the absence of ST elevation, quickly evaluate for non-cardiac causes (intracranial hemorrhage, respiratory failure, PE, sepsis), take into consideration Q waves (old scar?) and pronounced ST depression (active ischemia?), and consider urgent echocardiography. Coronary angiography does not need to be performed immediately, unless: (a) myocardial ischemia appears likely, with (b) persistent shock and (c) no poor neurological predictors.
Note that, when indicated, immediate coronary angiography is performed in patients who are successfully resuscitated and whose systemic pressure is maintained on reasonable and stable doses of vasopressors. The performance of PCI in patients actively receiving chest compressions, using an external compression device, did not improve the grim mortality in one study and was not recommended in an expert viewpoint.176,184
Note: 5–15% of patients with ST elevation and OHCA do not have acute coronary occlusion.179-181 In those cases, ST elevation is related to a myocardial injury from the cardiac arrest itself, hyperkalemia, PE, or intracranial hemorrhage. One Korean study has shown that up to 19% of OHCA patients with ST elevation or, more so, ST depression have intracranial hemorrhage as a cause of the OHCA.
B. Role of post-resuscitation echocardiography
Echo often shows LV dysfunction that is non-specific, as it may be secondary to acute ischemia but also post-cardiac arrest myocardial stunning or chronic cardiomyopathy. Echo may be more specific in some settings, particularly when segmental dysfunction is present: (i) segmental akinesis of a thin myocardium with Q waves and no ST elevation suggests an old infarct and a scar-related VF, rather than acute ischemia VF; (ii) segmental akinesis without Q waves suggests acute ischemia; (iii) preserved LV function with akinetic or dilated RV suggests massive PE.
C. Role of extra-corporeal membrane oxygenation (ECMO) in ongoing VF arrest
PCI is futile in patients who are actively undergoing cardiac compressions, but a select group of these patients with refractory VF arrest may qualify for emergent ECMO placement to provide organ and cerebral perfusion (in the emergency room or the catheterization suite), followed by PCI. This is considered in patients with: (1) witnessed VF arrest that is refractory to 3 shocks and amiodarone (may have evolved to PEA/asystole), (2) near immediate initiation of bystander resuscitation, (3) resuscitation ongoing for <45 min, and (4) young age (<75).177
D. No role for thrombolysis during the resuscitation of cardiac arrest
In patients undergoing cardiopulmonary resuscitation for an arrest of presumed cardiac origin, the administration of tenecteplase during resuscitation did not improve the 30-day survival, the return of spontaneous circulation, or the neurological outcome, and increased intracranial hemorrhage. During cardiac arrest, the poor systemic perfusion may preclude the delivery of the fibrinolytic agent to its target, explaining the lack of efficacy; also, frequently, there is no acute coronary thrombosis, or thrombosis is not totally occlusive. Bleeding, including intracranial hemorrhage, may be a cause of arrest in a small proportion of patients and is aggravated by thrombolysis.185 However, after the return of spontaneous circulation in a patient with STEMI, fibrinolytics may be appropriate, as suggested by a small analysis.186
E. Mild therapeutic hypothermia
Two randomized trials of resuscitated post-cardiac arrest patients have shown that mild therapeutic hypothermia drastically improves sur- vival with appropriate neurological recovery (49% vs. 26% in one trial, 55% vs. 39% in the other trial).187,188 Based on the inclusion criteria of these trials, patients with the following features have a class I recommendation for hypothermia:
Patients with VF/VT arrest who had return of spontaneous circulation within 60 minutes of cardiac arrest. Hypothermia may be used in patients with asystole or PEA (less evidence and generally poorer outcomes in comparison to VT/VF).
Persistent coma with Glasgow Coma scale <8.
Cardiac arrest is not due to trauma or drug overdose.
Exclusion criteria:
Persistent hypotension (mean pressure <60 mmHg) despite the use of one vasopressor. The requirement for IABP is not a contraindication.
Uncontrolled active bleeding or intracranial hemorrhage ± severely abnormal coagulation studies or platelets <50 × 109/l.
Patients in the hypothermia protocol should have hypothermia induced as soon as possible after arrival to the emergency department, with a temperature goal of 32–36 °C within 6 hours after return of spontaneous circulation. The temperature is reduced by 0.5–1 °C per hour. In one of the trials, hypothermia was initiated as late as several hours after restoration of circulation, and the goal temperature was achieved at a mean of 8 hours (interquartile range, 4–16 hours).188 However, hypothermia should not be initiated later than 6 hours, as there is probably no benefit beyond this point.
In the control group of the two major hypothermia trials, the post-arrest temperature was close to 38 °C. A later study suggested that the mere prevention of this post-arrest hyperthermia with a low normal temperature of 36 °C is as effective as a temperature goal of 33 °C, which was used in the two early trials.189
Hypothermia is achieved using ice packs, cold intravenous saline, or a cooling blanket with adjustable settings. The patient may be given paralytic agents to prevent the counterproductive shivering during induction of hypothermia. Paralytic agents are not usually necessary once the goal temperature is reached. Sedation is also administered. Hypothermia is maintained for 24 hours, then the patient is rewarmed very slowly, at a rate no faster than 0.5 °C per hour. Since the patient is sedated, the neurologic prognosis of patients undergoing hypothermia may not be properly assessed until 72 hours after rewarming.
During hypothermia, the patient is monitored for the following side effects:190
Metabolic: hypokalemia (resulting from intracellular K shift), hyperglycemia, mild reduction of GFR, cold-induced diuresis. Hypokalemia should not be aggressively replaced, as severe hyperkalemia may occur during rewarming.
Bradyarrhythmia, VT.
Bleeding (coagulation factors are less effective during hypothermia).
Increased infectious risk; seizures.
Hypotension is multifactorial in these patients but may be worsened by hypothermia. Hypothermia reduces cardiac output and increases systemic vascular resistance.
The early initiation of hypothermia does not preclude the early performance of coronary angiography and PCI. The induction of hypothermia prior to or on arrival to the catheterization laboratory has been shown to be safe in several studies.176 In fact, PCI should be performed urgently, and hypothermia started as soon as possible, preferably before the initiation of PCI (international consensus recommendation).191 Antithrombotic therapies may also be used and have not significantly increased bleeding risk in hypothermic patients, but the patient should still be carefully monitored for bleeding.190
F. Hemodynamic status post cardiac arrest
Hemodynamic instability after a cardiac arrest may be secondary to myocardial infarction, myocardial stunning that results from the arrest itself, or post-cardiac arrest syndrome, which is a form of systemic inflammatory response syndrome (SIRS) with systemic vasodilatation similar to sepsis. Post-cardiac arrest syndrome is managed similarly to sepsis with an early goal-directed therapy. The SBP goal is usually >90 mmHg; one study has shown that a mean blood pressure >70 mmHg in the first 6 hours is associated with better neurological outcomes.192 1–2 liters of isotonic fluid is initially administered, followed by dopamine or norepinephrine.
QUESTIONS