(For neonatal resuscitation, see Neonatal Resuscitation; for resuscitation in infants and children, see Cardiopulmonary Resuscitation in Infants and Children.)
CPR is an organized, sequential response to cardiac arrest, including
Prompt initiation of uninterrupted chest compression and early defibrillation (when indicated) are the keys to success. Speed, efficiency, and proper application of CPR determine successful outcome; the rare exception is profound hypothermia caused by cold water immersion, when successful resuscitation may be accomplished even after prolonged arrest (up to 60 min).
Guidelines for health care professionals from the American Heart Association are followed (see Fig. 1: Adult comprehensive emergency cardiac care.). If a person has collapsed with possible cardiac arrest (see Cardiac Arrest), a rescuer first establishes unresponsiveness and confirms absence of breathing or the presence of only gasping respirations. Then, the rescuer calls for help. Anyone answering is directed to activate the emergency response system (or appropriate in-hospital resuscitation personnel) and, if possible, obtain a defibrillator. If no one responds, the rescuer first activates the emergency response system and then begins basic life support by giving 30 chest compressions at a rate of 100/min and then opening the airway (lifting the chin and tilting back the forehead) and giving 2 rescue breaths. The cycle of compressions and breaths is continued (see Table 1: CPR Techniques for Health Care Practitioners) without interruption; preferably each rescuer is relieved every 2 min. When a defibrillator (manual or automated) becomes available, a person in ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) is given an unsynchronized shock. If the cardiac arrest is witnessed and a defibrillator is on the scene, a person in VF or VT is immediately defibrillated; early defibrillation may promptly convert VF or pulseless VT to a perfusing rhythm. Defibrillation is further discussed in Airway and Breathing. It is recommended that untrained bystanders begin and maintain continuous chest compressions until skilled help arrives.
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For children, unless collapse is sudden and witnessed, the first step if no one answers the call for help is to do 5 cycles of CPR (see Fig.: Cardiopulmonary Resuscitation in Infants and Children) before activating the emergency response system.
Airway and Breathing
In a change from previous recommendations, opening the airway is given 2nd priority (see Clearing and Opening the Upper Airway) after beginning chest compressions. For mechanical measures regarding resuscitation in children, see Table 4: Guide to Pediatric Resuscitation—Mechanical Measures.
Mouth-to-mouth (adults and children) or combined mouth-to-mouth-and-nose (infants) rescue breathing or bag-valve-mask ventilation is begun for asphyxial cardiac arrest. If available, an oropharyngeal airway may be inserted. Cricoid pressure is no longer recommended.
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, patients are positioned on their side, the epigastrium is compressed, and the airway is cleared.
When qualified providers are present, an advanced airway (endotracheal tube or supraglottic device) is placed without interruption of chest compression as described under Airway Establishment and Control (see Airway Establishment and Control). A breath is given every 6 to 8 sec (8 to 10 breaths/min) without interrupting chest compression. However, chest compression and defibrillation take precedence over endotracheal intubation. Unless highly experienced providers are available, endotracheal intubation may be delayed in favor of ventilation with bag-valve-mask, laryngeal mask airwaysee Laryngeal mask airways (LMAs), or similar device.
In witnessed cardiac arrest, chest compression should be done until defibrillation is available. In an unresponsive patient whose collapse was unwitnessed, the trained rescuer should immediately begin external (closed chest) cardiac compression, followed by rescue breathing. Chest compressions must be interrupted as little as possible (eg, for intubation, central IV catheter placement, or transport). A compression cycle should consist of 50% compression and 50% release. Mechanical chest compression devices are available; these devices are no more effective than properly executed manual compressions but can minimize effects of performance error and fatigue and can be helpful during patient transport. After several minutes of chest compression, rhythm interpretation and defibrillation are done.
Ideally, external cardiac compression produces a palpable pulse with each compression, although cardiac output is only 20 to 30% of normal. However, palpation of pulses during chest compression is difficult, even for experienced clinicians, 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. Restoration of spontaneous breathing or eye opening indicates restoration of spontaneous circulation (ROSC).
Open-chest cardiac compression may be effective but is used only in patients with penetrating chest injuries, shortly after cardiac surgery (ie, within 48 h), in cases of cardiac tamponade, and most especially after cardiac arrest in the operating room when the patient's chest is already open. However, thoracotomy requires training and experience and is best done only within these limited indications.
Complications of chest compression:
Laceration of the liver is a rare but potentially serious (sometimes fatal) complication and is usually caused by compressing the abdomen below the sternum. Rupture of the stomach (particularly if the stomach is distended with air) is also a rare complication. Delayed rupture of the spleen is very rare. An occasional complication, however, is regurgitation followed by aspiration of gastric contents, causing life-threatening aspiration pneumonia in resuscitated patients.
Costochondral separation and fractured ribs often cannot be avoided because 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 after a penetrating rib fracture may occur. Serious myocardial injury caused by compression is very unlikely, with the possible exception of injury to a preexisting ventricular aneurysm. Concern for these injuries should not deter the rescuer from doing CPR.
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.
Prompt direct current 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 use by first responders (police and fire services) and their prominent availability in public locations has increased the likelihood 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 defibrillator paddles are used with conducting paste; pads have conductive gel incorporated into them. Only 1 initial countershock is now advised (the previous recommendation was 3 stacked shocks), after which chest compression is resumed. Energy level for biphasic defibrillators is between 120 and 200 joules (2 joules/kg in children); monophasic defibrillators are set at 360 joules. Postshock rhythm is not checked until after 2 min of chest compression. 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 receive continued chest compression and ventilation and optional drug therapy as discussed in Drugs for ACLS.
Monitor and IV
ECG monitoring is established to identify the underlying cardiac rhythm. An IV line may be started; 2 lines minimize the risk of losing IV access during CPR. Large-bore peripheral lines in the antecubital veins are preferred. In adults and children, if a peripheral line cannot be established, a subclavian or internal jugular see Procedurecentral line can be placed provided it can be done without stopping chest compression (often difficult). Intraosseous and femoral lines (see Intraosseous Infusion) are the preferred alternatives, especially in children. Femoral vein catheterssee Procedure, preferably long catheters advanced centrally, are an option because CPR does not need to be stopped and they have less potential for lethal complications; however, 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 Intravenous Fluid Resuscitation).
In accidental electrical shock, rescuers must be certain that the patient is no longer in contact with the electrical source to avoid shocking themselves. 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 is not likely to be effectively done until the patient is placed horizontally on a firm surface, such as a surfboard or float.
If cardiac arrest follows traumatic injury, airway opening maneuvers and a brief period of external ventilation after clearing the airway have the highest priority because airway obstruction is the most likely treatable cause of arrest. To minimize cervical spine injury, jaw thrust, but not head tilt and chin lift, is advised. Other survivable causes of traumatic cardiac arrest include cardiac tamponade and tension pneumothorax, for which immediate needle decompression is lifesaving. However, most patients with traumatic cardiac arrest have severe hypovolemia due to blood loss (for which chest compression may be ineffective) or nonsurvivable brain injuries.
Drugs for ACLS
Despite widespread and long-standing use, no drug or drug combination has been definitively shown to increase survival to hospital discharge in patients with cardiac arrest. Some drugs do seem to improve the likelihood of ROSC and thus may reasonably be given (for dosing, including pediatric, see Table 2: Drugs for Resuscitation*). Drug therapy for shock and cardiac arrest continues to be researched.
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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 drug 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. During administration of a drug via endotracheal tube, compression should be briefly stopped.
First-line drugs include
Epinephrine has been the main drug used in cardiac arrest, although, as noted previously, its benefit is increasingly challenged. It may be given q 3 to 5 min. Epinephrine has combined α-adrenergic 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, in addition to interrupting precordial compression, pneumothorax, coronary artery laceration, and cardiac tamponade may occur.
A single dose of vasopressin 40 units, which has a duration of activity of 40 min, is an alternative to epinephrine (adults only); it has not been proved more effective than epinephrine.
Amiodarone 300 mg can be given once if defibrillation is unsuccessful after epinephrine or vasopressin, followed by 1 dose of 150 mg. It is also of potential value if VT or VF recurs after successful defibrillation; a lower dose is given over 10 min followed by a continuous infusion. There is no persuasive proof that it increases survival to hospital discharge.
A range of additional drugs may be useful in specific settings.
Atropine sulfate is a vagolytic drug that increases heart rate and conduction through the atrioventricular node. It is given for symptomatic bradyarrhythmias and high-degree atrioventricular nodal block. It is no longer recommended for asystole or pulseless electrical activity.
Ca chloride is recommended for patients with hyperkalemia, hypermagnesemia, hypocalcemia, or Ca channel blocker toxicity. In other patients, 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 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, patients with protracted diarrhea).
Procainamide is a 2nd-line drug for treatment of refractory VF or VT. However, procainamide is not recommended for pulseless arrest in children.
Phenytoin may rarely be used to treat VF or VT, but only when VF or VT is due to digitalis toxicity and is refractory to other drugs. A dose of 50 mg/min is given until rhythm improves or the total dose reaches 18 mg/kg.
NaHCO3 (sodium bicarbonate) is no longer recommended unless cardiac arrest is caused by hyperkalemia, hypermagnesemia, or tricyclic antidepressant overdose with complex ventricular arrhythmias. In children, NaHCO3 may be considered when cardiac arrest is prolonged (> 10 min); it is given 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 recommended for management of cardiac arrest.
VF or pulseless VT is treated with one direct current shock, preferably with biphasic waveform, immediately after witnessed arrest and after 2 min of chest compression in patients with unwitnessed arrest; 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 treatment is unsuccessful, epinephrine 1 mg IV is administered and repeated q 3 to 5 min. Alternatively, vasopressin 40 U IV may be given only once (not in children), although its value is questioned. Cardioversion at the same energy level is attempted 1 min after each drug administration. 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. Current versions of AEDs provide a pediatric cable that effectively reduces the energy delivered to children. (For pediatric energy levels, see Table 4: Guide to Pediatric Resuscitation—Mechanical Measures; for drug doses, see Table 2: 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 done 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 not successful in other settings. Pacing and atropine, however, are contraindicated in children 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. Epinephrine may be given in amounts of 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 disorder usually occurs in patients after thoracotomy and in patients with known pericardial effusion or major chest trauma. In such settings, immediate pericardiocentesis or thoracotomy is done (Fig. 2: Pericardiocentesis.). Tamponade is rarely an occult cause of cardiac arrest but, if suspected, can be confirmed by ultrasonography or, if ultrasonography is unavailable, pericardiocentesis.
Termination of Resuscitation
CPR should 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 is thought to be due to hypothermia, CPR should be continued until the body is rewarmed to 34° C.
The decision to terminate resuscitation is a clinical one, and clinicians take into account duration of arrest, age of the patient, and prognosis of underlying medical conditions. The decision is typically made when spontaneous circulation has not been established after CPR and ACLS measures have been done.
Restoration 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 a good outcome, clinicians must provide good supportive care (eg, provide therapeutic hypothermia, manage BP and cardiac rhythm) and treat underlying conditions. In adults, it is particularly important to recognize ST-segment elevation MI (STEMI—see Acute Coronary Syndromes (ACS)) and institute reperfusion therapy, preferably percutaneous coronary interventions (PCI), promptly. The decision to do cardiac catheterization after resuscitation from cardiac arrest should be individualized based on the interventional cardiologist's clinical impression and the patient's prognosis.
Postresuscitation laboratory studies include ABG, CBC, and blood chemistries, including electrolytes, glucose, BUN, creatinine, and cardiac markers. (Creatine kinase is usually elevated because of skeletal muscle damage caused by CPR; troponins, which are unlikely to be affected by CPR or defibrillation, are preferred.) Arterial Pao2 should be kept near normal values (80 to 100 mm Hg). Hct should be maintained at ≥ 30, and glucose at < 200 mg/dL; electrolytes, especially K, should be within the normal range.
Between 8% and 30% of adults have CNS dysfunction after resuscitation from cardiac arrest. Hypoxic brain injury is a result of ischemic damage and cerebral edema (see Pathophysiology). Both damage and recovery may evolve over 48 to 72 h after resuscitation.
Maintenance of oxygenation and cerebral perfusion pressure (avoiding hypotension) may reduce cerebral complications. Both hypoglycemia and hyperglycemia may damage the postischemic brain and should be treated.
Therapeutic hypothermia, in which core body temperature is reduced to between 32° and 34° C, has been shown to improve outcome and is recommended for patients who remain unresponsive after spontaneous circulation has returned. Cooling is begun as soon as spontaneous circulation has returned. Techniques to induce and maintain hypothermia can be either external or invasive. External cooling methods are easy to apply and range from the use of external ice packs to several commercially available external cooling devices that circulate high volumes of chilled water over the skin. For internal cooling, chilled IV fluids (4° C) can be rapidly infused to lower body temperature, but this method may be problematic in patients who cannot tolerate much additional fluid volume. Also available are external heat-exchange devices that circulate chilled saline to an indwelling IV heat-exchange catheter using a closed-loop design in which chilled saline circulates through the catheter and back to the device, rather than into the patient. Another invasive method for cooling uses an extracorporeal device that circulates and cools blood externally then returns it to the central circulation. Regardless of the method chosen, it is important to cool the patient rapidly and to maintain the core temperature between 32° C and 34° C.
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 proved effective in human trials.
Current recommendations are to maintain a mean arterial pressure (MAP) of > 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 prearrest level. MAP is best measured with an intra-arterial catheter. Use of a flow-directed pulmonary artery catheter for hemodynamic monitoring has been largely discarded.
BP support includes
Patients with low MAP and low central venous pressure should have IV fluid challenge with 0.9% saline infused in 250-mL increments.
Although use of inotropic and vasopressor drugs has not proved to enhance long-term survival, older adults with moderately low MAP (70 to 80 mm Hg) and normal or high central venous pressure may receive an infusion of an inotrope (eg, dobutamine started at 2 to 5 mcg/kg/min). Alternatively, amrinone or milrinone is used (see Table 2: Drugs for Resuscitation*). If this therapy is ineffective, the inotrope and vasoconstrictor dopamine may be considered. Alternatives are epinephrine and the peripheral vasoconstrictors norepinephrine and phenylephrine (see Table 2: Drugs for Resuscitation*). However, vasoactive drugs should be used at 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 of the heart at a time when its capability is decreased because of postresuscitation myocardial dysfunction. If MAP remains < 70 mm Hg in patients who may have sustained an MI, intra-aortic balloon counterpulsation should be considered. Patients with normal MAP and high central venous pressure 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 that is 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, ventricular septal defect).
Although VF or VT may recur after resuscitation, prophylactic antiarrhythmic drugs do not improve survival and are no longer routinely used. However, patients manifesting such rhythms may be treated with procainamide or amiodarone (see First-line drugs).
Postresuscitation rapid supraventricular tachycardias occur frequently because of high levels of β-adrenergic catecholamines (both endogenous and exogenous) during 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 mcg/kg/min.
Patients who had arrest caused by VF or VT not associated with acute MI are candidates for an implantable cardioverter-defibrillator (ICD). Current ICDs are implanted similarly to pacemakers and have intracardiac leads and sometimes subcutaneous electrodes. They can sense arrhythmias and deliver either cardioversion or cardiac pacing as indicated.
Last full review/revision February 2013 by Robert E O'Connor'Connor, MD, MPH
Content last modified October 2013