Electrolyte disturbances Pathophysiology, diagnosis and clinical management
HYPOKALEMIA and K+ DEPLETION HYPERKALEMIA
Bert Bammens UZ Leuven KU Leuven 1
Hypokalemia and K+ depletion • Definition hypokalemia: plasma [K+] < 3.5 mmol/L (normal plasma [K+] 3.5-5.1 mmol/L*)
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*reference values
lab UZ Gasthuisberg 3-2011
Hypokalemia and K+ depletion • Definition K+ depletion: negative (external) K+ balance • Relationship plasma [K+] and K+ balance not linear!
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Hypokalemia: pathogenesis
LOW INTAKE
K+ depletion
EXCESSIVE LOSSES K+ depletion
SHIFT TO INTRACELLULAR COMPARTMENT not necessarily K+ depletion
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Hypokalemia: pathogenesis LOW INTAKE Causes RARE in case of normal oral intake, except when combined with EXCESSIVE LOSSES Renal K+ excretion can be reduced to 5 à 25 mmol/day! Adaptation to low K+ diet takes ± 14 days. Kalium: fysiologie K+ transport in nefron BIJ LAGE K+ INTAKE PT en Lis van Henle reabsorptie
DCT, CNT, ICT, CCT reabsorptie
MCD beperkte reabsorptie
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Hypokalemia: pathogenesis LOW INTAKE Causes Parenteral feeding with insufficient amounts of K+ Geofagia: clay ingestion, clay binds K+ in gastrointestinal tract
cultural heritage vs. psychiatric eating disorder?
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes GASTRO-INTESTINAL LOW gastro-intestinal losses: 20-50 mmol/L K+. bv. diarrhea, enema, laxatives, cation exchangers low gastro-intestinal fistulisation/stoma, ileus villous adenoma VIPoma (vasoactive intestinal peptide) Particularly when long-lasting!
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes GASTRO-INTESTINAL HIGH (gastric) losses: only 5-10 mmol/L K+. Gastric losses metabolic alkalosis à renal K+ loss volume contraction à aldosterone à renal K+ loss Kalium: fysiologie
Zuur-base: pathogenese/oorzaken metabole alkalose met ECV contractie
Kalium: fysiologie
Externe K+ balans
• Alkalose (metabool of respiratoir) = hogere pH à hogere intracellulaire pH principal cells à actievere Na+-K+-ATPase en apicale K+-kanalen à meer K+ secretie • Alkalose (metabool of respiratoir) à hogere flow door meer HCO3à meer K+ secretie
Oorzaken GASTRO-INTESTINAAL INITIEREND: verlies van H+ braken van maagvocht, afzuigen van maagvocht, maagfistels
• Mineralocorticoiden: aldosterone, DOCA (synth.) 4 effecten -Stimulatie Na+-K+-ATPase -Toename aantal Na+-K+-ATPase -Stimulatie ENaC -Stimulatie K+-kanalen K+-secreterend effect van aldosterone werkt voornamelijk bij groot distaal Na+ aanbod!
DUS: beide renale effecten van alkalose versterken effect op interne balans 48
Externe K+ balans
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25
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes RENAL = increased K+ secretion by “DISTAL K+ SECRETORY SYSTEM” à in other words: high aldosterone and/or high flow / high Na+
Kalium: fysiologie LUMINALE en PERITUBULAIRE invloeden op “DISTAL K+ SECRETORY SYSTEM”
Peritubulaire factoren
Externe K+ balans
nierfunctie
Luminale factoren
zuur-base Samengevat, de belangrijkste factoren die de renale eliminatie van K+ beïnvloeden:
aldosterone
Na+ aanbod en flow thv “distal K+ secretory system”
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes RENAL DIURETICS carbo-anhydrase inhibitors (acetazolamide) loop diuretics (furosemide, bumetanide) thiazide diuretics (hydrochloorthiazide, chloortalidon) osmotic diuretics
DIURETICA
inhibitie Na+ reabsorptie door blokkade Na+ transport in specifieke nefronsegmenten 30
MECHANISM - Site of action = proximal à increased flow and Na+ delivery to “DISTAL K+ SECRETORY SYSTEM” - Decrease of ECF volume stimulates RAAS à high aldosterone 10
Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes RENAL non-resorbable anions in glomerular filtrate more Na+ retained in lumen of PT increased Na+ delivery to distal tubule bv. HCO3- in case of high gastro-intestinal losses in proximal RTA (type 2) β-hydroxybutiric acid in diabetic keto-acidosis Hippuric acid (toluene derivative) in glue addicts
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes RENAL Mineralocortoicoid excess (for other reasons than dehydration) primary (hyper)aldosteronism (Conn’s syndrome) Cushing syndrome (glucocorticoid excess) licorice (glycyrrhetinic acid) secondary to renovascular disease secondary to stress (bv. post-surgery)
Na+ balans: RAAS
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Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes RENAL RENAL TUBULAR DEFECTS Bartter’s syndrome (defect NKCC2 à mimics loop diuretics) Gitelman’s syndrome (defect NCC à mimics thiazide diuretics) RTA (type 1 and 2) Liddle’s syndrome Liddle’s syndrome (autosomal dominant) Overexpression of ENac in principal cells Na+ retention K+ secretion Mimics primary aldosteronism with hypertension, hypokalemia and alkalosis, but NO increased renine or aldosterone levels (pseudo-aldosteronism) 13
Hypokalemia: pathogenesis EXCESSIVE LOSSES Causes SWEATING, BURN WOUNDS VERY RARE cause of hypokalemia, except when excessive and combined with low intake or other causes of excessive losses.
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes ALKALOSIS
Kalium: fysiologie Interne K+ balans
Zuur-base afwijkingen beïnvloeden interne K+ balans. K+
“VUISTREGEL” wisselt uit voor H+
ACIDOSE à hyperkalemie ALKALOSE à hypokalemie12 15
Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes GLUCOSE ± INSULIN
Kalium: fysiologie Interne K+ balans Insuline, β-adrenerge agonisten (adrenaline), aldosterone stimuleren Na+-K+-ATPase à K+ naar intracellulair
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes GLUCOSE + INSULIN = essential part of treatment of diabetic keto-acidosis Zuur-base: pathogenese/oorzaken high anion gap METABOLE ACIDOSE Oorzaken DIABETISCHE KETO-ACIDOSE
K
(ook hyperglycemie + osm.diurese)
tekort aan insuline therapie-stop intercurrerende ziekte die insuline-nood verhoogt
overmaat aan glucagon (door wegvallen inhibitie insuline) hoger aanbod vrije vetzuren, aminozuren, glucose aan lever vanuit vet- en spierweefsel 16
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes GLUCOSE + INSULIN = essential part of treatment of diabetic keto-acidosis Zuur-base: pathogenese/oorzaken Dehydratatie: pathogenese high anion gap METABOLE ACIDOSE primair waterverlies = hyperosmolaire dehydratatie Renale oorzaken Oorzaken DIABETISCHE KETO-ACIDOSE
K
(ook hyperglycemie + osm.diurese)
Osmotische diurese: rijk aan “deeltjes”
tekort aan insuline
glomerulair gefilterde therapie-stop intercurrerende ziekte die insuline-nood verhoogt
abnormale osmolen
exogeen: mannitol, sorbitol… overmaat aan glucagon (door wegvallen inhibitieglucose insuline) (ongecontroleerde diabetes) endogeen: ureum (hoog eiwit dieet, CNI) hoger aanbod vrije vetzuren, aminozuren, glucose calcium (hypercalcemie) aan lever vanuit vet- en spierweefsel 16
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes GLUCOSE + INSULIN = essential part of treatment of diabetic keto-acidosis Zuur-base: pathogenese/oorzaken Dehydratatie: pathogenese Hypokalemie: pathogenese/oorzaken high anion gap METABOLE ACIDOSE primair waterverlies TE GROOT VERLIES = hyperosmolaire dehydratatie Renale oorzaken Oorzaken RENAAL Oorzaken DIABETISCHE KETO-ACIDOSE DIURETICA DIURETICA (ook hyperglycemie + osm.diurese) Osmotische diurese: rijk aan “deeltjes” koolzuuranhydrase inhibitoren (acetazolamide)
K
tekort aan insuline
glomerulair gefilterde therapie-stop intercurrerende ziekte die insuline-nood verhoogt
lisdiuretica (furosemide, ethacrynezuur) thiazide diuretica (hydrochloorthiazide, chloortalidon) abnormale osmolen osmotische diuretica
inhibitie Na+ reabsorptie door blokkade Na+ transport in specifieke nefronsegmenten 30
exogeen: mannitol, sorbitol… overmaat aan glucagon (door wegvallen inhibitieglucose insuline) (ongecontroleerde endogeen: MECHANISME diabetes) Door proximaal ureum (hoog eiwit dieet, CNI) te werken, verhogen ze flow en Na+ aanbod thv “DISTAL K+ SECRETORY SYSTEM” hoger aanbod vrije vetzuren, aminozuren, glucose calcium (hypercalcemie) - Door daling ECF volume, stimuleren ze aldosterone vrijzetting. aan lever vanuit vet- en spierweefsel 16
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes GLUCOSE + INSULIN = essential part of treatment of diabetic keto-acidosis Risk of life threatening hypokalemia as a consequence of K+ shift to intracellular compartment in already K+ depleted patient (osmotic diuresis, non-resorbable anions).
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes β-ADRENERGIC AGONISTS e.g.
Kalium: fysiologie Interne K+ balans Insuline, β-adrenerge agonisten (adrenaline), aldosterone stimuleren Na+-K+-ATPase à K+ naar intracellulair
- treatment of astma - treatment of preterm labor - stress usually only problematic if combined with 11
EXCESSIVE LOSSES 21
Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT http://www.youtube.com/user/vlivings
Causes FAMILIAL HYPOKALEMIC PERIODIC PARALYSIS autosomal dominant defect of Ca2+ of Na+ channels in striated muscle cells (sometimes acquired form, e.g. associated with hyperthyroidism)
Attacks of painless muscle weakness, triggered by physical excercise, calory-rich meal (insuline+glucose) Hypokalemia during attacks. Normal kalemia in-between attacks. (DD other forms of hypokalemic paralysis) 22
Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes ANABOLIC CONDITIONS with INCREASED CELL GROWTH uptake of K+ by “new” cells hypokalemia e.g.
treatment of anemia with Vit B12 of folic acid treatment of neurtropenia with GM-CSF
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Hypokalemia: pathogenesis SHIFT TO INTRACELLULAR COMPARTMENT Causes HIGH VOLUME TRANSFUSION OF RBC Mechanisms - alkalosis due to preservative à hypokalemia - cold storage: Na+ K+ ATPase inhibited; reactivation by warming à hypokalemia
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Hypokalemia: symptoms • Definition hypokalemia: plasma [K+] < 3.5 mmol/L (normal plasma [Na+] 3.5-5.1 mmol/L*)
• Symptoms usually only when [K+] < 3.0 mmol/L or in case of ACUTE onset. Muscle weakness due to change of resting membrane potential (hyperpolarisation) increased activation status of Na+ channels
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*reference values van lab UZ Gasthuisberg 3-2011
Hypokalemia: symptoms Muscle weakness Striated muscle decreased tendon reflexes paralysis (from lower limbs, through trunk to upper limbs) rhabdomyolysis Smooth muscle nausea, anorexia abdominal distension and paralytic ileus bladder paralyse 26
Hypokalemia: symptoms Muscle weakness Heart muscle
prolonged action potential à slow ventricular repolarisation à prolonged relative refractory period
arrhythmias (ectopic pacemakers and reentry phenomena) VES, VFib… hyperpolarisation resting potential à increased excitability of normal pacemaker and ectopic ventricular pacemakers
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Hypokalemia: symptoms Muscle weakness Heart muscle typical ECG changes ST depression, inversion T, U wave
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Hypokalemia: symptoms Glucose intolerance Hypokalemia inhibits insulin secretion by pancreatic β-cells and increases peripheral insulin resistance.
Cause of diabetogenic effect of thiazide diuretics?
FBG = fasting blood glucose
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Hypokalemia: symptoms Renal problems loss of urine concentrating abilities, ao by lower aquaporin-2 expression inhibition NKCC2 in TAL Dehydratatie: pathogenese
decreased ADH effect
nefrogene diabetes insipidus Water balans: NIEREN
renaal: te weinig respons op ADH
Activiteit van ADH op principal cells van ICT tot IMCD
nefrogenic diabetes insipidus
Oorzaken - Idiopathisch - Familiaal (genetisch) - Chronische hypoK+ of hyperCa - Medicatie: lithium, colchicine - Sommige nierziekten, bv. bij Sickle Cell Anemia 55
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Hypokalemia: symptoms Renal problems increased synthesis NH3, increased reabsorption HCO3alkalosis Hypokalemia • Door interne K+ balans: hypokaliemie à daling pHi
• à zelfde effect als bij chronische acidose via (pHo en) pHi door stimulatie NHE3, electrogene H+ pomp, NBC, ammoniagene enzymes (glutaminase, PEPCK), Na/citraat cotransporter à niet-titreerbaar/titreerbaar zuur stijgt! • K+ depletie stimuleert ook apicale K-H uitwisselaar in α-intercalated cells van ICT en CCT (Omgekeerde effecten bij hyperkaliemie. Bovendien competitie K+ en NH4+ voor Na/K/Cl cotransport in TAL à minder NH4+ accumulatie in interstitium medulla)
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Hypokalemia: symptoms Renal problems vacuolisation tubular epithelial cells, interstitial edema interstitial nephritis (acute and) chronic renal insufficiency
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Hypokalemia: symptoms Mental disturbances drowsiness, apathy, confusion, coma
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Electrolyte disturbances Pathophysiology, diagnosis and clinical management
HYPOKALEMIA and K+ DEPLETION HYPERKALEMIA
Bert Bammens UZ Leuven KU Leuven 34
Hyperkalemia • Definition hyperkalemia: plasma [K+] > 5.0 mmol/L (normal plasma [K+] 3.5-5.1 mmol/L*)
HIGH INTAKE
INSUFFICIENT (RENAL) ELIMINATION
SHIFT TO EXTRACELLULAR COMPARTMENT 35
*reference values van lab UZ Gasthuisberg 3-2011
Hyperkalemia: pathogenesis HIGH INTAKE Causes RARE with normal oral intake, except if combined with INSUFFICIENT RENAL ELIMINATION
thanks to early intracellular buffering followed by renal elimination. Kalium: fysiologie K+ intake kan aanzienlijk groter zijn dan hoeveelheid extracellulair K+.
Om extracellulaire [K+] constant te houden, is “opvang” van deze externe kaliumbelasting nodig. interne K+ balans = shift van K+ van extra- naar intracellulair snel (< 1uur), “eerste opvang” voor 4/5 van K + belasting externe K+ balans = eliminatie van K+ uit het lichaam trager (uren) 90-95% renaal 5-10% gastrointestinaal (+ zweet)
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Hyperkalemia: pathogenesis HIGH INTAKE Causes Parenteral: (too fast) infusion of K+ containing substances (= iatrogenic hyperkalemia, cave renal insufficiency) bv.
kalium penicilline glucion®
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION Causes = insufficient K+ secretion by “DISTAL K+ SECRETORY SYSTEM” In other words: renal insufficiency and/or low aldosterone and/or low flow / low Na+ delivery
Kalium: fysiologie LUMINALE en PERITUBULAIRE invloeden op “DISTAL K+ SECRETORY SYSTEM”
Peritubulaire factoren
Externe K+ balans
nierfunctie
Luminale factoren
zuur-base Samengevat, de belangrijkste factoren die de renale eliminatie van K+ beïnvloeden:
aldosterone
Na+ aanbod en flow thv “distal K+ secretory system”
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Hyperkalemia: pathogenesis
INSUFFICIENT RENAL ELIMINATION Causes Acute (oliguric, anuric) kidney injury Late stages of chronic kidney disease Hyperkalemic RTA METABOLE ACIDOSE Hyperkalemie MAAR NIET ALTIJD!
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION Causes Addison’s disease + all other conditions with low aldosterone Kalium: fysiologie
Externe K+ balans
• Mineralocorticoiden: aldosterone, DOCA (synth.) 4 effecten -Stimulatie Na+-K+-ATPase -Toename aantal Na+-K+-ATPase -Stimulatie ENaC -Stimulatie K+-kanalen K+-secreterend effect van aldosterone werkt voornamelijk bij groot distaal Na+ aanbod!
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Conditions of low aldosterone
Palmer BF N Engl J Med 351: 585-592, 2004
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION Causes Dehydration with low effective circulating volume low flow and low Na+ delivery to “DISTAL K+ SECRETORY SYSTEM” Kalium: fysiologie
Kalium: fysiologie
Externe K+ balans
• Hogere flow in lumen à K+ in lumen laag à gradient apicaal principal cells hoog à hogere K+ secretie • Hogere flow in lumen à hoger Na+ aanbod distaal à stimulatie Na+-K+-ATPase à meer K+ secretie
Externe K+ balans
• Hoger Na+ in lumen à Na+ opname via ENaC à apicaal membraan depolariseert à electrische gradient stimuleert K+ secretie
• Laag Na+ in lumen à hyperpolarisatie à minder K+ secretie • Idem bij blokkade ENaC door amiloride (diureticum)
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION Causes USUALLY MULTI-CAUSALITY! e.g. heart failure patient with chronic use of ACE-inhibitor and spironolactone, getting dehydrated due to intercurrent illness.
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION
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Hyperkalemia: pathogenesis INSUFFICIENT RENAL ELIMINATION
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes ACIDOSIS
Kalium: fysiologie Interne K+ balans
Zuur-base afwijkingen beïnvloeden interne K+ balans. K+
“VUISTREGEL” wisselt uit voor H+
ACIDOSE à hyperkalemie ALKALOSE à hypokalemie12 46
Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes INSULIN RESISTANCE or LACK of INSULIN
Kalium: fysiologie Interne K+ balans Insuline, β-adrenerge agonisten (adrenaline), aldosterone stimuleren Na+-K+-ATPase à K+ naar intracellulair
11
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes INSULIN RESISTANCE or LACK of INSULIN
= why patients with diabetic keto-acidosis may present with hyperkalemia (despite K+ depletion) Hypokalemie: pathogenese/oorzaken SHIFT NAAR INTRA-CELLULAIR Oorzaken GLUCOSE + INSULINE TOEDIENING = essentieel bij behandeling diabetische keto-acidose
DUS risico op levensbedreigende hypokalemie door shift van K+ naar intracellulair bij patiënten die vaak reeds een K+ depletie hebben ontwikkeld!
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes β-ADRENERGIC ANTAGONISTS e.g. - treatment heart failure - treatment tachy-arrythmias
Kalium: fysiologie Interne K+ balans Insuline, β-adrenerge agonisten (adrenaline), aldosterone stimuleren Na+-K+-ATPase à K+ naar intracellulair
usually only problematic if combined with INSUFFICIENT RENAL ELIMINATION
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes CELL- or TISSUE INJURY bv. intravascular hemolysis tumorlysis syndrome physical exercise crush syndrome
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes PSEUDOHYPERKALEMIA K+ leaves cells after blood sample has been taken
e.g. traumatic venipuncture long interval between sampling and analysis thrombocytosis or leucocytosis (release during clotting) hereditary spherocytosis (temperature dependent K+ leakage)
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Hyperkalemia: pathogenesis SHIFT TO EXTRACELLULAR COMPARTMENT Causes FAMILIAL HYPERKALEMIC PERIODIC PARALYSIS usually autosomal dominant defect of Na+ channels striated muscle cells
Attacks of painless paralysis, sometimes triggered by cold, recovery after physical excercise, fasting, ingestion of K+ Slight hyperkalemia during attacks (or normal [K+]) Normokalemia in-between attacks. 52
Hyperkalemia: symptoms • Definition hyperkalemia: plasma [K+] > 5.0 mmol/L (normal plasma [Na+] 3.5-5.1 mmol/L*)
• Symptoms usually only when [K+] > 6.0 mmol/L or in case of ACUTE onset. Symptoms due to change of resting membrane potential (depolarisation) slight depolarisation increases neuromuscular excitability more pronounced depolarisation inhibits excitability (refractory)
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*reference values van lab UZ Gasthuisberg 3-2011
Hyperkalemia: symptoms Muscle weakness Striated muscle muscle weakness paralysis (lower limbs, through trunk up to upper limbs)
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Hyperkalemia: symptoms Heart muscle
arrhytmias (ectopic pacemakers and reentry phenomena) VES, VFib… depolarisation resting potential à decreased excitability normal pacemaker more ectopic ventricular pacemakers
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Hyperkalemia: symptoms Heart muscle typical ECG changes tented T-waves, prolonged PR-interval, loss of P-waves, broadened QRS-complex, bradycardia
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Hyperkalemia: symptoms Heart muscle typical ECG changes tented T-waves, prolonged PR-interval, loss of P-waves, broadened QRS-complex, bradycardia
flattened P-waves
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Hyperkalemia: symptoms Heart muscle typical ECG changes
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Hyperkalemia: Hypokalemiasymptoms
Renal problems • Door interne K+ balans: hypokaliemie à daling pHi decreased NH3 synthesis, decreased reabsorption HCO3• à zelfde effect als bij chronische acidose acidosis via (pHo en) pHi door stimulatie NHE3, electrogene H+ Hypokalemia pomp, NBC, ammoniagene enzymes (glutaminase, PEPCK), Na/citraat cotransporter • Door interne K balans: hypokaliemie à daling pH à niet-titreerbaar/titreerbaar zuur stijgt! • à zelfde effect als bij chronische acidose +
i
via (pHo en) pHi door stimulatie NHE3, electrogene H+ pomp, NBC, ammoniagene enzymes (glutaminase, PEPCK), Na/citraat cotransporter à niet-titreerbaar/titreerbaar zuur stijgt!
• K+ depletie stimuleert ook apicale K-H uitwisselaar in α-intercalated cells van ICT en CCT • K+ depletie stimuleert ook apicale K-H uitwisselaar in α-intercalated cells van ICT en CCT
(Omgekeerde effecten bij hyperkaliemie. Bovendien competitie K+ en (Omgekeerde effecten bij hyperkaliemie. Bovendien competitie K en NH voor Na/K/Cl cotransport in TAL à minder NH accumulatie in + accumulatie NH4+ voor Na/K/Cl cotransport in TAL à minder NH in 4 interstitium medulla) interstitium medulla) +
+ 4
+ 4
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Hyperkalemia: symptoms Mental disturbances drowsiness, apathy, confusion, coma
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Hyperkalemia: treatment Indication depends on severity of symptoms. But actively look for symptoms if >6 mmol/L. Ca2+ to “stabilize” the membrane of cardiac muscle cells Insulin + glucose Bicarbonate Beta-2-adrenergic agonists Diuretics (loop and thiazide) Rehydration Dialysis Resins (cation exchangers) 61
