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Pathogenesis of Hyperkalemic Cardiac Arrest in Anesthesia
Potassium is an important intracellular ion and the sodium-potassium adenosine triphosphatase (Na+K+ – ATPase) pump is responsible for maintaining the cell membrane potential in myocardial muscle cells as well as nerve and skeletal muscle cells.
The sodium-potassium pump is influenced, in turn, by insulin and beta-2-agonists like catecholamines. The normal K+ levels in serum range from 3 to 5.5. Hyperkalemia is defined as:
- Mild = K+ 5.5 – 6.0
- Moderate = K+ 6.1 – 6.9
- Severe > K+ 7.0
Agents used during anesthesia like succinylcholine for neuromuscular relaxation can cause sudden onset hyperkalemia in susceptible patients as these patients have an increased number of nicotinic acetylcholine receptors (AChRs) at their neuromuscular junctions. The degree of increase in the receptors depends on the duration of the patient’s underlying condition such as prolonged immobilization, chronic renal failure etc.
On administration of succinylcholine in these patients there is depolarization of all the AChRs including the junctional receptors throughout the muscle membrane with efflux of potassium in to the extracellular plasma resulting in hyperkalemia. In addition, as succinylcholine is metabolized slowly there is an exaggerated release of potassium. The consequent elevation in serum potassium levels results in cardiac conduction abnormalities and other clinical features of hyperkalemia.
Predisposing factors for hyperkalemia during anesthesia include:
- Massive muscle trauma, inflammation or tumor
- Thermal burns
- Myopathies like Duchenne muscular dystrophy
- Upper or lower motor neuron lesions
- Disuse atrophy, chronic immobilization
- Chronic renal failure
- Longstanding denervation e.g. with muscle relaxants, magnesium or clostridial toxins
Diagnosis of Hyperkalemic Cardiac Arrest in Anesthesia
In the operating room, the patient is under anesthesia and unable to vocalize any symptoms. So electrocardiographic (ECG) changes accompanied by cardiovascular dysfunction within 5 minutes of succinylcholine administration should alert the anesthesia provider to the possibility of hyperkalemia.
Cardiovascular dysfunction can occur with serum potassium levels between 8 and 12 mEq/l. ECG changes, on the other hand, are usually proportional to the potassium levels and the changes seen include tall T waves, small, broad or absent P waves with wide QRS complex, sinusoidal QRST and atrioventricular dissociation or ventricular fibrillation. Occasionally, ECG changes as well as cardiovascular dysfunction may not be obvious in hyperkalemia making diagnosis difficult.
Laboratory tests like arterial blood gas (for acidosis), serum potassium, serum calcium (hypocalcemia can aggravate cardiac conduction anomalies), serum glucose, serum digoxin levels (digoxin can cause hyperkalemia) can be performed to confirm the diagnosis as well as to determine the etiology.
- Malignant hyperthermia (MH): Hyperkalemic cardiac arrest in the operating room is often mistaken for MH and dantrolene is administered. But MH usually occurs during anesthesia administration unlike hyperkalemia and is characterized by a rapid increase in end-tidal carbon dioxide, muscle rigidity, hyperthermia and acidosis. Cardiac arrest in MH is due to metabolic or respiratory acidosis and not due to hyperkalemia.
- Acute pericarditis
- Acute myocardial infarction
- Left bundle branch block
- Pulmonary embolism
Treatment of Hyperkalemic Cardiac Arrest in Anesthesia
It is important to remember that the management of hyperkalemic cardiac arrest does not follow the standard Advanced Cardiac Life Support (ACLS) guidelines for asystole. The anesthesia provider must be aware of this and has to institute treatment as soon as electrocardiographic changes or cardiovascular dysfunction are noted on administration of succinylcholine, especially in susceptible patients.
The aim of the treatment is to antagonize the action of K+ and move it into the intracellular compartment. This is achieved with calcium chloride/gluconate infusion under continuous electrocardiographic monitoring.
Calcium chloride is the preferred antidote as calcium gluconate is associated with tissue necrosis if it extravasates. Other drugs which are administered to manage hyperkalemia include glucose with insulin, catecholamines, and sodium bicarbonate as they increase the K+ uptake by the cells, thereby decreasing the extracellular levels.
Prevention of Hyperkalemic Cardiac Arrest in Anesthesia
Preoperative assessment of the patient by a pediatrician or a physician is essential to determine whether a child has occult myopathy or whether an adult has neurological disease (multiple sclerosis/AML) or chronic renal failure which can predispose the patient to hyperkalemia during anesthesia.
Anesthesiologists should be notified so that adequate precautions can be taken to avoid drugs like succinylcholine which can precipitate hyperkalemia. In addition, anesthesia providers should always be alert to the possibility of this condition and start aggressive management to improve outcomes.