Adult Resuscitation

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Chapter 9

Adult Resuscitation

Kevin R. Ward, Michael C. Kurz and Robert W. Neumar

Perspective

Epidemiology

It is estimated that 236,000 to 325,000 patients are treated for out-of-hospital cardiac arrest each year in the United States. The proportion of emergency medical services (EMS)–treated cardiac arrest patients with an initial rhythm of ventricular fibrillation (VF) has declined over time to one third or less in recent U.S. studies.1–4 Furthermore, the number of patients receiving bystander cardiopulmonary resuscitation (CPR) remains low, averaging only 26% in the home and 45% in public locations.⁵ Bystander automated external defibrillators (AEDs) are applied in 1% of home arrests and 8% of arrests in public settings.⁵

There is tremendous variability in survival to hospital discharge after EMS-treated cardiac arrest, ranging from 3 to 16.7% with a median of 7.9%.¹ For the subset of patients who achieve return of spontaneous circulation (ROSC) long enough to be admitted to the hospital, there is significant interinstitutional variability in survival ranging from 19 to 59%.⁶ Of patients surviving to hospital discharge, one third have persistent neurologic deficits, and less than half return to prearrest function. In patients meeting the inclusion criteria for clinical therapeutic hypothermia trials, favorable outcome has been reported in approximately 50% of comatose cardiac arrest survivors treated with hypothermia.^7,8 Subsequent studies implementing therapeutic hypothermia as part of a goal-directed post–cardiac arrest treatment protocol have reported rates of survival with good neurologic outcome ranging from 44 to 56%.^9,10 It is important to recognize that the entire system of care affects patient outcomes, and the variability in outcomes across the country likely reflects variability in how well these systems function.

Principles of Disease

Etiology

Understanding the causes of cardiac arrest helps direct therapy and diagnostic testing during resuscitation and in the immediate post–cardiac arrest period (Table 9-1). Cardiac arrest from a primary cardiac origin typically manifests as VF or much less often as pulseless ventricular tachycardia (VT). Coronary artery disease is the most common pathologic condition found in patients who die suddenly from VF; autopsy studies show a 75% incidence of previous myocardial infarction (MI) and a 20 to 30% incidence of acute MI.¹¹ Other anatomic abnormalities associated with sudden cardiac death caused by VF or VT include myocardial hypertrophy, cardiomyopathy, and specific structural abnormalities. Pulseless electrical activity (PEA) and asystole are less common presenting rhythms in patients with a cardiac cause of arrest. These rhythms most often occur as a deterioration of VF or VT or develop in response to resuscitation treatments, such as defibrillation.

Table 9-1

Common Causes of Nontraumatic Cardiac Arrest

CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

Primary respiratory failure generally causes initial hypertension and tachycardia, followed by hypotension and bradycardia and progressing to PEA, VF, or asystole. Circulatory obstruction (e.g., tension pneumothorax, pericardial tamponade) and hypovolemia generally manifest with initial tachycardia and hypotension, progressing through bradycardia to PEA, but also may deteriorate to VF or asystole.

The most common metabolic cause of cardiac arrest is hyperkalemia, which is seen most frequently in patients with renal failure. Hyperkalemia results in progressive widening of the QRS complex, which can deteriorate to VT, VF, asystole, or PEA. Other electrolyte abnormalities (e.g., hypomagnesemia, hypermagnesemia, hypokalemia) may lead to significant dysrhythmias, but the frequency with which they cause cardiac arrest is not documented.

Cardiac arrest from drug toxicity has specific characteristics depending on the drug involved. Specific therapy directed at drug toxicity is essential but may not be immediately effective. Prolonged resuscitation efforts involving a method that provides adequate perfusion may be needed.

Electrocution causes cardiac arrest through primary dysrhythmias or apnea. Alternating current in the range of 100 mA to 1 A generally causes VF, whereas currents greater than 10 A can cause ventricular asystole. Lightning produces a massive direct current electrocution that can result in asystole and prolonged apnea.

Hypothermia-induced cardiac arrest can manifest with any electrocardiogram (ECG) rhythm, and successful resuscitation depends on rapid rewarming, which often requires aggressive and invasive measures (e.g., intravascular rewarming, peritoneal lavage, cardiopulmonary bypass [CPB], open-chest cardiac massage [OCCM]). Drowning is a form of asphyxia usually resulting in bradyasystolic arrest. Because drowning often is accompanied by hypothermia, the victim may benefit from prolonged resuscitation efforts similar to resuscitation efforts for hypothermia.

Clinical Features and Management

Most cardiac arrest cases managed in the emergency department (ED) initially occur outside the hospital. An increasing number of first responders, nontraditional providers, and public venues are being equipped with AEDs. Dramatic resuscitation rates have been achieved when these programs enable providers and the lay public to deliver defibrillation within the first few minutes of arrest.12–15 Programs that fail to enable a significant number of patients to be defibrillated within this critical time window have limited or no effect on survival.^16,17

Advanced life support (ALS) units staffed by paramedics often have standing orders to follow advanced protocols. Because quality of CPR and time to defibrillation are the two most important determinants of outcome, there is no evidence to support interrupting properly performed advanced measures to transport a patient who is still in cardiac arrest. In cases of cardiac arrest refractory to properly performed advanced measures, the patient may be pronounced dead at the scene if appropriate protocols have been outlined within the system.¹⁸

Simultaneous assessment and management of cardiac arrest occurs in an orchestrated effort by a health care team led by an emergency physician who can make an ongoing assessment and monitor the efficacy and response to therapeutic interventions. It is often difficult or impossible to determine the cause of cardiac arrest at presentation. Although a differential diagnosis can be formulated based on history, physical examination, and ECG rhythm on arrival, key information often is not available or is unreliable.¹⁹ The differential diagnosis potentially can be narrowed by the patient’s age, underlying diseases, and medications when known.

History and Physical Examination

Historical information from the family, bystanders, and EMS personnel provides key information regarding cause and prognosis. Information surrounding the event includes whether the arrest was witnessed, the time of arrest, what the patient was doing (e.g., eating, exercising, trauma), the possibility of drug ingestion, time of initial CPR, initial ECG rhythm, and interventions by EMS providers. Important past medical history includes baseline health and mental status; previous heart, lung, renal, or malignant disease; hemorrhage; infection; and risk factors for coronary artery disease and pulmonary embolism. The patient’s current medications and allergies also should be obtained, if possible.

Physical examination of a cardiac arrest patient is necessarily focused on a few key goals: (1) ensure adequacy of airway maintenance and ventilation, (2) confirm the diagnosis of cardiac arrest, (3) find evidence of cause, and (4) monitor for complications of therapeutic interventions. This examination occurs in descending order of importance, simultaneously with therapeutic interventions, and is repeated frequently to assess for response to therapy and occurrence of complications (Table 9-2).

Table 9-2

Physical Examination Findings Indicating Potential Cause of Cardiac Arrest and Complications of Therapy

Cardiopulmonary arrest is defined by the triad of unconsciousness, apnea, and pulselessness. The pulse is palpated for in a large artery (carotid or femoral). If any question exists as to the diagnosis of pulselessness, CPR should be initiated. With sudden onset of cardiac arrest, as in VF, loss of consciousness occurs within 15 seconds, although agonal gasping respirations may persist for several minutes. A brief seizure may result from cessation of cerebral blood flow. Primary respiratory arrest results in transient tachycardia and hypertension that progress to loss of consciousness, bradycardia, and pulselessness.

After the initial minutes of cardiac arrest, physical examination may provide little evidence of the duration of arrest. Pupils dilate within 1 minute but constrict if CPR is initiated immediately and performed effectively. Dependent lividity and rigor mortis develop after hours of cardiac arrest. Temperature is an unreliable predictor of duration of cardiac arrest because it does not decrease significantly during the first hours of arrest. Moderate to severe hypothermia may cause cardiac arrest or may be caused by prolonged arrest, with opposite prognostic implications.

Monitoring

Traditional monitoring during CPR has relied on evaluation of the ECG in one or more leads and palpation of carotid or femoral artery pulses. Although the lack of a palpable pulse during CPR may indicate inadequate forward flow, the degree of forward flow cannot be estimated accurately in the presence of a palpable pulse because pressures generated during CPR may be transmitted equally to the venous and the arterial vasculatures. In addition, myocardial blood flow does not depend on the palpated arterial pressure during chest compression (CPR systole), but rather on the difference between aortic and right atrial pressure during relaxation (CPR diastole), which is defined as the coronary perfusion pressure (CPP). ECG monitoring during cardiac arrest indicates the presence or absence of electrical but not mechanical activity. Although these two monitoring modalities may be the best attainable in certain circumstances, they do not provide reliable information regarding the effectiveness of CPR and interventions or prognosis.

Unfortunately, no ideal monitoring technique provides all the information that might be desired during resuscitation, and even the modalities discussed next are often difficult or impossible to establish or interpret during CPR. A brief overview is provided of CPP, end-tidal carbon dioxide (ETCO₂), and central venous oxygen saturation (ScvO₂) monitoring, which if available can be used to detect inadequate CPR with high specificity (Table 9-3). In addition, several of these techniques are useful in the immediate post–cardiac arrest period.

Table 9-3

Indicators of Inadequate Blood Flow During Cardiopulmonary Resuscitation

MONITORING TECHNIQUE	INDICATOR
Carotid or femoral pulse	Not palpable
CPP	<15 mm Hg
Arterial relaxation (diastolic) pressure	<40 mm Hg
PETCO₂	<10 mm Hg (before vasopressor)
ScvO₂	<40%

CPP, coronary perfusion pressure; PETCO₂, partial pressure of CO₂ in exhaled air at the end of expiration; ScvO₂, central venous oxygen saturation.

Arterial Blood Pressure and Coronary Perfusion Pressure

Successful resuscitation of the arrested heart depends on generating adequate CPP during CPR, which has been directly correlated with myocardial blood flow.²⁰ Animal and human studies indicate that a minimum CPP of 15 mm Hg is necessary to achieve ROSC if initial defibrillation attempts have failed.^20,21 Unfortunately, CPP monitoring is rarely feasible in ED resuscitations of cardiac arrest patients, because it requires both an indwelling arterial pressure catheter and a central venous catheter, both transduced properly to provide simultaneous readings.

Invasive arterial blood pressure monitoring alone can be helpful in guiding resuscitation and should be used when an indwelling arterial pressure catheter is already in place. When adequate personnel are available, it is often feasible to cannulate the femoral artery during CPR, especially with ultrasound guidance. Human studies have shown that radial or femoral arterial relaxation pressures reliably reflect aortic relaxation pressures during CPR.22,23 Researchers have also reported that a CPP of 15 mm Hg or more was required to achieve ROSC and that no patient with an aortic relaxation pressure of less than 17 mm Hg achieved ROSC.^21,24 Titrating resuscitation efforts to arterial relaxation (diastolic) pressure is less reliable than CPP because improper CPR (e.g., leaning on chest during CPR diastole and hyperventilation) can cause undetected elevations in right atrial pressure, reducing coronary perfusion. Despite this limitation, it is reasonable to titrate resuscitation efforts to achieve an arterial relaxation (diastolic) pressure of 40 mm Hg or more when invasive arterial pressure monitoring is available. Invasive arterial pressure monitoring during CPR may also be useful to facilitate distinguishing PEA that does or does not result in mechanical heart contraction, to detect ROSC, and to assist in serial arterial blood gas monitoring. Although arterial and central venous catheters are most often placed in the post–cardiac arrest phase of care, a significant number of patients initially achieving ROSC will rearrest in the ED, making these modalities helpful during the patient’s subsequent resuscitation.

End-tidal Carbon Dioxide

The partial pressure of CO₂ in exhaled air at the end of expiration (PETCO₂) can be a reliable indicator of cardiac output during CPR. This is most reliably measured through waveform capnography after endotracheal intubation. PETCO₂ depends on CO₂ production, alveolar ventilation, and pulmonary blood flow (i.e., cardiac output) and correlates well with CPP and cerebral perfusion pressure during CPR.24,25 Therefore when minute ventilation is held constant (a desirable but often unmet goal) and no exogenous CO₂ is introduced (e.g., sodium bicarbonate [NaHCO₃] administration), only increased cardiac output during CPR and ROSC significantly increases PETCO₂. Resuscitation after cardiac arrest is likely to fail if PETCO₂ values are less than 10 mm Hg,^26,27 and such values should prompt the clinician to enhance the quality of CPR (either rate or force of compression) or consider more invasive maneuvers such as extracorporeal membrane oxygenation (ECMO) if the situation warrants and a good neurologic outcome is believed to be possible.²⁸

PETCO₂ monitoring also can aid in the diagnosis and treatment of PEA. Patients in a state of PEA with mechanical heart activity may have pulsatile flow that simply cannot be detected by palpation of a pulse. In such circumstances, PETCO₂ levels may be elevated even without compressions. Use of cardiac ultrasound in such cases can prove to be helpful in identifying corresponding cardiac activity. In such cases, volume expansion or the use of vasopressors and inotropes should be considered. PETCO₂ monitoring also is useful in rapidly detecting success of tension pneumothorax decompression, pericardiocentesis for pericardial tamponade, and fluid resuscitation for hypovolemia. ROSC causes immediate and significant increases in PETCO₂. Therefore PETCO₂ monitoring can detect ROSC at any time during the chest compression cycle, providing valuable guidance for pharmacologic therapies and minimizing the need for a pulse check when organized rhythms are detected (Fig. 9-1).

Figure 9-1 Capnogram tracings of end-tidal carbon dioxide partial pressure (PETCO₂) during human cardiopulmonary resuscitation (CPR). 1, Effect of rescuer fatigue is shown at point A. Point B shows the effect of changing to a fresh rescuer. 2, Patient with pseudoelectromechanical dissociation. At point A, the patient is pulseless but has a persistent PETCO₂ value of 20 mm Hg without CPR; at point B, CPR is restarted; at point C, dopamine infusion is started; and at point D, CPR is stopped and a pulse is palpated. 3, Sudden increase in PETCO₂ (point A) heralds the return of spontaneous circulation; pulses are palpated at point B. 4, Point A shows a transient increase in PETCO₂ such as occurs during bolus administration of sodium bicarbonate.

Finally, PETCO₂ monitoring is valuable in patients after ROSC to monitor endotracheal tube placement (waveform capnography recommended), titrate minute ventilation to avoid hyperventilation, and detect sudden hemodynamic deterioration.

Interventions are performed rapidly and efficiently to maximize the chances of a good neurologic outcome. The quality of CPR is perhaps the most underappreciated component of the resuscitation effort.³² Important quality performance measures include compression rate (at least 100 per minute), compression depth (>5 cm), duty cycle (CPR being performed at >50% of pulseless interval) full relaxation, and minimum pauses, especially before and after defibrillation.³³ Furthermore, hyperventilation has been shown to be common and reduces cardiac output during CPR.^34,35 A 30 : 2 compression-to-ventilation ratio is currently recommended for health care professionals in all adult resuscitation scenarios until an advanced airway has been established.³⁶ Once the airway is secured, CPR should be performed continuously without pausing, while providing six to eight ventilations every minute.³⁶ As indicated earlier, if PETCO₂ is to be helpful as an indicator of cardiac output during CPR, minute ventilation should be relatively constant. Although recent evidence suggests that chest-compression–only CPR is as effective as traditional CPR when performed by bystanders in the out-of-hospital setting, there is inadequate evidence to recommend this as an alternative strategy for heath care professionals. Whereas oxygen uptake from the lungs is low during CPR, oxygen remaining in the functional residual capacity of the lung will reach a critically low value as CPR progresses if not replenished. The exception to this is when inadequate personnel are present to provide compressions, ventilation, and other resuscitative activites.³⁷ Intubation should be performed only when capable personnel are available and without interruption of chest compressions. Use of supraglottic airway adjuncts such as the esophageal tracheal Combitube or laryngeal mask airway may be good alternatives for airway management in the out-of-hospital phase of resuscitation, with the main disadvantage being the inability to use the trachea as a route of drug administration and lack of evidence regarding the reliability of use of PETCO₂ to monitor cardiac output during CPR. In addition to monitoring specific CPR performance parameters, physiologic monitoring, if available, can help optimize CPR quality for the individual patient (see Table 9-3). If the inadequacy of CPR is recognized early in the resuscitation despite optimized therapy, the physician in charge may consider more invasive measures such as ECMO if ROSC and a good neurologic outcome are possible. After prolonged arrest, however, clear indications that CPR is inadequate (based on appropriate monitoring techniques) should prompt cessation of resuscitation efforts. Figure 9-2 is an algorithm for management of cardiac arrest. Interventions specific to each rhythm are discussed in the following sections.

Figure 9-2 Emergency treatment algorithm for treatment of cardiac arrest. ^aIf arrest is witnessed and known to be of short duration, immediate rhythm assessment and defibrillation or ventricular fibrillation/ventricular tachycardia (VF/VT) precede cardiopulmonary resuscitation (CPR). In cases of prolonged untreated VF/VT, 1 to 2 minutes of CPR before defibrillation may enhance the ability to achieve return of spontaneous circulation. EMD, electromechanical dissociation; PEA, pulseless electrical activity. ^bBiphasic defibrillation should use manufacturer-recommended energy versus monophasic defibrillation (360 J). ^cSee Table 9-4. ^dEndotracheal intubation or supraglottic airway when feasible with minimal interruption in chest compressions. ^eEpinephrine, initial dose of 1 mg intravenously (IV) or intraosseously (IO) or 2.5 mg by endotracheal tube (ETT). Repeat every 3 to 5 minutes. Subsequent doses may be increased up to 0.1 mg/kg. An alternative to epinephrine is vasopressin, 40 U via intravenous push. Vasopressin is potentially more effective if the presenting rhythm is asystole. The dose (40 U) can be repeated once in 3 minutes, followed by administration of epinephrine every 3 to 5 minutes. ^fAmiodarone, 300 mg via intravenous push followed by 150 mg every 30 minutes. Lidocaine is an alternative antidysrhythmic if amiodarone is not available. Magnesium sulfate, 1 to 2 g via intravenous push in torsades de pointes or known hypomagnesemia. ^gAtropine, 1 mg via intravenous push or 2.5 mg by ETT. Repeat dose every 3 to 5 minutes to a total dose of 0.04 mg/kg. AoDP, aortic diastolic pressure; ECG, electrocardiogram; ScvO₂, central venous oxygen saturation. ^hChanges in the partial pressure of end-tidal carbon dioxide (PETCO₂) may not be predictive of myocardial blood flow in the setting of high-dose vasopressor therapy. ⁱInvasive monitoring should be performed only if adequate personnel are available and if it would not delay therapeutic interventions.

Ventricular Fibrillation and Pulseless Ventricular Tachycardia

VF and pulseless VT are treated identically because they are generally caused by the same mechanisms and respond to the same interventions. Traditional monophasic defibrillators that use either a monophasic truncated exponential (MTE) or a monophasic dampened sinusoidal (MDS) waveform have almost completely been replaced by defibrillators that use biphasic waveforms. With biphasic defibrillation, the energy required for successful defibrillation, or the “defibrillation threshold,” is less than with monophasic defibrillation. When used, the biphasic waveform increases the likelihood of initial defibrillation success and decreases the likelihood of postcountershock myocardial dysfunction. Despite documented advantages of lower defibrillation threshold and reduced myocardial injury with use of biphasic defibrillation, data are currently inadequate to conclude that any specific waveform (biphasic or monophasic) is superior to any other in achieving ROSC or survival to hospital discharge. New defibrillation technologies have stimulated reevaluation of optimal defibrillation strategies. Current consensus suggests that the most effective strategy is delivery of single countershocks at optimal energy levels with minimal pauses in CPR both before and immediately afterward.³⁸ This is facilitated by placement of defibrillation pads early in the resuscitation sequence, thus not requiring a pause while defibrillation paddles and conducting gel are placed for each shock. Manufacturer-recommended countershock energies range from 120 to 360 J for biphasic defibrillators.³⁸ Health professionals should use the manufacturer-recommended countershock energies for biphasic defibrillator(s). The recommended energy for single monophasic defibrillation is 360 J.³⁶

A patient who develops VF or pulseless VT while on a cardiac monitor may remain conscious for 15 to 30 seconds. The patient should be encouraged to cough vigorously until a defibrillator is available. This “cough CPR” has been demonstrated to keep patients conscious for up to a minute or more. If the patient is unresponsive, chest compressions should be initiated immediately and continued until a defibrillator is available. Defibrillation without antecedent CPR is most likely to result in ROSC when administered in the early minutes of arrest. If the duration of untreated arrest is prolonged (>4-5 minutes), a brief period of chest compressions and ventilations (90-180 seconds) before defibrillation may improve the likelihood of ROSC and survival.34,39,40 The current consensus favors delivering a single countershock with minimal pause in chest compressions before defibrillation.³⁸ Defibrillation is followed immediately by resumption of chest compressions for 2 minutes before a rhythm check and additional defibrillation as appropriate.³⁶

VF and pulseless VT refractory to initial defibrillation should be treated with assisted ventilation and chest compression. Intravenous access and vasopressor therapy (epinephrine or vasopressin) should be administered and repeated every 3 to 5 minutes. Simultaneous administration of epinephrine and vasopressin does not improve outcome relative to epinephrine alone regardless of presenting rhythm.⁴¹

Defibrillation attempts should be preceded and followed by minimal interruptions of chest compression.³⁶ Subsequent therapy for refractory VF and pulseless VT includes continued administration of vasopressors and antidysrhythmic agents, followed by repeated countershocks. Antidysrhythmics should be administered up to their maximum loading dose. The use of magnesium sulfate during VF and pulseless VT is of no proven efficacy except in torsades de pointes and possible hypomagnesemia. Beyond the specific indications for NaHCO₃ therapy of hyperkalemia and tricyclic antidepressant overdose, there is no evidence to support use of NaHCO₃ or other buffers as empirical treatment for metabolic acidosis during cardiac arrest. If a patient is defibrillated into a different pulseless rhythm, such as PEA or asystole, subsequent treatment should be modified to address those specific rhythms.

Pulseless Electrical Activity

PEA is defined as coordinated electrical activity of the heart (other than VT/VF) without a palpable pulse. This group of dysrhythmias includes electromechanical dissociation (EMD), in which no myocardial contractions occur, and pseudo-EMD, in which myocardial contractions occur but no pulse can be palpated. Although distinguishing EMD from pseudo-EMD may be useful in determining cause and guiding treatment, in most cases of primary PEA there is a natural progression from hypotension to pseudo-EMD to EMD.

True EMD is the result of a primary disorder of electromechanical coupling in myocardial cells. It often is associated with abnormal automaticity and conduction resulting in bradycardia and a wide QRS complex. Although the mechanism of uncoupling is unclear, it most often is associated with global myocardial energy depletion and acidosis resulting from ischemia or hypoxia. True EMD typically occurs after defibrillation following prolonged VF and is associated with hyperkalemia, hypothermia, and drug overdose.

Pseudo-EMD caused by global myocardial dysfunction is a transient state in the progression to EMD and has the same cause. An additional cardiac cause of pseudo-EMD is papillary muscle and myocardial wall rupture, in which the ventricle continues to contract, but forward flow is greatly diminished. Pseudo-EMD also may be caused by primary supraventricular tachycardia. Additional extracardiac causes of pseudo-EMD include hypovolemia, tension pneumothorax, pericardial tamponade, and massive pulmonary embolism. Pseudo-EMD of extracardiac origin most often has narrow-complex tachycardia initially, which can progress to bradycardia with conduction abnormalities and QRS widening.

Treatment of PEA requires all general resuscitation measures, including CPR, intubation with assisted ventilation, intravenous access, and repeated administration of vasopressors. Initial assessment also should include vascular Doppler ultrasound, echocardiography, or PETCO₂ monitoring to distinguish EMD from pseudo-EMD. This is important because volume loading or continuous vasopressor infusion, which is not typically used in routine cardiac arrest resuscitation, may be helpful in cases of pseudo-EMD. In contrast, routine use of atropine during PEA, previously a mainstay of drug therapy, is unlikely to have a therapeutic benefit.³⁸ PEA thought to result from supraventricular tachycardia should be immediately cardioverted. These interventions alone are generally inadequate, unless the underlying cause of PEA is primary respiratory arrest or supraventricular tachycardia. Successful resuscitation of patients with PEA hinges on rapid diagnosis and treatment of the underlying cause. Physical examination may provide valuable clues to the underlying cause (Table 9-4). In hypoxia and hypovolemia, the diagnosis is based on response to empirical therapy, whereas other causes, such as pericardial tamponade, tension pneumothorax, and hypothermia, can be definitively diagnosed during resuscitation. Physical examination and monitoring are used to guide ongoing resuscitation efforts.

Table 9-4

Diagnosis and Treatment of Common Causes of Pulseless Electrical Activity

CPB, cardiopulmonary bypass; OCCM, open-chest cardiac massage.

Asystole

Asystole represents complete cessation of myocardial electrical activity. Although asystole may occur early in cardiac arrest as a consequence of progressive bradycardia, asystole generally represents the end-stage rhythm after prolonged cardiac arrest caused by VF or PEA. Because the potential exists for an organized rhythm or VF to appear as asystole in a single lead (if the rhythm vector is completely perpendicular to the lead vector), asystole should be confirmed in at least two limb leads. Although asystole may be difficult to distinguish from extremely fine VF, routine countershock of asystole has not been shown to improve survival.

Treatment of asystole requires all general resuscitation measures, including CPR, intubation with assisted ventilation, intravenous access, and repeated administration of vasopressors. In one randomized prospective out-of-hospital trial, improved survival to hospital admission and discharge was observed in patients in asystole when two doses of vasopressin (40 IU) were given initially during resuscitation compared with standard-dose epinephrine (1 mg), followed by additional epinephrine if needed.⁴² In a more recent study, simultaneous administration of epinephrine and vasopressin did not improve outcome relative to epinephrine alone, regardless of presenting rhythm.⁴¹ Available evidence indicates that routine administration of atropine is not beneficial.³⁶ Extensive research has shown that asystole in the out-of-hospital setting seldom responds to pacing. To be effective, pacing must be initiated within several minutes of arrest.

Post–Cardiac Arrest

Resuscitation of a cardiac arrest victim does not end with ROSC. Management includes rapid diagnosis and treatment of the disorders that caused the arrest and the complications of prolonged global ischemia. Simultaneous management of these two entities makes caring for a post–cardiac arrest patient particularly challenging. A comprehensive goal-driven program of post–cardiac arrest care is most successful in affecting survival and neurologic status.9,10

Induction of prolonged therapeutic hypothermia in comatose survivors of cardiac arrest has been shown to improve survival and functional outcome in two prospective randomized clinical trials.7,8 Both studies enrolled only out-of-hospital patients with witnessed arrest and an initial rhythm of VF. The time to achieve target temperature (<34° C) ranged from less than 2 hours to a median of 8 hours (interquartile range 4-16 hours),^7,8 suggesting a broad therapeutic window. Hypothermia was maintained for 12 to 24 hours, followed by gradual rewarming over 12 to 24 hours. Although these parameters provide guidelines within which post–cardiac arrest hypothermia is effective, additional preclinical and clinical data are needed to determine the optimal temperature, time to achieve target temperature, and duration of therapy. In both studies, the rates of complications were not statistically different between groups. Although there are no absolute contraindications, relative contraindications include severe cardiogenic shock, life- threatening dysrhythmias, uncontrolled bleeding, preexisting coagulopathy, pregnancy, another obvious reason for coma (e.g., drug overdose or status epilepticus), known end-stage terminal illness, and a preexisting do-not-resuscitate status. Thrombolytic therapy does not preclude the use of hypothermia.⁸ Finally, whereas initial studies were limited to patients with witnessed VF out-of-hospital cardiac arrest, evidence is accumulating that induced post–cardiac arrest therapeutic hypothermia is effective in patients with other presenting rhythms including PEA and asystole.^43,44

When the decision is made to treat the patient with therapeutic hypothermia, cooling efforts should be initiated as soon as possible. Practical methods of rapidly inducing hypothermia include ice packs (applied to the neck, inguinal areas, and axilla), fan cooling of dampened exposed skin, cooling blankets underneath and on top of the patient, and disabling of ventilator warming circuits. Rapid intravenous infusion of limited volumes (1-2 L) of 4° C saline facilitates rapid cooling, but additional measures are needed to maintain hypothermia as this initial cold fluid bolus will lose its heat transfer properties during circulation.⁴⁵ A number of automated surface cooling devices are now available that use chest and thigh pads and continuous temperature feedback from bladder or esophageal temperature probes. Although these devices were developed to make cooling less labor intensive and faster, some difficulties inherent with surface cooling remain, including overshooting and maintaining target temperature (SD usually > 1° C),⁴⁶ uncontrolled rewarming with frequent rebound hyperthermia, and inability to assess skin for cutaneous reactions and injury.⁴⁷ Automated endovascular cooling systems are also available that require placement of a central venous catheter. Although more invasive, cooling with a heat exchange catheter inserted in the inferior vena cava is the most rapid practical method of cooling and offers the tightest control of temperature at target (SD usually < 0.3° C) and during controlled rewarming.⁴⁸ Endovascular systems are far less nursing labor-intensive than surface cooling because they monitor core temperature and are automatically controlled through a feedback loop.⁴⁹ No one cooling strategy or device has been demonstrated to result in superior clinical outcomes.

Shivering, which inhibits cooling, can be prevented with sedation and neuromuscular blockade. If neuromuscular blockade is continued during the maintenance phase of therapeutic hypothermia, continuous electroencephalographic monitoring is strongly encouraged because seizures are common in post–cardiac arrest patients (5-20%).⁹ Target core body temperature is 32 to 34° C and is best monitored by an indwelling temperature-sensitive bladder catheter or esophageal temperature probe.⁵⁰ When the patient is stabilized and cooling efforts are initiated, transfer to a critical care unit should occur as soon as possible. Although the optimal duration of post–cardiac arrest hypothermia is unknown and may be related to the total ischemic time,⁵¹ target temperatures are typically actively maintained for at least 12 to 24 hours, followed by gradual rewarming over 8 to 12 hours.⁵² Effective application of therapeutic hypothermia in comatose cardiac arrest survivors requires a coordinated interdisciplinary effort and is best carried out through use of a predetermined goal-directed algorithm developed with input from emergency medicine, cardiology, and critical care physicians and nurses.

A simultaneous immediate concern in a comatose cardiac arrest survivor is whether the patient has an acute coronary syndrome. Diagnosing acute coronary syndrome in an unconscious patient after cardiac arrest presents a unique challenge. A standard 12-lead ECG should be obtained as soon as feasible after ROSC, with additional right-sided and/or posterior leads as indicated. In one study, 50% of patients achieving ROSC after out-of-hospital cardiac arrest were found to have acute coronary occlusion on cardiac catheterization; 10% of them did not have ST segment elevation.¹⁹ Subsequent studies have reported that successful immediate percutaneous coronary intervention (PCI) is associated with improved hospital survival in post–cardiac arrest patients with or without ST segment elevation.⁵³

Immediate PCI is indicated in post-ROSC patients with ST segment elevation MI or new left bundle branch block (LBBB), or high clinical suspicion of acute MI, and can be performed during therapeutic hypothermia.54–58 When PCI is indicated but not available, either early transfer of post–cardiac arrest patients to a center capable of PCI or fibrinolytic therapy should be considered.⁵⁹ Relative exclusion criteria for fibrinolytic therapy unique to the post–cardiac arrest patient include evidence of significant CPR trauma (e.g., pneumothorax, flail chest, pulmonary contusion with hemorrhage), but the effects of therapeutic hypothermia on the efficacy and complications of fibrinolytic therapy in postarrest patients have not been formally studied.

Antiplatelet and anticoagulant therapy should be administered to all patients after ROSC, whether or not therapeutic hypothermia is induced, if no evidence of hemorrhage exists and profound hypertension is absent. The choice of antiplatelet and anticoagulant therapy depends in part on the presence of active ischemia, renal function, and plans for acute angioplasty.⁶⁰ There is no proven benefit of prophylactic antiarrhythmic therapy or continuous infusion of an antiarrhythmic drug that has been associated with restoration of a stable rhythm during CPR. Concomitant therapies (e.g., nitrates, beta-blockers) are best performed in conjunction with careful hemodynamic monitoring. If indicated, intravenous preparations of nitrates and short-acting beta-blockers (e.g., esmolol) should be used because they have a brief duration of action and are easily titrated. In patients with new LBBB, right bundle branch block with left anterior or posterior hemiblock, second-degree type II block, or third-degree block, transthoracic pacing pads are immediately applied in case they are needed to treat bradycardic rhythms. Placement of transvenous pacing catheters also can be considered but is less often done with the increasing use and demonstrated efficacy of transthoracic cardiac pacing.⁶¹

Inadequate oxygen delivery (DO₂) causes cells to convert to anaerobic metabolism, resulting in increased lactate production (dysoxia). Continued resuscitation efforts to optimize DO₂ may help to stabilize the patient and potentially prevent subsequent multiorgan dysfunction and recurrent arrest. However, supranormal arterial oxygen partial pressure can exacerbate oxidative brain injury during the first minutes to hours after cardiac arrest. Therefore the fraction of inspired oxygen (FIO₂) can be titrated to the minimum concentration required to maintain an arterial oxyhemoglobin saturation around 94%. This level of oxygenation avoids detrimental hyperoxia while ensuring appropriate oxygen delivery.⁶²

During cardiac arrest and CPR, DO₂ is well below necessary levels. On ROSC, resuscitation efforts should continue to establish adequate systemic DO₂. Serum lactate levels provide an indirect measure of whether DO₂ is adequate to prevent anaerobic metabolism. A single lactate level is almost universally elevated after resuscitation from cardiac arrest. Detection of ongoing lactate production requires monitoring of serial lactate levels. Insufficient DO₂ also causes increased oxygen extraction, resulting in decreased . Low coupled with persistently elevated lactate levels indicates inadequate DO₂. Patients with prolonged duration of CPR and those who have received high-dose vasopressor therapy during CPR may develop impaired tissue oxygen extraction^. In such patients, is abnormally high (venous hyperoxia) in the face of inadequate DO₂ and likely represents a state of severe systemic shunting resulting in an increase in non-nutritive blood flow. Lactate levels in these circumstances continue to be elevated. Thus the combination of sustained elevated lactate levels along with normal or elevated ScvO₂ levels indicate severe systemic shunting. Treatments for this include carefully reducing any continuous infusion of vasopressors and more aggressive volume loading. The use of guided vasodilator therapy to open up underperfused tissue beds as well as consideration of mechanical adjuncts such as intra-aortic balloon pumping may also be necessary in this situation.

The use of combined hemodynamic and metabolic endpoints to guide resuscitation in the ED has been shown to improve the outcome of patients with septic shock states.⁶³ Because the post–cardiac arrest condition represents a complex state of cardiovascular shock, the use of such goal-directed therapy is inherently valuable to reduce mismatches of oxygen delivery and consumption that cannot be determined by simple physical examination and vital signs. Use of goal-directed hemodynamic therapy is relatively straightforward and requires only the insertion of a supradiaphragmatic central venous catheter. ScvO₂ can be used as a reliable surrogate for , which eliminates the need for a pulmonary artery catheter.²⁹ If ScvO₂ is abnormally low (<65%) but hemoglobin and SaO₂ values are normal, cardiac output is insufficient. Central venous pressure (CVP) is used to deduce whether inadequate cardiac output is secondary to hypovolemia or impaired myocardial function. Augmenting CVP to levels between 10 and 15 mm Hg ensures adequate preload in most patients. If CVP is adequate and the patient has a mean arterial pressure of at least 70 mm Hg, therapy with an inotropic agent, such as dobutamine, should be initiated while reperfusion strategies are considered. CVP measurements may decrease rapidly on initiation of dobutamine therapy. Additional volume expansion while the hemoglobin value is kept at least at 10 g/dL should be provided as needed to maintain an adequate CVP.