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Heart failure
Heart failure is defined as a structural or functional impairment of the heart that prevents it from maintaining an adequate blood supply to meet the body's needs. It can be caused by conditions that overload or damage the heart such as hypertension, heart attacks, and cardiomyopathy. Heart failure is classified as acute or chronic and as forward or backward based on its location and symptoms. While compensatory mechanisms initially help the heart function, long term they cause further damage and worsening of heart failure over time. Diagnosis involves tests like echocardiograms, EKGs and blood tests, and treatment focuses on diuretics, ACE inhibitors and beta blockers to manage symptoms and slow progression of the disease.
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Heart failure
- 1.
- 2. Definition • structural orfunctional CD • impairs the blood filling/ejecting ability of ventricles • inability to maintain the metabolic needs of the body
- 3. Causes Heart performance (CO) dependson: • Contractility • Preload • Afterload • Heart Rate Causes: • Abnormal loading conditions • Abnormal muscle function • Conditions that limit ventricular filling Congenital defects Valvular heart diseases Septal defects Hypertension Myocardial infarction Myocarditis Cardiomyopathy Alcoholism Mitral or tricuspid stenosis Pericarditis Ischaemic heart disease Drugs Thyrotoxicosis CO = SV x HR
- 4. Classifications Backward Failure ForwardFailure High Output Low Output RSHF LSHF
- 5. Acute vs. Chronic Acute •Develops rapidly • Can be immediately life threatening • Dramatic drop in cardiac output • May be new (e.g. acute MI, sepsis) or an exacerbation of chronic disease Chronic • Long term • More insidious • Associated with the heart undergoing adaptive responses (e.g. dilation, hypetrophy) to a precipitating cause
- 7. Symptoms • Fatigue • Activitydecrease • Cough (especially supine) • Edema • Shortness of breath
- 8. Symptoms RVF – Fatigue – Weakness –Lethargy – Weight gain – Anorexia – RUQ pain – Hepatomegaly – Neck vein pulsations – Jugular veinous distension – Pitting edema LVF – Fatigue – Anxiety – Insomnia – Tachycardia – Gallop heart sounds (S3, S4) – Pulmonary crackles, rales – Orthopnea PND – Cheyne Stokes – Cough
- 9. Pathophysiology Compensatory mechanism: 1. Hemodynamicalterations 2. Neurohormonal responses (SNS, RAAS, Vasopressin) 3. Ventricular dilation 4. Ventricular hypertrophy
- 10. Response Short-Term Effects Long-Term Effects Salt andWater Retention Augments preload Pulmonary Congestion, Anasarca Vasoconstriction Maintains BP for perfusion of vital organs Exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure Simpathetic stimulation Increases HR and ejection Increases energy expenditure
- 11. Frank-Starling Mechanism • Theability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. • In heart failure, there is a compensatory increase in venous return which is augmented by neurohormonal mechanisms. • Due to increase in venous return, there is a temporary increase in stroke volume.
- 12. Diagnostic Studies • X-ray(Kerley B lines) • ECG • Echocardiography (EF) • Laboratory data (cardiac enzymes, BNP, serum chemistries ,liver function studies ,thyroid function studies and complete blood count) • Stress testing (exercise or medicine) • Cardiac catheterization- determine heart pressures ( inc.PAW )
- 13. ECG ECG findings arenot diagnostic, but: • Old MI or recent MI • Arrhythmia • Some forms of tachycardia related cardiomyopathies • LBBB
- 14. Approach to thePatient with HF • Diagnose – Etiology – Severity (LV dysfunction) • Initiate – Diuretic/ACE inhibitor – -blocker – Spirololactone – Digoxin • Educate – Diet – Exercise – Lifestyle – CV Risk • Titrate – Optimize ACE inhibitor – Optimize -blocker