Introduction:> most common CVS disease | > elevated arterial BP damages vessels in renal, heart and brain | Complications: | Renal failure, Coronary disease, Heart failure, Stroke, Diamentia |
Classification:Classification: | Systolic BP | Diastolic BP: | Normal: | <120 | <80 | Pre-hypertension: | 120-139 | 80-89 | Stage 1 HTN: | 140-159 | 90-99 | Stage 2 HTN: | >= 160 | >=100 |
Types of Hypertension:Essential Hypertension (85-90%): | Primary hypertension, no identifiable cause (genetic), can't be cured, can be controlled | Secondary Hypertension (10-15%): | Specific identified cause (comorbid disease or drug), can be cured when cause is eliminated |
Secondary Causes of HTN:> Genetic factors | > Psychological stress | > Environmental and Dietary Factors: | high salt diet, decreased calcium and phosphate intake, sedentary lifestyle | > Diseases: | renal, endocrine, vascular, renal diseases | > Drugs: | sympathomimetic amines, amphetamines, oral decongestants (eg. pseudoehedrine), corticosteroids, osteogens (C0Cs), NSAIDs, COX-2 inhibitors |
Clinical presentation:- Often incidental finding | - Adults should get BP checks once a year | - Severe cases: | Headaches, visual disturbances, target organ damage (stroke, ischemic heart disease, renal failure) |
Potential Mechanisms of Parthogenesis:BP= CO x PVR | Increased Cardiac output: | Increased fluid volume from excessive sodium intake or renal sodium retention Venous constriction: due to excess stimulation of RAAS | Increased Peripheral resistance: | Excess stimulation of RAAS Sympathetic nervous system over-activity |
Antihypertensive Drugs:
| | Classes of Antihypertensive Agents:> Diuretics: | Reduce blood volume=Depletes the body of sodium, Venodilation | > Sympathoplegic agents: | Reduce peripheral vascular resistance, Inhibit cardiac function, Increase venous pooling capacitance vessels | > Direct vasodilators: | Reduce peripheral vascular resistance, Increase venous pooling capacitance vessels | > Angiotensin antagonists: | Reduce peripheral vascular resistance, Reduce blood volume |
Diuretics:- Reduce blood volume and cardiac output | - Cardiac output returns to normal | But peripheral vascular resistance declines | - Sodium | Contributes to vascular resistance = Increase vessel stiffness | - Venodilation | Altered sodium-sodium calcium exchange |
Vasodilation mechanism by Diuretics:
Use of Diuretics:> Lower BP by 10-15 mmHg in most patients | > Thiazide diuretics –mild to moderate HTN | > Loop diuretics – severe HTN and hypertensive emergencies |
Adverse Effects (Thiazide Diuretics):
Potassium depletion – hypokalemia
Magnesium depletion
Hyperuricemia- gouty attacks
Glucose intolerance
Increase serum lipid concentrations Sympathoplegic Drugs: Centrally-acting Drugs: | Methyldopa, clonidine | Adrenoceptor antagonists | Beta-blockers, alpha-1 blockers | Ganglionic-blocking Agents: | No longer used clinically ; hexamethonium | Adrenergic neuron blocking agents: | Block the release of noradrenaline, Reserpine, guanethidine, debrisoquin, Not/rarely used clinically |
Centrally-Acting Drugs:- Methyldopa, clonidine | rarely used except clondine | - Reduces sympathetic outflow | - Compensatory response mechanism: | salt retention | - Clonidine, guanabenz, guanfacine | Stimulate central alpha-2 adrenoceptors | - Methyldopa – anologue of L-dopa | Results in the synthesis of a false neurotransmitter | | | Alpha-methylnoradrenaline = Stimulates central alpha-2 adrenoceptors |
Clonidine:
Reduces cardiac output, PVR, relaxation of capacitance vessels
Rarely causes postural hypotension
Adverse effects:
- Dry mouth
- Sedation
Contraindication: Patients with depression
Caution: Abrupt discontinuation can lead to hypertensive crisis | | Adrenoceptor antagonists: Beta-blockersNon-selective: Propranolol | Beta-1 selective: “BBEAM” | Betaxolol, bisoprolol, esoprolol, atenolol, metoprolol, Cardioselective | Vasodilator beta-blockers | Also block alpha-1 receptors,Labetolol, carvidelol, nebivolol |
Decrease cardiac output
Decrease peripheral vascular resistance
Inhibit stimulation of renin production by catecholamines
Adverse effects= Heart block, bronchoconstriction, diabetes, vivid dreams Alpha-1 blockers:Prazosin, terazosin, doxazosin | Block alpha-1 receptors in arterioles and veins | Vasodilation | Reduce peripheral resistance | Compensatory mechanism: | salt and water retention |
More effective when used with other drugs Calcium Channel Blockers:> Dihydropyridines | amlodipine, isradipine, nicardipine, nimodipine, felodipine, nisoldipine, lacidipine | > Non-dihydropyridines | Verapamil, diltiazem, hydralazine | | | Benzothiazepine (diltiazem) |
Mechanism of action:
- Inhibit calcium influx through voltage-dependent L-type calcium channels
- Relax arteriolar smooth muscle, reduce peripheral vascular resistance
- Cause coronary and peripheral vasodilation CCB: Mechanisms of Action:Dihydropyridine CCBs | Primary vasodilators (reduce PVR), All decrease cardiac contractility except amlodipine and felodipine | Non-dihydropyridines (diltiazem, verapamil) | directly block the AV node, decrease heart rate,decrease cardiac contraction | Adverse effects: | 1. Flushing, peripheral oedema, tachycardia, bradycardia, heartblock |
2. Headache, flushing, dizziness, palpitations, hypotension
occur within a few hours of dosing, Associated w high initial doses or rapid increase in dose, Common with short-acting preparations
3. Ankle oedema: Due to a rise in intracapillary pressure as a result of selective dilatation of precapillary arterioles, NOT due to sodium retention, Relieved by bed rest
4. Gum Hypertrophy: dihydropyridines
5. GIT: constipation (verapamil), nausea, and vomiting Inhibitors of Angiotensin:Angiotensin converting enzyme inhibitors (ACEIs) | Captopril, enalapril, Ramipril, fosinopril, trandopril | Angiotensin receptor blockers (ARBs) | Losartan, valsartan, telmisartan, irbesartan, candesartan | Renin-inhibitors | Aliskiren |
Inhibitors of Angiotensin:Adverse Effects
ACEIs =
Dry cough
Can cause hyperkalemia – potassium monitoring essential
Angioedema (substance P?)
ARBs =
No dry cough
Hyperkalemia
Angiodema is less common than ACEIs
Contraindicated in pregnancy Combination Treatment: Vasodilators:
| | Management Approach:First-line agents: “ACD” drugs:
- A: ACEIs and ARBs
- C: Calcium channel antagonists
- D: Diuretics (Thiazides)
Second-line agents:
- Beta-adrenoceptor blockers
- Aldosterone antagonists (spironolactone, eplerenone)
- Alpha-blockers (doxazosin, prazosin, terazosin)
- Loop diuretics (frusemide, torsemide)
- Direct vasodilators (hydralazine, minoxidil) [last-line of therapy]
- Central α-2 agonists (clonidine)
- Adrenergic antagonists (reserpine) |
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