LT® and iGel® for airway management in cardiac arrest is becoming more widely adopted. These devices are inserted blindly in the airway without the need for direct laryngoscopy and can typically be placed very quickly without pausing compressions (see Chapter 3). Several EMS agencies have chosen this method for the initial approach, reasoning that they cannot perform traditional intubation without compromising chest compressions. Others may make an initial attempt at intubation and if unsuccessful turn to a supraglottic device [42]. A subanalysis of the ROC PRIMED trial demonstrated a higher rate of survival with good functional status in patients receiving endotracheal intubation rather than supraglottic airway placement (OR 1.40; 95% CI 1.04, 1.89) during the resuscitation [42]. The AIRWAYS trial compared endotracheal intubation with the iGel supraglottic airway. There was no difference in survival or favorable neurologic outcome [43]. A second randomized trial comparing the King LT with endotracheal intubation demonstrated higher survival and higher survival with good neurologic outcome in the King LT group [44]. It is important to note that in the latter trial, intubation success was low (52%). Based on these findings, EMS agencies with high intubation success rates may favor endotracheal intubation for airway management while agencies with low intubation success rates (or infrequent intubation attempts) should favor supraglottic airway use.
Ventilation
Another important consideration is the role of ventilation during chest compressions. The need for ventilation with bystander CPR for patients with short‐duration VF has been questioned [745–49]. The theoretical bases for this approach include: 1) the distractions posed by multiple interventions; 2) the subsequent reduction in number of chest compressions; 3) the adverse effect of hyperventilation on CPP; and 4) bystander reluctance to perform mouth‐to‐mouth ventilation [38,50–52]. Although “no ventilation” has practical value for bystander care, it is not clear how or if these principles should be applied to EMS care. There is some evidence that prearrival instruction for compression‐only CPR by emergency medical dispatchers results in delivery of earlier and more chest compressions, but not to an increase in survival [53, 54]. Some EMS systems have adopted protocols making active ventilation optional during the initial resuscitation, instead placing an oral airway and oxygen mask until sufficient rescuers are on scene. This allows the first‐arriving crew to focus on compressions and defibrillation. However, recent studies support that chest compressions alone do not provide clinically significant ventilation, and that outcomes are improved with adequate ventilation during resuscitation [55, 56].
Considerable scientific data have highlighted the importance of controlled ventilation during resuscitation. During cardiac arrest resuscitation, hyperventilation increases intrathoracic pressure, resulting in decreased preload and CPP [38]. Furthermore, inadvertent hyperventilation occurs frequently during resuscitation efforts, despite specific training to avoid this phenomenon. Ventilation during cardiac arrest should consist of tidal volumes of 500‐600 mL at a respiratory rate of 8‐10 breaths/min.
The impedance threshold device (ITD) is a ventilation adjunct that may be attached to either a facemask or an endotracheal tube. It contains a one‐way valve that permits exhalation during the downstroke of chest compression but prevents passive inhalation during the upstroke of chest compression. As a result, the ITD generates increased negative intrathoracic pressure during chest recoil, increasing cardiac preload and CPP. While preclinical and small trial data were favorable, a large randomized trial of the ITD versus sham device yielded similar rates of survival with good neurologic outcome between groups (ITD 5.8% vs. sham device 6.0%; p = 0.71) [57–62].
Medications
Although numerous medications may be used during treatment of cardiac arrest, the primary agents are vasopressors (e.g., epinephrine and vasopressin) and antiarrhythmics (e.g., lidocaine and amiodarone). ACLS algorithms provide specific guidelines for the use and doses of these agents [1].
The majority of studies suggest no drug in isolation improves outcome following cardiac arrest in humans [63–66]. The continued use of these drugs is based on tradition, theory, and animal research, and the selection of specific agents in each class is largely a matter of individual choice. EMS physicians must be aware that the only medications evaluated by randomized clinical trials are epinephrine, amiodarone, lidocaine, vasopressin, and magnesium [64, 67, 68]. However, these studies are mostly confounded by drug administration at prolonged times after onset of cardiac arrest.
Vasopressors serve two intended purposes during cardiac arrest: vasoconstriction, and exerting positive inotropy and chronotropy. Alpha‐agonists increase peripheral resistance, shunting blood flow to the brain and heart. Beta‐agonists increase inotropy and chronotropy. In clinical context, these agents are used to help to sustain coronary and cerebral perfusion before restoration of pulses. AHA guidelines suggest administering 1 mg of IV epinephrine every 3‐5 minutes [1]. Vasopressin may be administered alone or in combination with epinephrine.
Compelling animal data indicate increased ROSC with the early delivery of epinephrine or vasopressin [69–72]. Although several small clinical series have reported increases in ROSC and survival to admission for patients treated with vasopressin, a randomized trial comparing vasopressin with epinephrine versus epinephrine alone did not demonstrate additional benefit from vasopressin use [67,73–75]. Recent studies have demonstrated improved ROSC and survival to hospital discharge in patients receiving epinephrine. Also, the point estimate number of survivors (with both good and poor neurologic outcome) at 90 days was higher in those receiving epinephrine [76, 77].
With vasopressors, there is a trade‐off between increased coronary perfusion and reduced cerebral perfusion (possibly via increased cerebral vasoconstriction). A once‐popular ACLS approach was the use of high‐dose epinephrine (5–7 mg IV) [63]. Although clinical trials using high‐dose epinephrine demonstrated increased rates of ROSC, this did not translate into survival to discharge [63].
Antiarrhythmics are commonly used in cases of VT/VF cardiac arrest. They may increase the likelihood of conversion to a perfusing rhythm. Lidocaine and amiodarone are currently recommended antiarrhythmics for shock‐refractory VF [1]. EMS physicians may choose between an IV bolus of 300 mg of amiodarone or 1–1.5 mg/kg of lidocaine for patients suffering pulseless VT/VF. The largest randomized controlled trial comparing amiodarone, lidocaine, and placebo demonstrated higher survival to hospital admission in the amiodarone and lidocaine arms (when compared to placebo), but no difference in survival to hospital discharge. However, in the subgroup of bystander‐witnessed cardiac arrest, amiodarone demonstrated a 5% increase in survival to hospital discharge when compared with placebo (p = 0.04), and lidocaine demonstrated a 5.2% increase in survival to hospital discharge when compared with placebo (p = 0.03) [78]. This phenotype of patient may derive additional benefit from antiarrhythmic medication.
Epidemiologic studies suggest that pulseless electrical activity (PEA) and asystole are increasingly common in out‐of‐hospital cardiac arrests [79–82]. Atropine is a vagolytic and reverses cholinergic‐mediated decreases in heart rate, blood pressure, and vascular resistance [1]. Although traditionally it has been used in bradycardic PEA or asystolic cardiac arrest, the limited available research does not suggest any benefit, and this drug is no longer recommend for routine use. Epinephrine should be administered, and potentially treatable causes (the “5 Hs and 5 Ts” of ACLS) should be considered (Table 13.1).
An additional drug worth comment is sodium bicarbonate. For years, sodium bicarbonate was administered routinely during cardiac arrest to reverse the metabolic acidosis of cardiac arrest and, it was hoped, increase the effectiveness of vasopressors and antiarrhythmics. In formal trials, this drug did not improve survival [83]. Sodium bicarbonate may be reasonable in scenarios of suspected hyperkalemic arrest (such as individuals with known renal failure) and in prolonged resuscitations with adequate ventilation. Calcium (chloride or gluconate), however, is the most effective medication in cases of severe hyperkalemia affecting cardiac conduction.