When Dead Is Only Mostly Dead: Understanding which causes of sudden cardiac death have good outcomes - Patient Care - @ JEMS.com


When Dead Is Only Mostly Dead: Understanding which causes of sudden cardiac death have good outcomes

 

 
 
 

Andrew Muck, MD Michael Hilliard, MDBruce D. Adams, MD | From the March 2009 Issue | Sunday, March 8, 2009


My firsthand experience, every emergency medical professional knows just how common cardiac arrest is. To put it into perspective, 240,000 cases of out-of-hospital cardiac arrest occur in the U.S. each year. Despite advances in resuscitative medicine, widespread training in advanced cardiac life support (ACLS) and increased public education, the mortality rate for cardiac arrest has remained essentially unchanged during the past three decades. Survival from cardiac arrest ranges from 5-20%, with less than half of surviving patients discharged to live independently.

As a result of poor outcomes with cardiac arrest, EMS providers sometimes approach cardiac arrest with the belief that it inevitably ends poorly. However, certain causes of cardiac arrest, when treated appropriately, can result in excellent outcomes.

The goal of this article is to review those specific clinical scenarios in which cardiac arrest can have a good outcome despite prolonged CPR. We_ll review situations in which critical prehospital actions lead to dramatically improved outcomes. We_ll also review the role of thrombolytics in prehospital cardiac arrest, the rare "Lazarus phenomenon" and the role hypothermic resuscitation can play in improving morbidity and mortality in patients with the return of spontaneous circulation (ROSC) after CPR/ACLS. Understanding these situations will help EMS providers known when to "pull out all the stops"ƒwhen "dead" may be only "mostly dead."

Hypothermic Cardiac Arrest

Approximately 650 deaths in the U.S. each year are attributed to hypothermic cardiac arrest. Hypothermia has a myriad of cardiopulmonary effects, starting with simple tachycardia. But with prolonged hypothermia, bradydysrhythmias may develop. Bradycardia, atrial fibrillation and ventricular dysrhythmia can occur as core temperatures fall below 30_ C. Asystole and ventricular fibrillation are much more likely to occur at temperatures below 25_ C. A classic ECG finding in the setting of hypothermia is Osborn (J) waves seen at the junction of the QRS complex and ST segment, appearing at temperatures less than 32_ C.

Hypothermic cardiopulmonary arrest patients require aggressive resuscitation despite very low core temperatures (see Table 1). Multiple studies and case reports describe excellent outcomes despite severe hypothermia. Although invasive techniques for rewarming, such as extracorporeal membrane oxygenation (ECMO), have shown dramatic benefit, simple techniques, such as warmed intravenous fluids (IVF) and external rewarming techniques, en route to the hospital begin appropriate resuscitation. External rewarming with environmental controls, warm blankets and warmed IVF can all be life-saving interventions. An impressive resuscitation case report relied on ECMO for a core body temperature below 21 C. Extracorporeal blood warming has been used to great benefit in other studies, including a Switzerland study where 15 of 32 patients survived with core temperatures below 28 C and in Finland, where a mean CPR time of 70 minutes was noted.

A concept that must be noted is the recommendation to refrain from defibrillation or aggressive pharmacologic interventions in the setting of a hypothermic patient in cardiac arrest. A hypothermic patient does not have a normal myocardium. The patient truly needs re-warming more than aggressive ACLS interventions. A hypothermic patient will likely have little response to most ACLS measures, or may even have an overly sensitive cardiac reaction that could lead to an even more malignant arrhythmia.

Cold-Water Drowning

Cardiac arrest from cold-water submersion has a relatively high rate of survival even with a lengthy time of submersion. It_s difficult to predict whether a patient can survive the insult at the time of initial evaluation. Larger studies have shown it_s appropriate to perform prolonged resuscitations in victims of cold-water submersions. A study in Ontario, Canada, demonstrated that 55 near-drowning victims admitted to the ICU over a five-year period had a survival rate of 58%. In this study, all intact survivors had been submerged in cold water for prolonged periods and all underwent prolonged CPR. Notably, all patients with a detectable pulse at presentation, regardless of temperature, survived without neurologic sequelae.

Other available literature highlights many amazing stories and great saves. Extreme examples of successful resuscitations include a nine-hour resuscitation in the setting of a core temperature of 13.7 C in a 29-year-old female, a case of CPR that lasted more than six hours with successful resuscitation, and a child with a core temperature below 20 C who survived neurologically intact in the setting of cardiac arrest of over 85 minutes.

Sometimes, it_s unclear whether resuscitation should be undertaken in the setting of drowning when time and water temperature aren_t clear. Erring on the side of prolonged resuscitation is most appropriate as supported by a study of cold water immersions in Scotland between 1991 and 1997. In this study, it was noted that EMS providers sometimes failed to both initiate and continue prehospital resuscitation for victims of near drowning in cases where patients may have benefited.

Toxicologic Cardiac Arrest

Five major drugs will induce cardiac arrest that will respond to specific and potentially very beneficial therapies: 1) tricyclic antidepressants, 2) beta-adrenergic blockers, 3) calcium channel blockers, 4) digitalis and 5) cocaine (See Table 2).

1. Tricyclic antidepressants (TCA):The predominant systems involved in TCA overdose are cardiovascular and neurologic. These patients may present with hypotension, ECG changes and cardiac arrest. Patients with a TCA overdose may also have altered mental status, findings consistent with an anticholinergic toxidrome and seizures.

If hypotension occurs, be aggressive with fluid resuscitation. Classic ECG findings include sinus tachycardia, a classic prolongation of the QRS complex (> 100 msec) and a prolongation of the QT interval. Also notable is the rightward deviation of the terminal 40-msec QRS axis. Of the utmost importance is the use of sodium bicarbonate for any arrhythmias and for QRS widening. If the QRS widens beyond 100 msec, then sodium bicarbonate should be administered because the patient is at risk of progressing to cardiac arrest. If you suspect TCA overdose during a case of refractory cardiac arrest, empirically administer sodium bicarbonate (50 mEq) and repeat as needed to maintain QRS < 100 msec.

Hypertonic saline has been evaluated and thought to possibly be effective in cases of refractory hypotension with QRS widening.

Definitive airway management, to include endotracheal intubation, may be used in the setting of depressed mental status. If seizures occur, standard therapy with benzodiazepines or midazolam boluses is indicated with advancement to phenobarbital if benzodiazepines are not effective. Phenytoin should not be used as it may lead to more malignant cardiac arrhythmias.

2. Beta-blockers:Beta-blocker overdose can cause bradycardia, hypotension, loss of consciousness, respiratory arrest, hypoglycemia, seizures, symptomatic bronchospasm and VT/VF. Immediate treatment should include atropine, glucagon and crystalline fluids. Further approaches to maintain circulation rely on other vasopressors, calcium and mechanical devices. In rare cases, circulatory assist devices, such as an interarterial balloon pump or emergency cardiac bypass, may prove lifesaving.

3. Calcium channel blockers:Overdoses related to calcium channel blockers are similar to beta-blocker toxicity in many ways. As with beta-blockers, multiple organ systems are affected. Hypotension and bradycardia are common. Cardiac conduction disturbances, including sinus arrest, AV blocks and asystole, occur. Depressed mental status is common, and respiratory status can be affected. As with beta-blocker therapy, immediate monitoring, fluids and atropine administration are vital.

Calcium administration is imperative with the administration of calcium gluconate (or calcium chloride as appropriate). Studies have shown the potential benefit of a hyper insulin-euglycemia therapy. As with beta-blocker therapy, vasopressors, glucagon, phosphodiesterase inhibitors and mechanical devices can play a role.

4. Digitalis:Digoxin continues to be a commonly prescribed medication. Digitalis toxicity can occur with nearly any type of arrhythmia, but bidirectional ventricular tachycardia is pathognomonic (which means this sign is so characteristic it makes the diagnosis). If patients are suspected to have a digitalis overdose with CPR in progress, empirically administer 10 vials of digoxin-specific antibody (Digibind). Patients short of cardiac arrest, such as those with life-threatening arrhythmias with pulse present, hyperkalemia greater than five or a massive overdose, may also require digoxin-specific antibodies and, at that point, you may have time to calculate the appropriate amount.

5. Cocaine:The most easily recognized signs of cocaine use involve the stimulation of the sympathetic nervous system. Cocaine can produce a variety of direct myocardial effects, as well as severe metabolic derangements, leading to hyperthermia, electrolyte imbalances, refractory seizures and cardiovascular collapse. The treatment is immediate supportive care.

Benzodiazepines in large doses are an important mainstay both for agitation and cardiovascular affects. For example, atrial dysrythmias from cocaine use are often sympathetically driven, and thus respond to treatment with benzodiazepines. Sodium bicarbonate is often necessary in the setting of wide-complex tachycardias (1-2 mEq/kg). The use of sodium bicarbonate addresses the cocaine-induced sodium channel blockage. Epinephrine should be avoided in cocaine toxicity because such patients are already sympathetically overactive. Also, avoid the use of beta-blockers, because of the risk of unopposed alpha-blockade.

The Role of Thrombolytics

Thrombolytics have an established role in the treatment of early stages of embolic cerebrovascular accident and potentially in massive pulmonary embolism manifested with refractory hypoxemia or shock. With a majority of cardiac arrest cases thought to be related to acute myocardial infarction/ischemic heart disease or pulmonary embolism, it_s reasonable to suggest that in cases of refractory cardiac arrest, empiric thrombolytics could be considered. Although we can_t offer definitive recommendations on this topic, we_ll discuss possible interventions with thrombolytics.

Case reports suggest thrombolytics should be considered in undifferentiated out-of-hospital cardiac arrest. A pilot trial was conducted to look at giving thrombolytics in the prehospital environment in the setting of undifferentiated cardiac arrest. The findings of a pilot randomized trial of thrombolysis in cardiac arrest (TICA Trial) suggest that using thrombolytics in this environment is feasible and beneficial.

A study from Wake Forest found empiric use of tenecteplase (TNK) in cardiac arrest is associated with increased ROSC, short-term survival and survival to hospital discharge with good neurological function in patients who fail to respond to ACLS. In another case series, Tiffany et al found a benefit from the use of bolus of thrombolytics in the setting of cardiac arrest refractive to treatment. However, not all studies, including a study of more than 1,000 patients in Austria, show a benefit in using thromblytics in undifferentiated cardiac arrest.

There seems to be no harm in giving thrombolytics when you have performed or expect to perform CPR. Initial concerns for increased risk of thoraco-abdominal trauma from compressions have not been borne out in multiple case studies. Few adverse outcomes have been noted. Outcomes have included no significant increase in bleeding complications and only scattered case reports of chest wall hematomas, hepatic lacerations and Mallory-Weiss tears.

The Lazarus Phenomenon

Prognosticating the effects of CPR can be extremely difficult, as experienced by physicians and prehospital providers alike. Even in cases where patients have undergone prolonged CPR and have no signs of life, some have had ROSC after stopping CPR. The Lazarus Phenomenon, named after the Biblical story, raises the question of whether prolonged CPR and observation is always appropriate.

More than 20 cases are reported in the literature, including eight patients who survived neurologically intact. Each year, news articles report on such cases that aren_t always written up in the medical literature. Many of these patients experienced a premonitory gap prior to the patient auto-resuscitating. Two mechanisms are thought to potentially play a role: 1) dynamic hyperinflation of the lungs, and 2) delayed delivery of ACLS drugs.

Based on the rarity of such events, and the clearly poor outcomes of patients with prolonged asystole, we do not recommend any changes from current ACLS protocols, but rather encourage resuscitation providers to monitor patients closely for at least 10 minutes after CPR. Of note, the impedance threshold device (ITD, or ResQPod from Advanced Circulatory Systems Inc.) may help prevent the first mechanism (dynamic hyperinflation of the lungs) by lowering the intrathoracic pressure that draws more venous blood back to the heart.

After Resuscitation

All too commonly, patients will survive sudden cardiac death but will be left with significant neurological deficits. The most exciting therapy of late to improve outcomes is induced therapeutic hypothermia. Two important studies appeared in theNew England Journal of Medicine in 2002.

The first was an Australian series of 77 comatose patients after ROSC. In this study, patients were cooled using a protocol of 33_ C for 12 hours by placing ice packs around the head, neck, torso and limbs. Although there was no significant difference in hospital mortality, there was a very meaningful (49% versus 26%) difference in the number of patients with good neurologic function in the hypothermic group at the time of discharge.

A second study at that time found similar results. The Hypothermia After Cardiac Arrest Study Group studied whether mild systemic hypothermia could increase the rate of neurologic recovery after resuscitation from cardiac arrest due to ventricular fibrillation. In this multicenter trial, patients who had been resuscitated after cardiac arrest due to ventricular fibrillation were randomly assigned to undergo therapeutic hypothermia (target temperature of 32_ C to 34_ C, measured in the bladder) over a period of 24 hours or to receive standard treatment with normothermia. In the hypothermia group, 55% had a favorable neurologic outcome. In the normothermia group, 39% had a favorable neurologic outcome. Mortality was also improved in the hypothermia group; the hypothermia group had a 41% mortality rate at six months as compared with 55% in the normothermia group.

More recent studies have been done and even more are underway. To date, it remains evident that hypothermia is beneficial in ventricular tachycardia/ventricular fibrillation, and now the question is whether it is appropriate for other forms of cardiac arrest.

The overall conclusion from the studies described here is that there is a role for hypothermia and there are interventions that improve outcomes after ROSC in the setting of sudden cardiac arrest. Because cooled IVF and even possibly cooling blankets can be started in the field, prehospital protocols are a vital component of hypothermia protocols.

Conclusion

It_s important to recognize that all causes of sudden cardiac death are not created equal. The potential for a good clinical outcome varies based on the etiology. It_s imperative that basic and advanced prehospital providers recognize that specific causes and clues should guide resuscitation management. Once ROSC is achieved, the work is not done. Prehospital systems need to consider development and implementation of therapeutic hypothermia protocols for cardiac arrest patients, because this intervention can improve outcomes and quality of life.

Capt. Andrew E. Muckis the assistant director of EMS at Wilford Hall Medical Center at Lackland Air Force Base in Texas. He has served in the United States Air Force for five years and much of this article was written while deployed in Iraq. His recent work has included coordinating a hypothermia protocol for cardiac arrest at his institution. Contact him at Andrew.Muck@lackland.af.mil.

LTC Michael Hilliardis the transitional year program director and staff emergency medicine physician at the San Antonio Uniform Health Education Consortium at Brooke Army Medical Center. He has enjoyed a wide variety of assignments in his career, including time in Baghdad, Iraq, and is currently assigned to the teaching center in San Antonio, Texas.

COL Bruce Adamsis the chief of emergency medicine and also chief of clinical research at William Beaumont Army Medical Center in Texas. He has enjoyed a wide variety of assignments in his career, ranging from combat assignments to teaching centers. His research and teaching interests focus on resuscitation, trauma and combat casualty care.

To reviewthe reversible causes of cardiac arrest, read˙Arresting PEA.Ó

References

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Related Topics: Patient Care, Cardiac and Circulation, cardiac arrest, sudden cardiac death, Jems Features

 
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