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By: yessabel (85 month(s) ago)

VERY good presentation..i wish i could have this for my presentation...thank you

By: mufidah (88 month(s) ago)

interactive. I wish i can have this slide

By: mufidah (88 month(s) ago)

interactive. I wish i can have this slide

By: jeddahlyn (91 month(s) ago)

can i have thisCHF presentation for my report.?thank u so mucH....

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very good

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Presentation Transcript



Congestive heart failure : : 

Congestive heart failure : It is the state that develops when heart cannot maintain an adequate cardiac output/ can do so only at the expense of an elevated filling pressure. CARDIAC OUTPUT : Cardiac output is a function of preload(the volume & pressure of blood in ventricles & the end of diastole) the after load (the arterial resistance) & myocardial contractility.

Structure of heart :- : 

Structure of heart :-

Innervations of nerves :- : 

Innervations of nerves :-

etiology :- : 

etiology :- It is a common end point for many disease of cardiovascular system. It can be caused by : Inappropriate work load (volume or pressure overload) Restricted filling Myocyte loss


PATHOPHYSIOLOGY :- Hemodynamic changes Neurohormonal changes Cellular changes

Slide 8: 

Impaired ventricular function Heart failure Neuroharmonal activation Sympathetic activation Renin-angiotensin-aldosterone activation Vasoconstriction. Sodium & fluid retention. Increased preload & after load Further stress on ventricular wall and dilatation leading to deterioration of ventricular function. Further heart failure




CELLULAR CHANGES :- Changes in adrenergic receptors: •Slight  in α1 receptors •β1 receptor desensitization followed by down regulation Changes in contractile proteins Program cell death(Apoptosis) Increase amount of fibrous tissue

Types of heart failure : 

Types of heart failure Acute & chronic heart failure. Left, Right & Biventricular heart failure. Forward & Backward heart failure. Diastolic & systolic dysfunction. High output failure.

Clinical features :- : 

Clinical features :- The clinical picture depends on the nature of the underlying heart disease, the type of heart failure that it has evoked, and the neural and endocrine changes it has developed. A low cardiac output causes fatigue, listleness and poor effort tolerance. Poor renal perfusion may lead to oliguria and uraemia. Pulmonary oedema due to left heart failure may present with breathlessness, orthopnea, paroxysmal nocturnal dyspnoea and inspiratory crepitations over the lung bases. In contrast, right heart failure produces high jugular venous pressure, with hepatic congestion and dependent peripheral oedema. Chronic heart failure is some times associated with marked weight loss caused by a combination of anorexia and impaired absorption due to gastrointestinal congestion. Poor tissue perfusion due to low cardiac output; and skeletal muscle atrophy due to immobility.

Complications :- : 

Complications :- In advanced heart failure a number of non-specific complications occur. Uraemia. Hypokalaemia. Hyperkalameia. Hyponatraemia. Impaired liver function. Thromboembolism.

Management of heart failure :- : 

Management of heart failure :- GENERAL MEASURES : Effective education of patients and their relatives about the causes and treatment of heart failure Education Diet Alcohol Smoking Exercise Vaccination In patients with coronary heart disease secondary preventive measures such low dose of aspirin and lipid lowering therapy is appropriate.

Management of heart failure :- : 

Management of heart failure :- DRUG THERAPY :- Cardiac function can be improved by increasing contractility, optimizing preload or decreasing after load etc., by using.. Diuretics. Vasodilators. Angiotensin-converting enzyme (ACE) inhibitors. Angiotensin II receptor antagonists. Beta-adrenoreceptor antagonists.

Neuroharmonal activation and sites of action of drugs used in treatment of heart failure : 

Neuroharmonal activation and sites of action of drugs used in treatment of heart failure Angiotensinogen Renin Bradykinin Nitrous oxide Non- prostaglandin ACE Angiotensin I path- angiotensin ways converting in active Vasodilation Angiotensin II enzyme peptides Aldosterone Vasoconstriction Enhanced sympathetic Salt & water activity retention Β-blocker diuretic spironolactone ACE Inhibitors

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