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Hyperkalemia Vs Hypokalemia ( EASY TO REMEMBER )Potassium and metabolism -
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Metabolism of potassium and its clinical significance 1. Metabolism of Potassium and its clinical significance Dr. Rohini C Sane. Major intracellular cation 2. Transmission of nerve impulse 4.
Acid base balance 5. Intracellular potassium concentration is necessary for protein biosynthesis by ribosomes. preanalytical error. Homoeostasis of Potassium by Transcellular movement 2.
Role of gastrointestinal tract in Homoeostasis of Potassium 3. Role of Kidney in Homoeostasis of Potassium. Potassium ions transport across the cell membrane. It action is by constricting arterioles and increasing heartbeats.
Angiotensin II later hydrolyzed by Angiotensinase. Availability of sodium ions for exchange with potassium ions 2. The relative amount of hydrogen and potassium ions in the distal tubular cells 3. Plasma Aldosterone 4. In acidosis , hydrogen ions excreted and potassium ions reabsorbed.
Homeostasis of potassium in human body. Clinical significance of Potassium Metabolism. Disorders of potassium metabolism 1. Hypokalemia: low serum potassium deceases heartbeats and interferes with vital muscles such as those involved in respiration 2.
Hypokalemia results from abnormal losses, transcellular shifts, or insufficient intake Table 1. Diuretic use is a common cause of renally mediated hypokalemia. GI losses are another common cause of hypokalemia, particularly among hospitalized patients.
As a portion of daily potassium is excreted in the colon, lower GI losses in the form of persistent diarrhea can also result in hypokalemia and may be accompanied by hyperchloremic acidosis.
Hypokalemia is often asymptomatic. Evaluation begins with a search for warning signs or symptoms warranting urgent treatment Figure 1. Identification and treatment of concurrent hypomagnesemia are also important because magnesium depletion impedes potassium repletion and can exacerbate hypokalemia-induced rhythm disturbances.
A focused history includes evaluation for possible GI losses, review of medications, and assessment for underlying cardiac comorbidities. A history of paralysis, hyperthyroidism, or use of insulin or beta agonists suggests possible transcellular shifts leading to redistributive hypokalemia.
The physical examination should focus on identifying cardiac arrhythmias and neurologic manifestations, which range from generalized weakness to ascending paralysis.
The diagnosis should be confirmed with a repeat serum potassium measurement. Other laboratory tests include serum glucose and magnesium levels, urine electrolyte and creatinine levels, and acid-base balance. The most accurate method for evaluating urinary potassium excretion is a hour timed urine potassium collection; normal kidneys excrete no more than 15 to 30 mEq per L 15 to 30 mmol per L of potassium per day in response to hypokalemia.
A more practical approach is calculation of the urine potassium-to-creatinine ratio from a spot urine specimen; a ratio greater than 1. Typically, the first ECG manifestation of hypokalemia is decreased T-wave amplitude. Further progression can lead to ST-interval depression, T-wave inversions, PR-interval prolongation, and U waves.
Arrhythmias associated with hypokalemia include sinus bradycardia, ventricular tachycardia or fibrillation, and torsade de pointes. The immediate goal of treatment is the prevention of potentially life-threatening cardiac conduction disturbances and neuromuscular dysfunction by raising serum potassium to a safe level.
Further replenishment can proceed more slowly, and attention can turn to the diagnosis and management of the underlying disorder. Careful monitoring during treatment is essential because supplemental potassium is a common cause of hyperkalemia in hospitalized patients.
Because serum potassium concentration drops approximately 0. For example, a decline in serum potassium from 3. Additional potassium will be required if losses are ongoing. Concomitant hypomagnesemia should be treated concurrently. For hypokalemia associated with diuretic use, stopping the diuretic or reducing its dosage may be effective.
It is appropriate to increase dietary potassium in patients with low-normal and mild hypokalemia, particularly in those with a history of hypertension or heart disease.
Because use of intravenous potassium increases the risk of hyperkalemia and can cause pain and phlebitis, intravenous potassium should be reserved for patients with severe hypokalemia, hypokalemic ECG changes, or physical signs or symptoms of hypokalemia, or for those unable to tolerate the oral form.
Rapid correction is possible with oral potassium; the fastest results are likely best achieved by combining oral e. When intravenous potassium is used, standard administration is 20 to 40 mmol of potassium in 1 L of normal saline. Correction typically should not exceed 20 mmol per hour, although higher rates using central venous catheters have been successful in emergency situations.
In children, dosing is 0. Nonurgent hypokalemia is treated with 40 to mmol of oral potassium per day over days to weeks.
For the prevention of hypokalemia in patients with persistent losses, as with ongoing diuretic therapy or hyperaldosteronism, 20 mmol per day is usually sufficient.
Hyperkalemia is caused by excess potassium intake, impaired potassium excretion, or transcellular shifts Table 2. Renally mediated hyperkalemia results from derangement of one or more of the following processes: rate of flow in the distal nephron, aldosterone secretion and its effects, and functioning potassium secretory pathways.
Hyperkalemia secondary to decreased distal delivery of sodium and water occurs with congestive heart failure, cirrhosis, acute kidney injury, and advanced chronic kidney disease. Conditions that cause hypoaldosteronism, such as adrenal insufficiency and hyporeninemic hypoaldosteronism a common complication of diabetic nephropathy and tubulointerstitial diseases , can lead to hyperkalemia.
Various mechanisms promote the exit of potassium from cells or impede its entrance, thereby raising the plasma potassium concentration redistributive hyperkalemia. Increased plasma osmolality, such as with uncontrolled diabetes mellitus, establishes a concentration gradient wherein potassium follows water out of cells.
Relative insulin deficiency or insulin resistance, which also occurs in persons with diabetes, prevents potassium from entering cells. In response to acidosis, extracellular hydrogen is exchanged for intracellular potassium, although the net result is highly variable and depends in part on the type of acidosis; metabolic acidosis produces the greatest effect.
Medication use is a common cause of hyperkalemia, particularly in patients with baseline renal dysfunction or hypoaldosteronism. Also, the administration of potassium to treat or prevent hypokalemia can inadvertently cause hyperkalemia.
As with hypokalemia, the immediate danger of hyperkalemia is its effect on cardiac conduction and muscle strength, and initial efforts should focus on determining the need for urgent intervention Figure 2. Because of their increased risk of developing hyperkalemia, patients with underlying renal dysfunction merit special attention.
Severe hyperkalemia more than 6. Chronic kidney disease, diabetes, heart failure, and liver disease all increase the risk of hyperkalemia.
Clinicians should review patients' medications to identify those known to cause hyperkalemia, and ask patients about the use of salt substitutes that contain potassium.
The physical examination should include assessment of blood pressure and intravascular volume status to identify potential causes of kidney hypoperfusion, which can lead to hyperkalemia.
Neurologic signs of hypokalemia include generalized weakness and decreased deep tendon reflexes. Repeat measurement of serum potassium can help identify pseudohyperkalemia, which is common and typically results from potassium moving out of cells during or after sample collection.
Further evaluation may include measurement of serum glucose to evaluate for hyperglycemia, and measurement of serum renin, aldosterone, and cortisol to further investigate kidney and adrenal function.
ECG should be considered if the potassium level is greater than 6 mEq per L; if there are symptoms of hyperkalemia; if there is suspicion of rapid-onset hyperkalemia; or among patients with underlying kidney disease, heart disease, or cirrhosis who have a new case of hyperkalemia.
Findings on ECG are neither sensitive nor specific for hyperkalemia. Therefore, although ECG changes should trigger urgent treatment, treatment decisions should not be based solely on the presence or absence of ECG changes. Peaked T waves are the prototypical, and generally the earliest, ECG sign of hyperkalemia.
Other ECG changes include P-wave flattening, PR-interval prolongation, widening of the QRS complex, and sine waves. The goals of acute treatment are to prevent potentially life-threatening cardiac conduction and neuromuscular disturbances, shift potassium into cells, eliminate excess potassium, and resolve the underlying disturbance.
Patients with chronic hyperkalemia should be counseled to reduce dietary potassium. Although redistributive hyperkalemia is uncommon, a cautious approach is warranted because treatment may not involve attempts to eliminate potassium, and correction of the underlying problem can provoke rebound hypokalemia.
Indications for prompt intervention are symptoms of hyperkalemia, changes on ECG, severe hyperkalemia greater than 6. Figure 3 is an algorithm for the management of hyperkalemia, and Table 3 22 , 30 , 36 summarizes medications used in the treatment of the condition.
Intravenous Calcium. Intravenous calcium, which helps prevent life-threatening conduction disturbances by stabilizing the cardiac muscle cell membrane, should be administered if ECG changes are present. If after five minutes, follow-up ECG continues to show signs of hyperkalemia, the dose should be repeated.
Insulin and Glucose. The most reliable method for shifting potassium intracellularly is administration of glucose and insulin. Typically, 10 units of insulin are administered, followed by 25 g of glucose to prevent hypoglycemia.
Patients with a serum glucose level of more than mg per dL Inhaled Beta Agonists. Albuterol, a beta 2 agonist, is an underutilized adjuvant for shifting potassium intracellularly. It should be noted that the recommended dose of nebulized albuterol 10 to 20 mg is four to eight times greater than the typical respiratory dose.
There is an additive effect when albuterol is combined with insulin. Sodium Bicarbonate. Although sodium bicarbonate is often used to treat hyperkalemia, the evidence to support this use is equivocal, showing minimal to no benefit. It may have a role as adjuvant therapy, particularly among patients with concurrent metabolic acidosis.
Potassium can be removed via the GI tract or the kidneys, or directly from the blood with dialysis. Dialysis should be considered in patients with kidney failure or life-threatening hyperkalemia, or when other treatment strategies fail.
Currently available cation exchange resins, typically sodium polystyrene sulfonate Kayexalate in the United States, are not beneficial for the acute treatment of hyperkalemia but may be effective in lowering total body potassium in the subacute setting. However, case reports linking the concomitant use of sodium polystyrene sulfonate and sorbitol to GI injury prompted a U.
Food and Drug Administration boxed warning. There is no evidence supporting the use of diuretics for the acute treatment of hyperkalemia.
However, diuretics, particularly loop diuretics, may play a role in the treatment of some forms of chronic hyperkalemia, such as that caused by hyporeninemic hypoaldosteronism. Strategies to prevent chronic hyperkalemia include instructing patients to eat a low-potassium diet, discontinuing or adjusting medications, avoiding nonsteroidal anti-inflammatory drugs, and adding a diuretic if the patient has sufficient renal function.
Data Sources : An Essential Evidence search was conducted. Searches of PubMed, the Cochrane Database of Systematic Reviews, and the National Guideline Clearinghouse were completed using the key terms hypokalemia and hyperkalemia.
The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Search dates: February, September, and December Paice BJ, Paterson KR, Onyanga-Omara F, Donnelly T, Gray JM, Lawson DH.
Record linkage study of hypokalaemia in hospitalized patients. Postgrad Med J. Lippi G, Favaloro EJ, Montagnana M, Guidi GC. Prevalence of hypokalaemia: the experience of a large academic hospital.
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Am J Med. Shemer J, Modan M, Ezra D, Cabili S. Incidence of hyperkalemia in hospitalized patients. Isr J Med Sci. Paice B, Gray JM, McBride D, Donnelly T, Lawson DH.
Hyperkalaemia in patients in hospital. Br Med J Clin Res Ed. Weiner ID, Wingo CS. Hypokalemia—consequences, causes, and correction. J Am Soc Nephrol. Gennari FJ. Disorders of potassium homeostasis.
Hypokalemia and hyperkalemia. Crit Care Clin. Reid A, Jones G, Isles C. Hypokalaemia: common things occur commonly - a retrospective survey.
JRSM Short Rep. Schulman M, Narins RG. Hypokalemia and cardiovascular disease. Am J Cardiol. Dhalla IA, Gomes T, Yao Z, et al. Chlorthalidone versus hydrochlorothiazide for the treatment of hypertension in older adults: a population-based cohort study.
Ann Intern Med. Morgan DB, Davidson C. Hypokalaemia and diuretics: an analysis of publications. Br Med J. Mount DB, Zandi-Nejad K. Disorders of potassium balance. In: Taal MW, Chertow GM, Marsden PA, Brenner BM, Rector FC, eds.
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