I Heart Failure a Heart unable to maintain sufficient cardiac output to meet tissue metabolic demands Increasing incidence b c Most common reason for hospitalization in people over 65 years of age d Etiological factors i Cardiac disorders myocardial ischemia HT dilated cardiomyopathy e Pathogenesis i Impaired ability of myocardial fibers to contract systolic failure relax diastolic failure both ii Results in blood flow congestion in systemic pulmonary venous circulations f Compensatory Mechanisms i Restore cardiac output to normal ii Mechanisms Increased preload 1 SNS activation 2 3 Myocardial hypertrophy remodeling 4 Sympathetic nervous system activation a Due to baroreceptor reflex stimulation baroreceptors detect falls in blood pressure b CNS increases sympathetic nerve activity to the heart causing venoconstriction c Renal juxtaglomerular cells release renin to activate the RAAS cascade leading to increase Na and water retention a Due to reduced EF with resultant increase in residual ESV b Decreased CO to kidney will reduce glomerular filtration causing fluid conservation c Activates RAAS cascade leading to elevated blood 5 Increased preload 6 Myocardial hypertrophy and remodeling a Due to chronic elevation of myocardial wall volume pressure b High systolic pressure in the ventricle is needed to overcome a high afterload c Neurohormonal factors hypertrophy d Angiotensin II remodeling iii Detrimental to cardiac tissue in the long term 1 Current heart failure management is aimed at reducing long term effects g Clinical Manifestations i LV failure is most common ii Often leads to RV failure h Left Sided i Backward effects blood accumulates in pulmonary circulation 1 Pulmonary congestion dyspnea ii Forward effects insufficient CO with diminished oxygen and nutrient delivery to peripheral tissues and organs i Right Sided i Pulmonary disorders result in increased pulmonary vascular resistance This leads to high afterload and resultant right ventricular hypertrophy ii Backward effects congestion in systemic venous system iii Forward effects low output to left ventricle leads to low CO j Biventricular i Most often due to primary left sided HF which progresses to right sided HF ii Clinical manifestations iii Reduced CO iv Pulmonary congestion LHF v Systemic venous congestion RHF k Diagnosis of breath iv B type natriuretic peptide level v X ray and echocardiography l Treatment i Classification and staging ii According to symptom severity iii FACES fatigue activity limitation congestion edema shortness i Improve Co while minimizing congestive symptoms and cardiac workload 1 Decrease preload ii Reduce preload reduce intravascular volume 1 Diuretics ACE I iii Reduce afterload 1 blockers iv Increase contractility Digoxin 1 Digitalis other cardiac glycosides v Pacemakers synchronize ventricular contraction II Cardiac Dysrhythmia a Arrhythmia b Abnormal cardiac rhythm impulse generation or conduction c 3 major types i Abnormal sinus rhythm rates tachy brady ii Abnormal impulse generation sites ectopic sites iii Disturbed conduction pathways d Can indicate underlying pathophysiological disorders e Can impair CO f Treatment i When symptomatic or progressive ii Anti arrhythmic drugs can cayse arrhythmias too iii Increase CO pacemakers pro contractile drugs iv Ablation procedures get rid of other nodes to retain to normal PQRST v Heart Attack give patient nitroglycerin under the tongue vasodialate coronary arteries 1 Give aspirin blood thinner break up any small blood clots