What ECG changes occur in patients with hyperkalemia?
The characteristic ECG changes seen in hyperkalemia progress from peaked T waves initially,
followed by lengthening of the PR interval and QRS prolongation, leading to the QRS
progressively widening to a “sine wave,” which eventually results in cardiac standstill.
As in hypokalemia, the actual potassium concentration associated with the progression
of ECG changes varies widely from patient to patient, and continual monitoring of the ECG is
essential when managing patients with hyperkalemia.
9. What are some of the signs and symptoms of hypokalemia?
In addition to arrhythmias, hypokalemia can induce systemic symptoms. In mild hypokalemia
(serum potassium 3.0–3.5 mEq/L), patients are often asymptomatic. As hypokalemia
progresses, nonspecific symptoms develop, such as weakness and malaise. When serum
potassium drops below 2.0 mEq/L, it can precipitate muscle necrosis and paralysis, causing
respiratory failure.
10. What are some of the signs and symptoms of hyperkalemia?
Similar to hypokalemia, hyperkalemia can cause systemic symptoms in addition to cardiac
arrhythmias. Symptoms usually do not become clinically apparent until serum potassium
levels are very high (more than 7.0 mEq/L) and include ascending muscle paralysis
progressing to a flaccid paralysis.
11. What is pseudohyperkalemia and what are some of its causes?
Pseudohyperkalemia is the elevation of the serum potassium level in the absence of either cell
shifts or an increase in total body potassium. It can be present in the setting of thrombocytosis,
leukocytosis, and hemolysis. It results from the movement of potassium out of cells during or
after the blood sample has been drawn.
12. How can one determine if an elevated serum potassium is “real”?
Obtaining a plasma potassium, rather than a serum potassium, will differentiate
pseudohyperkalemia from true hyperkalemia.
13. What factors determine renal potassium excretion?
Renal potassium excretion is dependent on distal nephron sodium delivery, aldosterone, and
urine flow.
14. How does distal delivery of volume and sodium increase potassium
excretion?
Sodium is reabsorbed in the collecting duct via epithelial sodium channels, which stimulates
the basolateral Na-K-ATPase, which in turn facilitates the movement of potassium into the
collecting duct (i.e., into the urine) via potassium channels. With poor urine flow or distal
sodium delivery, the gradient for potassium to be secreted into the collecting duct is too steep
and there is insufficient sodium for uptake by sodium channels.
15. How does aldosterone effect renal potassium excretion?
Aldosterone increases renal potassium excretion by acting on principal cells in the collecting
duct. Aldosterone stimulates renal uptake of sodium and renal secretion of potassium.
16. What conditions stimulate release of aldosterone in a normal person?
Aldosterone is released in response to hypotension and hyperkalemia.
The characteristic ECG changes seen in hyperkalemia progress from peaked T waves initially,
followed by lengthening of the PR interval and QRS prolongation, leading to the QRS
progressively widening to a “sine wave,” which eventually results in cardiac standstill.
As in hypokalemia, the actual potassium concentration associated with the progression
of ECG changes varies widely from patient to patient, and continual monitoring of the ECG is
essential when managing patients with hyperkalemia.
9. What are some of the signs and symptoms of hypokalemia?
In addition to arrhythmias, hypokalemia can induce systemic symptoms. In mild hypokalemia
(serum potassium 3.0–3.5 mEq/L), patients are often asymptomatic. As hypokalemia
progresses, nonspecific symptoms develop, such as weakness and malaise. When serum
potassium drops below 2.0 mEq/L, it can precipitate muscle necrosis and paralysis, causing
respiratory failure.
10. What are some of the signs and symptoms of hyperkalemia?
Similar to hypokalemia, hyperkalemia can cause systemic symptoms in addition to cardiac
arrhythmias. Symptoms usually do not become clinically apparent until serum potassium
levels are very high (more than 7.0 mEq/L) and include ascending muscle paralysis
progressing to a flaccid paralysis.
11. What is pseudohyperkalemia and what are some of its causes?
Pseudohyperkalemia is the elevation of the serum potassium level in the absence of either cell
shifts or an increase in total body potassium. It can be present in the setting of thrombocytosis,
leukocytosis, and hemolysis. It results from the movement of potassium out of cells during or
after the blood sample has been drawn.
12. How can one determine if an elevated serum potassium is “real”?
Obtaining a plasma potassium, rather than a serum potassium, will differentiate
pseudohyperkalemia from true hyperkalemia.
13. What factors determine renal potassium excretion?
Renal potassium excretion is dependent on distal nephron sodium delivery, aldosterone, and
urine flow.
14. How does distal delivery of volume and sodium increase potassium
excretion?
Sodium is reabsorbed in the collecting duct via epithelial sodium channels, which stimulates
the basolateral Na-K-ATPase, which in turn facilitates the movement of potassium into the
collecting duct (i.e., into the urine) via potassium channels. With poor urine flow or distal
sodium delivery, the gradient for potassium to be secreted into the collecting duct is too steep
and there is insufficient sodium for uptake by sodium channels.
15. How does aldosterone effect renal potassium excretion?
Aldosterone increases renal potassium excretion by acting on principal cells in the collecting
duct. Aldosterone stimulates renal uptake of sodium and renal secretion of potassium.
16. What conditions stimulate release of aldosterone in a normal person?
Aldosterone is released in response to hypotension and hyperkalemia.
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