Emergency Laboratory Tests
If spontaneous circulation does not return after the first round of antiarrhythmic drug therapy, the resuscitation team must also endeavor to identify and treat the clinically relevant conditions causing or contributing to the cardiac arrest [see Table 7]. In theory, the interventions conducted to this point should have resulted in a perfusing rhythm. The code team must ask why this has not occurred and then attempt to answer this question as the resuscitation continues. Emergency laboratory studies that may prove helpful include a stat ABG measurement and measurements of hemoglobin, potassium, magnesium, and blood glucose levels (most of which can be obtained from the ABG specimen).
Figure 1 The sudden cardiac arrest arrhythmias. (a) Ventricular tachycardia. (b) Ventricular fibrillation. Pulseless electrical activity encompasses any of several forms of organized electrical activity in the pulseless patient; these include (c) normal sinus rhythm, (d) junctional rhythm, (e) bradycardic junctional rhythm, and (f idioventricular rhythm. (g) Asystole.
Choice of Antiarrhythmic Drugs
Four antiarrhythmic drugs are used in cardiac resuscitation: amiodarone, lidocaine, magnesium (if the patient is thought or proved to be hypomagnesemic), and procainamide (for intermittent or recurrent VT or VF that initially responds to defibril-lation).72 It is not known which one of these drugs or which combination of them will optimize the chances of patient survival to hospital discharge. Despite many years of routine use, there are no controlled studies demonstrating a survival benefit with lido-caine, versus placebo, in the management of VF or pulseless VT. Two studies in patients with shock-refractory prehospital VF showed that survival to hospital admission was better with amiodarone than with placebo (44% versus 34%; P = 0.03)73 or with lidocaine (22.8% versus 12.0%; P = 0.009).74 Neither of these studies demonstrated an improved survival to hospital discharge in the amiodarone groups, but neither study had the statistical power to demonstrate such a difference. Amiodarone is also considerably more expensive than lidocaine.
The optimal role and the exact benefit of antiarrhythmic medications in cardiac resuscitation are yet to be fully elucidated. According to AHA guidelines, either amiodarone or lidocaine is an acceptable initial antiarrhythmic drug for the treatment of patients with VF or pulseless VT that is unresponsive to initial shocks, CPR, airway management, and administration of epi-nephrine or vasopressin plus shocks. On the basis of available evidence, however, amiodarone may be the antiarrhythmic agent of first choice in the setting of prehospital refractory VF, allowing for optimal survival to hospital arrival.72-74
Pulseless electrical activity
Community ACLS providers are encountering nonventricu-lar arrhythmias (i.e., PEA and asystole) with increasing frequency. Classically, the prognosis for PEA has been poor, with outpatient survival rates generally reported as 0% to 7%.75,76 The sequence of resuscitation steps in the management of PEA is as follows: activation of the emergency medical or code response, primary survey (CPR and rhythm evaluation), and secondary survey (intubation and confirmation of correct ET tube placement, optimal oxygenation and ventilation, establishment of I.V. access, epinephrine administration, and, finally, problem solving for technical difficulties and establishment of the cause of the cardiac arrest) [see Figure 2]. The two core drugs for PEA management are epinephrine (repeated every 3 to 5 minutes for as long as the patient is pulseless) and atropine (up to 3 mg over time if the PEA rhythm on the monitor is inappropriately slow). Although not currently on the AHA PEA algorithm, vaso-pressin is probably a reasonable alternative to epinephrine. The best hope for a successful resuscitation is to find and treat the cause of PEA; therein lies the exceptionally challenging aspect of PEA resuscitation management [see Tables 6 and 7]. Because coronary artery thrombosis and pulmonary thromboembolism are common causes of cardiac arrest, a trial evaluated the efficacy of tissue plasminogen activator (t-PA) in the setting of PEA of unknown or presumed cardiovascular cause in 233 patients in pre-hospital and emergency department settings.77 No benefit was found with thrombolytic therapy for PEA in this study; the proportion of patients with return of spontaneous circulation was 21.4% in the t-PA group and 23.3% in the placebo group.
Figure 2 Treatment algorithm for patients with VT, VF, PEA, or asystole. (PEA—pulseless electrical activity; VF—ventricular fibrillation; VT—ventricular tachycardia)
Asystole
The prognosis for asystole is generally regarded as dismal unless the patient is hypothermic or there are other extenuating but treatable circumstances. The sequence of resuscitation steps in the management of asystole is as follows: activation of the emergency medical or code response, primary survey (CPR, rhythm evaluation, and asystole confirmation), and secondary survey (intubation and confirmation of correct ET tube placement, optimal oxygenation and ventilation, I.V. access with epinephrine and atropine administration, immediate transcutaneous pacing, if available, and problem solving for technical difficulties and establishment of the cause of cardiac arrest) [see Figure 2]. The two core drugs for asystole management are epinephrine (repeated every 3 to 5 minutes for as long as the patient is pulseless) and atropine (up to 3 mg over time). As with PEA, vasopressin appears to be a reasonable and possibly beneficial substitute for epinephrine in asystole. A single dose of aminophylline (250 mg I.V.) may also be beneficial in atropine-resistant asystole.78 Potentially treatable causes of asystole include hypoxia, acidosis, hypothermia, hypokalemia, hyperkalemia, and drug overdose. Resuscitation efforts should stop if asystole persists for longer than 10 minutes despite optimal CPR, oxygenation and ventilation, and epinephrine or atropine administration; if extenuating circumstances (e.g., hypothermia, cold-water submersion, or drug overdose) are not present; and if no other readily treatable condition is identified.
Immediate Postresuscitation Care
Even when the resuscitation is successful, the patient’s situation remains tenuous and continued meticulous patient care is essential. When the cardiac monitor indicates what should be a perfusing rhythm, the rescuer should immediately confirm that the patient has a palpable pulse. If there is a pulse, the patient’s blood pressure is then obtained. Simultaneously, resuscitation team members need to quickly reassess the adequacy of the patient’s airway, the ET tube position, oxygenation and ventilation, and the patient’s level of consciousness and comfort.
If the patient is hypotensive, appropriate blood pressure management depends on the presence or absence of fluid overload, as judged at the bedside. If the patient is clinically volume overloaded or in frank pulmonary edema and hypotensive, dopamine is started at inotropic doses (5 ^g/kg/min I.V.) and titrated to a target systolic blood pressure of 90 to 100 mm Hg. If the patient’s clinical status suggests normovolemia or hypo-volemia, intravenous crystalloid boluses (in 250 to 500 ml increments) can be administered instead of dopamine to support adequate tissue perfusion. In patients who are regaining consciousness, their level of comfort mandates careful assessment and administration of analgesia and sedation, as appropriate.
If the arrest rhythm was either VT or VF, the parenteral an-tiarrhythmic drug used immediately before the return of spontaneous circulation is continued as a maintenance infusion (amiodarone, 1 mg/min for 6 hr, then 0.5 mg/min for 18 hr as blood pressure allows; or lidocaine, 2 to 4 mg/min). If an antiar-rhythmic drug has not yet been administered, it is usually started at this point to prevent the recurrence of VF or pulseless VT. There are important exceptions to this guideline, however. If the perfusing postarrest arrhythmia is an idioventricular rhythm or third-degree heart block accompanied by an idioventricular escape rhythm, an antiarrhythmic medication should not be started at this time, because the antiarrhythmic agent could eliminate the ventricular perfusing focus and return the patient to a pulseless state.
Initial postresuscitation studies usually include an ECG; portable chest radiography; and measurement of ABGs, a serum electrolyte panel, fingerstick or blood glucose, serum magnesium and cardiac enzyme levels, and hemoglobin and hemato-crit. The resuscitated patient requires urgent transfer to the optimal site for continued definitive care. Depending on the circumstances, this may be either the cardiac catheterization laboratory or the intensive care unit.
Ongoing research continues to look at optimal postresuscita-tion management strategies to improve neurologic outcome and survival to hospital discharge.79 Hyperthermia and hyperglyce-mia compromise postresuscitation neurologic outcome, whereas mild to moderate induced hypothermia appears to improve neurologic outcome and decrease mortality.80-83
Ending a Resuscitation Attempt
Throughout the resuscitation, the team leader must speak with calmness and authority, and all resuscitations should be orchestrated with clarity and finesse. If possible, the code captain should make clinical decisions without directly performing specific procedures. Cardiac arrests are emotionally charged, but the leader must insist on a composed, orderly, and technically sound resuscitation. It is appropriate to invite suggestions from team members and to ensure that all members are comfortable with the decision to stop the resuscitation, should that time arrive.
The decision whether to stop a cardiac resuscitation is burdensome. Clearly, the circumstances of the event, patient comor-bidities, the nature of the lethal arrhythmia, and the resuscitation team’s ability to correctly identify and treat potential contributing causes of the arrest are all important considerations. Resuscitation efforts beyond 30 minutes without a return of spontaneous circulation are usually futile unless the cardiac arrest is confounded by intermittent or recurrent VF or pulseless VT, hypothermia, cold-water submersion, drug overdose, or other identified and readily treated contributing conditions.
With nontraumatic cardiac arrest in the prehospital setting (assuming proper equipment and medications are available and no extenuating circumstances suggest otherwise), full resuscitation efforts take place at the scene of the arrest in preference to rapid transport to an emergency department. A prehospital resuscitation that has been appropriately conducted but has not resulted in at least temporary return of spontaneous circulation to the patient may be discontinued. It is important that certain criteria are adhered to, however, including the following: high-quality CPR provided, an adequate airway successfully placed, appropriate oxygenation and ventilation delivered, intravenous access established, appropriate medications specific to the arrest scenario administered, and resuscitation attempted for at least 10 minutes; in addition, the patient must not be in persistent VF, and there can be no extenuating circumstances that mandate in-hospital continuation of the resuscitation (e.g., hypothermia, drug overdose). The decision whether to cease resuscitation efforts in the field is bolstered by direct discussion with EMS physicians. It is also essential that social services be available to provide immediate assistance and support to the family and loved ones of the patient who has now died.
Discontinuing in-hospital resuscitations is advisable when three criteria are met: (1) the arrest was unwitnessed, (2) the initial rhythm was other than VF or VT, and (3) spontaneous circulation does not return after 10 minutes of ongoing resuscitation.86 In a study of this three-component decision rule, only 1.1% of patients (three out of 269) who met these criteria survived to hospital discharge, and none of the three survivors were capable of independent living.87 In a study of 445 prospectively recorded resuscitation attempts in hospitalized patients, no patient survived who suffered a cardiac arrest between 12 A.M. and 6 A.M. if the arrest was unwitnessed and if it occurred in an unmoni-tored bed.38
A resuscitation attempt in a persistently asystolic patient should not last longer than 10 minutes, assuming all of the following conditions apply: asystole is confirmed through proper rhythm monitoring and assessment; high-quality CPR is taking place; ET intubation is correctly performed and confirmed; adequate oxygenation and ventilation are provided; intravenous access is secured; appropriate medications (epinephrine or vaso-pressin and atropine) have been administered; and the patient is not the victim of hypothermia, cold-water submersion, drug overdose, or other readily identified and reversible cause.
After all resuscitation attempts, the code-team captain should debrief the team so that all may learn from the experience. Finally, marked empathy and skill are needed to carefully and compassionately inform family members about the outcome of the resuscitation.
