Cardiopulmonary Resuscitation and Critical Care After Cardiac Arrest

Epidemiology and Outcomes of Cardiac Arrest

Out-of-hospital cardiac arrest (OHCA) affects nearly 1000 adult Americans each day; when including in-hospital cardiac arrest (IHCA), more than 500,000 adults suffer cardiac arrest each year in the United States. The most common cause of OHCA is cardiac disease, particularly coronary artery disease (CAD) and other structural heart diseases, such as cardiomyopathy. Cardiac arrest may be the initial manifestation of cardiac disease in up to half of patients dying from cardiovascular causes. IHCA etiology varies according to the type and location of patient, but progression of respiratory distress to cardiac arrest is most common in many hospitals.

Survival after cardiac arrest has increased steadily over the past 15 years despite the lack of novel therapeutics as a result of multiple improvements in the systems of care. Only 25% to 30% of patients with OHCA initially achieve return of spontaneous circulation (ROSC) and are admitted to the hospital. About 40% to 50% of IHCA patients achieve ROSC initially. The majority (approximately 60% to 70%) of cardiac arrest patients (either OHCA or IHCA) who initially achieve ROSC subsequently die in the hospital, with rates of survival in the United States of approximately 12% for OHCA and 24% for IHCA. Marked regional differences in initial ROSC rates and subsequent hospital and overall mortality exist for patients with both OHCA and IHCA, attributable to differences in baseline patient characteristics, cardiac arrest circumstances, and peri-arrest care.

Predictors of favorable and unfavorable cardiac arrest outcomes have been identified ( Table 51.1 ). These variables are often not available or reliable in clinical practice, limiting their utility for clinical decision making. The most important clinical distinction in cardiac arrest patients is between those with shockable rhythms, such as ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), and those with nonshockable rhythms, such as asystole or pulseless electrical activity (PEA). Patients with shockable arrest rhythms generally have more favorable outcomes, higher rates of underlying (reversible) cardiac etiology, lower rates of comorbidities, and fewer clinical adverse prognostic signs. Nonshockable rhythms may result from prolonged VF or cardiac failure after defibrillation of VF, but also may result from noncardiac etiologies such as hypoxia, sepsis, pulmonary embolus, hypovolemia, or other toxic-metabolic derangements. These situations are associated with worse outcomes, lower rates of reversible etiology, and higher rates of comorbidities. Over time, rates of shockable rhythms in OHCA have declined and now account for only 25% to 30% of initial rhythms reported. Rates of shockable rhythms are higher in witnessed OHCA and OHCA occurring in public places.

Intensive Care Implications of Initial Cardiopulmonary Resuscitation

Evidence-based guidelines have been widely disseminated for cardiopulmonary resuscitation (CPR), electrical therapy, pharmacologic therapy, and mechanical support to reverse cardiac arrest. Cardiac intensivists should understand how different parts of the initial resuscitation can influence subsequent organ dysfunction or recovery. During cardiac arrest, the heart is not generating adequate forward flow to maintain brain and organ perfusion, leading to tissue ischemia and progressive metabolic abnormalities. Immediately after restoration of pulses, there is potential for reperfusion injury when oxygenated blood arrives in acidotic, metabolically depleted tissues.

Cardiopulmonary Resuscitation

Closed-chest cardiac massage (chest compressions) can produce enough forward blood flow to the brain and organs to decrease the extent of ischemic injury and to delay metabolic deterioration. The quality of chest compressions varies between providers; minimizing interruptions of chest compressions is now recognized as an important determinant of patient survival. High-quality chest compressions are defined as a rate between 100 and 120 compressions per minute with a depth of at least 2 inches in adults, including full recoil. Minimizing interruptions of compressions required to deliver a defibrillation shock or to place an airway are examples of preventable decrements to organ perfusion during CPR.

Recent guidelines recommend a 30 : 2 ratio of chest compressions to rescue breaths during CPR prior to placement of an advanced airway with continuous chest compressions performed thereafter. One logical step to further reduce interruptions of CPR is to provide continuous chest compressions with no rescue breaths, sometimes called compression-only CPR or cardiocerebral resuscitation. Initial observational studies suggested that OHCA victims treated with continuous chest compressions rather than standard CPR had improved outcomes. However, a subsequent randomized clinical trial showed that continuous compressions with no interruptions prior to advanced airway placement is not superior to a 30 : 2 ratio.

Mechanical chest compression devices have been developed to prevent a decrease in CPR quality over time from rescuer fatigue. While safe and effective, in randomized studies these devices are not superior to manual CPR from highly trained providers. The role for these devices probably includes prolonged resuscitation efforts, CPR in settings in which manual CPR is difficult or dangerous (e.g., under fluoroscopy or in a moving ambulance), or when there are insufficient personnel to perform all procedures.

Another factor to consider during CPR is the adverse hemodynamic consequences of positive-pressure breathing. Increased intrathoracic pressure resulting from positive-pressure ventilation impairs venous return and forward cardiac flow, particularly with high inspiratory pressures or prolonged inflation. For this reason, rescue breaths should be given quickly and should not be excessively large; the rate of rescue breaths should only be 10 to 12 per minute with an advanced airway in place to avoid hyperventilation. At the time of arrest, the lungs are full of oxygenated air and a patient may tolerate longer pauses between rescue breaths. As cardiac arrest progresses, the oxygen reservoir in the lungs is depleted, but pulmonary blood flow is low during CPR; thus relatively minimal ventilation can still provide adequate gas exchange. In many cases, the amount of air entry into the lungs produced by the mechanical effect of chest compressions is adequate for gas exchange if supplemental oxygen is applied with or without positive-pressure breathing using a bag-valve mask.

Physiologic monitoring during resuscitation, which may be available particularly in cardiac intensive care unit (CICU) patients, can help guide the quality of CPR. End-tidal carbon dioxide monitoring is particularly useful once an advanced airway is placed. End-tidal carbon dioxide in the setting of CPR primarily reflects the amount of pulmonary blood flow; low end-tidal carbon dioxide readings imply poor pulmonary blood flow from ineffective CPR. Therefore a low end-tidal carbon dioxide reading (<10 to 20 mm Hg) not only suggests the need to improve CPR quality but also portends a poor prognosis for achieving ROSC. Failure to detect any significant end-tidal carbon dioxide suggests esophageal intubation and requires assessment of the endotracheal tube position. An abrupt, sustained increase in end-tidal carbon monoxide (>40 mm Hg) typically reflects ROSC. During prolonged CPR, maintenance of a relatively high end-tidal carbon dioxide suggests acceptable forward flow and a more favorable prognosis. Arterial blood pressure monitoring can directly demonstrate the pressure generated by chest compressions; restoring and maintaining an adequate diastolic blood pressure (perhaps >40 mm Hg, which is a surrogate for aortic relaxation pressure and partly determines coronary perfusion pressure) appears to be a major determinant of ROSC. Bedside cardiac ultrasound can often be performed using a subxiphoid (subcostal) imaging window at the time of pulse/rhythm check during CPR, but providers must be cautious that attempts to gain better images do not compromise or interrupt the ongoing life-saving interventions. For pulseless patients with an organized cardiac rhythm (i.e., PEA), absence of detectable cardiac contraction portends a very low likelihood of gaining ROSC. Specific complications, such as cardiac tamponade from pericardial effusion, can be readily identified. Several diagnostic algorithms using cardiac ultrasound in PEA have been proposed; in practice, however, interpretation of ultrasound images during CPR can be challenging.

Defibrillation

Timely defibrillation for patients with shockable rhythms is essential for achieving successful ROSC. The success rate of defibrillation decreases over time, accompanied by changes in the VF waveform morphology. VF waveform analysis may predict defibrillator shock success and prognosis. Immediately after initiation of VF, VF is high amplitude with much power in lower frequencies (“coarse VF”). This early VF is readily defibrillated; this early period is called the electrical phase of VF. After several minutes, myocardial ischemia causes VF to become lower amplitude with power distributed among both high and low frequencies (“fine VF”). This situation is less likely to result in successful defibrillation with rescue shocks, but it can be improved with CPR and perfusion. This period is called the circulatory phase of VF. With very prolonged VF, the metabolic phase of VF develops due to accumulation of metabolic by-products of anaerobic metabolism and successful defibrillation becomes far less likely. Within several minutes of VF onset, modern biphasic defibrillators have an 85% to 90% first-shock success rate for converting VF with little increase in success when shock energies are increased. For this reason, multiple “stacked” shocks are not recommended if the first shock fails. Different manufacturers have differing recommendations about escalating energy levels if the first shock fails. Regardless of cardiac arrest duration, defibrillation should be performed as soon as possible for patients with an initial rhythm of VF. Randomized trials failed to show a benefit of a predefined period of chest compressions with the goal of improving coronary perfusion prior to defibrillation, even for patients with unwitnessed OHCA. Using automated VF waveform analysis to guide a shock-first or CPR-first strategy likewise failed to improve survival in OHCA. On the contrary, continuation of chest compressions during defibrillator charging with immediate resumption of chest compressions after defibrillation may be beneficial.

Airway Management

Optimal airway management during cardiac arrest remains controversial. Various observational studies report either improvement or worsening of outcomes in patients receiving an advanced airway, including either supraglottic airways (such as laryngeal mask airways [LMA] and laryngeal tubes) or endotracheal tube, during CPR when compared to bag-valve mask alone. These studies are difficult to interpret because arrest duration, the need for CPR interruption for airway placement, and whether specific airways were selected because of skill level of the providers or the anatomy of the patient are often not known or not taken into account in the analyses. Given the aforementioned adverse hemodynamic effects of positive-pressure ventilation and the fact that supplemental oxygen alone is adequate during the early phases of cardiac arrest, advanced airways are unlikely to provide a significant benefit during the initial stages of resuscitation. For prolonged resuscitation, placement of an advanced airway is likely appropriate to ensure adequate gas exchange and allow measurement of end-tidal carbon dioxide. Supraglottic airways are employed more often by prehospital providers or during early CPR owing to the ease and rapidity of placement when compared to a standard endotracheal tube. Supraglottic airways can be placed blindly without laryngoscopy, eliminating any need to interrupt chest compressions. After return of pulses, emergency airways may be replaced with an adequate endotracheal tube for anticipated intensive care support.

Drug Therapy

Drug therapies for cardiac arrest are largely unproven. Studies comparing prehospital providers who can administer intravenous drugs to providers who cannot administer drugs failed to show a difference in outcome for OHCA. Similarly, placement of an intravenous (IV) line for medication administration failed to improve OHCA outcomes in a randomized study. No specific drug has been shown to improve survival compared to placebo when applied to all OHCA patients. It is important to note that drug circulation is markedly reduced during CPR, leading to reduced medication efficacy. Placement of a peripheral or central IV line can be time consuming during CPR; use of a rapidly deployable intraosseous (IO) cannulation kit is preferable.

For patients with persistent VF after one or more defibrillation attempts, use of an antidysrhythmic drug may increase the success of subsequent defibrillation. Amiodarone 300 mg (5 mg/kg) and lidocaine 100 mg (1.5 mg/kg) are the antidysrhythmics most studied. Initial trials suggested a higher VF conversion and ROSC rate with amiodarone compared to placebo and compared to lidocaine. These data only indicate that amiodarone can lead to a higher hospital admission rate but not any improvement in long-term survival; amiodarone was more frequently associated with hypotension and/or bradycardia than lidocaine. A recent large randomized controlled trial of amiodarone versus lidocaine versus placebo did not detect any difference in survival among these drugs across the entire study population, though there was higher survival in subgroups of patients treated with antidysrhythmic drugs. Among patients with a witnessed collapse, either amiodarone or lidocaine increased survival compared with placebo, perhaps indicating that these drugs are more effective when administered earlier. Alternative antidysrhythmic agents, such as sotalol and nifekalant, have not shown clear superiority to the standard antidysrhythmic agents. Multiple trials found no effect of magnesium sulfate as an adjunctive antidysrhythmic agent for drug-refractory VF. Atropine is not effective for restoring ROSC in patients with asystole or bradycardic PEA but still remains a first-line therapy for hemodynamically unstable bradyarrhythmias with a pulse.

Vasopressor drugs can increase coronary artery perfusion during CPR. Achieving return of pulses requires adequate coronary perfusion pressure (typically >15 mm Hg), which may be difficult to achieve with chest compressions alone. Vasopressor drugs constrict peripheral vessels, increase central aortic and coronary pressure, and improve rates of ROSC. Vasopressor agents have not been shown to improve survival, however, either compared to each other or to placebo. Epinephrine remains the standard vasopressor recommended based largely on its short-term effects, with bolus doses of 1 mg recommended because of tradition and demonstrated lack of superiority from higher doses. The limited placebo-controlled trials of epinephrine during CPR clearly show an increased rate of ROSC and hospital admission but lacked power to detect any difference in long-term survival. In support of epinephrine administration, observational studies in both OHCA and IHCA have shown that a longer time to first epinephrine dose in nonshockable rhythms is associated with worse outcomes.

Epinephrine has potentially deleterious physiologic effects. The potent β-adrenergic agonist effects may facilitate defibrillation of VF in some circumstances but can trigger myocardial ischemia and promote recurrent arrhythmias. Excessive β-adrenergic activation may contribution to cardiac stunning in post-arrest myocardial dysfunction (PAMD). Interestingly, despite the favorable effect of early epinephrine in nonshockable rhythms, more rapid administration of epinephrine is associated with worse outcomes in shockable rhythms. Epinephrine may also have direct injurious effects on other organs: its primary mechanism of action is to constrict blood flow in tissues in order to divert flow to the heart. This may also restrict perfusion of the brain. Observational studies find worse neurologic and overall outcomes in patients who receive epinephrine during CPR. Total cumulative dose of epinephrine is clearly associated with worse neurologic outcomes. This effect may be due to a direct harmful effect of epinephrine itself or simply a marker for more severe or prolonged cardiac arrest.

Vasopressin is a nonadrenergic vasopressor that is more effective during acidemia and therefore could be more efficacious during cardiac arrest. Initial studies suggested that use of vasopressin as an alternative or a supplement to epinephrine during cardiac arrest may be associated with better outcomes, but larger subsequent studies failed to show any clinical difference between the drugs. Therefore vasopressin remains an alternative to epinephrine but is equally unproven regarding its benefit.

Other resuscitation drugs have theoretical benefit based on physiologic arguments but lack supporting clinical data ( Table 51.2 ). Intravenous calcium is recommended only as an adjunctive therapy during cardiac arrest owing to hyperkalemia. Metabolic acidosis (and often superimposed respiratory acidosis) typically develops during prolonged cardiac arrest owing to reduced tissue perfusion with anaerobic lactic acidosis that is exacerbated by markedly reduced ventilation during CPR owing to limited pulmonary blood flow. Reversal of acidosis can improve cardiovascular responsiveness to catecholamines and improve cardiac performance and vascular tone, but there is no clinical trial evidence supporting the use of intravenous bicarbonate or other buffers as part of advanced life support. One theoretical concern regarding the use of intravenous bicarbonate is that it triggers overproduction of carbon dioxide, which can exacerbate intracellular and systemic acidosis if it is not cleared by ventilation (which is typically inadequate during CPR). Use of thrombolytic therapy—when there is no availability of primary percutaneous coronary intervention (PCI)—is a logical strategy for suspected pulmonary embolus or acute myocardial infarction (MI), which are among the most common causes of cardiac arrest. Despite this, clinical trials of empiric thrombolytic therapy during cardiac arrest have not shown a clinical benefit.

Team Management

Potentially more important than the specific medical therapies during resuscitation is team management. Cardiac arrest is inherently a chaotic circumstance; an organized approach to management provides the best likelihood of successful resuscitation. One of the most crucial aspects is ensuring minimally interrupted, high-quality CPR. Regularly rotating rescuers performing chest compressions maintains CPR quality by avoiding fatigue. For multi-provider resuscitation, having a team leader who provides team members with clearly defined roles to avoid duplication of effort is essential. Clear, efficient, closed-loop communication is essential to prevent errors; team members must be empowered to provide feedback to each other.

Overview of Post–Cardiac Arrest Care

Immediately after restoration of pulses, patients remain fragile and may have ongoing organ injury. In many cases, the precipitating cause of the cardiac arrest may not have been reversed during resuscitation. In fact, only primary dysrhythmias, hypoxia, or large airway obstructions are likely to have been completely resolved by the time that pulses are restored. Therefore post–cardiac arrest care has two major priorities: (1) damage control and resuscitation of the injured organ systems, particularly the heart and brain; and (2) identification and treatment of the precipitating cause of cardiac arrest. Implementing post–cardiac arrest intensive care is best organized with an understanding of the post–cardiac arrest syndrome.