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72 Cards in this Set
- Front
- Back
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Potassium distribution in the body
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50meq/kg. body wt. (3500 meq/70 kg person)
98% of the total body potassium is intracellular (140-150 meq/l) 2% of the total body potassium is extracellular (3.5-5.0 meq/l) |
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Factors affecting the intracellular to extracellular K+ concentration
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Na+-K+ ATPase pump
Acid base balance Plasma tonicity-osmolarity Plasma insulin level Aldosterone concentration Epinephrine concentration |
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Potassium Intake
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Only 50% K+ load excreted by kidneys in the first 4-6 hours
80% retained K+ translocated into cells translocation enhanced by insulin & beta-2 adrenergic receptors which increase Na-K-ATPase pump activity. |
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Renal regulation of K+ excretion
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600-700 meq K+ filtered/day
70-80% reabsorbed in the proximal tubule 15-20% reabsorbed in the loop of henle 10% filtered K+ presented to early distal tubule Most K+ found in urine is a result of tubular secretion Tubular secretion of K+ occurs mid-late distal tubule and collecting tubule by the principal cells |
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Hyperkalemia definition
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Elevation of serum potassium >5.0meq/L obtained by venous stick
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Tubular K+secretion stimulated by:
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Increase in K+ concentration
Rise in aldosterone Enhanced delivery of Na+ and water |
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Pathogenesis of Hyperkalemia
list them |
I – Movement of K+ from intracellular to extracellular space
II – Decreased renal K+ excretion III- acute K+ load |
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Pathogenesis of Hyperkalemia
TYpe 1 |
Movement from the intracellular to extracellular compartment
Metabolic acidosis Hyperglycemia / hyperosmolarity Insulinopenia Beta-2 blockade hypoaldosteronism Exercise (vigorous) Tissue catabolism Digitalis overdose Succinylcholine Hyperkalemic periodic paralysis |
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Pathogenesis of Hyperkalemia
Type 2 |
Decreased renal K+ excretion
Inadequate Na+ delivery to distal nephron Decreased distal tubular urine flow Defect in R-A-A axis Primary renal tubular secretory defect Inhibition of distal K+ secretion by acute metabolic acidosis, drugs, or toxins |
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Differential Diagnosis of Hyperkalemia
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Factitious
Acidemia Increased input Inadequate distal delivery of Na and/or decrease in distal tubular urinary flow Renal failure Impaired R-A-A axis Primary renal tubular K+ secretory defect Inhibition of tubular secretion of K+ Abnormal K+ distribution |
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I. Factitious causes of hyperkalemia
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Lab error
Pseudohyperkalemia |
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II. Acidemia and Hyperkalemia
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Acute
Chronic |
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Factors influencing effect of acidosis on K+ concentration
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Origin of acidosis
Accompanying anion Duration Change in plasma HCO-3 concentration |
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III. Increased input of potassium
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Endogenous- rhabdomyolysis, burns, post-chemotherapy, hemolysis, GI bleed, and increased cellular catabolism
Exogenous – K+ supplements, KCL infusion, salt substitutes, low sodium diet |
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IV. Inadequate sodium delivery to distal tubule or decreased urine flow
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Acute pulmonary edema in patient with CKD
Decreased vascular volume in patient with CKD Addisons disease with GI losses and subsequent decrease in vascular volume Decreased distal Na+ delivery- uncommon cause of hyperkalemia (urinary Na+ must be < 10meq/day to be a factor) |
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V. Renal failure
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Acute oligo-anuric renal failure often associated with hyperkalemia
Etiologies: Decreased urine flow Decreased GFR ATN/acute interstitial nephritis Lack of time for adaptation Increased tissue catabolism Metabolic acidosis Chronic renal failure – K+ typically normal due to adaptation but increased K+ can occur under certain conditions |
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VI. Impaired renin-angiotensin-aldosterone axis
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Addisons disease
Enzyme deficiencies Primary hypoaldosteronism Primary hyporeninism Hyporeninemic hypoaldosteronism Drugs – NSAIDS, beta-blockers, ACEI’s, ARB’s, or heparin |
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VII. Primary renal tubular secretory defect
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Sickle cell disease
SLE Renal transplantation Obstructive uropathy Amyloidosis Hyperkalemic form of distal RTA |
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VIII. Inhibition of tubular secretion of K+
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Spiranolactone
Amiloride Triamterene Digitalis (toxic levels) |
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IX. Abnormal Potassium Distribution
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Metabolic acidosis
Insulinopenia Hypertonicity B-blockers Exercise Familial hyperkalemic periodic paralysis Aldosterone deficiency Tissue damage Digitalis, arginine, succinylcholine |
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Diagnostic approach to Hyperkalemia
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Recheck potassium level if clinical condition not supportive
ABG’s--- optional Evaluate renal function Assess urine output Check for drugs that may cause hyperkalemia Rule out hyperglycemia/hypertonicity as a cause |
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Signs and Symptoms of Hyperkalemia
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The presence of S&S is dependent upon severity and rapidity of development
Symptoms are related to impaired neuromuscular transmission Paresthesias may occur in extremities Muscle weakness which typically begins in the lower extremities Untreated it may progress to involve the trunk and upper extremities Cardiac rhythm disturbances may occur Significant variability among patients regarding ECG changes and potassium levels Modifying factors include hyponatremia, hypocalcemia and acidemia Ongoing clinical assessment and ECG monitoring are recommended |
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Treatment CDK
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Aimed at antagonizing the effects of hyperkalemia on the cell membrane
Enhancing cellular uptake of K+ Accelerate K+ elimination from the body |
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Therapeutic Measures all of them
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Calcium (gluconate-normal kidney or chloride-abnormal kidney)- antagonizes membrane actions of hyperkalemia
Onset: 1-3 minutes Duration: 30-60 minutes Insulin and glucose will increase uptake of K+ by the cells by enhancing Na+-K+-ATPase pump in skeletor muscle (and liver) Onset: 15 minutes Duration: 4-6 hours NO DM- give both insulin and glucagon DM- give only insulin Sodium Bicarbonate: will raise the systemic pH causing H+ to move out of the cells and potassium will move into the cells. Also, increasing the plasma bicarbonate level will have a direct effect on lowering potassium independent of pH. Onset: 15-30 minutes Duration: 2-3 hours Beta- 2 adrenergic agonists Enhance K+ uptake/movement into the cells via increasing Na-K-ATPase activity i.e. albuterol- IV or nebulizer Avoid in patients with known cardiac disease Cation Exchange Resin Sodium polystyrene sulfonate (Kayexalate) Effective in the gut for removal of K+ from the body Typical dose: 30gms Can be given orally or by rectum Every gram of Resin will bind approximately 1meq of potassium. Onset: 1-2 hours Duration: 4-6 hours Diuretics If renal function intact and patient euvolemic to hypervolemic Dialysis May be indicated if: conservative measures ineffective severe hyperkalemia (K+ > 7.0meq/l) marked tissue damage or necrosis with ongoing release of K+ from the cells May remove up to 50meq K+ per hour by standard hemodialysis CRRT, peritoneal dialysis, effective however slower |
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Therapeutic Measures all of them
Calcium?onset/duration |
(gluconate or chloride)- antagonizes membrane actions of hyperkalemia
Onset: 1-3 minutes Duration: 30-60 minutes |
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Therapeutic Measures all of them
Insulin and glucose/onset/duration |
Insulin and glucose will increase uptake of K+ by the cells by enhancing Na+-K+-ATPase pump in skeletor muscle (and liver)
Onset: 15 minutes Duration: 4-6 hours |
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Therapeutic Measures Hyperkalemia
Sodium bicarbonate/onset/duration |
Sodium Bicarbonate: will raise the systemic pH causing H+ to move out of the cells and potassium will move into the cells. Also, increasing the plasma bicarbonate level will have a direct effect on lowering potassium independent of pH.
Onset: 15-30 minutes Duration: 2-3 hours |
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Therapeutic Measures all of them
Beta- 2 adrenergic agonists |
Beta- 2 adrenergic agonists
Enhance K+ uptake/movement into the cells via increasing Na-K-ATPase activity i.e. albuterol- IV or nebulizer Avoid in patients with known cardiac disease |
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Therapeutic Measures all of them
Cation Exchange Resin/onset/duration |
Cation Exchange Resin
Sodium polystyrene sulfonate (Kayexalate) Effective in the gut for removal of K+ from the body Typical dose: 30gms Can be given orally or by rectum Every gram of Resin will bind approximately 1meq of potassium. Onset: 1-2 hours Duration: 4-6 hours |
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Therapeutic Measures all of them
diuretics |
If renal function intact and patient euvolemic to hypervolemic
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Therapeutic Measures all of them
Dialysis |
Dialysis
May be indicated if: conservative measures ineffective severe hyperkalemia (K+ > 7.0meq/l) marked tissue damage or necrosis with ongoing release of K+ from the cells May remove up to 50meq K+ per hour by standard hemodialysis CRRT, peritoneal dialysis, effective however slower |
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Hypokalemia
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Defined as potassium less than 3.5
Transcellular shifts Gastrointestinal causes Skin Loss Renal Losses |
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Transcellular Shifts
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Alkalosis- H+ move out of cells in effort to correct acid/base disturbance
Potassium then enters the cells to maintain electroneutrality. This leads to hypokalemia Insulin stimulates Na/K atpase and increases the cellular uptake of potassium Catecholamines- stimulate B adrenergic receptors which causes K to enter the cells |
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Therapeutic Measures all of them
Dialysis |
Dialysis
May be indicated if: conservative measures ineffective severe hyperkalemia (K+ > 7.0meq/l) marked tissue damage or necrosis with ongoing release of K+ from the cells May remove up to 50meq K+ per hour by standard hemodialysis CRRT, peritoneal dialysis, effective however slower |
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Hypokalemia- GI Losses
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Severe reduction such as anorexia, alcoholism can lead to K depletion despite renal conservation
Vomiting- causes volume contraction, alkalosis, which can lead to increased aldosterone production and K depletion Colonic fluid high in K; diarrhea, laxative abuse can cause significant K loss. Aldosterone production is increased as volume loss stimulates production |
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Hypokalemia- Renal Losses
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Increased distal sodium delivery
Thiazides, Loop diuretics increase distal of sodium and subsequent K secretion Diuretics also cause volume depletion which stimulates aldosterone production Hereditary disorders such as Barrter’s syndrome and Gitelman syndrome haver defects as well which mimic diuretics Bicarb and poorly absorbable anion such as sulfate, ketoanions promotes K secretion Proximal RTA Type II- inability to absorb bicarb causes negative lumen charge causing K secretion distally Type I RTA –reduced H+ secretion into the tubular lumen is compensated by increased K secretion Chronic metabolic acidosis from ketosis or hyperglycemia can lead to volume depletion which causes aldosterone production and subsequent K secretion |
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Hypokalemia
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Defined as potassium less than 3.5
Transcellular shifts Gastrointestinal causes Skin Loss Renal Losses |
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Consequences of Hypokalemia
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When level drops below 3 patients may develop muscular weakness, fatigue, malaise, and myalgias
In severe potassium depletion, muscular paralysis, rhabdomyolysis may occur. Results in hyperpolarization of the membrane, leads increase threshold of action potential, leading to weakness. Sodium channels may be inactivated, causing paralysis |
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Transcellular Shifts
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Alkalosis- H+ move out of cells in effort to correct acid/base disturbance
Potassium then enters the cells to maintain electroneutrality. This leads to hypokalemia Insulin stimulates Na/K atpase and increases the cellular uptake of potassium Catecholamines- stimulate B adrenergic receptors which causes K to enter the cells |
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Hypokalemia- Cardiac Complications
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Levels less than 3, may cause ECG changes
Hyperpolarization of cardiac muscle, delayed repolarization which leads to prominent U waves Prolonged QT intervals can lead to PVC’s and V-Tach Patients should be placed on a cardiac monitor |
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Therapeutic Measures all of them
Dialysis |
Dialysis
May be indicated if: conservative measures ineffective severe hyperkalemia (K+ > 7.0meq/l) marked tissue damage or necrosis with ongoing release of K+ from the cells May remove up to 50meq K+ per hour by standard hemodialysis CRRT, peritoneal dialysis, effective however slower |
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Hypokalemia- GI Losses
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Severe reduction such as anorexia, alcoholism can lead to K depletion despite renal conservation
Vomiting- causes volume contraction, alkalosis, which can lead to increased aldosterone production and K depletion Colonic fluid high in K; diarrhea, laxative abuse can cause significant K loss. Aldosterone production is increased as volume loss stimulates production |
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Hypokalemia- Renal Losses
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Increased distal sodium delivery
Thiazides, Loop diuretics increase distal of sodium and subsequent K secretion Diuretics also cause volume depletion which stimulates aldosterone production Hereditary disorders such as Barrter’s syndrome and Gitelman syndrome haver defects as well which mimic diuretics Bicarb and poorly absorbable anion such as sulfate, ketoanions promotes K secretion Proximal RTA Type II- inability to absorb bicarb causes negative lumen charge causing K secretion distally Type I RTA –reduced H+ secretion into the tubular lumen is compensated by increased K secretion Chronic metabolic acidosis from ketosis or hyperglycemia can lead to volume depletion which causes aldosterone production and subsequent K secretion |
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Hypokalemia
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Defined as potassium less than 3.5
Transcellular shifts Gastrointestinal causes Skin Loss Renal Losses |
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Hypokalemia- Metabolic Effects
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Hypokalemia blunts insulin secretion
Reduction in aldosterone production Important growth factor- can lead to growth retardation if chronically low |
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Therapeutic Measures all of them
Dialysis |
Dialysis
May be indicated if: conservative measures ineffective severe hyperkalemia (K+ > 7.0meq/l) marked tissue damage or necrosis with ongoing release of K+ from the cells May remove up to 50meq K+ per hour by standard hemodialysis CRRT, peritoneal dialysis, effective however slower |
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Hypokalemia- Renal Effects
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K depletion stimulates thirst, impairs urinary concentrating ability
Polyuria, polydipsia may be notedetabolic Disruption of K dependent countercurrent multiplier system Metabolic alkalosis from increased ammonia production, H+ enters proximal tubule to replace K , increased ammonium and acid secretion as a result Non renal losses result in renal conservation of K within 5-10 days, with urinary K less than 20meq/liter Renal losses result in urinary K greater than 20meq/liter Potassium depletion results in proximal and distal tubular cell degeneration and vacuolization |
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Transcellular Shifts
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Alkalosis- H+ move out of cells in effort to correct acid/base disturbance
Potassium then enters the cells to maintain electroneutrality. This leads to hypokalemia Insulin stimulates Na/K atpase and increases the cellular uptake of potassium Catecholamines- stimulate B adrenergic receptors which causes K to enter the cells |
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Consequences of Hypokalemia
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When level drops below 3 patients may develop muscular weakness, fatigue, malaise, and myalgias
In severe potassium depletion, muscular paralysis, rhabdomyolysis may occur. Results in hyperpolarization of the membrane, leads increase threshold of action potential, leading to weakness. Sodium channels may be inactivated, causing paralysis |
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Hypokalemia
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Defined as potassium less than 3.5
Transcellular shifts Gastrointestinal causes Skin Loss Renal Losses |
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Hypokalemia-Replacement
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Mild hypokalemia about 3.5 can increase dietary intake
Less than 3.0 will need supplement Oral best choice unless having dysrythmias IV replacement should not exceed 10-20meq/hour Very caustic on peripheral veins |
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Hypokalemia- GI Losses
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Severe reduction such as anorexia, alcoholism can lead to K depletion despite renal conservation
Vomiting- causes volume contraction, alkalosis, which can lead to increased aldosterone production and K depletion Colonic fluid high in K; diarrhea, laxative abuse can cause significant K loss. Aldosterone production is increased as volume loss stimulates production |
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Hypokalemia- Cardiac Complications
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Levels less than 3, may cause ECG changes
Hyperpolarization of cardiac muscle, delayed repolarization which leads to prominent U waves Prolonged QT intervals can lead to PVC’s and V-Tach Patients should be placed on a cardiac monitor |
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Hypokalemia- Renal Losses
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Increased distal sodium delivery
Thiazides, Loop diuretics increase distal of sodium and subsequent K secretion Diuretics also cause volume depletion which stimulates aldosterone production Hereditary disorders such as Barrter’s syndrome and Gitelman syndrome haver defects as well which mimic diuretics Bicarb and poorly absorbable anion such as sulfate, ketoanions promotes K secretion Proximal RTA Type II- inability to absorb bicarb causes negative lumen charge causing K secretion distally Type I RTA –reduced H+ secretion into the tubular lumen is compensated by increased K secretion Chronic metabolic acidosis from ketosis or hyperglycemia can lead to volume depletion which causes aldosterone production and subsequent K secretion |
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Transcellular Shifts
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Alkalosis- H+ move out of cells in effort to correct acid/base disturbance
Potassium then enters the cells to maintain electroneutrality. This leads to hypokalemia Insulin stimulates Na/K atpase and increases the cellular uptake of potassium Catecholamines- stimulate B adrenergic receptors which causes K to enter the cells |
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Hypokalemia- Metabolic Effects
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Hypokalemia blunts insulin secretion
Reduction in aldosterone production Important growth factor- can lead to growth retardation if chronically low |
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Hypokalemia- GI Losses
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Severe reduction such as anorexia, alcoholism can lead to K depletion despite renal conservation
Vomiting- causes volume contraction, alkalosis, which can lead to increased aldosterone production and K depletion Colonic fluid high in K; diarrhea, laxative abuse can cause significant K loss. Aldosterone production is increased as volume loss stimulates production |
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Consequences of Hypokalemia
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When level drops below 3 patients may develop muscular weakness, fatigue, malaise, and myalgias
In severe potassium depletion, muscular paralysis, rhabdomyolysis may occur. Results in hyperpolarization of the membrane, leads increase threshold of action potential, leading to weakness. Sodium channels may be inactivated, causing paralysis |
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Hypokalemia- Renal Effects
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K depletion stimulates thirst, impairs urinary concentrating ability
Polyuria, polydipsia may be notedetabolic Disruption of K dependent countercurrent multiplier system Metabolic alkalosis from increased ammonia production, H+ enters proximal tubule to replace K , increased ammonium and acid secretion as a result Non renal losses result in renal conservation of K within 5-10 days, with urinary K less than 20meq/liter Renal losses result in urinary K greater than 20meq/liter Potassium depletion results in proximal and distal tubular cell degeneration and vacuolization |
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Hypokalemia- Renal Losses
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Increased distal sodium delivery
Thiazides, Loop diuretics increase distal of sodium and subsequent K secretion Diuretics also cause volume depletion which stimulates aldosterone production Hereditary disorders such as Barrter’s syndrome and Gitelman syndrome haver defects as well which mimic diuretics Bicarb and poorly absorbable anion such as sulfate, ketoanions promotes K secretion Proximal RTA Type II- inability to absorb bicarb causes negative lumen charge causing K secretion distally Type I RTA –reduced H+ secretion into the tubular lumen is compensated by increased K secretion Chronic metabolic acidosis from ketosis or hyperglycemia can lead to volume depletion which causes aldosterone production and subsequent K secretion |
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Hypokalemia- Cardiac Complications
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Levels less than 3, may cause ECG changes
Hyperpolarization of cardiac muscle, delayed repolarization which leads to prominent U waves Prolonged QT intervals can lead to PVC’s and V-Tach Patients should be placed on a cardiac monitor |
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Hypokalemia-Replacement
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Mild hypokalemia about 3.5 can increase dietary intake
Less than 3.0 will need supplement Oral best choice unless having dysrythmias IV replacement should not exceed 10-20meq/hour Very caustic on peripheral veins Potassium chloride for concomitant alkalosis, potassium citrate or bicarb with acidosis |
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Consequences of Hypokalemia
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When level drops below 3 patients may develop muscular weakness, fatigue, malaise, and myalgias
In severe potassium depletion, muscular paralysis, rhabdomyolysis may occur. Results in hyperpolarization of the membrane, leads increase threshold of action potential, leading to weakness. Sodium channels may be inactivated, causing paralysis |
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Hypokalemia- Metabolic Effects
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Hypokalemia blunts insulin secretion
Reduction in aldosterone production Important growth factor- can lead to growth retardation if chronically low |
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Hypokalemia- Cardiac Complications
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Levels less than 3, may cause ECG changes
Hyperpolarization of cardiac muscle, delayed repolarization which leads to prominent U waves Prolonged QT intervals can lead to PVC’s and V-Tach Patients should be placed on a cardiac monitor |
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Hypokalemia- Metabolic Effects
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Hypokalemia blunts insulin secretion
Reduction in aldosterone production Important growth factor- can lead to growth retardation if chronically low |
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Hypokalemia- Renal Effects
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K depletion stimulates thirst, impairs urinary concentrating ability
Polyuria, polydipsia may be notedetabolic Disruption of K dependent countercurrent multiplier system Metabolic alkalosis from increased ammonia production, H+ enters proximal tubule to replace K , increased ammonium and acid secretion as a result Non renal losses result in renal conservation of K within 5-10 days, with urinary K less than 20meq/liter Renal losses result in urinary K greater than 20meq/liter Potassium depletion results in proximal and distal tubular cell degeneration and vacuolization |
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Hypokalemia-Replacement
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Mild hypokalemia about 3.5 can increase dietary intake
Less than 3.0 will need supplement Oral best choice unless having dysrythmias IV replacement should not exceed 10-20meq/hour Very caustic on peripheral veins Potassium chloride for concomitant alkalosis, potassium citrate or bicarb with acidosis |
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Hypokalemia- Renal Effects
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K depletion stimulates thirst, impairs urinary concentrating ability
Polyuria, polydipsia may be notedetabolic Disruption of K dependent countercurrent multiplier system Metabolic alkalosis from increased ammonia production, H+ enters proximal tubule to replace K , increased ammonium and acid secretion as a result Non renal losses result in renal conservation of K within 5-10 days, with urinary K less than 20meq/liter Renal losses result in urinary K greater than 20meq/liter Potassium depletion results in proximal and distal tubular cell degeneration and vacuolization |
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Hypokalemia-Replacement
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Mild hypokalemia about 3.5 can increase dietary intake
Less than 3.0 will need supplement Oral best choice unless having dysrythmias IV replacement should not exceed 10-20meq/hour Very caustic on peripheral veins Potassium chloride for concomitant alkalosis, potassium citrate or bicarb with acidosis |
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Summary- Main points for Potassium
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Hyperkalemia is a very common electrolyte disturbance encountered in the hospitalized patient.
Depending upon the severity and/or rapidity of development, it may be life threatening. With an understanding of the normal physiology of Potassium, the clinician is better prepared to deal with the pathogenesis and differential diagnosis of Hyperkalemia. This will allow for a more appropriate and expedient approach in regards to treatment of your patient. |
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Hypokalemia- main points
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Look for underlying cause
Treat orally when possible Limit IV bolus K given burning in veins and possible dysrthymias |
