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Cardiac arrest is the terminal event in any fatal disorder. It also may occur suddenly (defined as within 24 h of onset of symptoms in a previously functioning person), and as such occurs outside the hospital in about 400,000 people/yr in the US, with a 90% mortality.
Etiology
In adults, sudden cardiac arrest results primarily from cardiac disease (of all types, but especially coronary artery disease). In a significant percentage, sudden cardiac arrest is the first manifestation of heart disease. Other causes include circulatory shock from noncardiac disorders (especially pulmonary embolism, GI hemorrhage, trauma), ventilatory failure, and metabolic disturbance (including drug overdose).
In children, cardiac causes of sudden cardiac arrest are much less common (< 15 to 20%). Instead, predominant causes include trauma, poisoning, and various respiratory disorders (eg, airway obstruction, smoke inhalation, drowning, infection, sudden infant death syndrome).
Pathophysiology
Cardiac arrest produces global ischemia with consequences at the cellular level that adversely affect patients following resuscitation. The main consequences involve direct cellular damage and edema formation. Edema is particularly harmful in the brain, which has no room to expand, resulting in increased intracranial pressure and corresponding decrease in cerebral perfusion post-resuscitation. A number of successfully resuscitated patients have short- or long-term cerebral dysfunction.
Decreased ATP production leads to loss of membrane integrity with efflux of K and influx of Na and Ca. Excess Na produces cellular edema. Excess Ca damages mitochondria (depressing ATP production), increases nitric oxide production (leading to formation of damaging free radicals), and in certain circumstances, activates proteases that damage cellular contents.
In neurons, the abnormal ion flux additionally causes depolarization, releasing neurotransmitters. A particularly damaging neurotransmitter is glutamate, which activates a specific Ca channel, worsening intracellular Ca overload.
Inflammatory mediators (eg, IL-1B, tumor necrosis factor-α) are elaborated, some of which lead to microvascular thrombosis and loss of vascular integrity with further edema formation. Apoptosis is activated in severe ischemia by numerous mediators, resulting in accelerated cell death.
Symptoms and Signs
In critically or terminally ill patients, cardiac arrest is often preceded by a period of clinical deterioration with rapid, shallow breathing, arterial hypotension, and a progressive decrease in mental alertness. In other cases of cardiac arrest, collapse occurs without warning, occasionally accompanied by a brief (< 5 sec) seizure.
Diagnosis
and Treatment
Diagnosis is by clinical findings of apnea, pulselessness, and unconsciousness. Arterial pressure is not measurable. A cardiac monitor may indicate ventricular fibrillation, ventricular tachycardia, or asystole. Sometimes a perfusing rhythm (eg, sinus bradycardia) is present; this may represent true pulseless electrical activity (electromechanical dissociation) or extreme hypotension with failure to detect a pulse.
In children, the presenting rhythm is typically bradyarrhythmia followed by asystole; however, about 15 to 20% of children present with ventricular tachycardia or fibrillation. Thus, the need for rapid defibrillation should be considered in any child with sudden cardiac arrest not preceded by respiratory symptoms.
The patient is evaluated for potentially treatable causes, such as hypoxia, massive volume loss, cardiac tamponade, tension pneumothorax, or massive pulmonary embolus. Unfortunately, many causes will not be identified during CPR. Clinical examination and chest x-ray can detect tension pneumothorax. If available, immediate cardiac ultrasound can detect cardiac contractions and also recognize cardiac tamponade, extreme hypovolemia (empty heart), right ventricular overload suggestive of pulmonary embolism, and focal wall motion abnormalities suggestive of MI. Primary causes must be promptly treated. If no treatable conditions are present but cardiac motion is detected or pulses are present by Doppler, severe circulatory shock is identified and IV pressors (eg, norepinephrine , dopamine , or epinephrine ) are given in addition to volume infusion.
Further treatment is with cardiopulmonary resuscitation. Rapid intervention is essential.
Cardiopulmonary
Resuscitation (CPR)
(For neonatal resuscitation, see Perinatal Problems: Neonatal Resuscitation.)
Cardiopulmonary resuscitation (CPR) is an organized, sequential response to cardiac arrest, including recognition of absent breathing and circulation, basic life support (BLS) with chest compressions and rescue breathing, advanced cardiac life support (ACLS) with definitive airway and rhythm control, and post-resuscitative care. Rapid initiation of chest compression and early defibrillation (if indicated) are the keys to success. Speed, efficiency, and proper application of CPR directly determine successful neurologic outcome; the rare exception is in profound hypothermia from cold water immersion, in which successful resuscitation may be accomplished even after prolonged arrest (up to 60 min).
After establishing unresponsiveness (tap, shake, or shout) and absence of breathing, the rescuer calls for help (including a defibrillator) and begins basic life support following the mnemonic ABC (Airway, Breathing, Circulation, see
Fig. 6: Respiratory and Cardiac Arrest: Adult comprehensive emergency cardiac care. ). Next, defibrillation (D) with a manual or automated defibrillator is used to try to convert ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) to a perfusing rhythm.
The techniques used in basic 1- and 2-rescuer CPR are listed in
Table 2: Respiratory and Cardiac Arrest: Techniques of CPR for Health Care Professionals ; their mastery is best acquired by hands-on training such as that provided in the US under the auspices of the American Heart Association (1‑800-AHA-USA1) or similar organizations in other countries.
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Table 2
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Techniques of CPR for Health
Care Professionals
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One-Rescuer CPR
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Two-Rescuer CPR
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Breath Size
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Adults
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2 breaths (1 sec each) after every 30 chest compressions at 100/min
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2 breaths (1 sec) after every 30 chest compressions at 100/min*
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Each breath about 500 mL (caution against hyperventila-tion)
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Children (1 to 8)
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2 breaths (1 sec duration) after every 30 chest compressions at 100/min
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2 breaths (1 sec duration) after every 15 chest compressions at 100/min*
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Smaller breaths than for adults (enough to make chest rise)
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Infants (1< yr)
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2 breaths (1 sec duration) after every 30 chest compressions at 100/min
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2 breaths (1 sec duration) after every 15 chest compressions at 100/min*
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Only small puffs from rescuer's cheeks
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*With an advanced airway in place, give 8 to 10 breaths/min without pause of chest compressions.
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Airway
and Breathing
Except in witnessed cardiac arrest when a defibrillator is available in < 3 min, opening the airway is the first priority (see Respiratory and Cardiac Arrest: Clearing and Opening the Upper Airway).
Mouth-to-mouth (adults and children) or combined mouth-to-mouth-and-nose (infants) rescue breathing is begun. Cricoid pressure may be applied continuously by a 2nd rescuer until airway control is achieved by endotracheal intubation. Firm pressure on the rigid cartilaginous rings of the trachea occludes the esophagus, minimizing the chance of gastric inflation from ventilations and blocking the exit of gastric contents if regurgitation occurs; pressure must be much lighter in young children to avoid collapsing the trachea. If abdominal distention develops, the airway is rechecked for patency and the amount of air delivered during rescue breathing is reduced. Nasogastric intubation to relieve gastric distention is delayed until suction equipment is available because regurgitation with aspiration of gastric contents may occur during insertion. If marked gastric distention interferes with ventilation and cannot be corrected by the above methods, the patient is positioned on his side, the epigastrium compressed, and the airway cleared.
The trachea is intubated as described under Airway Establishment and Control (see Respiratory and Cardiac Arrest: Airway Establishment and Control). However, defibrillation is not delayed to perform endotracheal intubation, and, if possible, chest compression continues uninterrupted during intubation.
Circulation
Chest
compression:
In an unresponsive patient whose collapse was unwitnessed, the rescuer should immediately begin external (closed chest) cardiac compression, alternating with rescue breathing. In witnessed cardiac arrest, defibrillation precedes chest compression, if available within 3 min.
Ideally, external cardiac compression produces a palpable pulse with each compression, although cardiac output is only 30 to 40% of normal. However, palpation of pulses during chest compression is difficult and often unreliable. End-tidal CO2 monitoring provides a better estimate of cardiac output during chest compression; patients with inadequate perfusion have little venous return to the lungs and hence a low end-tidal CO2. Normal-sized, light-responsive pupils signal adequate brain circulation and oxygenation. Light-responsive but dilated pupils may indicate inadequate cerebral oxygenation although brain injury may not have occurred. However, persistently dilated, nonreactive pupils do not prove brain injury or death because high doses of cardioactive drugs, other drugs, or cataracts may modify pupil size and reaction. Restoration of spontaneous breathing or eye opening may indicate restoration of spontaneous circulation.
Open-chest cardiac compression may be effective, but its use is restricted to patients after penetrating chest injuries, cardiac tamponade, and cardiac arrest in the operating room with the patient's chest already open. However, thoracotomy requires training and experience and is best performed only with these limited indications.
Complications
of chest compression:
Laceration of the liver is the most serious (sometimes fatal) complication and is usually caused by compressing below the sternum. Rupture of the stomach is a rare complication (particularly if the stomach is distended with air). Delayed rupture of the spleen is very rare. A more frequent complication is regurgitation followed by aspiration of gastric contents, producing aspiration pneumonia that may be fatal.
Costochondral separation and fractured ribs sometimes cannot be avoided for it is important to compress the chest deeply enough to produce sufficient blood flow. Fractures are quite rare in children because of the flexibility of the chest wall. Bone marrow emboli to the lungs have rarely been reported after external cardiac compression, but there is no clear evidence that they contribute to mortality. Lung injury is rare, but pneumothorax secondary to rib fracture can occur. Serious myocardial injury does not occur, with the possible exception of injury to a preexisting ventricular aneurysm. Concern for these injuries should not deter the rescuer from performing CPR.
Monitor and IV:
ECG monitoring is established to identify the underlying cardiac rhythm. An IV line is started; 2 lines minimize the risk of losing IV access during CPR. Large-bore peripheral lines in the antecubital veins are preferred. In adults, a subclavian or internal jugular central line can be placed if a peripheral line cannot be established. Intraosseous and femoral lines (see Approach to the Critically Ill Patient: Intraosseous Infusion) are the preferred alternatives in children. Femoral vein catheters (preferably long catheters advanced centrally) are practical because CPR need not be interrupted and they have less potential for lethal complications, but they may have a lower rate of successful placement because no discrete femoral arterial pulsations are available to guide insertion.
The type and volume of fluids or drugs given depend on the clinical circumstances. Usually, IV 0.9% saline is given slowly (sufficient only to keep an IV line open); vigorous volume replacement (crystalloid and colloid solutions, blood) is required only when arrest results from hypovolemia (see Shock and Fluid Resuscitation: Intravenous Fluid Resuscitation).
Defibrillation
The most common rhythm in witnessed adult cardiac arrest is VF; rapid conversion to a perfusing rhythm is essential. Pulseless VT is treated the same as VF.
A precordial thump is advised only when a defibrillator is not available. A forceful precordial thump can rarely convert VF or VT to a functional cardiac rhythm, and there is no evidence of deleterious effect (eg, converting VT to VF) in the cardiac arrest setting. However, it is not recommended in children. One or 2 blows can be delivered to the junction of the middle and lower third of the sternum with a clenched fist held 20 to 25 cm above the chest.
Prompt direct current (DC) cardioversion is more effective than antiarrhythmic drugs; however, the success of defibrillation is time dependent, with about a 10% decline in success after each minute of VF (or pulseless VT). Automated external defibrillators (AEDs) allow minimally trained rescuers to treat VT or VF. Their placement with 1st responders (police and fire vehicles) and in public locations appears to increase the rate of resuscitation.
Defibrillating paddles or AED pads are placed between the clavicle and the 2nd intercostal space along the right sternal border, and over the 5th or 6th intercostal space at the apex of the heart. Conventional defibrillators are used with conducting paste or gel pads; the conducting material is incorporated into AED pads. Only 1 initial countershock is given (previously recommended 3 stacked shocks). Energy level for biphasic defibrillators is between 120 and 200 joules (2 joules/kg in children); monophasic defibrillators are set at 360 joules. CPR resumes immediately. Post-shock rhythm is not checked until after 2 min of CPR; this may be done earlier in continuously monitored patients. Any subsequent shocks are delivered at the same or higher energy level (maximum 360 joules, 2 to 4 joules/kg in children). Patients remaining in VF or VT are given drug therapy as described below.
Special Circumstances
In accidental electrical shock, the rescuer must be certain that the patient is no longer in contact with the electrical source to avoid shock to himself. Use of nonmetallic grapples or rods and grounding of the rescuer allows for safe removal of the patient before starting CPR.
In near-drowning, rescue breathing may be started in shallow water, although chest compression cannot be effectively performed until the patient is horizontal on a firm surface. Placing the patient on a surfboard or float may help.
If cardiac arrest follows traumatic injury, airway opening maneuvers and a brief period of external ventilation after clearing the airway take priority to exclude airway obstruction as the cause of arrest. To minimize cervical spine movement, only jaw thrust, not head tilt and chin lift, is used. However, because most patients with traumatic cardiac arrest have marked hypovolemia due to blood loss, or nonsurvivable brain injury, chest compressions will be ineffective. The main survivable causes of traumatic cardiac arrest include cardiac tamponade and tension pneumothorax, which require immediate needle decompression; if this is unavailable or ineffective, BLS measures are futile.
Drugs
for ACLS
Despite widespread and long-standing use, no drug has definitively been shown to increase survival to hospital discharge in patients with cardiac arrest. Some drugs do appear to improve the return of spontaneous circulation and thus may reasonably be given (for dosing, including pediatric, see
Table 3: Respiratory and Cardiac Arrest: Drugs for Resuscitation* ).
In a patient with a peripheral IV line, drug administration is followed by a fluid bolus (“wide open” IV in adults; 3 to 5 mL in young children) to flush the agent into the central circulation. In a patient without IV or intraosseous access, atropine and epinephrine , when indicated, may be given via the endotracheal tube at 2 to 2.5 times the IV dose.
First-line drugs:
Epinephrine is the main drug used in cardiac arrest although its benefit is increasingly challenged. It is given q 3 to 5 min. Epinephrine has combined α- and β-adrenergic effects. The α-adrenergic effects may augment coronary diastolic pressure, thereby increasing subendocardial perfusion during chest compressions. Epinephrine also increases the likelihood of successful defibrillation. However, β-adrenergic effects may be detrimental because they increase O2 requirements (especially of the heart) and cause vasodilation. Intracardiac injection of epinephrine is not recommended because pneumothorax, coronary artery laceration, and cardiac tamponade may occur.
A single dose of vasopressin 40 units is an alternative to epinephrine (adults only); it is not proven superior to epinephrine .
Atropine sulfate is a parasympatholytic drug that increases heart rate and conduction through the atrioventricular node. It is given for asystole (except in children), bradyarrhythmias, and high-degree atrioventricular nodal block, although no survival benefit has been demonstrated.
Amiodarone can be given once if defibrillation is unsuccessful following epinephrine or vasopressin . It is also of potential value if VT or VF recurs following successful defibrillation; a lower dose is given over 10 min followed by a continuous infusion.
Other drugs:
Ca chloride is recommended for patients with hyperkalemia, hypermagnesemia, hypocalcemia, or Ca channel blocker toxicity. In others, because intracellular Ca is already higher than normal, additional Ca is likely to be detrimental. Because cardiac arrest in patients on renal dialysis is often a result of or accompanied by hyperkalemia, these patients may benefit from a trial of Ca if bedside K determination is unavailable. Caution is necessary because Ca exacerbates digitalis toxicity and can of itself cause cardiac arrest.
Mg sulfate has not been shown to improve outcome in randomized clinical studies. However, it may be helpful in patients with torsades de pointes or known or suspected Mg deficiency (ie, alcoholics, protracted diarrhea).
Procainamide is a 2nd-line drug for treatment of refractory VF or VT. However, procainamide is not recommended in pulseless arrest in pediatric patients.
Phenytoin may rarely be used to treat VF or VT, but only when it is due to digitalis toxicity and is refractory to other drugs. Dose is 50 mg/min given until rhythm improves or total dose reaches 18 mg/kg.
NaHCO3 is no longer recommended unless cardiac arrest is caused by hyperkalemia, hypermagnesemia, or tricyclic antidepressant overdose with complex ventricular arrhythmias. In pediatric patients, NaHCO3 should be considered when cardiac arrest is prolonged (> 10 min); it is administered only if there is good ventilation. When NaHCO3 is used, arterial pH should be monitored before infusion and after each 50-mEq dose (1 to 2 mEq/kg in children).
Lidocaine and bretylium are no longer used during CPR.
Dysrhythmia Treatment
VF/pulseless
VT is treated with one DC shock, preferably with biphasic waveform; chest compression is interrupted as little as possible. Recommended energy levels vary: 120 to 200 joules for biphasic waveform and 360 joules for monophasic. If this is unsuccessful, epinephrine 1 mg IV is administered and repeated q 3 to 5 min. Alternatively, vasopressin 40 U IV can be given only once (not in pediatric patients). Cardioversion at the same energy level is attempted 1 min after each drug administration (the role of escalating biphasic energy levels is unclear). If VF persists, amiodarone 300 mg IV is given. Then, if VF/VT recurs, 150 mg is given followed by infusion of 1 mg/min q 6 h, then 0.5 mg/min. (For pediatric energy levels, see
Table 4: Respiratory and Cardiac Arrest: Guide to Pediatric Resuscitation—Mechanical Measures; for drug doses, see Table 3: Respiratory and Cardiac Arrest: Drugs for Resuscitation* .)
Asystole can be mimicked by a loose or disconnected monitor lead; thus, monitor connections should be checked and rhythm viewed in an alternative lead. If asystole is confirmed and heart block is suspected, transcutaneous pacing is performed and the patient is given epinephrine 1 mg IV repeated q 3 to 5 min, and atropine 1 mg IV repeated q 3 to 5 min to a total dose of 0.04 mg/kg. Electrical pacing is rarely successful, but if it is to work it must be instituted early. Note, atropine and pacing are contraindicated in pediatric patients with asystole. Defibrillation of apparent asystole (because it “might be fine VF”) is discouraged because electrical shocks injure the nonperfused heart.
Pulseless
electrical activity is circulatory collapse that occurs despite satisfactory electrical complexes on the ECG. Patients with pulseless electrical activity receive 500- to 1000-mL (20 mL/kg) infusion of 0.9% saline and epinephrine 0.5 to 1.0 mg IV, repeated q 3 to 5 min. If the heart rate is < 60/min, atropine 0.5 to 1 mg IV is given. Cardiac tamponade can cause pulseless electrical activity, but this usually occurs in patients with known pericardial effusion or major chest trauma. In such settings, immediate pericardiocentesis is performed (see Fig. 2: Pericarditis: Pericardiocentesis.). Tamponade is rarely an occult cause of cardiac arrest but, if suspected, can be confirmed by pericardiocentesis or, if immediately available, ultrasound.
Termination of
Resuscitation
CPR must be continued until the cardiopulmonary system is stabilized, the patient is pronounced dead, or a lone rescuer is physically unable to continue. If cardiac arrest occurs in hypothermic patients, CPR should be continued until the body is rewarmed to 34° C.
Decision to pronounce death is somewhat subjective, taking into account duration of arrest before treatment, age, prior medical conditions, and other factors, but typically is made following failure to establish spontaneous circulation after 30 to 45 min of CPR and ACLS measures.
Post-Resuscitative
Care
Return of spontaneous circulation (ROSC) is only an intermediate goal in resuscitation. Only 3 to 8% of patients with ROSC survive to hospital discharge. To maximize the likelihood of good outcome, physiologic parameters must be optimized and underlying conditions addressed. In adults, it is particularly important to recognize MI (see Coronary Artery Disease: Acute Coronary Syndromes (ACS)) and institute reperfusion therapy (eg, thrombolysis, percutaneous transluminal coronary angioplasty) rapidly. Caution: Thrombolysis following
aggressive CPR sometimes causes cardiac tamponade.
Post-resuscitation laboratory studies include ABG, CBC, and blood chemistries, including electrolytes, glucose, BUN, creatinine, and cardiac markers. (Creatine phosphokinase will usually be elevated due to skeletal muscle damage from CPR.) Arterial Pao2 should be kept near normal values (80 to 100 mm Hg). Hct should be maintained ≥ 30, glucose at 80 to 120 mg/dL, and electrolytes, especially K, should be within the normal range.
BP
support:
Mean arterial pressure (MAP) should be maintained > 80 mm Hg in older adults, or > 60 mm Hg in younger and previously healthy patients. In patients known to be hypertensive, a reasonable target is systolic BP 30 mm Hg below pre-arrest level.
Patients with low MAP or signs of left ventricular failure may benefit from pulmonary artery catheter monitoring (see Approach to the Critically Ill Patient: Pulmonary Artery Catheter Monitoring) to measure cardiac output, pulmonary artery occlusion pressure (PAOP), and mixed venous O2 saturation (a measure of peripheral perfusion) allowing optimal titration of therapy. Mixed venous O2 saturation should be > 60%.
Patients with low MAP and low central venous pressure or PAOP should have IV fluid challenge with 0.9% saline infused in 250-mL increments. Older adults with moderately low MAP (70 to 80 mm Hg) and normal or high central venous pressure/PAOP may receive infusion of an inotrope, dobutamine started at 2 to 5 μg/kg/min. Alternatively, amrinone or milrinone is used (see Table 3: Respiratory and Cardiac Arrest: Drugs for Resuscitation* ). If this is ineffective, the inotrope and vasoconstrictor dopamine should be considered. Alternatives are epinephrine and the peripheral vasoconstrictors norepinephrine and phenylephrine (see Table 3: Respiratory and Cardiac Arrest: Drugs for Resuscitation* ). Vasoactive drugs should be used in the minimal dose necessary to achieve low-normal MAP because they may increase vascular resistance and decrease organ perfusion, especially in the mesenteric bed. They also increase the workload on the heart at a time when its capability is decreased due to post-resuscitation myocardial dysfunction. If MAP remains < 70 mm Hg in patients who may have sustained MI, intra-aortic balloon counterpulsation should be considered. Patients with normal MAP and high central venous pressure/PAOP may improve with either inotropic therapy or afterload reduction with nitroprusside or nitroglycerin .
Intra-aortic balloon counterpulsation can assist low-output circulatory states due to left ventricular pump failure refractory to drugs. A balloon catheter is introduced via the femoral artery, percutaneously or by arteriotomy, retrograde into the thoracic aorta just distal to the left subclavian artery. The balloon inflates during each diastole, augmenting coronary artery perfusion, and deflates during systole, decreasing afterload. Its primary value is as a temporizing measure when the cause of shock is potentially correctable by surgery or percutaneous intervention (eg, acute MI with major coronary obstruction, acute mitral insufficiency, or ventricular septal defect).
Dysrhythmia
treatment:
Although VF or VT may recur after resuscitation, prophylactic antiarrhythmic drugs do not improve survival and are no longer indicated. However, patients manifesting such rhythms may be treated with procainamide or amiodarone as described above.
Post-resuscitation rapid supraventricular tachycardias occur frequently due to high levels of β-adrenergic catecholamines (both endogenous and exogenous) associated with cardiac arrest and resuscitation. These rhythms should be treated if extreme, prolonged, or associated with hypotension or signs of coronary ischemia. An esmolol IV infusion is given, beginning at 50 μg/kg/min.
Patients who had arrest from VF or VT not associated with an acute MI are candidates for an implantable cardioverter-defibrillator (ICD). Current devices are implanted similar to pacemakers and have intracardiac leads and sometimes subcutaneous electrodes. They can sense arrhythmias and deliver either cardioversion or cardiac pacing as indicated.
Neurologic
support:
Between 8 and 20% of adults have some degree of CNS dysfunction following resuscitation from cardiac arrest. Hypoxic brain injury is a result of direct neuronal ischemic damage and cerebral edema (see Respiratory and Cardiac Arrest: Pathophysiology). Damage may evolve over 48 to 72 h after resuscitation.
Maintenance of oxygenation and cerebral perfusion pressure (avoiding hypotension) can reduce cerebral complications. Also, because hyperglycemia may damage the postischemic brain, it should be treated vigorously and glucose administration should be avoided except for documented hypoglycemia.
Additionally, there is now persuasive evidence of the benefits of inducing mild hypothermia. Surface cooling with ice packs can reduce core body temperature to between 30° and 34° C. Alternative methods of cooling include cardiopulmonary bypass or newly available intravascular cooling devices.
Numerous pharmacologic treatments, including free radical scavengers, antioxidants, glutamate inhibitors, and Ca channel blockers, are of theoretic benefit; many have been successful in animal models, but none have proven effective in human trials.
CPR
in Infants and Children
Despite the use of CPR, mortality rates for cardiac arrest are 80 to 97% for infants and children. The mortality rate is almost 25% for respiratory arrest alone. Neurologic outcome is often severely compromised.
About 50 to 65% of children requiring CPR are < 1 yr; of these, most are < 6 mo. About 6% of neonates require resuscitation at delivery (see Perinatal Problems: Neonatal Resuscitation); the incidence increases significantly if birth weight is < 1500 g.
Standardized outcome guidelines should be followed in reporting outcomes of CPR in children; eg, the modified Pittsburgh Outcome Categories Scale reflects cerebral and overall performance (see
Table 5: Respiratory and Cardiac Arrest: Pediatric Cerebral Performance Category Scale*).
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Table 5
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Pediatric Cerebral Performance
Category Scale*
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Score
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Category
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Description
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1
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Normal
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Age-appropriate level of functioning; preschool-aged child developmentally appropriate; school-aged child attends regular classes
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2
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Mild disability
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Can interact at an age-appropriate level; minor neurologic disease that is controlled and does not interfere with daily functioning (eg, seizure disorder); preschool-aged child may have minor developmental delays, but more than 75% of all daily living developmental milestones are above the 10th percentile; school-aged child attends regular school, but grade is not appropriate for age, or child is failing appropriate grade because of cognitive difficulties
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3
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Moderate disability
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Below age-appropriate functioning; neurologic disease that is not controlled and severely limits activities; most activities of preschool-aged child's daily living developmental milestones are below the 10th percentile; school-aged child can perform activities of daily living but attends special classes because of cognitive difficulties or a learning deficit
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4
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Severe disability
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Preschool-aged child's activities of daily living milestones are below the 10th percentile, and child is excessively dependent on others for provision of activities of daily living; school-aged child may be so impaired as to be unable to attend school; school-aged child is dependent on others for provision of activities of daily living; abnormal motor movements for preschool- and school-aged children may include nonpurposeful, decorticate, or decerebrate responses to pain
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5
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Coma or vegetative state
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Unawareness
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6
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Death
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*Worst level of performance for any single criterion is used for categorizing. Deficits are scored only if they result from a neurologic disorder. Assessments are made on the basis of medical records or interview with caretaker.
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From Recommended Guidelines for Uniform Reporting of Pediatric Advanced Life Support: The Pediatric Utstein Style; Statement for Health Care Professionals from the Task Force of the American Academy of Pediatrics, the American Heart Association, and the European Resuscitation Council; Pediatrics 96(4):765–779, 1995.
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Major Differences
Between Pediatric and Adult CPR
Pre-arrest:
Bradycardia in
a distressed child is a sign of impending cardiac arrest. Neonates, infants, and young children are more likely to develop bradycardia from hypoxemia, whereas older children initially tend to have tachycardia. An infant or child with a heart rate < 60/min and signs of poor perfusion that do not rise with ventilatory support should have cardiac compressions (see
Fig. 7: Respiratory and Cardiac Arrest: Chest compression.). Bradycardia secondary to heart block is unusual, although it may occur.
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Fig. 7
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Chest compression.
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A: Side-by-side thumb placement for chest compressions is preferred for neonates and small infants whose chest can be encircled. Thumbs should overlap if used in very small neonates. B: Two fingers are used for infants. Fingers should be maintained in the upright position during compression. For neonates, this technique will result in too low a position, ie, at or below the xiphoid; the correct position is just below the nipple line. C: Hand position for chest compression for a child. (Adapted from American Heart Association: Standards and Guidelines for CPR. Journal of the American Medical Association 1992; 268:2251–2281. Copyright 1992, American Medical Association.)
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After adequate oxygenation and ventilation, epinephrine is the drug of choice.
BP should be measured with an appropriate-sized cuff, but direct invasive arterial BP monitoring is mandatory in severely compromised children.
Since BP varies with age, an easy guideline to remember the lower limits of normal (< 5th percentile) by age is as follows: < 1 mo, 60 mm Hg; 1 mo to 1 yr, 70 mm Hg; > 1 yr, 70 + 2 × age in yr. Thus, in a 5 yr old, hypotension would be defined by a BP of < 80 mmHg (70 + 2 × 5). Of significant importance is that children maintain BP longer because of stronger compensatory mechanisms (increased heart rate, increased systemic vascular resistance). Once hypotension occurs, cardiorespiratory arrest may rapidly follow. All effort should be made to treat signs of shock (increased heart rate, cool extremities, capillary refill > 2 sec, poor peripheral pulses) before hypotension develops.
Equipment and
environment:
Equipment size, drug dosage, and CPR parameters vary with patient age and weight (see Table 3: Respiratory and Cardiac Arrest: Abdominal thrusts with victim standing or sitting (conscious). and Table 4: Respiratory and Cardiac Arrest: Expired air ventilation—child.). Size-variable equipment includes defibrillator paddles or electrode pads, masks, ventilation bags, airways, laryngoscope blades, endotracheal tubes, suction catheters. Weight should be measured rather than guessed; alternatively, commercially available measuring tapes that are calibrated to read standard patient weight based on body length can be used. Some tapes are printed with the recommended drug dose and equipment size for each weight. Dosages should be rounded down; eg, a 2 1⁄2 yr old should receive the dose for a 2 yr old.
Susceptibility to heat loss is greater in infants and children because of a large surface area relative to body mass and less subcutaneous tissue. A neutral external thermal environment is crucial during CPR and post-resuscitation and may range from 36.5° C in a neonate to 35° C in a child. Hypothermia with core temperature < 35° C makes resuscitation more difficult (distinct from the beneficial effects of post-resuscitation hypothermia discussed above).
Airway:
Upper airway anatomy is different in children. The head is large with a small face, mandible, and external nares, and the neck is relatively short. The tongue is large relative to the mouth, and the larynx lies higher in the neck and is angled more anteriorly. The epiglottis is long, and the narrowest portion of the trachea is inferior to the vocal cords at the cricoid ring, allowing the use of uncuffed endotracheal tubes. In younger children, a straight laryngoscope blade generally allows better visualization of the vocal cords than a curved blade, since the larynx is more anterior and the epiglottis is more floppy and redundant.
Rhythm disturbances:
In asystole, atropine and pacing are not used.
VF and pulseless VT occur in only about 15 to 20% of cardiac arrests. Vasopressin is not indicated. When cardioversion is used, the absolute energy dose is less than for adults, and should be 2 to 4 joules/kg monophasic (see Table 4: Respiratory and Cardiac Arrest: Guide to Pediatric Resuscitation—Mechanical Measures). It is recommended to start at 2 joules/kg and increase to a maximum of 4 joules/kg by the 3rd defibrillatory shock, if necessary. The pediatric dose for biphasic defibrillation is likely to be lower but has not yet been determined.
Automated external defibrillators (AEDs) with adult cables may be used for children as young as 1 yr, but an AED with pediatric cables (maximum biphasic shock of 50 joules) is preferred for children between 1 and 8 yr.
Last full review/revision November 2005
Content last modified November 2005
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