Chest Compressions

In CPR, chest compressions are used to circulate blood to the heart and brain until a pulse can be restored. The mechanism by which chest compressions generate cardiac output is through an increase in intrathoracic pressure plus direct compression of the heart. With the patient lying in the supine position, the rescuer applies compressions to the patient’s sternum. The heel of one hand is placed over the lower half of the sternum and the heel of the other hand on top in an overlapping and parallel fashion. The recommended compression depth in adults is 2 inches. The recommended rate of compression is 100 or more per minute. “Push hard, push fast” is now the American Heart Association (AHA) mantra for CPR instruction. This underscores the importance of vigorous chest compressions in achieving return of spontaneous circulation (ROSC).⁵ In addition, incomplete recoil of the chest impairs the cardiac output that is generated, and thus the chest wall should be allowed to recoil completely between compressions. Owing to rescuer fatigue, the quality of chest compressions predictably decreases as the time providing chest compressions increases, and the persons providing chest compressions (even experienced HCPs) may not perceive fatigue or a decrease in the quality of their compressions.⁶ Therefore, it is recommended that rescuers performing chest compressions rotate every 2 minutes.

The quality of CPR is a critical determinant of surviving a cardiac arrest event.⁷ Minimization of interruptions in chest compressions is imperative. Interruptions in chest compressions during CPR have been quite common historically, and the “hands off” time has been shown to take up a substantial amount of the total resuscitation time.⁷ Potential reasons for “hands off” time include pulse checks, rhythm analysis, switching compressors, procedures (e.g., airway placement), and pauses before defibrillation (“preshock pause”). All of these potential reasons for interruptions must be minimized. Pauses related to rotating compressors or pulse checks should take no longer than a few seconds.⁵ Eliminating (or minimizing) preshock pauses has been associated with higher likelihood of ROSC and improved clinical outcome.⁸

Defibrillation

The next critically important action in the resuscitation of patients with cardiac arrest due to pulseless ventricular arrhythmias (i.e., VF or pulseless VT) is rapid defibrillation. Delays in defibrillation are clearly deleterious, with a sharp decrease in survival as the time to defibrillation increases.⁹ With the advent of automatic external defibrillators (AEDs) and their dissemination into public places, both elements of effective CPR (both effective chest compressions and rapid defibrillation) can be performed by lay rescuers in the field for patients with out-of-hospital cardiac arrest. Figure 1.2 shows the importance of rapid defibrillation, with decreasing success of resuscitation with increasing time to defibrillation.

Rescue Breathing

The most recent AHA recommendations regarding ventilation during CPR depends on who the rescuer is (i.e., trained HCPs versus lay person).⁵ For trained HCPs, the recommended ventilation strategy is a cycle of 30 chest compressions to two breaths until an endotracheal tube is placed, and then continuous chest compressions with one breath every 6 to 8 seconds after the endotracheal tube is placed. Excessive ventilations can be deleterious from a hemodynamic perspective due to increased intrathoracic pressure and reduction in the cardiac output generated by CPR and thus should be avoided during resuscitation. Excessive ventilation could also potentially result in alkalemia.

For lay persons who are attempting CPR in the field for a victim of out-of-hospital cardiac arrest, rescue breathing is no longer recommended. Rather, the recommended strategy is compression-only (or “hands-only”) CPR.⁵ The rationale is that compression-only CPR can increase the number of effective chest compressions that are delivered to the patient (i.e., minimizes interruptions for rescue breaths), and does not require mouth-to-mouth contact. Mouth-to-mouth contact is one of the perceived barriers to CPR in the field. By removing this element, the hope is that an increase in attempts at bystander CPR will result. Hands-only CPR has been found to be not inferior to conventional CPR including rescue breaths for victims of out-of-hospital cardiac arrest,^10–12 and thus hands-only CPR has become the preferred technique to teach lay rescuers.

Figure 1.3 displays the AHA algorithm for adult basic life support.

Advanced Cardiac Life Support

There are several additional elements of resuscitation that are intended specifically for trained HCPs (e.g., advanced cardiac life support [ACLS]), and these elements include pharmacologic therapy. Figure 1.4 displays the AHA algorithm for ACLS.¹³

The primary goal of pharmacologic interventions is to assist the achievement and maintenance of spontaneous circulation. The mainstay of pharmacologic interventions is vasopressor drugs. Epinephrine (1 mg) is administered by intravenous (IV) or intraosseous (IO) route every 3 to 5 minutes during CPR until ROSC is achieved.¹³ If IV/IO access cannot be established, epinephrine could be administered via endotracheal tube, but at a higher dose (2-2.5 mg). Vasopressin (40 mg IV/IO) can be substituted for the first or second dose of epinephrine. Amiodarone is the preferred antiarrhythmic agent. In patients with VF/VT not responding to CPR, defibrillation, and vasopressor therapy, amiodarone is recommended (300 mg IV/IO for the first dose, 150 mg IV/IO for the second dose).¹³ Recently, the use of atropine for PEA/asystole was removed from the ACLS algorithm. Along these lines, there is also insufficient evidence to recommend routine administration of sodium bicarbonate during CPR.

It is notable that the impact of recommended ACLS therapies on outcome from cardiac arrest remains a matter of debate. Some studies have shown that ACLS interventions did not improve clinical outcomes when compared to basic life support alone.¹⁴

General Approach

Patients resuscitated from cardiac arrest should be admitted to a critical care unit with the following capabilities:¹⁶

Critical Care Support

I/R triggers profound systemic inflammation. In clinical studies, ROSC has been associated with sharp increases in circulating cytokines and other markers of the inflammatory response. Accordingly, some investigators have referred to the post–cardiac arrest syndrome as a “sepsis-like” state. The clinical manifestations of the systemic inflammatory response may include marked hemodynamic derangements such as sustained arterial hypotension similar to septic shock. Hemodynamic instability occurs in approximately 50% of patients who survive to intensive care unit admission after ROSC, and thus the need for aggressive hemodynamic support (e.g., continuous infusion of vasoactive agents and perhaps advanced hemodynamic monitoring) should be anticipated.¹⁷

In addition to a systemic inflammatory response, an equally important contributor to post-ROSC hemodynamic instability is myocardial stunning. Severe, but potentially reversible, global myocardial dysfunction is common following ROSC. The cause is thought to be I/R injury, but treatment with defibrillation (if applied) could also contribute. Although the myocardial dysfunction occurs in the absence of an acute coronary event, myocardial ischemia may be an ongoing component of myocardial depression if an acute coronary syndrome caused the cardiac arrest. Severe myocardial stunning may last for hours but often improves by the 24-hour mark after ROSC. An echocardiogram may be helpful in hemodynamic assessment after ROSC to determine if global myocardial depression is present, as this may impact decisions on vasoactive drug support (e.g., dobutamine) or mechanical augmentation (e.g., intra-aortic balloon counterpulsation) until the myocardial function recovers. However, when needed, clinicians should be aware that β-adrenergic agents may increase the likelihood of dysrrhythmia.

Although there are no data on whether specific blood pressure or other hemodynamic goals are beneficial,¹⁸ expert opinion (and clinical intuition) suggests that hemodynamics and organ perfusion should be optimized.¹⁵ Rapidly raising the blood pressure in patients who remain markedly hypotensive after ROSC is prudent, because postresuscitation arterial hypotension has been associated with sharply lower survival rate.¹⁷ Whether or not postresuscitation hypotension has a cause-and-effect relationship with worse neurologic injury or is simply a marker of the severity of the I/R injury that has occurred remains unclear.

Regarding respiratory system support, exposure to hyperoxia (excessively high partial pressure of arterial oxygen [PaO₂]) has been associated with poor clinical outcome among adult patients resuscitated from cardiac arrest and admitted to an intensive care unit.¹⁹ These data corroborate the findings of numerous laboratory studies in animal models in which hyperoxia exposure after ROSC worsens brain histopathologic changes and neurologic function.^20–24 A paradox may exist regarding oxygen delivery to the injured brain, where inadequate oxygen delivery can exacerbate cerebral I/R injury, but excessive oxygen delivery can accelerate formation of oxygen free radical and subsequent reperfusion injury. Although clinical data on this topic are few at the present time (and specifically no interventional studies have been performed), expert opinion advocates limiting unnecessary exposure to an excessively high postresuscitation PaO₂ by titrating the fraction of inspired oxygen down after ROSC as much as possible to maintain an arterial oxygen saturation of 94% or more.¹⁵

Seizures are not uncommon after anoxic brain injury, and it is important to be vigilant in clinical assessment for any motor responses that could represent seizure activity so that they can be treated promptly with anticonvulsant medications. Continuous electroencephalography monitoring (if available) can be useful, especially if continuous administration of neuromuscular blocking agents becomes necessary for any reason.

Cardiac Catheterization

Acute coronary syndrome is the most common cause of sudden cardiac arrest. Clinicians should have a high clinical suspicion of acute myocardial ischemia as the inciting event for the cardiac arrest when no other obvious cause of cardiac arrest is apparent. Although ST-segment myocardial infarction is an obvious indication for PCI, other more subtle electrocardiogram abnormalities may indicate that an acute ischemic event caused the cardiac arrest. In patients with no obvious noncardiac cause of cardiac arrest, a clinical suspicion of coronary ischemia, an abnormal electrocardiogram after ROSC, and consultation with an interventional cardiologist is warranted and coronary angiography should be considered. Recent studies and experience indicate that inducing hypothermia simultaneously with emergent PCI is feasible.

Therapeutic Hypothermia

Therapeutic hypothermia (TH), also called mild therapeutic hypothermia or targeted temperature management, is a treatment strategy of rapidly reducing the patient’s body temperature after ROSC for the purposes of protection from neurologic injury. The body temperature is typically reduced to 33° to 34° C for 12 to 24 hours. After ROSC the severity of the reperfusion injury can be mitigated, despite the fact that the initial ischemic injury has already occurred. Reperfusion injury refers to tissue and organ system injury that occurs when circulation is restored to tissues after a period of ischemia, and is characterized by inflammatory changes and oxidative damage that are in large part a consequence of oxidative stress. Neuronal cell death after I/R injury is not instantaneous, but rather a dynamic process. In animal models of cardiac arrest, brain histopathologic changes may not be found until 24 to 72 hours after cardiac arrest.¹⁵ This indicates that a distinct therapeutic window of opportunity exists. In theory, TH may protect the brain by attenuating or reversing all of the following pathophysiologic processes: disruption of cerebral energy metabolism, mitochondrial dysfunction, loss of calcium ion homeostasis, cellular excitotoxicity, oxygen free radical generation, and apoptosis. Two clinical trials of TH were published in 2002.^25,26 These trials showed improved outcomes with TH for comatose survivors of witnessed out-of-hospital cardiac arrest with VF as the initial rhythm. The survival data for the largest of these clinical trials (i.e., the Hypothermia After Cardiac Arrest Study Group) appear in Table 1.2 and Figure 1.5.

The current AHA guidelines for CPR and emergency cardiovascular care recommend 12 to 24 hours of TH for comatose survivors of out-of-hospital cardiac arrest due to VF or pulseless VT.¹⁶ TH may also be considered for victims of in-hospital cardiac arrest and other arrest rhythms. Figure 1.6 displays the AHA algorithm for post–cardiac arrest care including TH.¹⁶

Appropriate selection of candidates for TH is clearly important. If a patient does not follow verbal commands after ROSC is achieved, this indicates that the patient is at risk for brain injury and TH should be strongly considered. If a patient is clearly following commands immediately after ROSC, then significant brain injury is less likely and it is probably reasonable to withhold TH. There are multiple potential methods for inducing TH including specialized external or intravascular cooling devices for targeted temperature management, or a combination of conventional cooling methods such as ice packs, cooling blankets, and cold (4° C) IV saline infusion. Compared to the use of specialized cooling devices, overshoot (body temperature < 31° C) is a not uncommon occurrence with use of ice packs, cooling blankets, and cold saline.²⁷ Regardless of what method is used, effective achievement of target temperature may be aided by the use of a uniform physician order set for TH induction.²⁸ The current recommendation is to maintain TH for 12 to 24 hours.¹⁶ Whether or not a longer duration of therapy could be beneficial is currently unknown.

Shivering with TH induction is very common and should be anticipated. Shivering can be detrimental to the patient by making goal temperature more difficult (or impossible) to achieve. Therefore, immediate recognition and treatment of shivering is imperative. Adequate sedation and analgesics are an essential component of TH, especially the induction phase, and often the administration of additional sedative and opioid agents will be sufficient to ameliorate shivering. If shivering persists despite sedatives or opioid agents, neuromuscular blocking agents may be required. If neuromuscular blocking agents are used, they are often only necessary in the induction phase of TH when the temperature is dropping at a fast rate. Once target temperature is achieved, patients often stop shivering. It is prudent to try to limit neuromuscular blocking agents to the induction phase of TH, and they likely can be withheld thereafter. Unnecessarily prolonged neuromuscular blockade should be avoided because prolonged neuromuscular weakness may persist after discontinuation and could potentially make the patient’s neurologic assessment at a later time point more challenging. When using neuromuscular blocking agents for the induction of TH, their administration may be titrated to the resolution of shivering rather than complete paralysis, which may result in the administration of a much lower dose of neuromuscular blocker.

A number of potential complications are possible with TH including bradycardia, a “cold diuresis” resulting in hypovolemia and electrolyte derangements, hyperglycemia, coagulopathy, and perhaps increased risk of secondary infection. However, these potential complications are often not severe when they do occur, and in terms of risk-benefit determinations, the risk of anoxic brain injury usually greatly outweighs the risks of complications.

If TH is not initiated, fever must be avoided. Fever is not uncommon in the post–cardiac arrest population because of the intense proinflammatory response to I/R and must be treated aggressively with antipyretic therapies and other techniques (e.g., cooling blankets). Fever is clearly detrimental in brain-injured patients because it increases cerebral metabolic rate.

Neurologic Prognostication

Neurologic prognostication is often extremely difficult in the first few days after resuscitation from cardiac arrest.²⁹ Although some neurologic examination findings may suggest poor prognosis, few of these signs on examination are sufficiently reliable upon which to base treatment decisions (e.g., support withdrawal). These critically important decisions should hinge on neurologic examination findings in which the false-positive rate (FPR) (i.e., the rate of predicting a poor outcome that ultimately proves not to be poor) approaches zero. An abundance of clinical data exists on neurologic assessment after cardiac arrest, and few examination findings have a sufficiently low false-positive rate in the first 72 hours after ROSC to form the basis of a limitation of support decision.^15,30 In particular, neurologic prognostication immediately (e.g., first 24 hours) after resuscitation from cardiac arrest is especially unreliable. Among patients who are initially comatose after ROSC, one quarter to one half of patients could potentially have a favorable outcome, especially if TH is employed. In general, the recommended approach is to wait a minimum of 72 hours after ROSC before neurologic prognostication.³⁰ However, it is important to recognize that the vast majority of data on neurologic prognostication was generated before the era of TH, that is, before an effective therapy existed. In the population of patients treated with TH, the optimal time course for making neurologic prognostication may be significantly different, not only because the therapy could modulate the degree of brain injury, but also because low body temperature decreases the metabolism of sedative agents that are typically used during TH, and it may take much longer for the effects of the sedation to be eliminated. Recently published data have shown that good neurologic outcome can potentially occur even with unfavorable neurologic findings at 72 hours, suggesting that the optimal time interval to wait before attempting neurologic prognostication in the population treated with TH may be longer than 72 hours.³¹ Our general approach is to not make any final neurologic prognostication until 72 hours after ROSC. In the population treated with TH, we perform daily neurologic assessments beyond the 72-hour mark and we do not make final neurologic prognostication as long as the patient continues to improve. If there are zero signs of neurologic improvement over 2 or more consecutive days, we typically deem neurologic prognostication to be reliable at that time.

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