HEART FAILURE by Nancy Jenkins,The most common reason for hospitalization in adults 65 years old. 1 in 100 adults has HF,heart failure,Mild,Mild,Drugs Diet Fluid Restriction,Heart Failure,Uncompensated Heart Failure Pulmonary Edema-ADHF,Severe End Stage,Cardiogenic shock Cardiomyopathy,IrreversibleNeeds new ventricleVAD IABP,VAD IABP Heart Transplant,Control With,/Same as Mild with Morphine Sulfate,Heart Failure Pneumonic,U Upright Position N Nitrates L Lasix O Oxygen A Amiodorone, ACE, ARBs D Dig, Dobutamine M Morphine Sulfate E Extremities Up or Down,Definition Of Heart Failure,CO=SVxHR is insufficient to meet the metabolic needs of the body SV is determined by preload, afterload and myocardial contractility Systolic failure- dec. contractility Diastolic failure- dec. filling EF 40%,Heart Failure- Types Systolic versus Diastolic,Systolic failure is the most common cause ”poor pump” *Hallmark finding: Decrease in the left ventricular ejection fraction (EF) 40% Caused by Impaired contractility (e.g., MI) Increased afterload (e.g., hypertension) Cardiomyopathy Mechanical abnormalities (e.g., valve disease),http:/coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module15/Part02/M15L04S41a.html?hostType=undefined&authorName=Mccance&prodType=undefined,hypokinesis,EF- the % of total ventricular filling volume that is ejected during systole. EF- 55-65 normal90/140= 64%,Heart Failure Diastolic,Diastolic failure-”poor filling” stiff ventricles Impaired ability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and CO Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, normal ejection fraction (EF),diastolic failure,Heart Failure,Mixed systolic and diastolic failure Seen in disease states such as dilated cardiomyopathy (DCM) Poor EFs (35%) High pulmonary pressures Biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity),Your patient has a normal EF but shows signs of heart failure. Your patient most likely has:,Decreased cardiac output Systolic failure Diastolic failure LV hypertrophy,How the Body Responds:,Remember, a decrease in stroke volume leads to a decrease in cardiac output. Body attempts to increase cardiac output: Sympathetic Nervous System Neurohormonal Response Dilation of chambers of the heart Hypertrophy Natriuretic peptides,The Bodys Response:,Sympathetic Nervous System: Release of catecholamines (epinephrine and norepinephrine) Causes increased heart rate & increased contractilityWhat does this do to the workload on heart? What does this do to O2 need of the heart? What meds could we give to decrease this release?,The Body Responds (Contd):,Neurohormonal Response: As CO decreases, blood flow to kidneys _: Causes activation of (RAAS) RAAS causes _ & _ retention, peripheral vasoconstriction, increased BPLow CO decreases cerebral perfusion pressure: Posterior pituitary secretes more antidiuretic hormone (ADH) ADH causes more retention of _ & production of endothelin. Endothelin causes arterial vasocontriction & increased contractility of heart muscle,The Body Responds (Contd):,Neurohormal Response (Contd): Due to various types of cardiac injury (ie. MI), proinflammatory cytokines are released. Cause cardiac hypertrophy, pumping dysfunction, and death of cells in the heart muscle Over time, this process can lead to a systemic inflammatory response that further damages the heart,The Body Responds (Contd):,Hypertrophy: Increase in _ of heart Increases contractility at first However, hypertrophic muscle doesnt work as well, needs more _, greater risk for rhythm problems, and has poor circulation,The Body Responds (Contd):,Dilation: Chambers of the heart get larger Increase in stretch of muscle fibers due to increase in blood volume The greater the stretch, the greater the force of contraction (_ Law) Initially, causes increase in cardiac output. After time, muscle fibers are overstretched and contraction decreases .CHF,The Body Responds,Counter regulatory processes- these help protect the heart Natriuretic peptides: atrial natriuretic peptide (ANP) released with cardiac muscle stretch and b-type natriuretic peptide (BNP) released with increased pressure of LV Released in response to increases in atrial volume and ventricular pressure Act opposite of RAAS and block effect Promote venous and arterial vasodilation, reducing preload and afterload Increase GFR Prolonged HF leads to a depletion of these factors- Natrecor can be used for same effects,Which of the following are compensatory mechanisms for HF?,Tachycardia Hypotension RAAS LV hypertrophy,Pathophysiology Structural Changes,Decreased contractility Increased preload (volume) Increased afterload (resistance) Ventricular remodeling(ACE inhibitors can prevent this) Ventricular hypertrophy Ventricular dilation,END RESULT,