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Hypokalaemia
By Dr Nihal AbosaifConsultant acute physicianUHCW
Outline
Physiology of K+ transport
Factors modifying transcellular K+
distribution
Causes of Hypokalaemia
Diseases associated with it
Management of Hypokalaemia
Most abundant cation in human body
Regulates intracellular enzyme function and helps to determine neuromuscular & cardiovascular tissue excitability.
90 % of total body K+ : Intracellular
( predominantly in muscle ) 10 % : Extracellular fluid < 1 % : Plasma
Introduction : Potassium
Ratio of extracellular K+ to Intracellular K+ : determines the membrane potential
The acuity of changes in serum potassium concentration & membrane potential determines clinical symptoms and underlying signs
Plasma concentration varies from 3.5 to 5.3 mmol/l
Introduction : Potassium
K+ uptake into cells : actively driven by Na+/K+/ATPase
Leak back into ECF : opposed by electrical gradient
Physiology Of Potassium Homeostasis
Acid base statusPancreatic hormones : insulin ,
glucagonCatecholaminesAldosteronePlasma Osmolality ExerciseCellular K+ content
Factors modifying transcellular K+ distribution
Alkalosis promotes K+ uptake by cells
Acidosis diminishes K+ uptake by cells
Acute respiratory alkalosis, in contrast increase plasma K+ by 0.2 mmol/l per 0.1 pH unit due to increased adrenergic activity
Acid Base Status
Insulin stimulates cellular uptake of K+ by activating Na+/K+/ATPase
( decreasing plasma K+ )
Insulin affects K+ transport independently of glucose uptake
Glucagon increase plasma K+ independently of changes in plasma glucose / insulin
Pancreatic Hormones
Beta 2 adrenergic activity – hypokalaemia
Alpha adrenergic antagonists – hypokalaemia
Catecholamines
Invitro studies Aldosterone stimulates Na+/K+/ATPase and thereby activating Na + influx
Aldosterone
Hyperosmolality ( Mannitol infusion / hyperglycemia in DM ) : increase plasma K+
Each 10 mOsm / Kg rise in plasma osmolality, increases plasma K+ by 0.6 mmol/l
Osmolality
Recurrent contraction increases K+ egress from muscle
Modest exercise : high K+ in ECF in local environment produces vasodilatation & thereby increased regional blood flow
Severe exercise : increase plasma K+ modestly
Physical training increases Na+/K+/ATPase activity in skeletal muscle which helps skeletal muscle to take up K+ again
Exercise
Kidney is dominant in sustaining K+ balance
>90 % K+ : excreted in urine
Remainder through faeces
Decrease in GFR, K+ excretion via faeces increased
GI Loss : K+ secretion by proximal & distal colon
K+ Balance
Renal Handling of K+
Glomerulus: freely filtered
PCT, TAL, Loop of Henle : reabsorbed
Defined as plasma concentration of K+ < 3.5 mEq/L
Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic
Hypokalemia < 3.0 mEq/L : symptomatic
Clinical manifestations of hypokalemia vary greatly between individual patients &
their severity depends on degree of hypokalemia
Hypokalemia
Clinical features
Investigations
Diagnosis
Mild hypokalemia : generally asymptomatic
Increased risk of mortality for pts with cardiovascular disease – trigger ventricular tachycardia / ventricular fibrillation
(decrease K+ : d/t sympathetic stimulation)
Digitalis induced arrhythmias – can occur with
normal drug levels if hypokalemia is present
Diuretic induced hypokalemia & hypomagnesemia
must be avoided in pts on drugs that prolong QT
interval : as it predisposes to polymorphic VT /
Torsade de pointes
Hypokalemia < 3 mEq/L : Symptomatic
Clinical Features
Digitalis Intoxication : ventricular extrasystoles
ventricular tachycardia
ventricular fibrillation
partial-complete AV block
bradycardia
atrial flutter
atrial fibrillation
Ventricular arrhythmias : tachycardia / fibrillation
Cardiac
FatigueMyalgiaMuscular weakness involving
lower limbs
Severe Hypokalemia : Paralysis ( extremities ) Weakness of respiratory muscles ( dyspnea ) Rhabdomyolysis (exercise
induced)
Neuro-muscular
Constipation
Paralytic ileus
Gastro-intestinal
Chronic interstitial nephritis due to functional decrease in renal blood flow –
decreased GFR
Chronic renal failure
Renal Cysts
Renal
Polyuria ( nephrogenic diabetes insipidus )
Polydipsia ( nephrogenic diabetes insipidus )
Increased ammonia production ( intracellular acidosis ) precipitate hepatic coma in pts with advanced liver ds
EdemaChloride wasting Metabolic alkalosis HypercalciuriaPhosphaturia
Fluid – Electrolyte
Glucose intolerance ( decreased insulin secretion )
Growth retardation ( Reduced Growth hormone receptors, Reduced IGF-1 )
Hypertension ( increased renin secretion )
Endocrine
ECG : Initially : flattening of t wave depression of ST
Segment development of
prominent u waves Severe hypokalemia :
increased amplitude of p wave
increased QRS duration S.Potassium
Basic Investigations
Investigations – Causes
Urinary K+TTKG Urinary ChlorideCBC Peripheral SmearABG Echocardiogram Cardiac Enzymes
Serum aldosteroneSerum renin USG AbdomenCT / MRI AbdomenFBS / PPBS / Urine
KetonesTSH / free T3 / free
T4 Colonoscopy /
OGDscopy
Decreased net intake
Shift into cells
Increased net loss
Causes of hypokalaemia
Hypokalemia
True Hypokalemia Spurious
Hypokalemia
Decreased total body K+
Decreased intake
Renal loss of K+
Extra renal loss of K+
Occurs in patients with extreme leukocytosis
eg : in myeloproliferative disorders
Invitro WBC uptake potassium within the test tube
Spurious Hypokalemia
Starvation
Clay ingestion ( binds to dietary K+ & Iron )
Diarrhoea and vomiting
Decreased Intake or increased loss
Acid – Base Status : Metabolic Alkalosis
Hormonal : Increased Insulin Increased Beta 2
Adrenergic activity
Drugs : Beta 2 agonists Theophylline Barium Intoxication Chloroquine Calcium Channel Blockers
Transcellular shifts
Catecholamine release associated with :
Asthma
COPD – exacerbations
Heart failure
Myocardial infarction / angina
Drug withdrawal syndrome – alcohol / narcotics / barbiturates
Transcellular shift
Insulin administration – for treatment
of DKA
Refeeding Syndrome
Hypokalemic Periodic Paralysis
Thyrotoxic Periodic Paralysis
Treatment of anemia : Vit B12 / Folic
acid deficiency
Use of GM – CSF in patients with
Neutropenia
Transcellular shift
Urinary K+: > 20 mEq/L – Renal loss
Urinary K + : < 20 mEq/L – Extrarenal loss
TTKG : Transtubular Potassium Gradient
( Urine K+ / Plasma K+ )
( Urine Osm / Plasma Osm )
TTKG : Renal loss : > 4 Extra renal loss : < 4
Renal Vs Extra renal loss
Algorithm for diagnosis of Extra Renal Loss
Urinary K+ < 20 mEq/L
Metabolic Acidosis
GI Loss DiarrhoeaLaxative Abuse
Normal pH
Villous AdenomaLaxative Abuse
Metabolic Alkalosis
GI Loss: rareLaxative
abuse : rare
Urinary loss K+ > 20 mEq/L
Metabolic Acidosis
RTA DKA
Ureterosigmoidost
omy
Variable pHATN
recovery Post
obstructive
diuresis Drugs
Metabolic Alkalosis
Urinary chloride
level
Renal Loss
Urinary Chloride
< 20 mmol/L
DiureticsVomiting
> 20 mmol/L
Check BP
Renal Loss + Metabolic Alkalosis
Check BP, ECF
Low BP
Check Bicarb
Low - RTA
High : Bartter,
Gitelman
HTN , Increased ECF
Check Renin, Aldosterone
Renal loss +Urine Cl > 20 mEq/L
Amphotericin B : tubular damage increased
excretion of K+Aminoglycosides : renal wasting of
K+Thiazides, Furosemide,
Acetazolamide : renal loss K+Cisplatin
HYPOMAGNESEMIA : Significant renal K+ wasting
Renal loss - Drugs
Management of HypokalaemiaIf mild asymptomatic Oral KCl
If severe or symptomatic hypokalemia
IV KCl supplement
IV infusion rate for severe or
symptomatic hypokalemia
.
Standard IV replacement rate 10 - 20 mmol/h
Serum potassium < 2.5 meq/L, or Moderate-severe symptoms
20 - 40 mmol/h
Serum potassium < 2.0 Meq/L, or Life-threatening symptoms
> 40 mmol/h
If heart block, or Renal insufficiency exists
5 - 10 mmol/h
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