Hyperkalemia | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment

The video begins with an introduction to hyperkalemia, which is defined as an elevated potassium level in the blood. The speaker encourages viewers to follow along with comprehensive notes and illustrations provided on their website. They also ask viewers to like, comment, and subscribe if they find the content helpful. The primary causes of hyperkalemia are then outlined, including reduced excretion of potassium, with a focus on the role of kidney function in potassium regulation.

The second paragraph delves into the hormonal causes of hyperkalemia, particularly the role of aldosterone, a hormone produced by the adrenal cortex's zona glomerulosa. Aldosterone is crucial for regulating potassium excretion in the distal convoluted tubules of the nephron. The paragraph explains how hyperkalemia can result from a decrease in aldosterone production, which can be due to conditions like hypoaldosteronism or the use of certain medications such as NSAIDs, ACE inhibitors, angiotensin receptor blockers, and potassium-sparing diuretics.

The third paragraph discusses the concept of a transcellular shift of potassium as another cause of hyperkalemia. It highlights that most of the body's potassium is stored within cells, and hyperkalemia occurs when potassium moves from the intracellular fluid to the extracellular fluid. The speaker mentions insulin's role in regulating potassium levels and how conditions like diabetes mellitus can lead to decreased insulin, resulting in less potassium being taken up by cells. Additionally, the use of beta-blockers and other medications that affect the sodium-potassium ATPase is covered as contributing factors.

In the fourth paragraph, the focus is on how acidosis can lead to hyperkalemia. The speaker explains the exchange of protons for potassium ions in cells to maintain electroneutrality, which can cause potassium to shift out of cells and into the bloodstream, increasing blood potassium levels. Conditions like respiratory acidosis, metabolic acidosis, and hyperglycemic hyperosmolar state are discussed as potential causes for this shift.

The fifth paragraph addresses the final category of hyperkalemia causes, which includes increased potassium intake from food, medications, or replacement therapy, especially in individuals with kidney impairment. The speaker also introduces the concept of pseudohyperkalemia, where blood potassium levels appear elevated due to laboratory artifacts like hemolysis during blood draw or thrombocytosis, rather than true hyperkalemia.

The sixth paragraph explores the pathophysiology of hyperkalemia, explaining how it affects cell membrane potential and action potentials in excitable cells like cardiac, smooth, and skeletal muscle, as well as neurons. The speaker details how hyperkalemia can lead to decreased cell excitability, which manifests clinically as muscle weakness, decreased reflexes, constipation, nausea, vomiting, and cardiac issues like decreased contractility and various ECG changes.

The seventh paragraph is about the diagnosis of hyperkalemia, emphasizing the importance of confirming true hyperkalemia by ruling out pseudohyperkalemia caused by hemolyzed samples or thrombocytosis. The speaker outlines various clinical features and signs, such as muscle weakness, oliguria/anuria, respiratory distress, decreased cardiac contractility, ECG changes, and decreased reflexes, which can help identify the condition. A mnemonic, 'MURDER,' is provided to remember the clinical features.

The eighth paragraph details the investigative approach to determining the underlying cause of hyperkalemia. It covers the evaluation of kidney function, checking for hypoaldosteronism, reviewing medication history for potential culprit drugs, assessing for hyperosmolar states, and considering acidosis as a cause. The speaker also discusses the importance of identifying conditions like rhabdomyolysis, tumor lysis syndrome, and hemolysis as possible causes of hyperkalemia.

The ninth paragraph focuses on the ECG changes associated with hyperkalemia. The speaker describes how hyperkalemia affects cardiac excitability and contractility, leading to repolarization abnormalities and various ECG findings such as peaked T-waves, widened QRS complex, prolonged PR interval, flat or absent P-waves, junctional rhythm, sine wave pattern, and potentially cardiac arrest.

The tenth paragraph outlines the treatment strategies for hyperkalemia. It starts with stabilizing cardiac membranes using calcium gluconate or calcium chloride. The speaker then explains how to shift potassium back into cells using insulin and dextrose (D50), beta2 agonists like albuterol, and bicarbonate for acidosis. The paragraph also covers the use of diuretics, particularly furosemide, to enhance potassium excretion. In cases where patients cannot be treated with diuretics, sodium polystyrene sulfonate (Kayexalate) is discussed as an alternative. Lastly, the speaker mentions dialysis as a treatment option for patients who are refractory to other treatments.

The eleventh paragraph wraps up the discussion on hyperkalemia by emphasizing the importance of identifying and treating the underlying cause of the condition. The speaker advises on considering various treatments based on the cause, such as dialysis for kidney injury or discontinuation of certain medications. The video concludes with a reminder to always address the root cause of hyperkalemia for effective management.