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Treatment of Hypertension: 7 classification

Treatment of Hypertension: 7 classification. Categories. Risk factors. Age above 55 and 65 in Men and Woman respectively Family History Smoking DM and Dyslipidemia Hypertension Obesity Microalbuminuria. Treatment of Hypertension – . 7 compelling Indications : Heart failure

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Treatment of Hypertension: 7 classification

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  1. Treatment ofHypertension: 7 classification Categories Risk factors Age above 55 and 65 in Men and Woman respectively Family History Smoking DM and Dyslipidemia Hypertension Obesity Microalbuminuria

  2. Treatment of Hypertension – • 7 compelling Indications: • Heart failure • Coronary artery disease • H/o MI • H/o stroke • Diabetes • Chronic Renal failure

  3. Treatment of Hypertension

  4. Treatment of Hypertension – General principles • Stage I: • Start with a single most appropriate drug with a low dose. Preferably start with Thiazides. Others like beta-blockers, CCBs, ARBs and ACE inhibitors may also be considered. CCB – in case of elderly and stroke prevention. If required increase the dose moderately • Partial response or no response – add from another group of drug, but remember it should be a low dose combination • If not controlled – change to another low dose combination • In case of side effects lower the dose or substitute with other group • Stage 2: Start with 2 drug combination – one should be diuretic

  5. Treatment of Hypertension – combination therapy • In clinical practice a large number of patients require combination therapy – the combination should be rational and from different patterns of haemodynamic effects • Sympathetic inhibitors (not beta-blockers) and vasodilators + diuretics • Diuretics, CCBs, ACE inhibitors and vasodilators + beta blockers (blocks renin release) • Hydralazine and CCBs + beta-blockers (tachycardia countered) • ACE inhibitors + diuretics • 3 (three) Drug combinations: CCB+ACE/ARB+diuretic; CCB+Beta blocker+ diuretic; ACEI/ARB+ beta blocker+diuretic

  6. Treatment of Hypertension. • Never combine: • Alpha or beta blocker and clonidine - antagonism • Nifedepine and diuretic synergism • Hydralazine with DHP or prazosin – same type of action • Diltiazem and verapamil with beta blocker – bradycardia • Methyldopa and clonidine • Hypertension and pregnancy: • No drug is safe in pregnancy • Avoid diuretics, propranolol, ACE inhibitors, Sodium nitroprusside etc • Safer drugs: Hydralazine, Methyldopa, cardioselective beta blockers and prazosin

  7. Treatment guidelines (ESH/ESC 2007) Average risk Low added risk Moderate added risk High added risk Very high added risk ESH – ESC Guidelines Committee. J Hypertens 2007; 25: 1105–1187

  8. Complications of Hypertension:End-Organ Damage Hypertension Hemorrhage, Stroke LVH, CHD, CHF Peripheral Vascular Disease Renal Failure, Proteinuria Retinopathy CHD = coronary heart disease CHF = congestive heart failure LVH = left ventricular hypertrophy Chobanian AV, et al. JAMA. 2003;289:2560-2572.

  9. Conditions favouring the use of some antihypertensive drugs versus other • Subclinical organ damage: LVH ACEI, CA, ARB Asymptomatic Atherosclerosis CA, ACEI Microalbuminuria ACEI, ARB Renal dysfunction ACEI, ARB

  10. Conditions favouring the use of some antihypertensive drugs versus other • Clinical event: Previous stroke any BP lowering agent Previous MI BB, ACEI, ARB Heart failure diuretics, BB, ACEI, ARB, anti-aldosterone agents Tachyarrhythmias BB Periph.art.disease CA LV dysfunction ACEI

  11. Conditions favouring the use of some antihypertensive drugs versus other • Condition : ISH (elderly) diuretics,CA Metabolic syndrome ACEI,ARB,CA Diabetes mellitus ACEI, ARB Pregnancy CA,methyldopa,BB Glaucoma BB

  12. Monotherapy versus combination therapy • Monotherapy allows to achieve BP target only in a limited number of patients • Use of more than one agent is necessary to achieve target BP • Initial therapy: monotherapy or combination of two drugs in low doses with subsequent increase in drug doses or number

  13. Monotherapy versus combination therapy • Monotherapy in mild BP elevation with low or moderate total CV risk • Two drugs at low doses should be preferred as the first step when BP is in grade 2 or 3 or total CV risk is high or very high with mild hypertension • Fixed combination of two drugs simplify the treatment • If BP control is not achieved by two drugs, combination of three or more drugs is required

  14. Possible combinations of different classes of antihypertensive agents Diuretics AT1-receptorblockers β-blockers CCBs α-blockers ACE, angiotensin-converting enzyme AT, angiotensin CCB, calcium-channel blocker ACEinhibitors The preferred combinations in general hypertensive population are represented as thick lines. The frames indicate classes of agents proven to be beneficial in controlled interventional trials ESH – ESC Guidelines Committee. J Hypertens 2007; 25: 1105–1187

  15. Antihypertensive therapy in special groups • Elderly patients • Diabetic patients • Patients with renal dysfunction • Patients with cerebrovascular disease • Patients with coronary heart disease and heart failure • Patients with atrial fibrillation

  16. Beta-adrenergic blockers • Non selective:Propranolol (others: nadolol, timolol, pindolol, labetolol) • Cardioselective: Metoprolol (others: atenolol, esmolol, betaxolol) • All beta-blockers similar antihypertensive effects – irrespective of additional properties • Reduction in CO but no change in BP initially but slowly • Adaptation by resistance vessels to chronically reduced CO – antihypertensive action • Other mechanisms – decreased renin release from kidney (beta-1 mediated) • Reduced NA release and central sympathetic outflow reduction • Non-selective ones – reduction in g.f.r but not with selective ones • Drugs with intrinsic sympathomimetic activity may cause less reduction in HR and CO  

  17. Beta-adrenergic blockers • Advantages: • No postural hypotension • No salt and water retention • Low incidence of side effects • Low cost • Once a day regime • Preferred in young non-obese patients, prevention of sudden cardiac death in post infarction patients and progression of CHF • Drawbacks (side effects): • Fatigue, lethargy (low CO?) – decreased work capacity • Loss of libido – impotence • Cognitive defects – forgetfulness • Difficult to stop suddenly • Therefore cardio-selective drugs are preferred now

  18. Beta-adrenergic blockers • Advantages of cardio-selective over non-selective: • In asthma • In diabetes mellitus • In peripheral vascular disease • Current status: • JNC 7 recommends - 1st line of antihypertensive along with diuretics and ACEIs • Preferred in young non-obese hypertensive • Angina pectoris and post angina patients • Post MI patients – useful in preventing mortality • In old persons, carvedilol – vasodilatory action can be given

  19. The End

  20. Adrenergic ReceptorsReview of ANS • Sympathetic Nervous System • Alpha 1 = vasoconstriction • Alpha 2 = feedback/vasodilation • Beta 1 = increases heart rate • Beta 2 = bronchodilation

  21. Beta Adrenergic Blocking Agents • Known as Beta-blockers • Axn: Inhibit cardiac response to sympathetic nerve stimulation by blocking Beta receptors • Decreases heart rate and C.O. • Decreases blood pressure

  22. Beta Adrenergic Blocking Agents • Examples – “olol” names • Beta 1: Atenolol • Beta 1 and 2: Propranolol

  23. Nursing Implications • Can not be abruptly discontinued • Check baseline b.p. • Check hx. of resp. condition-aggravates bronchoconstriction

  24. Side effects • Bradycardia • Bronchospasm, wheezing • Diabetic: hypoglycemia • Heart failure: edema,dyspnea,rhales

  25. DIURETICS • MOA: • 1- ↑ renal excretion of Na & water ↓ plasma volume ↓ C.O. • 2- ↓ peripheral resistance ( desensitize smooth muscles to action of catecholamines )

  26. 1-Thiazide • Sulfonamide molecule • Prolonged action • Flat curve response • Potentiates action of other anti HTN • Eg: Hydrochlorothiazide ( Ezidrex ) , Bendrofluazide • SE: hypo K+ , hypo Na+, hyperuricemia, hyperglycemia, lipid profile disturb.

  27. 2- Loop Diuretics • Steep curve response • Restricted to CCF & CRF • Eg: Frusemide • SE: ↓ K+ , ↓ Na+ , hypotension, ototoxic in v.high doses

  28. 3- K+ sparing diuretics • Not effective alone, so used in combination • Eg: Spironolactone, Amiloride , Uniretic( HCT + Amiloride) • SE: ↑ K+, gynecomastia

  29. Beta Blockers • MOA: • Block beta receptors ↓sympathetic drive • 1- ↓ H.R. & contractility, ↑ P.R. ↓ C.O. • 2- ↓ Renin release & activity ↓ Ang II ↓BP Act as anti HTN within 3-7 days

  30. Beta Blockers • Metabolism: Hydroxylated in liver to water soluble compounds excreted in kidneys • Preferred in HTN with angina, SVT, HOCM, Thyrotoxicosis, Pheochromocytoma, Migraine and L.cirrhosis.

  31. Beta Blockers • SE: bradycardia, bronchospasm, cold extremeties, hypoglycemia, insomnia, bad dreams • Overdose: hypotension, bradycardia, bronchospasm, coma ( treated with Atropine, Isoprenaline, glucagon ) • C.I: HF, Asthma, DM, H.Block, Periph.vascular diseases , Hyperlipidemia

  32. Beta Blockers • Atenolol: less lipid soluble less CNS SE • Timolol: lipid soluble more CNS SE.

  33. Thiazides • Mechanism of action: • = lower blood pressure by reduction of blood volume and by direct • vascular effect • inhibition of sodium chloride transport in the early segment of the distal • convoluted tubule  natriuresis, decrease in preload and cardiac • output - renal effect • slow decrease of total peripheral resistance (raised initially) during • chronic treatment, suggesting an action on resistance vessels - • extrarenal effects • compensatory responses to pressor agents including angiotensin II and • noradrenaline are reduced during chronic treatment with thiazides • used with loop diuretic - synergistic effect occurs

  34. Thiazides Adverse effects: - Idiosyncratic reactions (rashes - may be photosensitiv, purpura) - Increased plasma renin (which limits the magnitude of their effect on BP) - Metabolic and electrolyte changes Hyponatremia Hypokalemia (combine with potassium-sparing diuretics) Hypomagnesemia Hyperuricemia(most diuretics reduce urate clearance) Hyperglycemia Hypercalcemia (thiazides reduce urinary calcium ion clearance  precipitate clinically significant hypercalcemia in hypertensive patients with hyperparathyroidism) Hypercholesterolemia (a small  in plasma cholesterol concentration)

  35. LOOP DIURETICS furosemid - useful in hypertensive patients with moderate or severe renal impairment, or in patients with hypertensive heart failure. - relatively short-acting (diuresis occurs over the 4 hours following a dose)  used in hypertension if response to thiazides is inadequate Mechanism of action: - they inhibit the co-transport of Na+, K+ and Cl- - of Ca2+ and Mg2+ excretion - they have useful pulmonary vasodilating effects (unknown mechanism)

  36. LOOP DIURETICS Toxicity: - hypokalemic metabolic alkalosis (increased excretion of K+) - ototoxicity (dose dependent, reversible) - decrease of Mg2+ plasma concentration (hypomagnesemia) - hyperuricemia (competition with uric acid about tubular secretion) - sulfonamide allergy - risk of dehydration (> 4 L urine/ 24 h) Imporatant drug interaction may occurs if loop diuretic is given with Li+ (thymoprofylactic drug). Decrease of Na+ reabsorption can lead to increase of Li+ reabsorption  toxicity.

  37. b -adrenoreceptor antagonists • Mechanism of action: • the fall in cardiac output   BP • - theyreduce renin secretion • CNS-effects ??? • additional mechanisms involve baroreceptors or other homeostatic • adaptations • Possible mechanisms include: • b-adrenoceptors located on sympathetic nerve terminals can promote • noradrenaline release, and this is prevented by b-receptor • antagonists • local generation of angiotensin II within vascular tissues is stimulated • by b2-agonists.

  38. b-adrenoreceptor antagonists cardio-selective: b1blockersatenolol, metoprolol b1blockers with ISAacebutol b1 + a1blockerslabetalol, carvedilol cardio non-selective: b1 + b2blockersmetiprolol, propranolol, nadolol b1 + b2blockers with ISApindolol, bopindolol Note: Partial agonist activity (intrinsic sympathomimetic activity – ISA) - may be an advantage in treating patients with asthma because these drugs will cause bronchodilation; they have moderate (lower) effect on lipid metabolism, cause lesser vasospasms and negative inotropic effect

  39. b-adrenoreceptor antagonists • Adverse effects • Cardiovascular adverse effects, which are extension of the beta • blockade, include: • bradycardia • antrioventricular blockade • congestive heart failure (unstable) • asthmatic attacks(in patients with airway disease) • premonitory symptoms of hypoglycemia from insulin overdosage • (eg, tachycardia, tremor and anxiety, may be marked) • CNS adverse effects - sedation, fatigue, and sleep alterations.

  40. Hypertension & regulation of blood pressure Baroreflexes (mediated by autonomic nerves) Humoral mechanisms (include: RAAS system and local release of hormones from vascular endothelium, such as, NO, endothelin 1) Anatomic sites of blood pressure control

  41. Hypertension & regulation of blood pressure A. Postural baroreflex: responsible for rapid , moment to moment adjustments in blood pressure. • Sense the stretch of the vessel walls • from a reclining to an upright posture; • reduction of peripheral vacular resistance; • Reduction in intravascular volume; -

  42. Hypertension & regulation of blood pressure B. Renin-Angiotensin-Adolsteron (RAAS) Angiotensin II Redistribution of renal blood flow This is responsible for long-term blood pressure control.

  43. Basic pharmacology of antihypertension drugs

  44. I. Basic pharmacology of antihypertension agents 1. Diuretics:depleting the sodium and reducing blood volume and perhaps by other mechanisms. 2. Sympathoplegic agents:reducing peripheral vascular resistance, inhibiting cardic output, increasing venous pooling. 3. Direct vasodilators:relaxing vacular smooth muscle, dilaing resistance vessels and/or increasing capacitance. 4. Agents that block RAAS:reduce peripheral vacular resistance and blood volume.

  45. 1. Diuretics • Sodium restriction is very preventive in the control of blood pressure. It is a nontoxic and therapeutic measure. 1) Pharmacological roles (1) Diurectic action: In the early stage: reducing blood volume and cardiac output; In the late stage: reduce peripheral vascular resistance (by reducing the Na+; reduce Na+-Ca2+ exchange in vascular smooth muscle cells (Ca2+i , peripheral resistance  ) (2) Non diurectic action: direct vasodilating, e.g. Indapamide, a non-thiazide sullfonamide diuretic with both diuretic and vasodilator activity; Amiloride inhibits smooth muscle responses to contractile stimuli.

  46. Diuretics commonly used

  47. Diuretics • Drugs causing net loss of Na+ and water in urine • Mechanism of antihypertensive action: • Initially: diuresis – depletion of Na+ and body fluid volume – decrease in cardiac output • Subsequently after 4 - 6 weeks, Na+ balance and CO is regained by 95%, but BP remains low! • Q: Why? Answer: reduction in total peripheral resistance (TPR) due to deficit of little amount of Na+ and water (Na+ causes vascular stiffness) • Similar effect is seen with sodium restriction (low sodium diet)

  48. Thiazide diuretics – adverse effects • Adverse Effects: • Hypokalaemia – muscle pain and fatigue • Hyperglycemia: Inhibition of insulin release due to K+ depletion (proinsulin to insulin) – precipitation of diabetes • Hyperlipidemia: rise in total LDL level – risk of stroke • Hyperurecaemia: inhibition of urate excretion • Sudden cardiac death – tosades de pointes (hypokalaemia) • All the above metabolic side effects – higher doses (50 – 100 mg per day) • But, its observed that these adverse effects are minimal with low doses (12.5 to 25 mg) - Average fall in BP is 10 mm of Hg

  49. Thiazide diuretics – current status • Effects of low dose: • No significant hypokalaemia • Low incidence of arrhythmia • Lower incidence of hyperglycaemia, hyperlipidemia and hyperuricaemia • Reduction in MI incidence • Reduction in mortality and morbidity • JNC recommendation: • JNC recommends low dose of thiazide therapy (12.5 – 25 mg per day) in essential hypertension • Preferably should be used with a potassium sparing diuretic as first choice in elderly • If therapy fails – another antihypertensive but do not increase the thiazide dose • Loop diuretics are to be given when there is severe hypertension with retention of body fluids

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