Hypokalemia and Hyperkalemia

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 07/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2826 times

Chapter 44 Hypokalemia and Hyperkalemia

Stuart L. Linas, MD , Shailendra Sharma, MD

Hypokalemia

1 Is serum potassium level an accurate estimate of total body potassium?

No. The majority of potassium is distributed in the intracellular fluid (ICF) compartment, with only approximately 2% of the total body potassium in the extracellular fluid (ECF) compartment. Alterations in serum potassium can result from transcellular potassium shift between ECF and ICF compartments or from actual changes in total body potassium.

2 When does serum potassium level falsely estimate total body potassium?

Transcellular potassium shifts between ECF and ICF compartments can have profound effects on serum potassium. Buffering of the ECF compartment, with reciprocal movement of potassium and hydrogen across the cell membrane, can result in a rise in serum potassium in the case of acidemia and a fall in serum potassium in the case of alkalemia. Two important hormones that are known to drive potassium into the ICF compartment are insulin and catecholamines.

The classic example of how serum potassium falsely estimates total body potassium is a patient with diabetic ketoacidosis. Insulin deficiency and acidemia cause potassium to shift to the ECF compartment so that serum potassium may be normal or high despite profound total body potassium depletion (due to osmotic diuresis and hyperaldosteronemic state). Only after proper treatment of insulin deficiency and acidosis does the total body potassium depletion become apparent.

3 Why is tight regulation of serum potassium concentrations so critical?

Although a small fraction of total body potassium is in the ECF compartment, changes in ECF potassium, either by compartmental shifts or by net gain or loss, significantly alter the ratio of ECF to ICF potassium, which determines the cellular resting membrane potential. As a consequence, small fluctuations in ECF potassium can have profound effects on cardiac and neuromuscular excitability.

4 How do you estimate the total body potassium deficit?

It is difficult to predict accurately the total body potassium deficit on the basis of serum potassium, but in uncomplicated potassium depletion a useful rule of thumb is as follows: For each 100 mEq potassium deficit, the fall in serum potassium level is 0.27 mEq/L. Thus, for a 70-kg patient, serum potassium of 3 mEq/L reflects a 300- to 400-mEq deficit, whereas potassium of 2 mEq/L reflects a 500- to 700-mEq deficit. In patients with acid-base disorders, this rule of thumb is not accurate because of shifts in compartmental potassium.

5 What is the relationship between potassium and magnesium?

Magnesium depletion typically occurs after diuretic use, sustained alcohol consumption, or diabetic ketoacidosis. Magnesium depletion can cause hypokalemia that is refractory to oral or intravenous (IV) potassium chloride therapy because severe magnesium depletion causes renal potassium wasting through undefined mechanisms. In the setting of severe magnesium and potassium depletion, magnesium and potassium must be replaced simultaneously.

Magnesium regulates activity of the renal outer medullary potassium (ROMK) channel. Intracellular magnesium is inversely proportional to the open ROMK channel pore. Therefore low intracellular magnesium causes more ROMK channels to open, allowing more K+ efflux into the urine.

Magnesium is also closely related to sodium-potassium–adenosine triphosphatase (Na+,K+-ATPase), possibly explaining failure to retain intracellular potassium in hypomagnesemia.

6 What factors are important in K+ balance?

K+ is mostly intracellular cation. Of 3500 mEq of total body potassium only approximately 60 mEq is in the extracellular compartment. Dietary K+ must be rapidly shifted from the vascular space into cells (internal K+ balance) before excretion by kidneys and GI tract (external balance). Internal balance is primarily regulated by insulin, whereas external balance is regulated by kidneys (85%) and gastrointestinal (GI) tract (15%).

7 What are the factors that dictate urine potassium excretion?

Key factors influencing potassium secretion include adequate sodium delivery to the distal nephron and increased aldosterone action.

8 What are the causes of hypokalemia?

image Redistribution: Intracellular potassium redistribution or shift can be caused by metabolic alkalosis, increased insulin availability, increased β2-adrenergic activity, and periodic paralysis (classically associated with thyrotoxicosis).

image GI loss: Diarrhea or poor K+ intake.

image Renal loss: Diuretics, vomiting, and states of mineralocorticoid excess (e.g., primary hyperaldosteronism, Cushing disease, European licorice ingestion, and hyperreninemia). Increases in distal sodium delivery in the setting of high plasma aldosterone levels (due to lower blood volume) result in increases in urinary potassium and subsequent hypokalemia. Other causes include hypomagnesemia and familial hypokalemic alkalosis syndromes (Bartter and Gitelman syndromes)

image Low intake: Poor oral intake or total parenteral nutrition with inadequate potassium supplement.

9 What are the clinical manifestations of hypokalemia?

By depressing neuromuscular excitability, hypokalemia leads to muscle weakness, which can include quadriplegia and hypoventilation. Severe hypokalemia disrupts cell integrity, leading to rhabdomyolysis. Among the most important manifestations of hypokalemia are cardiac arrhythmias, including paroxysmal atrial tachycardia with block, atrioventricular dissociation, first- and second-degree atrioventricular block with Wenckebach periods, and even ventricular tachycardia or fibrillation. Typical electrocardiographic (ECG) findings include ST-segment depression, flattened T waves, and prominent U waves.

10 Which drugs can cause hypokalemia?

The most common drugs are diuretics: loop diuretics, thiazides, and acetazolamide. Penicillin and penicillin analogs (e.g., carbenicillin, ticarcillin, piperacillin) also cause renal potassium wasting that is mediated by various mechanisms, including delivery of nonreabsorbable anions to the distal nephron, which results in potassium trapping in the urine. Drugs that damage renal tubular membranes such as amphotericin, cisplatin, and aminoglycosides cause renal potassium wasting even in the absence of decreases in glomerular filtration rate (GFR).

11 What is the diagnostic approach to a patient with hypokalemia?

After eliminating spurious causes (such as leukocytosis), the diagnosis of true hypokalemia can be approached on the basis of urine potassium concentration, systemic acid-base status, urine chloride level, and blood pressure (Fig. 44-1).

image

Figure 44-1 Algorithm for diagnosis of hypokalemia. ATN, Acute tubular necrosis; Cl, chloride; NG, nasogastric.

Urine potassium excretion is best measured by a 24-hour urine collection. A spot urine potassium concentration can also be measured (less accurate, but easier to obtain thus most commonly obtained) with a value of < 15 mEq/L indicating extrarenal loss (poor oral intake, GI loss, intracellular shift) and a value of > 15 mEq/L indicating renal potassium wasting. Low urine osmolality can interfere with interpretation of isolated urine potassium by diluting the urinary K+ concentration.

12 Why is serum K+ often low in patients with myocardial infarction or acute asthma?

Both conditions are associated with activation of the sympathetic nervous system. β2

Related posts:

Intensive Care Unit Organization, Management, and Value Status Epilepticus Bronchoscopy Skin and Soft Tissue Infections Ultrasound in the Intensive Care Unit Hemodynamic Monitoring