HYPERTENSION AND HYPOKALEMIA - API

1 HYPERTENSION AND HYPOKALEMIA . 3:5 Sekhar Chakraborty, Siliguri INTRODUCTION. HYPERTENSION and HYPOKALEMIA are two distinct clinical entities, whenever present in a single clinical setting of an individual, may or may not be related to each other. However it is mandatory for a treating physician to search for this clinical correlation. Detection of the underlying cause not only guides the treatment protocol but also dictates further steps for prevention of HYPERTENSION & HYPOKALEMIA , prevention for life threatening conditions like arrhythmias, sudden cardiac death, respiratory failure etc. & provides the insights for prognosis. Simple reason like diuretic induced HYPOKALEMIA for the treatment of HYPERTENSION may be overshadowed with complicated genetic disorders, channelopathies or endocrine disorders which need prolonged biochemical & genetic workup.

2 Therefore careful &. vigilant approach is warranted in this clinical setting. Potassium Homeostasis Approximately 98 % of total body stores are intracellular Normal Serum [K+] ranges from 5 mmol/ L. Insulin, aldosterone, catecholamine & acid base status influence movement of [K+] into the cells. K+ excretion is regulated at the distal nephron. K+ excretion is related to (Urine flow rate). The marked discrepancy between intracellular & extracellular content of potassium is illustrated Fig. 1. Total body potassium content in healthy adult is approx 50mEq/ kg, so a 70 kg adult will have 3500. mEq as 2% of total amount is in extracellular fluid, therefore ECF contain 70 mEq K+. As plasma 4000. Total Body K (mEq). 3000. 353500. 2000.

3 70 mEq 1000 . 0. Intracellular Potassium Extracellular Potassium Fig. 1 : Intracellular & extracellular content of potassium 128. HYPERTENSION and HYPOKALEMIA accounts for approx 20% of ECF volume, the potassium Extra renal loss gastrointestinal. content of plasma is about 15 mEq which is about of Definition of HYPOKALEMIA total body potassium. HYPOKALEMIA has been defined as Serum [K+] is < mEq/. This suggests that plasma potassium is an insensitive marker L. Severe HYPOKALEMIA where of changes in total body potassium stores. Serum [K +] = < mEq / L (Figs. 3 and 4). Serum level of K+ is regulated by- HYPERTENSION . Uptake of K+ into cells by altering activity of Na K- ATP's pump in the cell membrane. HYPERTENSION , more specifically systemic arterial HYPERTENSION is defined as the elevation of blood pressure (BP) to such a level Renal excretion mainly controlled by aldosterone.

4 That place patients at increased risk of target organ damage in several vascular beds including the retina, brain, heart, 10 kidneys and large condict arteries. In demographic studies the level has been observed above 120/80mHg. HYPERTENSION has 8. (70 kg Adult) been staged as High normal stage I & II, Hypertensive crisis, Serum K+ isolated systolic HTN according to level of elevation of BP, (mEq/ L). 6- rapidity of development of HTN, threat to vascular bed, etc. ACIDOSIS. 4- Prevalence Recent studies have reported a high prevalence of HYPERTENSION in both urban & rural areas, in India 2- In urban area the prevalence varies from 30 -45 % in ALKALOSIS different regions, which is consistent with the findings with other developing countries in Asia where prevalence is -900 -600 -300 +300 50% Epidemiological studies report that currently 70% of 0 HYPERTENSION in India is Stage I (140 159 / 90 99 mmHg.)

5 K+ Deficit (mEq) K+ Excess (mEq) & rest of are Stage II. Mechanism Fig. 2 : Relationship between the Serum potassium of HYPOKALEMIA concentration Prevalence of resistant HYPERTENSION in India is unknown. & changes in total body potassium content. HYPOKALEMIA : High K+ excretion Reason? (Can be both). High Flow Rate High [K+] CCD. Osmoles? ECFV? Lytes' Organics Not low = Low =. Faster Na+ Slower Cl - * High NaCl input * Glucose * Primary high * Bartter * Diuretics loop, * Urea aldosterone * Gitelman Thiazide, or * Mannitol * AME syndrome * Bicarbonaturia Cal types * GRA * Low Cl - delivery * Liddle * Amphotericin B. HYPOKALEMIA Fig. 3 : Mechanism of HYPOKALEMIA 129. +. Faster Na Slower Cl- * Liddle * Amphotericin B. HYPOKALEMIA Medicine Update 2012 Vol.

6 22. Faster Na + Slower Cl- Na +. Electro Electro- -negative negative Cl - K * TTKG * TTKG. Na * ECFV * ECFV. * Urine [Na + + Cl -] * Urine [Na + + Cl -]. if ECFV low not . Fig. 4 : HYPOKALEMIA 50 Table 1 : Causes of K+ depletion 40 Extrarenal (Urine K+ < 20mmol/ Renal (Urine K+> 20mmol/day). 30. day). Urban 20 Rural Inadequate intake Renal tubular acidosis 10 Copious perspiration Diabetic ketoacidosis 0 Gastrointestinal losses Chloride depletion Prevalence Awareness Treatment Control Diarrhoea Vomiting/gastric suction Fig. 5 : Status of HYPERTENSION prevalence, awareness, treatment &. Laxative abuse Diuretics control in India. Villous adenoma Bartter's syndrome Status of HYPERTENSION prevalence, awareness, treatment and Gitelman's syndrome control in India.

7 Mineralocorticoid excess states (4608 middle aged women, 35 70 years, in 4 urban and 5. Liddle's syndrome rural cites.). Glucocorticoid excess What is the relation between HYPERTENSION & HYPOKALEMIA ? Magnesium depletion HYPERTENSION & HYPOKALEMIA are two distinct clinical Antibiotic therapy syndromes which may or may not be associated. Relation Leukaemia between these two clinical syndromes can be established as Interstitial nephritis immune re- follows. lated 1. Aetiology of HYPERTENSION is associated with hypoka- Diuretic conditions. lemia. Endocrine cause . 2. Treatment of HTN may lead to HYPOKALEMIA Primary hyperaldostronism Aetiology of HTN associated with HYPOKALEMIA . Secondary hyperaldostronism Among all the causes of HTN, the following are related to Cushing Syndrome.

8 HYPOKALEMIA . Congenital adrenogenital syndrome 130. HYPERTENSION and HYPOKALEMIA Table 2 : Mineralocorticoid Excess States High aldosterone Low aldosterone and PRA. Low PRA High PRA Normal cortisol Low cortisol High cortisol Primary hyperaldosteronism Renovascular disease Exogenous Mineralocorticoid Adrenogenital syndrome Familial Glucocorticoid resistance Glucocorticoid-remediable Main renal arteries 11- -HSD deficiency 17- - Hydroxylase deficiency Aldosteronism (GRA) Small vessels Congenital 11- -Hydroxylase deficiency Renin secretory tumour Liquorice Carbenoxolone Liddle's syndrome MR activation mutation. Algorithm depicting the diagnostic approach to HYPOKALEMIA Exclude spurious/transcellular shift ileus occurs when smooth muscle function is affected.

9 More severe HYPOKALEMIA my lead to complete paraly- Decreased total body K+ sis, hypoventilation or rhabdomyolysis 3. K+ depletion is associated with increased risks of ar- Urine K+ < 25 mEq/d Urine K+ > 30 mEq/d rhythmias leading to palpitation or Syncope. 4. Polydipsia & Polyuria may result for HYPOKALEMIA in- Acid-base status Acid-base status duced NDI. Normal acid-base Metabolic acidosis Metabolic alkalosis Normal acid-base 5. Possible causes of transcellular shift should be sought, * Profound Lower GI loses Post ATN/post sweating obstructive diuresis such as use of bronchodilators in COPD. Diuretic &. * Prolonged Osmotic diuresis decreased intake Gentle diuretic use laxative abuse & recurrent vomiting should be excluded. * Remote diuretic, Urine [Cl-] < 20mEq/L Urine [Cl-]> 20mEq/L [Mg ++].

10 NG suction, or vomiting High-dose penicillin Polydipsia/DI 6. Sign of hypovolemia or hypervolemia, hypotension/ hy- * NG suction * Vomiting Blood pressure pertension provides the clue to the aetiology. 7. ECG changes of HYPOKALEMIA do not correlate well with Hypertensive Normotensive/ Metabolic acidosis the plasma [K+]. Early changes may include flattening or hypotensive inversion of T waves a prominent U wave (more than 1. Normal/low aldosterone High aldosterone Aggressive diuretic use Bartter's or Type 1 or 2 RTA. Amphotericin B. mm in height) depression and a prolonged Gitelman's Syndrome DKA. Acetazolamide Q u interval. Severe K+ depletion may result in a pro- * Cushing syndrome longed PR interval, decreased voltage and widening of * Apparent Mineralocorticoid excess * Primary hyperaldosteronism QRS complex.