of the FIO2 to 0.4 or less and of PEEP to 5 cm H2O or less is accomplished first.

To consider weaning from the ventilator, it is important to first ensure that the underlying problem leading to intubation has been rectified and the patient is hemodynamically stable.Then, one may make the "SOAP" assessment: (1) Are the Secretions too much for the patient to handle? (2) Is the patient Oxygenating adequately? (3) Can the patient protect his Airway?

(4) Is Pulmonary function adequate while breathing spontaneously?

Ideally, the patient is assessed while breathing spontaneously, and a number of parameters may be obtained to evaluate pulmonary function. Negative inspiratory force > - 25 cm H2O, minute ventilation < 10-15 L/min, tidal volume (Vt) > 5mL/kg and respiratory frequency (f) < 30/min are useful indicators. Perhaps the most reliable single test is the f/Vt ratio, or the “rapid shallow breathing index”. A value > 105 predicts failure of extubation with a 95% likelihood, whereas a value

< 80 predicts success in 95%.

Weaning parameters are:1. PaO2 > 60 mmHg (with FIO2 < 0.4 and PEEP < 8 cm H2O). 2. PaCO2 acceptable with normal pH.3. Tidal volume > 5 ml/kg. 4. Minute ventilation < 10-15 L/min. 5. Respiratory frequency < 30/min. 6. Negative inspiratory pressure > -25 cm H2O.

How should a hypoxic event be managed?

The first priority is to disconnect the ventilator and switch to bag ventilation using 100% oxygen. Increased airway pressures may indicate obstruction of the tube with secretions or a kink in the tube, bronchospasm, pneumothorax, or migration of the ET tube into a main-stem bronchus. Check the ET tube for patency and suction; if there is a partial obstruction, use large-volume saline lavage to clear the tube. If the obstruction is complete, change the ET tube. Listen closely for any change in breath sounds consistent with a pneumothorax, new lung consolidation, or pleural collection. A less common cause is pulmonary embolism. Check the ventilator's function and, if normal, return the patient to the ventilator, making any needed changes to ensure adequate ventilation and oxygenation. The results of an ABG and a chest x-ray are frequently helpful.

ACUTE CARDIAC DYSRHYTMIA1. Patient Is Hemodynamically Unstable

All patients who have ventricular fibrillation (VF) or pulseless ventricular tachycardia (pulseless VT) should be treated immediately by cardioversion.Cardioversion delivers sufficient electrical energy to the precordium to depolarize cells. In theory, after this massive depolarization, all the myocardial cells will repolarize simultaneously and then reinstitute a synchronous beat. The first cardioversion should be with 200 joules. If it fails, the second should be with 200-300 joules, and the third with 360 joules. If the first three attempts fail, epinephrine (1 mg IV) is administered and cardioversion with 360 joules is

attempted.

Epinephrine augments aortic diastolic blood pressure and increases heart perfusion, principally because of its alpha-receptor activity. The dose is 1 mg/3-5 min IV; it may be necessary to administer escalating doses (1, 3, and 5 mg) 3 minutes apart, continued at 5 mg/3-5 minutes thereafter.If peripheral line is used to administer epinephrine, the medication is followed by 50 ml IV fluid. If ET tube is used, 2-2.5 times the IV dose is administered by diluting in 10 ml saline and spraying down the tube, followed by quick insufflations to aerosolize the medication. If VF is resistant to cardioversion and epinephrine, lidocaine (1.5 mg/kg) is used and can be repeated once. After successful conversion to sinus rhythm, the myocardium remains electrically unstable; therefore, lidocaine infusion

(3 mg/min) is initiated.

Asystole often signals the end of the resuscitation effort. Whenever a flat-line or low-amplitude electrocardiogram is recorded, it is important to confirm the absence of pulses, to check for technical failures (low battery or disconnected monitor leads), and to rotate the monitoring leads 900. VF may masquerade as asystole, especially if the VF amplitude is low (fine VF), or if the polarity of the fibrillatory waves is at right angles to the monitoring lead. Epinephrine is given in escalating doses. Atropine can be used to a maximum of 3 mg. Cardioversion should be attempted only if the rhythm is unclear or if it

appears to be fine VF .

Pulseless electrical activity (PEA), or electro-mechanical dissociation (EMD), is almost fatal unless the underlying etiology can be treated. Keep in mind the potentially correctable causes that commonly cause PEA: tension pneumothorax and pericardial tamponade. PEA is also associated with hypovolemia, ventricular rupture (traumatic or secondary to MI), PE, and massive MI.The only hope in refractory PEA is to restore coronary perfusion; therefore,

epinephrine is given in escalating doses.

2 .Patient Is Hemodynamically Stable

Ventricular rate is slow

If the patient is bradycardic, 0.5 mg atropine is administeredI.V. This dose may be repeated at 2-minute intervals. Because the effects of atropine are transient, a temporary internal or external pacemaker should be used to maintain the heart rate. Insertion of an internal pacemaker consistently takes longer than predicted; an

external pacemaker is a very effective temporizing maneuver .

Ventricular rate is fast

When an impulse originates above the AV node, it can access the ventricles only through the AV node. The AV node connects with the Purkinje system, which conducts impulses rapidly (2 to 3 m/sec). A supraventricular impulse activates the ventricles rapidly (< 0.08 second, or two little boxes on the ECG paper), producing a narrow-complex beat. An ectopic ventricular impulse cannot access the Purkinje fibers rapidly; ventricular activation is therefore delayed and the QRS complex is wider.

The cardiac depolarization route. AVN: atrioventricular node; SAN: sinoatrial node.

Because the QRS complex in supraventricular tachycardia (SVT) is narrow, the width of the QRS can be used to distinguish SVT from ventricular tachycardia (VT). The ECG-signs of VT are heart rate > 90/min, wide QRS complex (> 0.14 second), and absence of P waves (or atrioventricular dissociation). When the ventricular rate is fast and the QRS is narrow, the 12-lead ECG should be searched for P waves. If P waves are absent and the QRS complexes occur at

irregular intervals, the patient probably has atrial fibrillation .

This tracing depicts frequent ventricular ectopic depolarizationsThis tracing depicts frequent ventricular ectopic depolarizations interspersed among depolarizations from a supraventricular sourceinterspersed among depolarizations from a supraventricular source . .

Note that the QRS depolarizations of supraventricular origin are narrowNote that the QRS depolarizations of supraventricular origin are narrow , ,whereas the QRS complexes of ectopic ventricular origin are widewhereas the QRS complexes of ectopic ventricular origin are wide..

In a wide-complex tachycardia, QRS complex is > 0.08 second and occupiesIn a wide-complex tachycardia, QRS complex is > 0.08 second and occupies > >two small boxes on the ECG papertwo small boxes on the ECG paper..

In a narrow-complex tachycardia, QRS complex is < 0.08 second and occupiesIn a narrow-complex tachycardia, QRS complex is < 0.08 second and occupies < <two small boxes on the ECG papertwo small boxes on the ECG paper..

A patient with a wide-complex tachycardia is treated by cardioversion, commonly followed by lidocaine infusion, whereas a patient with a narrow-complex tachycardia is treated with a calcium chammel blocker (verapamil or diltiazem) to retard impulse conduction through the AV node. For verapamil, 10 mg is mixed into 10 ml of saline, and 1 mg/min is given until the ventricular rate slows. For diltiazem, 15-20 mg is given over 2 minutes; the dose can be repeated in 15 minutes at 20-25 mg over 2 minutes. Because of its rapid onset and short duration of action, adenosine can be used diagnostically. If it is uncertain whether the tachycardia is supraventricular or ventricular, 6 mg adenosine I.V. is given, and repeated if necessary. If the tachycardia breaks, it was supraventricular. If it does not break, it was ventricular.