CONGESTED HEART FAILURE

Congested heart failure is a clinical syndrome described as the inability of the heart to pump enough oxygenated blood to meet the bodys demands (a decrease in cardiac output - CO).

Causes Weakened heart muscle Incompetent heart valves Atherosclerosis Acute MI Substance abuse (especially cocaine & alcohol) Infection Hypertension Pericardial effusion Congenital heart disease Prolonged serous arrhythmias

These causes can occur independently or in combination.

Clinical Manifestations The condition is marked by shortness of breath, oedema, poor tissue perfusion, circulatory congestion, pulmonary oedema, jugular vein distension, and liver congestion. Abnormal sodium levels and fluid overload are also present.

Pathophysiology When congested heart failure occurs there is a drop in CO and the SNS is stimulated. The catecholamines produced (norepinephrine/noradrenaline) activate the following compensatory measures in an attempt to he increase venous return to the heart: Increase heart rate Increase force of contraction Vasoconstriction Increase preload Increase afterload

Increase peripheral resistance

In addition to an increase in sympathetic activity, the kidneys also attempt to compensate for the initial decrease in CO. They do so by decreasing renal perfusion and activating the reninangiotensin-aldosterone-system (RAAS). When RAAS is activated, the following compensatory process begins: a. Angiotensin 11 and aldosterone are released and this leads to Na+ retention and vasoconstriction. b. This activates the release and increase of the anti-diuretic hormone (ADH). c. The release of ADH causes the kidneys to reabsorb more H2O. d. The combination of increased Na+ and H2O leads to further increase in preload. In both acute and chronic heart failure, these initial compensatory mechanisms eventually become counter-productive and maladaptive. When either the R/L ventricle loses the ability to handle the increase preload, there is a backup of fluid. If the L ventricle is involved, the fluid back-up reaches the lungs and causes symptoms such as: Shortness of breath Dyspnea on exertion Orthopnea Paroxysmal nocturnal dyspnea pulmonary oedema is present.

If the R ventricle is involved, the fluid backs up into the systemic circulation and produces symptoms such as: Jugular vein distension Hepatomegaly Ascites (abdomen oedema) Anorexia Increased central venous pressure (CVP) Peripheral oedema Anasarca (generalized oedema) is a possibility

CLASSIFICATION OF HEART FAILURE Classification 1 Systolic Failure -ejection fraction (amt. of blood the heart pumps out) < 35%-40%, best treated by Ace (Angiotensin converting enzyme) inhibitorse.g. Cataprel. Ace inhibitors attack RAAS preventing Na+ & H2O retention. -Beta blockerse.g. Coregare given to decrease the heart rate. -Diureticse.g. Lasixare given to reduce the amount of fluid. The above combination of medication is called the Gold Standard If the client remains symptomatic.. -Cardiac glycosidee.g. Digoxinis added to slow the heart rate and strengthen contractions. Classification 2 L ventricular Failure -capillary refill >3 sec -orthopnea -dyspnea on exertion -nocturnal dyspnea -cough with frothy sputum (indicative of pulmonary oedema) -tachypnea -diaphoresis -bascular crackles (crackles heard at the base of the lungs) or rhonchi -cyanosis -acidosis (because of increased CO2) -increased pulmonary artery pressure -S3 & S4 heart sounds -nocturia -confusion -weight gain -fatigue -enlarged L ventricle and atrium on chest x-ray -narrowing pulse pressure -pulsus alterans (alternating weak & strong pulse)

Diastolic Failure The right ventricle is resistant to filling, therefore stroke volume is decreased. Management includes managing - BP - Heart rate - Fluid overload Ace inhibitors, Beta blockers, & Calcium Antagonists (Ca+ channel blockers)

R ventricular Failure -Hepatomegaly -Splenomegaly -Abdominal distension -Pitting oedema of the legs -Venous distension -Oliguria (decreased amount of urine produced) -Arrhythmias -Increase CVP -Narrowing pulse pressure -S3 & S4 heart sounds -Kussmauls sign a paradoxic rise in venous pressure with distension of the jugular veins during inspiration.

-Fatigue -Abdominal pain due to -Ascites -Anorexia -Enlarged R ventricle & atrium on x-ray -Weight gain

Investigative Procedures Blood test for cardiac enzymes ABG ESR (Erythrocyte Sediment Rate) decreases in heart failure; increases for infection Creatinin levels Chest x-ray Echocardiogram ECG Cardiac catheterization may be necessary