Prolonged Resuscitation 

23 JUN 2014

Prolonged Resuscitation

Dr Faisal P.K, MEM Resident PGY - I
Dr Abdul Jaleel, EM Consultant and Faculty, MIEM
Dr Venugopal P.P., Director, Emergency Medicine, DM Healthcare

Editor: Dr Lajeesh Jabbar, MIEM

BRIEF NARATION OF EVENTS:A 58 year old female, a known case of CAD – Recent AWMI, DM, HTN, CKD was brought to our ED with h/o unresponsiveness since 10 minutes. On arrival she was gasping with no palpable central pulse. Resuscitation was started according to ACLS protocol. Initial rhythm was asystole. VBG done while resuscitating her revealed severe hyperkalemia which was aggressively corrected with insulin dextrose infusion, calcium gluconate and soda bicarbonate. She continued to be in asystole for 45 minutes, after which ROSC was obtained. Post ROSC she remained unresponsive, hypotensive and her ECG showed complete heart block with a heart rate of 30/min. She was intubated and ventilated, started to dopamine infusion and an emergency transcutaneous pacing was done from ED after which she became heamodynamically stable. She was then shifted to ICCU for further management.

Her sensorium dramatically improved with in 24 hours and was extubated the next day. She continued to be in TCP in ICCU as her relatives were not willing for PPI. Her rhythm reverted to normal sinus with control of hyperkalemia. Her subsequent hospital stay was uneventful except for post resuscitation chest pain and mildly elevated serum creatinine. She was discharged on the 8th day of admission in a stable condition.

ISSUES / CHALLENGES: Prolonged resuscitation (around 45 minutes) Hyperkalemia, Complete heart block, Metabolic acidosis, Hypotension.

CONCERNS: Hypoxic brain injury, Hyperkalemia induced arrhythmias, Ischemia induced arrhythmias.

Hyperkalemia is a common clinical condition that can induce deadly cardiac arrhythmias. Electrocardiographic manifestations of hyperkalemia vary from the classic sine-wave rhythm, which occurs in severe hyperkalemia, to nonspecific repolarization abnormalities seen with mild elevations of serum potassium.
Hyperkalemia is a common cause of the cardiac arrhythmias seen in clinical practice. The challenge in managing hyperkalemia comes from the fact that it can be difficult, if not impossible, to identify the condition solely on the basis of electrocardiographic information. Patients who present with hyperkalemia may have a normal electrocardiogram or have changes that are so subtle that physicians frequently have difficulty attributing these changes to increased potassium levels. In a study performed at the University of Pittsburgh Medical Center, only 46% of patients with potassium levels greater than 6.0 mEq/L had electro-cardiographic changes, and only 55% of patients with potassium levels greater than 6.8 mEq/L had changes consistent with hyperkalemia.2 In fact, there have been several reports in the literature of patients who had potassium levels greater than 7.5 mEq/L with no electrocardiographic manifestations of hyperkalemia. Even when there is evidence of hyperkalemia on a patient's electrocardiogram, physicians often miss the diagnosis. Wrenn and colleagues designed a study to determine the ability of physicians to predict the presence of hyperkalemia solely on the basis of their patients' electrocardiograms. The physicians in this study were able to predict hyperkalemia with a sensitivity of 35% to 43% and a specificity of 85% to 86%. This small study further emphasizes how difficult hyperkalemia can be to diagnose. Nevertheless, hyperkalemia can manifest with classic electrocardiographic changes that suggest its presence.
In experimental models, there is a very orderly progression of electrocardiographic changes induced by hyperkalemia. The earliest electrocardiographic manifestation of hyperkalemia is the appearance of narrow-based, peaked T waves. These T waves are of relatively short duration, approximately 150 to 250 msec, which helps distinguish them from the broad-based T waves typically seen in patients with myocardial infarction or intracerebral accidents. Peaked T waves are usually seen at potassium concentrations greater than 5.5 mEq/L and are best seen in leads II, III, and V2 through V4, but are present in only 22% of patients with hyperkalemia. It may be that increased myocyte excitability, shortening of the myocyte action potential, and an increase in the slope of phase 2 and 3 of the action potential account for the T wave peaking seen in mild hyperkalemia.
As serum potassium levels increase to greater than 6.5 mEq/L, the rate of phase 0 of the action potential decreases, leading to a longer action potential and, in turn, a widened QRS complex and prolonged PR interval. Electrophysiologically, this appears as delayed intraventricular and atrioventricular conduction. As the intraventricular conduction delay worsens, the QRS complex may take on the appearance of a left or right bundle branch block configuration. A clue that these electrocardiographic changes are due to hyperkalemia, and not to bundle branch disease, is that in hyperkalemia the conduction delay persists throughout the QRS complex and not just in the initial or terminal portions, as seen in left and right bundle branch block, respectively. As potassium levels reach 8 to 9 mEq/L, sinoatrial (SA) node activity may stimulate the ventricles without evidence of atrial activity, producing a sinoventricular rhythm. This occurs because the SA node is less susceptible to the effects of hyperkalemia and can continue to stimulate the ventricles without evidence of atrial electrical activity. The electrocardiographic manifestations of continued SA node function in the absence of atrial activity may be very similar to those of ventricular tachycardia, given the absence of P waves and a widened QRS complex .
As the hyperkalemia worsens and the potassium levels reach 10 mEq/L, sinoatrial conduction no longer occurs, and passive junctional pacemakers take over the electrical stimulation of the myocardium (accelerated junctional rhythm).If hyperkalemia continues unabated, the QRS complex continues to widen and eventually blends with the T wave, producing the classic sine-wave electrocardiogram. Once this occurs, ventricular fibrillation and asystole are imminent.
In addition to the previously mentioned arrhythmias, many other electrocardiographic abnormalities have been associated with hyperkalemia. In patients with acutely elevated serum potassium levels, a pseudomyocardial infarction pattern has been reported to appear as massive ST-T segment elevation develops secondary to derangements in myocyte repolarization. Early stages of hyperkalemia may manifest with only shortening of the PR and QT interval. Sinus tachycardia and bradycardia, idioventricular rhythm, and 1st-, 2nd-, and 3rd-degree heart block have all been described on the presenting electrocardiograms of patients with hyperkalemia. Given the vast array of electrocardiographic manifestations of hyperkalemia, the difficulty in consistently identifying hyperkalemia on the basis of electrocardiographic abnormalities, and the fact that the electrocardiogram during hyperkalemia may progress from normal to that of ventricular tachycardia and asystole precipitously, physicians need to consider this diagnosis in patients at risk.


1.    Always consider the reversible causes of cardiac arrest while resuscitating patients. Though AHA advocates the 5H’s and 5T’s as a must do, many people tend to ignore it.
2.    Never give up on resuscitating patients in view of multiple co-morbid conditions and advanced age.
3.    There is no substitute for a well coordinated resuscitation. Its is all about teamwork.
4.    Point of care saves lives!