Adult Resuscitation

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Chapter 9

Adult Resuscitation



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


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.

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).

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.


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

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).

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.

Central Venous Oxygen Saturation

ScvO2, when available, provides an additional method to monitor adequacy of resuscitative measures. The mixed venous blood oxygen saturation in the pulmonary artery (image) represents the oxygen remaining in the blood after systemic extraction. Studies have shown a close correlation between ScvO2 and image during CPR.29 Because oxygen consumption remains relatively constant during CPR, as do arterial oxygen saturation (SaO2) and hemoglobin, changes in ScvO2 reflect changes in oxygen delivery by means of changes in cardiac output.

Although used primarily in the intensive care unit (ICU) setting, multilumen oximetric ScvO2 catheters are placed in the same manner as regular central venous catheters and can be used to monitor ScvO2 continuously in real time. ScvO2 values normally range from 60 to 80%. During cardiac arrest and CPR, these values range from 25 to 35%, indicating greatly enhanced oxygen extraction of tissues owing to the inadequacy of oxygen delivery during CPR. Failure to achieve an ScvO2 of 40% or greater has a negative predictive value for ROSC of almost 100%.29 ScvO2 also helps to rapidly detect ROSC without interruption of chest compressions, as ROSC will result in a rapid increase in Scvo2 as a result of a dramatic increase in oxygen delivery to tissues. ScvO2 monitoring is also useful in the post–cardiac arrest period for hemodynamic optimization and for recognition of any sudden deterioration in the patient’s clinical condition.