INTRODUCTION
In 1960, an article was published in the Journal of the American Medical Association that became the single most influential study in twentieth-century medicine. The article, titled “Closed-Chest Cardiac Massage,” presented five cases of acute cardiopulmonary arrest. Although recovery in each case can be attributed to other interventions (e.g., intubation and cardioversion), the conclusion of the report stated, “Closed-chest cardiac massage has been proved to be effective in cases of cardiac arrest”. This report represents the birth of what is known today as cardiopulmonary resuscitation (CPR). CPR is far from successful as a life-saving intervention. Yet despite this poor performance, CPR not only is a universally accepted practice, but is considered a human right.
This chapter describes the mechanical and pharmacologic interventions involved in the management of cardiac arrest. Also included are recommendations for clinical monitoring during CPR and some concerns in the early postresuscitation period. A more detailed description of this topic is available in the American Heart Association guidelines for basic and advanced cardiac life support (see Suggested Readings at the end of the chapter).
BASIC LIFE SUPPORT
The ABCs of basic life support are Airway, Breathing, and Circulation. Clearing the airway is achieved by maneuvers such as the Heimlich maneuver that relieve airway obstruction. Breathing is achieved by mouth-to-mouth resuscitation. Circulation involves closed-chest cardiac massage. Circulation is the heart of basic life support, and it is performed as follows:
CHEST COMPRESSIONS
1. Place the heel of one hand on the lower half of the patient’s sternum so that the long axis of the hand runs perpendicular to the long axis of the sternum. Place the other hand, palm down, on top of the sternal hand, and interlace the fingers while keeping them off the chest.
2. Lock the elbows so that both arms are kept straight, and, with the shoulders positioned directly above the point of contact, depress the sternum by 1.5 to 2 inches at a rate of 80 to 100 times per minute. The duration of chest compression should take up half of the total compression-release cycle. The traditional ratio of chest compressions to lung inflations is 5:1.
3. If Steps 1 and 2 do not produce a palpable carotid or femoral pulse, increase the force of chest compressions.
Problems
The weak link in CPR is the inability of chest compressions to achieve adequate flow to the vital organs. In the original report in 1960, the ability to achieve a palpable pulse with chest compressions was mistakenly interpreted as indicating that chest compression could achieve adequate systemic blood flow. The pressure tracings in this figure are taken from a patient who received standard CPR with rhythmic chest compressions performed as just described. Note that similar pressures were achieved in the radial artery and the right atrium (the right-atrial pressure was recorded through a central venous catheter). Therefore, even though the chest compressions produced a systolic blood pressure slightly greater than 50 mm Hg, the arteriovenous pressure difference, which is the principal determinant of systemic and regional blood flow, is negligible. This is why blood flow in both systemic and regional (e.g., coronary) circulations is less than one-quarter of prearrest levels during closed-chest compressions. It also explains why CPR has had such a poor success rate. (If the original investigators had evaluated a venous pressure tracing during chest compressions, we may have been spared many of the false claims about CPR that predominate today.)
Coronary Perfusion Pressure
The difference between aortic pressure and right-atrial pressure, called coronary perfusion pressure (CPP), is the pressure gradient that drives coronary blood flow. Studies of CPR outcomes in humans show that a CPP of at least 15 mm Hg is necessary for a satisfactory outcome.
ACTIVE COMPRESSION-DECOMPRESSION CPR
In 1990, a case was reported where a cardiac arrest patient was resuscitated with a toilet plunger applied to the anterior chest wall. This led to the development of a plunger device that, when applied over the sternum, produces alternating chest compression and decompression. Although this device can produce higher cardiac outputs than standard chest compressions, clinical trials with this device have not resulted in higher survival rates in either out-of-hospital or in-hospital cardiac arrests.
OPEN-CHEST CARDIAC MASSAGE
Emergency thoracotomy with direct cardiac massage can achieve normal and even supranormal rates of blood flow during CPR. Unfortunately, the role of open-chest cardiac massage is limited by the reluctance to perform this procedure on cardiac arrest patients.
ADVANCED LIFE SUPPORT
Advanced life support (also called advanced cardiac life support, ACLS) includes maneuvers such as airway intubation, mechanical ventilation, and adjunctive measures (e.g., electric shock and drug administration) to enhance cardiac performance and promote blood flow. The following description focuses on the adjunctive measures used to promote cardiac output during CPR.
DEFIBRILLATION
Direct-current cardioversion is the single most effective resuscitative measure for improving survival in cardiac arrest. In patients with ventricular tachycardia and ventricular fibrillation, the time from cardiac arrest to defibrillation is the most important factor in determining outcomes. The data in this figure are taken from a study of 1667 cardiac arrest patients with ventricular fibrillation. Note that survival decreases linearly with increasing time to defibrillation. Survival decreased from 40% to less than 10% when defibrillation was delayed 15 minutes (from 5 to 20 minutes after arrest). These results emphasize the importance of avoiding delays in initiating defibrillation.
Dosage
The strength of defibrillation is usually expressed in units of energy (joules) rather than units of electric current (amperes). The recommended energy for three successive defibrillations (if necessary) is 200 J, then 300 J, then 360 J. If the initial three defibrillation attempts are unsuccessful, (e.g., epinephrine and lidocaine) are administered and the sequence of cardioversions is repeated. This pattern of defibrillations-drugs-defibrillations is the basic management strategy for ventricular tachycardia and fibrillation.
ROUTES OF DRUG ADMINISTRATION
Central versus Peripheral Veins
The initial site of venous cannulation for CPR should be the external jugular vein or the veins in the antecubital fossa (because these sites do not interfere with chest compressions and endotracheal intubation). Drug administration through peripheral veins should always be bolus injection, followed by a 20-mL saline flush. If spontaneous circulation does not return after the initial drug injection, central venous cannulation should be performed for subsequent drug administration. This latter maneuver reduces the circulation time for drug distribution by at least 2 minutes.
Endobronchial Drug Administration
When venous access is not readily available and an endotracheal tube is in place, certain drugs can be injected through the endotracheal tube. The drugs that can be given via the endobronchial route are atropine, epinephrine, and lidocaine. The endobronchial dose is twice the recommended intravenous dose for each drug. Epinephrine seems to be less effective when given via the endobronchial route, and more than twice the recommended intravenous dose of epinephrine may be necessary to produce the desired result when the drug is given endobronchially. All drugs injected into the airways should be diluted in 10 mL saline or sterile water, and the injection should be made through a long catheter (such as a 20-cm central venous catheter) whose tip extends beyond the tip of the endotracheal tube. Drugs should not be injected directly into the endotracheal tube. Chest compressions should be discontinued while the drug is injected into the upper airways, and the injection should be followed with a few manual lung inflations. This maneuver is effective in promoting drug absorption from the lung (13).
EPINEPHRINE
Intravenous epinephrine is a mainstay in ACLS and is indicated for pulseless ventricular tachycardiac and ventricular fibrillation, electromechanical dissociation, and ventricular asystole. The rationale for epinephrine administration is to promote systemic vasoconstriction and thereby direct blood flow to the coronary and cerebral circulations.
Dosage
The standard dose of epinephrine in ACLS protocols is 1 mg (10 mL of a 1:10,000 solution), repeated every 3 to 5 minutes if necessary. The optimal dose of epinephrine in CPR may actually be much higher, particularly in larger patients. In animal studies, the optimal hemodynamic dose of epinephrine is 0.045 to 2.0 mg/kg, which is considerably higher than the standard epinephrine dose recommended in human ACLS protocols. However, two clinical studies evaluating high-dose epinephrine (7 mg in one study, 0.2 mg/kg in the other) in CPR show no increase in survival with the high-dose regimens compared with standard-dose regimens. Despite the lack of evidence for improved outcomes with high-dose epinephrine, the American Heart Association now recommends that epinephrine doses can be increased to 5 mg if there is no response to an initial 1-mg dose of the drug.
ATROPINE
Atropine is probably one of the least effective drugs in the ACLS armamentarium. It is most effective for the management of bradycardias, but it is also recommended in the management of pulseless electrical activity and ventricular asystole.
Dosage
The recommended dose of atropine for electromechanical dissociation and asystole is 1 mg by intravenous injection, repeated every 3 to 5 minutes if necessary. A total dose of 3 mg (or 0.04 mg/kg) produces complete vagal blockade, so this dose should not be exceeded. Atropine doses that are less than 0.5 mg can have parasympathomimetic effects (i.e., they can promote bradycardia), and thus should be avoided.
BICARBONATE
The recommendations for bicarbonate administration in CPR have been revised considerably in recent years because of an accumulation of studies showing little benefit and possible harm associated with bicarbonate administration in metabolic acidoses. Of note is recent evidence showing that bicarbonate administration in doses recommended for CPR (1 mg/kg) does not result in enhanced vasopressor actions of epinephrine.
As indicated at the bottom of the table, bicarbonate is no longer recommended in patients with ischemic lactic acidosis. In fact, it is considered potentially harmful in this condition.
CALCIUM
Despite the fact that extracellular calcium enhances the contractile force of cardiac muscle, there is no evidence to indicate that calcium administration during CPR improves cardiac performance. In fact, ischemia promotes the intracellular accumulation of calcium, and this can lead to membrane disruption and uncoupling of oxidative phosphorylation. Because of the risk of calcium accumulation and subsequent cell injury during periods of tissue ischemia, the indications for calcium administration during CPR are restricted to cases of acute hyperkalemia, ionized hypocalcemia, and calcium channel blocker overdose.
DEXTROSE INFUSIONS
Although dextrose is a popular additive in intravenous fluids, dextrose administration can have deleterious effects in critically ill patients. Dextrose infusions can enhance the production of lactic acid in critically ill patients. The accumulation of lactic acid can itself promote cell injury, possibly by promoting the formation of toxic oxygen metabolites. This may explain why hyperglycemia enlarges infarct size in animal studies of cerebrovascular occlusion. The impact of carbohydrate infusions during CPR is not clear. However, the current recommendations from the American Heart Association are that dextrose infusions are a Class III intervention (harmful) and thus should be avoided.
CLINICAL MONITORING
The number one problem with CPR is the inability of chest compressions to maintain adequate organ blood flow. The number two problem is the inability to monitor the adequacy of organ perfusion during CPR. The presence of palpable pulses and arterial pressure waves is not an indication of blood flow (the difference between pressure waves and flow waves is described in Chapter 9). The measurements described in this section can provide a more accurate assessment of organ perfusion than the standard measures used to evaluate the response to CPR.
END-TIDAL CO2 PRESSURE
The excretion of carbon dioxide in exhaled gas is a function of pulmonary blood flow (cardiac output), and thus the level of CO2 in exhaled gas changes in direct proportion to changes in cardiac output. The CO2 pressure (PCO2) in end-expiratory gas (i.e., the end-tidal PCO2) is easy to measure at the bedside, and changes in end-tidal PCO2 can be used as a noninvasive marker of changes in cardiac output. End-tidal PCO2 has been used to monitor the cardiac output in hypovolemia and during cardiopulmonary resuscitation.
Prognostic Value
A progressive rise in end-tidal PCO2 during CPR indicates that the resuscitation effort is successful in promoting cardiac output. As such, a steady rise in end-tidal PCO2 during CPR is more likely to be associated with a successful outcome than a persistently low end-tidal PCO2. The initial end-tidal PCO2 measurement, obtained at the onset of CPR, is very low (11 to 12 mm Hg, compared to a normal end-tidal PCO2 of 40 to 45 mm Hg), and is similar in survivors and nonsurvivors. However, in the survivors, the end-tidal PCO2 increased considerably (from 12 to 31 mm Hg) after 20 minutes of CPR, whereas in the nonsurvivors the end-tidal PCO2 decreased further (from 10.9 to 3.9 mm Hg). These results are supported by the results of another study where CPR that failed to raise the end-tidal PCO2 above 10 mm Hg was universally unsuccessful.
The tendency of the end-tidal PCO2 to rise during CPR can thus be a valuable prognostic marker. When end-tidal PCO2 does not rise above 10 mm Hg after a resuscitation time of 15 to 20 minutes, the resuscitative effort is unlikely to be successful.
VENOUS BLOOD GASES
The common practice of monitoring arterial blood gases during CPR should be abandoned in favor of monitoring venous blood gases. The rationale for this switch is the greater propensity for venous blood to represent the oxygenation and acid-base status of peripheral tissues. The tendency for arterial blood gases to provide misleading information during CPR is demonstrated by the observation that arterial blood can show a respiratory alkalosis while venous blood shows a metabolic acidosis during CPR.
The superiority of venous blood gases for monitoring tissue events during CPR (or in any low-flow state) has been ignored for over a decade, resulting in suboptimal care for cardiac arrest patients.
HOW LONG TO RESUSCITATE
There is little doubt that CPR is inappropriately prolonged in a significant percentage of resuscitative efforts. The goal of prolonged CPR is to increase the chance for survival, but this is not a desirable goal if the survivor is mentally impaired, as is often the case in survivors of prolonged CPR.
Ischemic Time and Neurologic Recovery
The risk of functional impairment in any of the major organs is directly related to the duration of the ischemic insult. The ischemic time following cardiac arrest includes the time from onset of the arrest to onset of CPR (arrest time) and the duration of the resuscitative effort (CPR time). The data in this figure are taken from a multicenter study of patients who did not regain consciousness in the first hour following successful CPR. If the arrest time was less than 6 minutes and the CPR time did not exceed 30 minutes, half of the survivors had a satisfactory neurologic recovery. However if the arrest time exceeded 6 minutes, more than 15 minutes of CPR always produced neurologic impairment in the survivors. Thus, in witnessed cardiac arrest (when arrest time can be accurately determined), CPR can be continued for 30 minutes if the arrest time is less than 6 minutes, but if the arrest time is longer than 6 minutes, CPR should be terminated after 15 minutes.
POSTRESUSCITATION CONCERNS
When CPR is successful in restoring spontaneous circulation, two concerns deserve attention in the early postresuscitation period. The first is the potential for continued and progressive multiorgan damage (i.e., postresuscitation injury). The second is the likelihood of neurologic recovery in patients who do not regain consciousness immediately after CPR.
POSTRESUSCITATION INJURY
This condition is usually seen after prolonged ischemic times, and it is characterized by progressive dysfunction in multiple organs. Other, more familiar terms for this condition are multiple organ failure and multiple organ dysfunction syndrome. This condition is often fatal, and there is no effective therapy at present. Several mechanisms have been proposed for this condition, including persistent vasoconstriction (i.e., the no-reflow phenomenon) and the release of toxins produced during the period of ischemia (i.e., reperfusion injury). (See Chapter 31 for a more detailed description of the multiple organ failure and its management.)
NEUROLOGIC RECOVERY
Neurologic impairment is common in cardiac arrest patients who are successfully resuscitated. Many survivors do not regain consciousness immediately after CPR, and the following are some prognostic factors that help identify patients who are unlikely to awaken or achieve a satisfactory neurologic recovery.
Duration of Coma
Failure to regain consciousness in the first few hours after CPR is not a harbinger of prolonged or permanent neurologic impairment,. However, coma that persists longer than 4 hours after CPR carries a poor prognosis for full neurologic recovery. Although the recovery rates are low for all points on the graph, there is a linear decline in recovery rate as the duration of coma increases. After 1 day of persistent coma, only 10% of the patients achieved a satisfactory neurologic recovery. The recovery rate drops below 5% when the coma lasts 1 week, and no patient recovers neurologic function when the coma persists for 2 weeks.
Three days of persistent coma is my threshold for informing families of the poor prognosis for recovery. The actual time selected for informing families of a poor prognosis is a matter of individual preference. The important point is to keep the family informed and to provide guidance in decisions about future strategies.
Coma Scores
Scoring systems such as the Glasgow Coma Scale (GCS) can also provide valuable prognostic information. (This scoring method is described in Chapter 50.) A GCS below 5 on the third day of persistent coma is almost always associated with a poor outcome.
Pupillary Light Reflex
Several brainstem reflexes can have prognostic value in patients who do not regain consciousness after CPR, but none can match the predictive value of the pupillary light reflex. The importance of this reflex is its negative predictive value (i.e., the ability to identify a poor outcome). Absence of the pupillary light reflex after one or more days of coma indicates little or no chance for neurologic recovery. This reflex has no prognostic value in the first 6 hours after CPR because it can be transiently lost and then reappear. Finally, the resuscitation drugs atropine and epinephrine can produce pupillary dilation, but these agents do not interfere with the pupillary response to light.
