Handbook of Clinical Anesthesia

Chapter 59

Cardiopulmonary Resuscitation

The cardiopulmonary physiology, and pharmacology that form the basis of anesthesia practice are applicable to treating the victims of cardiac arrest (Otto CW: Cardiopulmonary resuscitation. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1532–1558).

  1. History

(Table 59-1)

  1. Scope of the Problem
  2. Cardiopulmonary resuscitation (CPR) is systematic therapy that is aimed at sustaining vital organ function until natural cardiac function can be restored.
  3. In clinical practice, the severity of underlying cardiac disease is the major determining factor in the success or failure of CPR.
  4. Brain adenosine triphosphate is depleted in 4 to 6 minutes of no blood flow. It returns nearly to normal within 6 minutes of starting effective CPR.
  5. Factors associated with poor outcomes are long arrest time before CPR is begun, prolonged ventricular fibrillation without definitive therapy, and inadequate coronary and cerebral perfusion during cardiac massage.
  6. Optimum outcome from ventricular fibrillation is obtained only if basic life support is begun within 4 minutes of arrest and defibrillation is applied within 8 minutes.
  7. Blood flow decreases rapidly with interruptions of chest compressions (checking the pulse, intubation, defibrillation attempts, starting intravenous [IV] lines) and resumes slowly with reinstitution of compressions,

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emphasizing the importance of continued chest compressions in overall outcome.

Table 59-1 History of Cardiopulmonary Resuscitation

Bible story of Elisha breathing life back into the son of a Shunammite woman
Andreas Versalius described tracheostomy and artificial ventilation in 1543
Teaching of resuscitation by the Society for the Recovery of Persons Apparently Drowned founded in London in 1774
Establishment of mouth-to-mouth ventilation as the only effective means of artificial ventilation in the 1950s by Elam, Safar, and Gordon
Successful use of the internal defibrillator in 1947
External defibrillation introduced in the late 1950s
Description by Kouwenhoven, Jude, and Knickerbocker of closed chest compression
Description by Redding and Pearson of the value of epinephrine

III. Ethical Issues: “Do not Resuscitate” Orders in the Operating Room

  1. The patient's right to limit medical treatment, including refusing CPR (with a “do not resuscitate” order) is firmly established in modern medical practice based on the ethical principle of respect for patient autonomy.
  2. There are ethically sound arguments on both sides of the issue of whether DNR orders should be upheld in the operating room.
  3. A desire by the anesthesiologist or surgeon to suspend DNR orders during surgery is often based on the knowledge that nearly 75% of cardiac arrests in the operating room are related to surgical or anesthetic complications and that resuscitation attempts are highly successful.
  4. A mutual decision to suspend or limit a DNR order in the perioperative period may be achieved by communication among the patient, family, and caregivers.
  5. Many interventions used commonly in the operating room (mechanical ventilation, vasopressors, cardiac antidysrhythmics, blood products) may be considered forms of resuscitation in other situations. The only modalities that are not routine anesthetic care are cardiac massage and defibrillation.

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  1. Specific interventions included in a DNR status must be clarified with allowance made for methods necessary to perform anesthesia and surgery.
  2. Components of Resuscitation

The major components of resuscitation from cardiac arrest are airway, breathing, circulation, drugs, and electrical therapy (ABCDE). Traditionally, these have been divided into basic life support (BLS) and advanced cardiac life support (ACLS) (Fig. 59-1). Recent advances in resuscitation (public access to automatic external defibrillators [AEDs]) have tended to blur the lines between BLS and ACLS.

  1. Airway Management.The techniques used for airway maintenance during anesthesia are also applicable to cardiac arrest victims (Table 59-2).
  2. Foreign body airway obstructionmust be considered in any person who suddenly stops breathing and becomes cyanotic and unconscious. (This occurs most commonly during eating and is usually caused by food, especially meat, impacting in the laryngeal inlet, at the epiglottis, or in the vallecula.)
  3. The signs of total airway obstruction are the lack of air movement despite respiratory efforts and the inability of the victim to speak or cough.
  4. Treatment is the abdominal thrust maneuver (chest thrusts are an alternative for parturients and massively obese individuals) and the finger sweep.
  5. In an awake victim, the rescuer reaches around the victim from behind, placing the fist of one hand in the epigastrium between the xiphoid and umbilicus. The fist is grasped with the other hand and pressed into the victim's epigastrium with a quick upward thrust. If the first attempt is unsuccessful, repeated attempts should be made because hypoxia-related muscular relaxation may eventually allow success.
  6. Ventilation(see Fig. 59-1). When ventilation is provided in the rescue setting, mouth-to-mouth or mouth-to-nose ventilation is the most effective immediately available method. Although inspired gas with this method contains only about 17% oxygen and nearly 4% carbon dioxide (composition of exhaled air), it is sufficient to maintain viability.

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Figure 59-1. Adult basic life support (BLS) provider algorithm. ACLS = advanced cardiac life support; AED = automatic external defibrillator; CPR = cardiopulmonary resuscitation.

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Table 59-2 Techniques Used for Airway Maintenance During Cardiopulmonary Resuscitation

Head tilt and chin lift (the head is extended by pressure applied to the brow while the mandible is pulled forward by pressure on the front of the jaw, lifting the tongue away from the posterior pharynx)
Jaw thrust (applying pressure behind the rami of the mandible)
Oropharyngeal or nasopharyngeal airway (danger of inducing vomiting or laryngospasm in a semiconscious victim)
Tracheal intubation (should not be performed until adequate ventilation and chest compression have been established)
Alternatives to tracheal intubation
   Laryngotracheal mask airway
   Airway Combitube
   Translaryngeal ventilation
   Tracheostomy

  1. Physiology of Ventilation During Cardiopulmonary Resuscitation
  2. Avoiding gastric insufflation requires that peak inspiratory airway pressures remain below esophageal opening pressure (~20 cm H2O). Partial airway obstruction by the tongue and pharyngeal tissues is a major cause of increased airway pressure contributing to gastric insufflation during CPR. Properly applied pressure to the anterior arch of the cricoid (Sellick maneuver) causes the cricoid lamina to seal the esophagus and can prevent air from entering the stomach at airway pressures up to 100 cm H2O.
  3. Achievement of an acceptable tidal volume during low inspiratory pressures characteristic of rescue breathing requires a slow inspiratory flow rate and long inspiratory time (breaths over 1.5–2.0 seconds during a pause in chest compressions).
  4. Techniques of Rescue Breathing(Table 59-3)
  5. Circulation
  6. Physiology of Circulation During Closed Chest Compression.Two theories of the mechanism of blood flow during closed chest compression have

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been suggested. The mechanism that predominates varies from victim to victim and even during the resuscitation of the same victim.

Table 59-3 Techniques of Rescue Breathing

Mouth-to-mouth ventilation (the rescuer delivers exhaled air to victim, and exhalation by the victim is passive)
Mouth-to-nose ventilation
Oropharyngeal airway with an external extension mouthpiece (it is often difficult to obtain a good mouth seal)
Mouth-to-mask ventilation (the mask may include one-way valve to direct the victim's exhaled gases away from the rescuer and a side port for delivery of supplemental oxygen)
Self-inflating resuscitation bag
Tracheal intubation (after placement of the tracheal tube, no pause should be made for ventilation because blood flow during CPR decreases rapidly when chest compressions are stopped)

CPR = cardiopulmonary resuscitation.

  1. The cardiac pump mechanismproposes that pressure on the chest compresses the heart between the sternum and spine. Compressions increase the pressure in the ventricular chambers (closing the atrioventricular valves) and eject blood into the lungs and aorta. During the relaxation phase of closed chest compression, expansion of the thoracic cage causes a subatmospheric intrathoracic pressure, facilitating blood return.
  2. The thoracic pump mechanismproposes that the increase in intrathoracic pressure caused by sternal compressions forces blood out of the chest (backward flow into veins is prevented by valves) with the heart acting as a passive conduit.
  3. Distribution of Blood Flow During Cardiopulmonary Resuscitation.Cardiac output is decreased between 10% to 33% of normal during CPR, and nearly all the blood flow is directed to organs above the diaphragm (abdominal viscera and lower extremity blood flow are decreased to <5% of normal).
  4. Myocardial perfusion is 20% to 50% of normal, and cerebral perfusion is maintained at 50% to 90% of normal.
  5. Total flow tends to decrease with time during CPR, but the relative distribution is not altered.

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Epinephrine may help sustain cardiac output over time during CPR.

  1. Gas Transport During Cardiopulmonary Resuscitation
  2. During the low-flow state of CPR, excretion of carbon dioxide is decreased to the same extent that cardiac output is reduced.
  3. Exhaled carbon dioxide concentrations reflect only the metabolism of the part of the body that is being perfused.
  4. When normal circulation is restored, carbon dioxide that has accumulated in nonperfused tissues is washed out, and a temporary increase in carbon dioxide excretion is seen.
  5. Although carbon dioxide excretion is decreased during CPR, measurement of blood gases reveals an arterial respiratory alkalosis and a venous respiratory acidosis, reflecting the severely reduced cardiac output.
  6. Technique of Closed Chest Compression
  7. Some circulation may be present in a “pulseless” patient (systolic blood pressure of about 50 mm Hg is necessary to palpate a peripheral pulse) with primary respiratory arrest. In such a patient, opening the airway and ventilation of the lungs may be sufficient for resuscitation. For this reason, a further search for a pulse should be made after artificial ventilation before beginning sternal compressions.
  8. Important considerations in performing closed chest compressions are the position of the rescuer relative to the victim, the position of the rescuer's hands, and the rate and force of compression (Table 59-4).
  9. Alternative Methods of Circulatory Support.Standard CPR can sustain most patients for only 15 to 30 minutes. If return of spontaneous circulation has not been achieved in that time, the outcome is dismal.
  10. Alternatives to standard techniques for CPR are based on the thoracic pump mechanism with the goal of improving hemodynamics. Unfortunately, none of these alternatives has proven reliably superior to the standard technique.
  11. Invasive Techniques.Open chest cardiac massage or cardiopulmonary bypass must be instituted

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early to improve survival. If open chest massage is begun after 30 minutes of ineffective closed chest compressions, there is no better survival even though hemodynamics are improved.

Table 59-4 Techniques of Closed Chest Compression

The rescuer should stand or kneel next to the victim's side.
The heel of one hand is placed on the lower sternum, and the other hand is placed on top of the hand on the victim. Pressing on the xiphoid, which can lead to liver laceration, should be avoided. Even with proper technique, costochondral separation and rib fractures are common.
Pressure is applied only with the heel of the hand (with the fingers free of contact with the chest) straight down on the sternum with the arms straight and the elbows locked into position so the entire weight of the upper body is used to apply force.
During relaxation, all pressure is removed, but the hands should not lose contact with the chest wall.
The sternum must be depressed 3.5 to 5.0 cm in the average adult (palpable pulse when systolic pressure >50 mm Hg).
The duration of compression should equal that of relaxation.
The compression rate should be 80 to 100/min.

  1. Assessing the Adequacy of Circulation During Cardiopulmonary Resuscitation(Table 59-5).
  2. The adequacy of closed chest compressions is usually judged by palpation of a pulse in the carotid or femoral artery (palpable pulse primarily reflects systolic blood pressure).
  3. The return of spontaneous circulation is greatly dependent on restoring oxygenated blood flow to the myocardium. Obtaining such flow depends on closed chest compressions developing adequate cardiac output and coronary perfusion

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pressure (diastolic blood pressure minus central venous pressure). Damage to the myocardium from underlying disease may preclude survival no matter how effective the CPR efforts.

Table 59-5 Critical Variables Associated with Successful Resuscitation

Myocardial blood flow

>15–20 mL/min/100 g

Aortic diastolic pressure

>40 mm Hg

Coronary perfusion pressure

>15–25 mm Hg

End-tidal carbon dioxide

>10 mm Hg

  1. During CPR with a tracheal tube in place, exhalation of carbon dioxide is dependent on pulmonary blood flow (cardiac output) rather than alveolar ventilation. End-tidal carbon dioxide concentrations can be used to judge the effectiveness of chest compressions. Attempts should be made to maximize the end-tidal carbon dioxide concentration by alterations in technique or drug therapy (epinephrine). It should be remembered that sodium bicarbonate produces a transient (3–5 minutes) increase in end-tidal carbon dioxide concentration.
  2. Pharmacologic Therapy (Table 59-6)

Establishing IV access and pharmacologic therapy should come after other interventions have been instituted. Of the drugs given during CPR, only epinephrine is acknowledged as being useful in helping restore spontaneous circulation. Asystole and pulseless electrical

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activity (electromechanical dissociation) are circumstances in which drugs are most frequently given.

Table 59-6 Adult Advanced Cardiac Life Support Drugs and Doses

 

Dose (IV)

Dosing Interval

Maximum Dose

Epinephrine

1 mg

3–5 min

None

3–7 mg*

3–5 min

Vasopressin

40 U

May replace first or second dose of epinephrine

Amiodarone

300 mg

Repeat 150 mg in 5 min

2 g

Lidocaine

1.0–1.5 mg/kg

Repeat 0.5–0.75 mg/kg in 5 min

3 mg/kg

Atropine

1 mg

3–5 min

0.04 mg/kg

Sodium bicarbonate

1 mEq/kg

As needed

Check pH

*Consider if there is no response to lower doses of epinephrine.

  1. Routes of Administration
  2. The preferred route of administration of all drugs during CPR is IV. (Central injection produces a higher drug level and more rapid onset than peripheral injection.) Because of poor blood flow below the diaphragm during CPR, drugs administered into the lower extremity may not reach sites of action.
  3. If venous access cannot be established, the endotracheal tube is an alternative route of administration for epinephrine, lidocaine, and atropine (not sodium bicarbonate). Doses 2 to 2.5 times the established IV dose administered in 5- to 10-mL volumes are recommended when the tracheal route of administration is used.
  4. Catecholamines and Vasopressors
  5. Mechanism of Action.The efficacy of epinephrine lies entirely in its α-adrenergic actions. (Peripheral vasoconstriction leads to an increase in aortic diastolic pressure, causing an increase in coronary perfusion pressure and myocardial blood flow.)
  6. It is commonly believed that the ability of epinephrine to increase the amplitude of ventricular fibrillation (α-adrenergic effect) makes defibrillation easier. There is no proof, however, that epinephrine improves the success or decreases the energy necessary for successful defibrillation.
  7. When added to chest compressions, epinephrine helps develop the critical coronary perfusion pressure necessary to provide myocardial blood flow for restoration of spontaneous circulation.
  8. Epinephrineis given 1 mg IV every 3 to 5 minutes in adults. If this dose remains ineffective, higher doses (3–7 mg IV) should be considered.
  9. Vasopressinis recommended as an alternative to epinephrine in a dose of 40 U IV as a one-time injection. If additional vasopressor doses are need, epinephrine should be administered.
  10. Amiodarone and Lidocaine
  11. These drugs are used during cardiac arrest to aid in defibrillation when ventricular fibrillation is refractory to electrical countershock or when ventricular fibrillation recurs. Amiodarone may be considered

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the first drug for treatment of ventricular fibrillation that is resistant to electrical countershock.

  1. Lidocaine has few hemodynamic effects when given IV.
  2. Amiodarone can cause hypotension and tachycardia, especially with rapid IV administration.
  3. Ventricular fibrillation threshold is decreased by acute myocardial ischemia or infarction, and this effect is partially reversed by lidocaine and amiodarone.
  4. To rapidly achieve and maintain therapeutic blood levels during CPR, relatively large doses of lidocaine or amiodarone are necessary (see Table 59-6).
  5. Atropine
  6. Atropine (1 mg IV repeated every 3 to 5 minutes to a total dose of 0.04 mg/kg, which is totally vagolytic) is commonly administered during cardiac arrest associated with a pattern of asystole or slow, pulseless electrical activity on the electrocardiogram (ECG). Atropine enhances sinus node automaticity and atrioventricular conduction via its vagolytic effects.
  7. Excessive parasympathetic tone probably contributes little to asystole or pulseless electrical activity in adults (most often caused by myocardial ischemia).
  8. Even in children, it is doubtful that parasympathetic tone plays a significant role during most cardiac arrests.
  9. Full vagolytic doses of atropine may be associated with fixed mydriasis after successful resuscitation confounding neurologic evaluation.
  10. Sodium Bicarbonate
  11. The use of sodium bicarbonate during CPR is based on theoretical considerations that acidosis lowers ventricular fibrillation threshold and respiratory acidosis impairs the physiologic response to catecholamines.
  12. Little to no evidence supports the efficacy of sodium bicarbonate treatment during CPR. The lack of effect of buffer therapy may be explained by the slow onset of metabolic acidosis during cardiac arrest. (Acidosis as measured by blood lactate concentrations does not become severe for 15–20 minutes of cardiac arrest.)

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  1. In contrast to the lack of evidence that buffer therapy during CPR improves survival, the adverse effects of excessive sodium bicarbonate administration are well documented and include metabolic alkalosis, hypernatremia, and hyperosmolarity.
  2. IV sodium bicarbonate combines with hydrogen ions to produce carbonic acid that dissociates into carbon dioxide and water. (PaCO2is temporarily increased until ventilation eliminates the excess carbon dioxide.)
  3. Tissue acidosis during CPR is caused primarily by low tissue blood flow and accumulation of carbon dioxide in the tissues. (Theoretically, there is concern that carbon dioxide liberated from sodium bicarbonate could worsen existing tissue acidosis.)
  4. Current practice restricts the use of sodium bicarbonate (1 mEq/kg IV initially with additional doses of 0.5 mEq/kg every 10 minutes [better if guided by blood gas determinations]) primarily to cardiac arrests that are associated with hyperkalemia, severe pre-existing metabolic acidosis, and tricyclic antidepressant overdose.
  5. Calcium
  6. The only indications for administration of calcium during CPR are hyperkalemia, hypocalcemia, or calcium blocker toxicity.
  7. When calcium is administered, the chloride salt (2–4 mg/kg of the 10% solution IV) is recommended because it produces higher and more consistent levels of ionized calcium than other salts. (Calcium gluconate contains one third as much molecular calcium as the chloride salt.)
  8. Electrical Therapy (see Fig. 59-1)
  9. Electrical Pattern and Duration of Ventricular Fibrillation.Ventricular fibrillation is the most common ECG pattern found during cardiac arrest in adults, and the only effective treatment is electrical defibrillation. Defibrillation should be performed as soon as the ventricular fibrillation is diagnosed and equipment is available. Immediate defibrillation is only effective when applied within 4 to 5 minutes of collapse. Otherwise, a brief period of 2 to 3 minutes of chest compressions before defibrillation is necessary.

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  1. The most important controllable determinant of failure to resuscitate a patient with ventricular fibrillation is the duration of fibrillation. (The fibrillating heart has a high oxygen consumption.)
  2. If defibrillation occurs within 1 minute of fibrillation, CPR is not necessary.
  3. Defibrillation should not be delayed for epinephrine administration. (There is no evidence that epinephrine improves the success of defibrillation or decreases the energy setting needed for defibrillation.)
  4. Fibrillation amplitude on an ECG lead varies with the orientation of that lead to the vector of the fibrillatory wave. (A flat line can be present if lead is oriented at right angles to the fibrillatory wave.)
  5. A nonfibrillatory rhythm will not respond to defibrillation.
  6. Defibrillators: Energy, Current, and Voltage
  7. The typical defibrillator consists of a variable transformer that allows selection of a variable voltage potential, an AC to DC converter to provide a direct current that is stored in a capacitor, a switch to charge the capacitor, and discharge switches to complete the circuit from the capacitor to the paddle electrodes.
  8. Defibrillation is accomplished by direct current passing through a critical mass of myocardium, resulting in simultaneous depolarization of the myofibrils.
  9. Even at a constant delivered energy, the delivered current (critical determinant of defibrillation) is decreased as impedance (resistance) increases.
  10. Transthoracic Impedance(Table 59-7)

Table 59-7 Determinants of Transthoracic Impedance

Diameter of electrode paddles (most common diameter, 8–10 cm)
Impedance between metal electrode and skin (decreased with gel designed to conduct electricity in the defibrillation setting)
Successive shocks (may decrease impedance and partially explain why an additional shock of the same energy can cause defibrillation when previous shocks have failed)
Lung volume (air is a poor electrical conductor, so impedance is slightly higher during inspiration)
Paddle pressure (pressure of at least 11 kg decreases resistance by improving contact between the paddle and the skin and by expelling air from the lungs)

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  1. Adverse Effects and Energy Requirements
  2. Repeated defibrillation with high-energy shocks, especially if repeated at short intervals, may result in myocardial damage.
  3. Current recommendations for adults are to use 200 J for the initial shock followed by a second shock at 200 to 300 J if the first is unsuccessful. If both fail to defibrillate the patient's heart, additional shocks should be given at 300 to 360 J.

VII. Putting it All Together

Specific guidelines for the teaching and practice of CPR are published periodically (Figs. 59-1 and 59-2). The two levels of CPR care are referred to as BLS for ventilation and chest compressions without additional equipment and ACLS for using all modalities available for resuscitation. Medical personnel need to be well versed in both levels of care.

  1. Cardiocerebral Resuscitation.An approach to victims of sudden cardiac death has been called cardiocerebral resuscitation or minimally interrupted cardiac resuscitation.
  2. Time-Sensitive Model of Ventricular Fibrillation.Untreated ventricular fibrillation has been described as a time-sensitive model consisting of the electrical (first 4–5 minutes), hemodynamic (next 10–15 minutes when perfusing the brain and heart with oxygenated blood is critical), and metabolic (not clear what intervention will be successful) phases.
  3. Prompt defibrillation during the electrical phaseis when CPR has had the most dramatic effect and why public access AED has proven beneficial. The longer ventricular fibrillation continues, the more difficult it is to defibrillate and the less likely successful resuscitation is.
  4. If an arrest is witnessed and a defibrillator or AED is immediately available, then defibrillation should be the first priority in resuscitation.
  5. The most important intervention during the hemodynamic phaseof cardiac arrest is producing coronary perfusion with chest compressions before any attempt to defibrillate.
  6. In the absence of prompt defibrillation, the most important intervention for neurologically normal survival from cardiac arrest is restoration and

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maintenance of cerebral and myocardial blood flow. This is the main principle behind the concept of cardiocerebral resuscitation.

 

Figure 59-2. Adult advanced cardiac life support pulseless arrest algorithm. AED = automatic external defibrillator; CPR = cardiopulmonary resuscitation; IV = intravenous; PEA = pulseless electrical activity; VF = ventricular fibrillation; VT = ventricular tachycardia.

  1. Bystander Cardiopulmonary Resuscitation.Restoration of cerebral and myocardial blood flow must begin at the scene of the cardiac arrest. Much of the reluctance

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to initiate CPR as a bystander is the concern of applying mouth-to-mouth ventilation on a stranger.

  1. If the airway remains patent during CPR, chest compressions cause substantial air exchange. Some data suggest that eliminating mouth-to-mouth ventilation early in the resuscitation of witnessed fibrillatory cardiac arrest is not detrimental to outcome and may improve survival.
  2. Recognizing the deleterious effects of prolonged pauses in chest compressions for ventilation, the 2005 American Heart Association's guidelines change the compression-to-ventilation ratio from 15:2 to 30:2, recommending that ventilation be done in 2 to 4 seconds.
  3. A public education program stresses an immediate call to 911 and prompt institution of continuous chest compressions without ventilation in the case of witnessed unexpected sudden collapse in adults.
  4. Cardiocerebral Resuscitation During Advanced Life Support
  5. The principle of not interrupting chest compressions to maintain cerebral and myocardial perfusion applies to resuscitation attempts by health care providers as well as lay bystanders.
  6. The adverse hemodynamic consequences of interrupting chest compressions have been well documented. Blood flow stops almost immediately with cessation of chest compressions and returns slowly when they are resumed. Consequently, in cardiocerebral resuscitation, the emphasis is that chest compressions are to be paused only when absolutely necessary and then for the shortest time possible.
  7. Positive pressure ventilation increases intrathoracic pressure, reducing venous return, cardiac output, and coronary perfusion pressure and adversely affecting survival.
  8. Rhythm Analysis and Defibrillation
  9. Defibrillation during the hemodynamic phase is counterproductive, usually producing either asystole or pulseless electrical activity.
  10. The success rate of a single shock is between 70% and 85%, with most monophasic waveform defibrillators and more than 90% with the newer biphasic waveform units.

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  1. In prolonged ventricular fibrillation, successful defibrillation almost always results in asystole or pulseless electrical activity. Immediately restarting chest compressions (without waiting to check a pulse or reanalyze the ECG rhythm) after defibrillation to provide coronary perfusion nearly always results in reversion to a perfusing rhythm.

VIII. Pediatric Cardiopulmonary Resuscitation

  1. The basic approach to pediatric cardiac arrest victims is the same as in adults (see Fig. 59-1).
  2. Cardiac arrest is less likely to be a sudden event and more likely related to progressive deterioration of ventilation and cardiac function in the pediatric age group.
  3. Effective ventilation of the lungs is critical because ventilatory problems are frequently the cause of cardiac arrest in this age group.
  4. Cardiac compression in infants is provided with two fingers on the midsternum or by encircling the chest with the hands and using the thumbs to provide compression.
  5. Defibrillation is less frequently necessary in children, but the same principles apply as in adults. (The recommended starting energy is 2 J/kg, which is doubled if defibrillation is unsuccessful.)
  6. Drug therapy is similar to that in adults but plays a larger role because electrical therapy is less often needed.
  7. Postresuscitation Care
  8. The major factors contributing to mortality after successful resuscitation are progression of the primary disease and cerebral damage experienced as a result of the cardiac arrest. Furthermore, even brief cardiac arrest causes generalized decreases in myocardial function (global myocardial stunning) and may require treatment with inotropic drugs.
  9. When cerebral blood flow is restored after a period of global cerebral ischemia, there are initially multifocal areas of the brain with no reflow (this may reflect the effects of epinephrine administered during CPR)

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followed within 1 hour by global hyperemia, which is followed quickly by global hypoperfusion.

  1. Support after resuscitation is focused on providing stable oxygenation (PaO2>100 mm Hg), ventilation (PaCO2 25–35 mm Hg), neuromuscular blockers to prevent coughing or restlessness, and optimal hemodynamics (hematocrit, 30%–35%).
  2. A brief (5 min) period of hypertension (mean arterial pressure, 120–140 mm Hg) may help overcome the initial cerebral no reflow.
  3. Hyperglycemia during cerebral ischemia results in increased neurologic damage. Although it is unknown if hyperglycemia in the postresuscitation period influences outcome, it seems prudent to maintain the blood glucose level between 100 and 250 mg/dL.
  4. Increased intracranial pressure (ICP) is unusual after resuscitation from cardiac arrest. (Ischemic injury may lead to cerebral edema and increased ICP in the ensuing days.)
  5. In contrast to general supportive care, specific pharmacologic therapy directed at brain preservation has not been shown to have further benefit.
  6. Most severely damaged victims die of multisystem organ failure within 1 to 2 weeks.
  7. It is recommended that unconscious patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32° to 34°C for 12 to 24 hours when the initial rhythm was ventricular fibrillation. Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest.
  8. Prognosis.Most patients who completely recover show rapid improvement in the first 48 hours.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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