ECG as a window of opportunity: For hyperkalemia

Wincy Marlene, S. Aravindakumar*

Department of Cardiology, Kauvery Hospital, Trichy

*Correspondence: aravindgowri@yahoo.co.in

Background

Hyperkalemia is a common electrolyte disorder observed in the emergency department. It is often associated with underlying predisposing conditions such as moderate or severe kidney disease, heart failure, diabetes mellitus and drugs or significant tissue trauma.

A 65-year-old female with multiple comorbidities and with a history of a kidney transplant, CAD- TVD (2022) who came to the emergency department with acute breathlessness ECG evaluation showed hyperkalemia changes and serum potassium was found to be high (7.2 mEq/l). In this article, we explored the ECG changes and management of hyperkalemia in an acute setup.

Hyperkalemia

Hyperkalemia is defined as serum or plasma potassium levels above the upper limits of normal, usually greater than 5.0 mEq/l. Symptoms usually develop at higher levels, 6.5 to 7 mEq/l. The goal of managing acute hyperkalemia is to prevent or minimize electrophysiologic effects on the heart to reduce the immediate risk of arrhythmias such as ventricular fibrillation and conduction defects such as sinoatrial and atrioventricular blocks, which can lead to complete heart block and asystole. Other common symptoms include neuromuscular weakness, paresthesia, areflexia, ascending paralysis and GI effects (nausea, vomiting, and diarrhea).

ECG Changes of The Patient

In this initial, ECG the classical findings can be seen such as prolonged PR interval, tall peaked T wave and short QT interval which are suggestive of hyperkalemia ranging [K+] 6.57.5 mEq/l.

Hyperkalemia-1

Repeat ECG after 2 has above shows features such as flattening of the P-wave and QRS widening seen in [K+] 7.58.0 mEq/l, which are highly suggestive of hyperkalemia.

Hyperkalemia

Approach Considerations

The severity of hyperkalemia therapy is closely connected to the rate at which the condition develops the absolute level of serum potassium and the presence of toxicity. The faster the potassium level rises higher the cardiotoxicity and requiring immediate aggressive therapy.

Based on the ECG changes in this patient and clinical findings, the diagnosis of severe hyperkalemia was made and aggressive treatments were initiated with serial monitoring of ECG mainly and other blood investigations.

Initial Emergency Management

In the prehospital setting, a patient with known hyperkalemia or a patient with kidney failure with suspected hyperkalemia should have IV access established and should be placed on a cardiac monitor.

Further workup should be initiated to determine the inciting cause and to prevent future episodes. Such a workup should include an evaluation of sources of potassium intake causes for decreased renal excretion and causes for decreased cell uptake of potassium. In most cases, all 3 of those etiologic factors contribute to hyperkalemia.

Step 1

  1. Administer intravenous (IV) calcium to ameliorate cardiac toxicity.
  2. Infuse calcium chloride or calcium gluconate (10 ml of a 10% solution over 2 to 3 min).
  3. The onset of action occurs within minutes.The duration of action is 30 min to an hour.

Step 2

  1. Identify and remove sources of potassium intake.
  2. Discontinue oral and parenteral potassium supplements.
  3. Remove potassium-containing salt substitutes.
  4. Examine the patient’s diet.
  5. Change the diet to a low-potassium tube feed or a 2 g potassium diet.

Step 3

  1. Enhance potassium uptake by cells to decrease the serum concentration.
  2. IV glucose and insulin infusions are very effective in enhancing potassium uptake.
  3. A typical regimen is 10 U of regular insulin and 50 ml of dextrose 50% in water (d50w).
  4. The onset of action is within 2030 minutes, and the duration is variable, ranging from 2 6 h.
  5. Continuous infusions of insulin and glucose-containing IV fluids can be used for prolonged effects.
  6. IV insulin (even when administered with dextrose) can cause hypoglycemia.
  7. Patients with acute kidney injury and chronic kidney disease are especially susceptible, particularly those with lower body weight and creatinine clearance.
  8. Sufficient dextrose in the treatment regimen can minimize the risk.
  9. Continue monitoring glucose and potassium levels every 2 h.

Beta-adrenergic agonists are likewise highly effective, but they are possibly more controversial and more prone to cause negative effects. The most widely utilized preparations are nebulized albuterol and salmeterol. The dose for treating hyperkalemia is larger than the standard amount for treating bronchospasm and requires the aid of a respiratory therapist. The maximum hypokalemic effect comes after 90 min.

In the absence of acidosis, sodium bicarbonate has only a little effect on plasma potassium content. It should be kept for hyperkalemia patients with accompanying metabolic acidosis after they have administered insulin and glucose, an adrenergic drug and calcium.

We must keep an eye out for potassium overcorrection. Extracellular potassium levels are increased in diabetic ketoacidosis (DKA) and many other kinds of metabolic acidosis, yet the patient may have a whole-body potassium deficiency. When a physician starts DKA treatment, the extracellular potassium level drops on its own.

Step 4

  1. Increase the body’s potassium excretion.
  2. Renal excretion is easily increased in persons with normal kidney function by providing IV saline with a loop diuretic (e.g., furosemide).
  3. Stop using potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBS), and any other medications that limit renal potassium excretion.
  4. Maintain euvolemia by monitoring volume status.
  5. The use of an aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate can increase renal excretion.

Sodium Polystyrene Sulfonate

The use of cation exchange resins such as sodium polystyrene sulfonate (SPS) can increase gastrointestinal excretion. Because the colon is the primary site of action for SPS, it can be taken orally or rectally (as a retention enema). For hyperkalemic crises, rectal administration is preferable. The efficiency of SPS is increased if the enema is kept for 1 h.

Step 5

Emergency dialysis is a last resort for patients with potentially fatal hyperkalemia who have not responded to more conservative therapies, or for patients with full kidney failure. Dialysis can typically take several hours to begin; therefore, even if dialysis is considered the other treatment modalities should be implemented as a bridge to dialysis.

The patient should be hospitalized following emergency management and hyperkalemia stabilization. Potassium-lowering therapies can be discontinued once the potassium level is restored to normal, and the serum potassium level can be monitored. Cardiac monitoring should be kept up at all times.

Result and Disscussion

To summarize, the primary cause in this patient was the known factor of immunocompromised kidney disease, leading to an acute severe hyperkalemic state that was diagnosed primarily based on acute ECG changes. Emergency aggressive hyperkalemic corrections was initiated.

Hyperkalemia-2

Serial ECG monitoring showed resolving hyperkalemic changes, and other supportive blood investigations.

Conclusion

The reports has proven that timely clinical diagnosis and management are crucial. Prevention of reversible risk factors is important. Basic ECG readings contribute a great deal to understanding the pathology of the underlying diseases. Awareness and understanding of electrolyte abnormality in ECG gives an opportunity for early detection, prevention and treatment of the life threatening condition.

Aravindakumar

Dr. S. Aravindakumar

Interventional Cardiologist

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