Hyperkalemia-Induced Bradydysrhythmias

Abstract

Hyperkalemia is an acute life-threatening metabolic imbalance that is commonly seen in emergency departments. The primary cause is renal disease, but it also results from increased potassium intake in the diet, severe volume contraction, some medications, and other metabolic disturbances. Signs and symptoms suggestive of hyperkalemia must be recognized early so that life-saving interventions can be initiated. Rapid acquisition of an electrocardiogram (ECG) is important for making an early diagnosis because it can provide clues to the diagnosis long before laboratory results become available. Acute care providers are trained in the progression of alterations on the ECG tracings that occur as serum potassium levels rise. The earliest signs of mild hyperkalemia (5.5–6.5 mmol/L) are tall, narrow-based T waves, best seen in the precordial leads. As the potassium level becomes moderately elevated (6.5–8.0 mmol/L), the PR and QRS intervals become progressively longer, and the P waves might be lost. Severe hyperkalemia (> 8.0 mmol/L) often produces fascicular and intraventricular blocks and an eventual “sine wave” appearance which leads to ventricular fibrillation or asystole if immediate treatment is not provided. Hyperkalemia also often produces bradycardic rhythms along the progression of ECG findings, but this manifestation is not well-known or commonly taught. As a result, life-threatening hyperkalemia may be easily missed until laboratory results reveal the diagnosis. Additionally, standard treatments for bradydysrhythmias, such as atropine and electrical pacing, are often ineffective in treating this life-threatening cause of bradycardia. With early recognition of bradyarrhythmia caused by hyperkalemia, however, the proper treatment can be expedited and clinical decline can be averted.

Introduction

Hyperkalemia is an acute life-threatening metabolic imbalance often seen in the emergency department (ED). Severe hyperkalemia is most commonly a result of reduced potassium (K+) excretion secondary to renal disease. In fact, 75% of cases of severe hyperkalemia are caused by renal failure. 1 Other causes of hyperkalemia are increased dietary intake, severe volume contraction, medications, and other metabolic disturbances.

In the ED, an electrocardiogram (ECG) should be available long before serum K+ levels return from the laboratory. Although the ECG is not considered 100% reliable for diagnosing hyperkalemia, a predictable progression of ECG findings is commonly taught to clinicians in training: peaked T waves, widening of the QRS intervals, a “sine wave” pattern, and eventual ventricular fibrillation or asystole. However, severe hyperkalemia is also associated with unusual bradydysrhythmias.

It is important for emergency physicians to quickly recognize the electrocardiographic changes associated with hyperkalemia, because prompt initiation of specific treatment can be life-saving. When clinicians fail to recognize hyperkalemia-induced bradydysrhythmias, delays in initiation of proper treatment occur and ineffective therapies are sometimes administered. Early recognition of bradydysrhythmias caused by hyperkalemia will dramatically alter the patient’s course of treatment and prevent a worsening clinical condition and death.

Case Presentations

Case One

A 58-year-old incarcerated man with a history of hypertension, hepatitis C, chronic renal insufficiency (not treated with dialysis), and congestive heart failure presented to the ED by ambulance with a complaint of chest pain. He was evaluated first at the prison and was found to have a heart rate in the 20s. He reported associated lightheadedness, recent decreased oral intake, and several episodes of non-bloody vomiting and diarrhea. His medications included multiple antihypertensive drugs, one of them being lisinopril, 40 mg daily. On examination, the patient appeared diaphoretic and in mild distress. He was afebrile, with a heart rate of 27 beats/min, a respiratory rate of 22 breaths/min, blood pressure of 133/56 mmHg, and a pulse oximetry reading of 99% on 2 L/minute via nasal cannula. His examination was notable for dry mucous membranes, marked bradycardia, and clear lungs. The patient was connected to a cardiac monitor, and transcutaneous pacemaker pads were applied. An ECG was obtained ( Fig. 1 ), showing atrial fibrillation with a very slow ventricular response. The T waves were minimally peaked. The patient had no prior history of atrial fibrillation. The patient was initially treated in the ambulance with 0.5 mg intravenous (IV) atropine because of the slow rhythm, and the dose was repeated upon arrival to the ED without any improvement in the heart rate. Transcutaneous pacing was initiated but mechanical capture was unsuccessful. At that point, the patient’s heart rate decreased to < 20 beats/min, he lost palpable pulses, and he became unconscious. At that point, given the patient’s known history of renal insufficiency and lisinopril use, empiric treatment for hyperkalemia was initiated. Administration of 2 grams of IV calcium gluconate resulted in a slight improvement of his heart rate to the 30s, and he regained consciousness.

Fig. 1 . Atrial fibrillation with slow ventricular response and minimally peaked T waves.

Point-of-care testing revealed a K+ concentration of 8.4 mmol/L. Formal laboratory analysis of his chemistries soon thereafter revealed the following values: sodium, 126 mmol/L; K+, 8.5 mmol/L; chloride, 108 mmol/L; bicarbonate, 18 mmol/L; blood urea nitrogen (BUN), 69 mg/dL; and creatinine, 4.85 mg/dL. The patient was treated with 10 units of IV insulin (with 25 grams of dextrose), 100 mEq of IV sodium bicarbonate, four 2.5-mL albuterol nebulizers; and 60 mg of oral sodium polystyrene sulfonate (Kayexalate) was administered after he was more awake. He was admitted to the medical intensive care unit, where he received emergent dialysis. His repeat K+ concentration after dialysis was 5.0 mmol/L, and a follow-up ECG showed a return to normal sinus rhythm with a heart rate in the 60s.

Case Two

A 65-year-old woman with history of dialysis-dependent renal failure, hypertension, diabetes mellitus, and left nephrectomy presented to the ED with the complaint of 1 day of shortness of breath, chest pain, and abdominal discomfort. Three days prior, the patient completed only half of her hemodialysis session because of a malfunction of her tunneled dialysis catheter. She had not been able to undergo hemodialysis since that time because the catheter had not yet been replaced. The patient’s medications included aspirin, hydralazine, lisinopril, and pravastatin.

Initial assessment revealed the patient was awake; alert; oriented to person, place, and time; in moderate respiratory distress; and diaphoretic. She was afebrile and had the following vital signs: heart rate, 30 beats/min; respiratory rate, 28 breaths/min; blood pressure, 107/51 mmHg; and pulse oximetry reading, 87% on room air. The physical examination was notable for bradycardia, rales at bilateral lung bases, and a soft, non-tender abdomen with a midline incisional scar. The patient was connected to a cardiac monitor and given supplemental oxygen, and two large-bore intravenous lines were placed. A 12-lead ECG was obtained ( Fig. 2 ), which showed an idioventricular rhythm with rate 27 beats/min and large peaked T waves. A portable chest X-ray film showed prominent vascular congestion and pulmonary edema.

Fig. 2 . Idioventricular rhythm.

This patient was treated for presumed hyperkalemia with 4 g of IV calcium gluconate, 10 units of IV insulin, and 25 grams of IV dextrose. Two doses of atropine (0.5 mg) had also been administered prior to the arrival in the ED without effect. Repeat vital signs were obtained 5 minutes later and read as follows: pulse of 65 beats/min, respiratory rate of 16 breaths/min, blood pressure of 90/54 mmHg, and pulse oximetry reading 93% on 15 L/minute supplemental oxygen.

Laboratory results obtained 45 minutes later revealed the following pre-treatment values: potassium, 9.6 mmol/L; bicarbonate, 18 mmol/L; BUN, 117 mg/dL; and creatinine, 12.7 mg/dL. The on-call nephrologist was contacted to perform emergent hemodialysis. The patient’s post-dialysis potassium concentration was 5.2 mmol/L, and the repeat ECG at that point was normal. The patient was admitted to the medical floor for further monitoring and treatment.

Case Three

A 55-year-old man presented to the ED moribund after having been found unresponsive at home by family members. The family reported that this patient had a history of end stage renal disease and but did not know if he had missed any dialysis sessions. The ambulance crew noted that the patient was minimally responsive to pain but was breathing spontaneously with a respiratory rate of 24 breaths/min. The pulse oximetry reading was 90% on room air, heart rate 25 beats/min, blood pressure 70/35 mmHg, and fingerstick glucose was normal. The patient was given 1 mg of IV atropine without any improvement in vital signs. He was placed on 15 L/min supplemental oxygen and transported to the ED. Intravenous fluids were administered in route.

Upon arrival to the ED, the patient’s blood pressure had improved slightly to 80/40 mmHg, but his mental status and other vital signs were unchanged. Laboratory studies, including a basic metabolic panel and a venous blood gas, were sent. An ECG was obtained ( Fig. 3 ) and interpreted to be a junctional bradycardia with a rate of 24 beats/min. Large, somewhat-peaked T waves are present but were not noticed by the treating team, as their main focus was the bradycardia. Standard treatment for unstable bradycardia was initiated with 1 mg IV atropine which had no effect. Transcutaneous pacing was attempted but failed to achieve mechanical capture. The ED providers, with the assistance of a cardiology fellow, then moved rapidly to place a transvenous pacer via a right internal jugular vein, but mechanical capture was still unsuccessful. The patient’s blood pressure slowly deteriorated, but at that point the treatment team received a call from laboratory personnel, who stated that the serum potassium level was 10.2 mmol/L. They also reported that the venous blood gas pH was 7.16.

Fig. 3 . Regular slow rhythm, diagnosed as a junctional bradycardia. (A) Large T waves are present but were not noticed by the treating team. (B) Sinus rhythm with slightly peaked T waves.

The treatment team discontinued attempts at electrical pacing and instead administered 100 mL of 8.4% sodium bicarbonate (2 ampules) as a rapid IV push. Within 1 minute, the heart rate was noted to increase and the blood pressure improved as well. A repeat ECG was obtained ( Fig. 3 ), demonstrating a return to sinus rhythm with slightly peaked T waves. This treatment was immediately followed by IV administration of 2 g of calcium gluconate, 10 units of insulin, and 25 g of dextrose. Other laboratory studies (pre-treatment) included BUN 90 mg/dL and creatinine 9.5 mg/dL. The nephrology service was consulted and the patient underwent emergent hemodialysis with a good outcome, including full neurologic recovery.

Discussion

Hyperkalemia is the most common deadly metabolic condition among patients presenting to the ED. The prevalence of hyperkalemia among patients admitted to hospitals is estimated to be between 1% and 10%. 1 The causes of this electrolyte imbalance include potassium redistribution, increased intake, decreased excretion, and medications that interfere with potassium homeostasis by promoting a transcellular shift or by impairing excretion. 2 In many patients, hyperkalemia often has several causes, the most common being renal failure and medications. 3 , 4

Pathophysiology and ECG Findings

The effects of hyperkalemia on the heart’s conduction system have been well studied and documented. 5 The normal extracellular level of K+ in the human body is 3.5 to 5.3 mmol/L. As the K+ level rises, a predictable pattern of electrocardiographic changes may be seen. The earliest signs of mild hyperkalemia (5.5–6.5 mmol/L) found on the ECG are tall, narrow-based T waves, which are best seen in the precordial leads as a result of acceleration of terminal repolarization. 6 - 8 Progressive prolongation of the PR and QRS intervals can be seen with moderate elevations of the K+ level (6.5–8.0 mmol/L). Fig. 4 demonstrates these classic ECG findings of hyperkalemia of which acute care providers are well-trained to recognize.

Fig. 4 . The classic and most recognized findings of hyperkalemia are demonstrated here: large peaked T waves (especially in the precordial leads) and widening of the QRS intervals. Prolongation of the PR interval, a well-described finding, is present here as well.

As the potassium level continues to rise, conduction of the atrial impulse to the atrioventricular node can occur without atrial contraction, resulting in loss of P waves. This occurs because atrial tissue is more sensitive to elevations in the serum K+ concentration than are other ventricular myocytes. The result is an ECG that has the appearance of a junctional escape rhythm if the QRS complexes remain narrow, or the appearance of a ventricular escape rhythm (“idioventricular rhythm”) if the QRS complexes are wide. The latter is often referred to as “sinoventricular conduction,” indicating atrial impulses without atrial contraction occur. Progressive hyperkalemia (> 8.0 mmol/L) often produces fascicular blocks with axis changes and intraventricular blocks with further widening of the QRS complexes ( Fig. 5 ), and an eventual “sine wave” pattern. 9 Further elevation inhibits ventricular conduction, producing ventricular fibrillation or, more often, asystole.

Fig. 5 . Progressive prolongation of the QRS intervals with rightward axis, approaching the “sine wave” pattern. Note the absence of P waves, typical of sinoventricular conduction.

Profound, often bizarre bradydysrhythmias are also frequently noted to occur with hyperkalemia and easily mislead health care providers into making incorrect diagnosis and treatment plans (Figs. 6 and 7). Unfortunately, the fact that hyperkalemia can produce these rhythms is rarely taught. As a result, these cases of hyperkalemia are often misdiagnosed or delayed in diagnosis. Textbooks in emergency medicine, internal medicine, and even cardiology provide minimal, if any, discussion of this critical finding. Cases 1 and 3 demonstrate this occurrence, whereby acute care providers did not initially recognize hyperkalemia, and there was a delay in proper treatment with near-disastrous results.

Fig. 6 . Unusual bradydysrhythmia with prolonged sinus pause in a patient with potassium level 8.0 mmol/L. Peaked T waves are noted only in one complex in lead V4 and led to a significant delay in proper diagnosis and treatment in this case.

Fig. 7 . Bizarre bradydysrhythmia demonstrating junctional rhythm with premature supraventricular complexes in a pattern of bigeminy. Mild peaked T waves were only noted in retrospect. The potassium level was 8.9 mmol/L.

The “rate of rise” of the potassium level seems to be an important modifying factor in the development of these bradydysrhythmias. Rapid administration of K+ in vitro appears to markedly depress cardiac conduction below the bundle of His, causing escape beats and escape rhythms. 10 This point is highlighted in Case 1: the patient in that scenario was acutely dehydrated as the result of recent decreased oral intake and multiple episodes of diarrhea. Similar reports have described patients presenting with hyperkalemia-induced bradycardia after starting K+-sparing medications or experiencing diarrhea. 11 , 12

Treatment

Traditional Advanced Cardiac Life Support guidelines for symptomatic bradycardia recommend 13 starting an intravenous line, connecting the patient to a cardiac monitor, and giving supplemental oxygen. An ECG should also be obtained to better define the rhythm. Transcutaneous pacemaker pads should be placed on the patient, and administration of atropine (0.5 mg, IV) should be considered as a first-line therapy. 13 Administration of atropine, however, is a common pitfall. Atropine is typically effective for bradydysrhythmias that are induced by excessive vagal tone, but as noted above hyperkalemia produces bradycardia through a different mechanism. Another common pitfall is initiation of early electrical (transcutaneous or transvenous) pacing, which is ineffective because of reduced myocardial cell electric potential. Published cases reports 14 , 15 have documented the failure of electrical pacing to achieve mechanical capture in patients with severe hyperkalemia, as demonstrated in Cases 1 and 3.

Treatment for acute or severe hyperkalemia is directed toward antagonizing the effect of K+ on excitable cell membranes, redistributing extracellular K+ into cells, and enhancing the elimination of K+ from the body. 16 If the emergency physician suspects hyperkalemia-induced bradycardia, rapid administration of IV calcium gluconate or calcium chloride will help stabilize the cardiac tissue while waiting for the laboratory report. The administration of IV sodium bicarbonate in patients with acidemia may be effective as well, as shown in Case 3, but the improvement in cardiac conduction is only temporary. Administration of nebulized albuterol and IV insulin (with dextrose) to shift K+ into the intracellular space should be initiated. If the patient still produces urine, consider giving IV fluids and a loop diuretic to promote excretion of excess K+. Traditionally, oral sodium polystyrene sulfonate was used to remove excess K+ by way of the gastrointestinal tract, but this approach has been associated with colonic necrosis, especially in patients with constipation. 17 , 18 Newer safer oral potassium binders have recently been introduced, but they work slowly and are not immediately effective in life-threatening cases of hyperkalemia. Emergent hemodialysis should be strongly considered for patients with refractory hyperkalemia.

Conclusion

Hyperkalemia is an acute life-threatening metabolic emergency that is commonly seen in the ED. Hyperkalemia should be strongly considered in ED patients with bradydysrhythmias, especially in those patients taking medications that increase K+, in those with known underlying renal disease, in the setting of unusual or bizarre-appearing slow rhythms, and when typical bradycardia therapies (e.g., atropine, electrical pacing) are ineffective. Appropriate treatment that is specific for hyperkalemia will be life-saving in these patients.

Acknowledgment

The manuscript was copyedited by Linda J. Kesselring, MS, ELS, the technical editor/writer in the Department of Emergency Medicine at the University of Maryland School of Medicine.