Download Free Medical Congestive Heart Failure PowerPoint Presentation

Congestive Heart Failure PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : CHF occurs when the cardiac output (CO) is inadequate to provide the oxygen needed by the body. It is a highly lethal condition, with a 5-year mortality rate conventionally said to be about 50%. The most common causes include Coronary artery disease (CAD) and hypertension.

Tags : Congestive Heart Failure, CHF

Published on : Nov 06, 2020 | Views : 19705 | Downloads : 203

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Congestive Heart Failure 1 Dr. Mohammed Samir Hussein BCs of Pharmaceutical Science MDs of Clinical Pharmacology
Slide 2-

Congestive Heart Failure (CHF) Definition: CHF occurs when cardiac output (CO) is inadequate to provide the oxygen needed by the body. It is a highly lethal condition, with a 5-year mortality rate conventionally said to be about 50%. The most common causes: Coronary artery disease (CAD), with hypertension. 2
Slide 3-

Heart Failure: Causes Cardiac defect Myocardial infarction Valvular disease Congenital heart disease Defect outside the heart Coronary artery disease Hypertension Diabetes 3
Slide 4-

Pathophysiology of CHF 4 Increased Load ↑ After load ↑Preload ↑ Blood Volume Decreased COP ↓ Contractility ↓ Stroke Volume
Slide 5-

Compensatory Physiological Mechanisms in HF 1-Increased sympathetic activity (Baroreceptors) ↑ HR and ↑ force of contraction Vasoconstriction  ↑ venous return and preload  ↑ stroke volume ↑ Cardiac output (CO) 2-Activation of the renin-angiotensin-aldosterone system ↓CO ↓ renal blood flow ↑renin-angiotensin-aldosterone system ↑ PVR (afterload) & blood volume 3-Myocardial hypertrophy ↑The heart size, stretching of muscles and chambers dilates 5
Slide 6-

6 Compensatory Responses during CHF
Slide 7-

Symptoms of CHF 7 Dyspnea Fatigue Fluid retention Exercise intolerance
Slide 8-

Classification and treatment of CHF 8
Slide 9-

Heart Failure (HF) Treatment Goals (1) Reducing symptoms (2)slowing progression as much as possible during relatively stable periods and (3) To improve survival Increase cardiac contractility Decrease preload (left ventricular pressure) Decrease after load (systemic vascular resistance) Normalize heart rate and rhythm 9
Slide 10-

STRATEGIES TO TREAT CHF 10
Slide 11-

Diet and Activity 11 Salt restriction Fluid restriction Daily weight Gradual exertion programs
Slide 12-

Drugs used in CHF 12 Drugs improving force of cardiac Contractility (Positive Inotropic) Cardiac glycosides (Digoxin,Digitoxin) Phosphodiestrase inhibitors (Inamrinone) BetaI agonists(Dobutamine) Drugs improving compensatory stresses upon the cardiac performance Diuretics(Thiazides) Vasodilators (Diazoxide, Minoxidil) ACE Inhibitors(Captopril) Angiotensin II receptor inhibitor (Losartan, Candisartan) Beta-blockers (Atenolol,Propranolol)
Slide 13-

13
Slide 14-

Drugs improving force of cardiac Contractility (Positive Inotropic) Cardiac glycosides (Digoxin,Digitoxin) Phosphodiestrase inhibitors (Inamrinone) BetaI agonists(Dobutamine) 14
Slide 15-

CARDIAC GLYCOSIDES Originally obtained from Digitalis plant Digoxin is the prototype Pharmacological Effects: Stimulates myocardial contractility (+ve inotropic) Decrease rate of electrical conduction of the heart Result: reduced heart rate and improved cardiac efficiency Improves ventricular emptying Increase cardiac output Promotes diuresis so lowers blood volume. Reduce cardiac size 15
Slide 16-

Mechanism of Action Inhibit Na +/K + -ATPase (Sodium pump) Increase of intracellular sodium concentration reduction of calcium expulsion from the cell by the sodium-calcium exchanger distinctive increase in cardiac contractility 16
Slide 17-

Digitalis 17
Slide 18-

Cardiac Glycosides: Indications 18 indicated in patients with heart failure and atrial fibrillation. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms.
Slide 19-

Cardiac Glycosides: Adverse Effects 19 Digoxin (Lanoxin) Very narrow therapeutic window (Drug levels must be monitored) Low potassium levels increase its toxicity Electrolyte levels must be monitored Cardiovascular Dysrhythmias, including bradycardia or tachycardia CNS Headaches, fatigue, malaise, confusion, convulsions Eye Colored vision (seeing green, yellow, purple), blurred vision, flickering lights GIT Anorexia, nausea, vomiting, diarrhea
Slide 20-

Conditions That Predisposing to Digoxin Toxicity 20 Hypokalemia Hepatic dysfunction Hypercalcemia Dysrhythmias Advanced age Treatment: Digoxin Immune Fab (Digibind) therapy
Slide 21-

OTHER POSITIVE INOTROPIC DRUGS 21
Slide 22-

PHOSPHODIESTRASE ENZYME INHIBITORS Inamrinone and Milrinone Used in acute or refractory HF Given when patient has not responded to treatment with digoxin, diuretics, and/or vasodilators Short-term management of heart failure Improve quality of life Decrease remissions for heart failure episodes MOA: - Selectively inhibits phosphodiesterase (PDE) III (enzyme that catalyzes the breakdown of cAMP) increased cAMP - Increased intracellular calcium concentration and myocardial contractility 22
Slide 23-

BETA-ADRENOCEPTOR AGONISTS Dobutamine (parenteral): The selective β1 agonist (Chronic) Widely used agent in patients with heart failure. Given by IV infusion Dopamine (Non selective ẞ1, ɑ1 ) has also been used in HF (acute) particularly when BP need to raise. MOA Increase cAMP thus causing positive inotropic effect and vasodilation leading to improved cardiac performance. Adverse Effects: Tachycardia ---- arrhythmias Increase in myocardial oxygen consumption ---- angina 23
Slide 24-

Drugs improving compensatory stresses upon the cardiac performance 24 DIURETICS ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS ANGIOTENSIN RECEPTOR BLOCKERS VASODILATORS BETA-ADRENOCEPTOR BLOCKERS
Slide 25-

Diuretics The most effective symptomatic relief (dyspnea) in Heart Failure Relieve pulmonary congestion and peripheral edema Do not improve survival in HF 25 ↓ Plasma Volume ↓ Venous Return (↓ Preload) ↓ Blood Pressure (↓ Afterload)
Slide 26-

LOOP Diuretics Furosemide, Bumetanide, Torsemide A drug of choice in CHF No direct effect on cardiac contractility MOA : Na-K-Cl transporter Inhibitors This results in reduction of salt and water retention and edema and its symptoms. The reduction of cardiac size, which leads to improved pump efficiency, is of major importance in systolic failure. Overdose can induce hypovolemia 26
Slide 27-

Potassium Sparing Diuretics… Spironolactone and Eplerenone Have the additional benefit of decreasing morbidity and mortality in patients with severe HF who also receiving ACE inhibitors and other standard therapy. One possible mechanism is to antagonize aldosterone action Aldosterone cause myocardial and vascular fibrosis and baroreceptor dysfunction 27
Slide 28-

ACE Inhibitors Example: Captopril Reduce total peripheral resistance Reduce sodium water retention by inhibiting aldosterone Reduce blood volume Reduce after load and some how preload Excellent drug for long term remodeling of heart and blood vessels Used in patients with left ventricular dysfunction but no edema 28
Slide 29-

Angiotensin AT 1 receptor blockers ARBs Losartan They should be considered in patients intolerant of ACE inhibitors because of incessant cough. In some trials, candesartan was beneficial when added to an ACE inhibitor. 29
Slide 30-

VASODILATORS Reduction of afterload ------ (Hydralazine) Arteriolar vasodilatation  reduce systemic arteriolar resistance Reduction of preload ------ (Nitrate) Venous dilation  ↓ the venous return ↓ the load on both ventricles. Usually the maximum benefit is achieved by using agents with both action. 30
Slide 31-

Nesiritide A Recombinant brain natriuretic peptide (BNP) Approved for use in acute (not chronic) HF It increases cGMP in smooth muscle cells and reduces venous and arteriolar tone It also causes diuresis & has short half-life of about 18 minutes Administered as a bolus IV dose followed by continuous infusion ADRs: Excessive hypotension & a significant renal damage and deaths It should be used with great caution 31 VASODILATORS
Slide 32-

Vasopressin Antagonists A small subset of patients in AHF have dilutional hyponatremia, due to increased vasopressin activity. Vasopressin Antagonists have a beneficial effect in some patients with acute heart failure and hyponatremia. Examples Conivaptan, V1a and V2 receptor antagonist Tolvaptan, V2 antagonists 32
Slide 33-

BETA-ADRENOCEPTOR BLOCKERS Bisoprolol, Carvedilol, Metoprolol, and Nebivolol Blocks beta I receptors on heart Relax cardiac muscle by reducing cardiac work Decreased heart rate Reduced remodeling 33
Slide 34-

Chronic Failure and Acute Failure: 34 Chronic Heart Failure (CHF): Typically observed in patients with dilated cardiomyopathy or multivalvular heart diseases that develops or progresses slowly Acute Heart Failure (AHF): Sudden development of a large myocardial infarction or rupture of a cardiac valve in a patient who previously was entirely well, usually predominant systolic dysfunction
Slide 35-

35 THANK YOU FOR YOUR ATTENTION