Vasodilator Lecture

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Information about Vasodilator Lecture

Published on February 23, 2008

Author: guest9bc2b8

Source: slideshare.net

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Vasodilator Lecture

Drugs Used In the Treatment of Congestive Heart Failure(Cont)

 

 BLOCKERS AT 1 BLOCKERS

DETERMINANTS OF VENTRICULAR FUNCTION STROKE VOLUME PRELOAD CONTRACTILITY CARDIAC OUTPUT HEART RATE AFTERLOAD - Synergistic LV contraction - LV wall integrity - Valvular competence

 

 

 

 

Venous Vasodilatation MIXED  -adrenergic Blockers ACEI Angiotensin II inhibitors K + channel activators Nitroprusside VENOUS Nitrates Molsidomine ARTERIAL Minoxidil Hydralazin VASODILATORS CLASSIFICATION Arterial Vasodilatation

1- VENOUS VASODILATATION Preload 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others Pulmonary congestion Ventricular size Vent. Wall stress MVO 2 NITRATES HEMODYNAMIC EFFECTS • Cardiac output • Blood pressure

 

 

Placebo Enalapril 12 11 10 9 8 7 6 5 PROBABILITY OF DEATH MONTHS 0.1 0.8 0 0.2 0.3 0.7 0.4 0.5 0.6 p< 0.001 p< 0.002 CONSENSUS N Engl J Med 1987;316:1429 ACEI SURVIVAL 4 3 2 1 0

VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ ACEI MECHANISM OF ACTION A.C.E.

ACEI HEMODYNAMIC EFFECTS Arteriovenous Vasodilatation - PCWP and LVEDP - SVR and BP - CO and exercise tolerance No change in HR / contractility MVO 2 Renal, coronary and cerebral flow Diuresis and natriuresis

ACEI ADVANTAGES Inhibit LV remodeling post-MI Modify the progression of chronic CHF - Survival - Hospitalizations - Improve the quality of life In contrast to others vasodilators, do not produce neurohormonal activation or reflex tachycardia Tolerance to its effects does not develop

Inhibit LV remodeling post-MI

Modify the progression of chronic CHF

- Survival

- Hospitalizations

- Improve the quality of life

In contrast to others vasodilators, do not produce neurohormonal activation or reflex tachycardia

Tolerance to its effects does not develop

ACEI UNDESIRABLE EFFECTS Inherent in their mechanism of action - Hypotension - Hyperkalemia - Angioneurotic edema Due to their chemical structure - Cutaneous eruptions - Neutropenia, thrombocytopenia - Digestive upset - Dry cough - Renal Insuff. - Dysgeusia - Proteinuria

ANGIOTENSIN II INHIBITORS MECHANISM OF ACTION RENIN Angiotensinogen Angiotensin I ANGIOTENSIN II ACE Other paths Vasoconstriction Proliferative Action Vasodilatation Antiproliferative Action AT1 AT2 AT1 RECEPTOR BLOCKERS RECEPTORS

AT1 RECEPTOR BLOCKERS DRUGS Losartan Valsartan Irbersartan Candesartan Competitive and selective blocking of AT1 receptors

0.6 PROBABILITY OF DEATH 0 Placebo (273) Prazosin (183) Hz + ISDN (186) MONTHS 0.7 0.5 0.3 0.4 0.2 0.1 VHefT-1 N Engl J Med 1986;314:1547 NITRATES SURVIVAL 0 6 12 18 24 30 36 42

 

 

CARDIAC GLYCOSIDES SYMPATHOMIMETICS Catecholamines ß-adrenergic agonists PHOSPHODIESTERASE INHIBITORS Amrinone Enoximone Others Milrinone Piroximone POSITIVE INOTROPES

CARDIAC GLYCOSIDES

SYMPATHOMIMETICS

Catecholamines

ß-adrenergic agonists

PHOSPHODIESTERASE INHIBITORS

Amrinone

Enoximone

Others

 

 

Inamrine&Mirinone

3. Nesiritide:  natriuretic peptide a. New treatment for acute congestive heart failure and dyspnea at rest

 

 

 

 

 

ß-ADRENERGIC BLOCKERS INDICATIONS and UTILIZATION Not clearly established Begin with very low doses Slow augmentation of dose Slow withdrawal ?

ß-ADRENERGIC BLOCKERS POSSIBLE BENEFICIAL EFFECTS  Density of ß 1 receptors Inhibit cardiotoxicity of catecholamines  Neurohormonal  activation  HR Antihypertensive and antianginal Antiarrhythmic Antioxidant Antiproliferative

ALDOSTERONE Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Collagen deposition Fibrosis - myocardium - vessels Spironolactone Edema Arrhythmias Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) ALDOSTERONE INHIBITORS

 BLOCKERS AT 1 BLOCKERS

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