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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