Lecture 15-Heart Pathology I
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40 terms
Terms | Definitions |
|---|---|
What are four types of congestive heart failure? | 1. Systolic Dysfunction2. Diastolic Dysfunction 3.Valve Disease 4.High Demand Failure |
Charactierized by progressive pump failure. Deteriorating myocardial contractile fxn-IHD and HTN. | Systolic Dysfunction |
Diastolic Dysfunction | myocardium cannot relax (cannot fill). females with HTN.DM. |
High Output Failure | -metabolic demand exceeds output-can be caused by hyperthyroidism or anemia |
2 conditions under which cardiac dysfunction occurs... | 1. when the heart cannot generate sufficient output to meet the metabolic demands of tissue2. heart can only meet metabolic demands at ELEVATED FILLING PRESSURES (starlings law) |
2 effects of elevated filling pressure | 1. elevated cvp...higher volumes filling ventricle2. dilated ventricle...greater stretch |
Heart can no longer pump the blood delivered to it by venous circulation. 2 outcomes: | 1. forward failure- inadequate cardiac output2.backward failure-increased congestion of venous circulation |
Pathogenesis of Heart Failure | LV myocardium fails> EDV increased> ED pressure increased>increased venous pressure causes elevated CVP,& pulmonary/systemic Venous pooling |
Decreased CO from CHF leads to: | -diminished tissue perfusion-CO2 builds up in tissues -hypoxia in tissues -acidosis (H+) build up in tissues |
Compensatory Mechanisms to make up for decreased perfusion | -Frank-Starling Mechanism-Activation of Neuro-hormonal axis -Myocardial Hypertrophy (these methods further disease cycle) |
Frank-Starling Compensation Mechanism | -Increased EDV dilates the hear, stretches cardiac myocytes, and increases CO-increases demand for O2 |
Decompensation and Frank-Starling | -eventually overstreches CO falls anyway-congestion results (elevated venous pressures) -symptoms develop |
2 neuro-hormornal axis compensatory mechanisms | 1. Symp Stim2. Renin Angiotensin |
Sympathetic Stimulation | Noepinephrine release- increased contractility and increased heart rate |
Renin-Angiotensin | -renin release-salt and water retention -increased volume elevates preload and results in higher filling pressures |
2 Myocardial Changes to comp. for CHF | 1) Compensatory Dilation- dilated cardiomyopathy, new sarcomeres added2) Compensatory Hypertrophy- thickened ventricle *both changes require more O2 and are vulnerable to ischemia |
-occurs in hypertension-monocyte enlargement -higher O2 demands -poor capillary perfusion relative to thickness | hypertrophy |
2 types of hypertrophy | 1. pathologic comp.2. aerobic/physiologic comp. |
Hypertrophy: Pathologic Compensation | -increased mortality-poor capillary density relative to thickness -poor perfusion -high O2 demand |
Hypertrophy: Aerobic/Physiologic Compensation | -volume related hypertrophy-regular aerobic exercise -increased capillary density -decreased HR -decreased BP -reduced overall morbidity and mortality |
Left Sided CHF | -predominate-high EDV in LV -backs up in lung-pulmonary venous cirulation-elevated PCWP -Fluid spills into lung tissue-pulmonary edema |
Causes of Left Sided CHF | -IHD (AMI)-Chronic HTN -Malignant HTN -Aortic or Mitral Dz -Cardiomyopathy -Myocarditis |
Symptoms of Pulmonary Edema | -Dyspnea (SOB)-exertional,cough, at rest-Orthopnea-SOB supine, increases venous return -Paraoxysmal Nocturnal Dysnea-suffocation at night -Pulmonary Edema |
Left-Sided Heart Failure (LONG) | pumping efficiency failure>chambers fail to empty completelyat systole and dilate>progressive rise is pressure> back up into chamber or vessels preceding it in the circulation> LA dilates>dilation and increase in pressure in pulmonary veins>increase in pressure in pulmonary capillaries> fluid component of blood in alveolar air sacs (pulmonary edema) |
__________ ____________ leads to acute breathlessness due to fluid in air sacs | pulmonary edema |
Left sided Heart Failure causes insufficient blood to be pumped into the aorta and arterial system..... | hypotension, poor perfusin of tissue, and poor oxygenation |
cyanosis, fatigue, exertional dyspnea,tachycaria, orthopnea, confusion, restlessness, pulonmary congestion (cough, crackeles, wheezes, blood in sputum), elevated pulmonary capillary wedge pressure, paraoxysmal dyspnea | Symp of Left sided hF |
#1 cause of R sided HF | left side heart failure |
____________ ____________ is an enlargement of the right ventricle due to high blood pressure in the lungs usually caused by chronic lung disease. | Cor pulmonale (right sided heart failure) |
Clinical presentation of right sided CHF | -few if any respiratory symptoms-peripheral edema -liver (hepatic) congestion -ascites -high CVP and Venous Congestions b/c compliance of venous system has capacity to become engorged with excess volume |
What is right-sided CHF? | severe pulmonary hypertension, dilated and hypertrophic RV |
What causes right-sided CHF? | pulmonic stenosis, tricuspid regurgitation |
dependent edema, weight gain, anorexia, complaints of gi distress, distedned jug. vein, secondary to chronic pulmonary problems, enlarged liver and spleen, ascites, increased peripheral venous pressure, fatigue | right sided heart failure |
dilated tortuous veins | varicose veins |
what causes varicose veins? | -prolonged increase in intraluminal pressure-dependent for long periods -10x normal pressure -valves incompetent: stasis, congestion, edema, thrombosis |
varicose veins can lead to... | -venous stasis dermatitis-ischemic changes, ulcerations, edema, poor would healing-embolism but rarely bc with superfical veins embolism isn't really a concern |
Deep Vein Thrombosis Risk Factors | CHFneoplasia pregnancy obesity post op immobilization |
Triangle Leading to Deep Vein Thrombosis | venous stasishypercoagulation vessel injury |
What is DVT? | -deep leg veins responsible for 95% if thrombophlebitis-thrombus can move to emoblism |
Superior Vena Cava Syndrome | -tumor obstructs SVC-distention and increase pressure in jugular vein, subclavian vein, axillary vein -swelling and distention of head, neck and right arm -cyanosis, dyspnea |
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