The Pathophysiology of Congestive Heart Failure

Legend: Manifested by JC Applied Intervention

PREDISPOSING FACTORS Age (Over 65 years old) Sex (Both Sexes) Genetics

PRECIPATIONG FACTORS Hyperthyroidism Hypertension Diabetes Mellitus Dyslipidemia Obesity Cardiovascular Disease Myocardial Infarction Valvular Disease Arrhythmias

It decreases myocardial contractions and filling Myocardial Dysfunction

Systemic Heart Failure Decrease blood volume ejected from the ventricle Activation of Baroreceptors in the Aortic and Carotid Bodies

Diastolic Heart Failure

Develop as result of continuous decrease of heart workload

Ventricular Hyperthrophy and altered cellular functioning Resistance to Ventricular Filling

Sympathetic Nervous System Stimulated

Release of Epinephrine and nonEpinephrine Vasoconstriction of the Skin Vasoconstriction of Gastrointestinal Tract Vasoconstriction of the kidneys Activates Renin-angiotensinaldosterone system

Decrease ventricular filling pressures despite of a normal or reduced blood volume Less Blood in the Ventricle Low cardiac output Cause some neurohormonal response described in systolic heart failure

Renin

Angiotensin

Angiotensin converting Enzyme (Lungs) Angiotensin II

Stimulates release of Aldosterone from Adrenal Cortex

Sodium and fluid retention by the Renal Tubules Fluid Volume Overload Increase Stress on Ventricular wall

Increase Work Load of the Heart Release of counter regulatory mechanism through the release of Natriuretic Peptides (ANP) and (BNP) Heart workload Increase

Contraction of myocardial muscle fiber decreases Increase end-diastolic blood volume in the ventricle Ventricular Dilation Further increase in the stress in the ventricular wall Additional increase workload of the heart To compensate, it increases the thickness of heart muscles Ventricular Hypertrophy Proliferate abnormal myocardial cells

Ventricular Remodeling

Clinical Manifestations

Left-sided Heart Failure

Right-sided Heart Failure

Increase left ventricular and diastolic blood volume

Cannot exert blood and cannot accommodate all the blood that normally returns to it from venous circulation

Increase blood flow from left atrium and left ventricle during diastole Increase blood volume and pressure on the left atrium Increase blood flow from the pulmonary vessels Congestion of the Peripheral Tissues and the Viscera Increase venous pressure

Jugular vein distention and increase hydrostatic pressure through venous system

Increase pulmonary venous blood volume and pressure

Pulmonary Congestion

Signs and Symptoms: Dyspnea on Exertion Cough ( Dry non-productive) Pulmonary Crackles (Bibasilar) Decrease Oxygen Saturation S3 Gallop Auscultated Fatigue

Systemic Clinical Manifestations: Dependent Edema Hepatomegaly Ascites Anorexia Nausea Weight Gain

Without intervention Heart does not pump sufficient blood in the body Surgical Management: Coronary Bypass Surgery PTCA Innovative Therapies (e.g. mechanical assistive devices, Transplantation Nutritional Management Low Sodium Intake Fluid Restriction

With Intervention Early Assessment of Ventricular Functioning and Performing Diagnostic Procedures: Electrocardiogram Echocardiogram (Ejection Fraction) Exercise testing to detect CAD Laboratory Studies (Blood, Urea nitrogen, creatinine, CBC, thyroid stimulating hormone, urinalysis)

Stimulates the heart to work harder Heart cannot respond Heart failure worsen Bad Prognosis

Death

Medical Management: Ace Inhibitors (Lisinopril) (ARBs) Angiotensin II Receptor Beta Blockers (Carvedilol) Calcium Channel Blockers Diuretics (Lasix) Digitalis antihypertensive Anticoagulant (Warfarin) Antilypidemic ( Simvastatin)

Promotes vasodilation and diuresis

Reducing systemic vascular resistance

Reducing Afterload and Preload

Diminishing hearts work load Preventing exacerbation of heart failure

Good Prognosis