Heart Failure
- 1. Heart Failure Prepared by: malek ahmad University of Malaya
- 2. Outline Definition and Epidemiology Pathophysiology Aetiological factors and Risk factors Clinic al manifestation Investigation Differential diagnosis Management and treatment Complication and prognosis
- 3. Definition • Inability in which heart cannot provide sufficient cardiac output to vital organ to satisfy the metabolic body needs or only can do so with filling pressure are higher than normal • Due to any structural or functional cardiac abnormalities • Can be divided to LVF , RVF • Always cause circulatory failure Epidemiology • Num 1 cause of hospitalization among Medicare patients • Cause more hospitalization than all form of cancer combined
- 6. Terms • Deterioration of myocardial contraction function Systolic dysfunction • Normal contraction but abnormal relaxation Diastolic dysfunction • Inadequate CO Forward failure • Congestion of venous system Backward failure • Low CO and fails to increase normally with exertion Low-output failure • Greatly increase tissue demands result to failure High-output failure • Dilated ventricle able to maintain CO at level that meets body needsCompensated HF • Dilated ventricle unable to maintain and propel sufficient blood at level that meets body needsDecompensated HF
- 8. Mechanism of adaptation • SNS>NA>Incrs HR, Incrs contractality, VasoC • Activation of RAAS • ANP>VasoD, natriuresis, diuresis Activation of neurohormonal system • Incrs EDV> Incrs EDP > muscle fibers strech > Incrs cardiac chamber V > contract more forcibly • However, incrs dilatation>incrs ventricular wall tension >incrs O2 demand Frank-starling mechanism (heamodynamic changes) • Pressure overload>incrs fiber diameter>concenteric hyperthrophy (incrs wall thckness w/o incrs chamber size) • Volume overload>incrs fiber length>eccenteric hyperthrophy>incrs heart size, incrs wall thickness Myocardial structural changes (cellular)
- 9. Aetiological causes • Structural abnormalities (congenital /acquired) that affect the circulation, pericardium, myocardium, valves. Underlying causes • Biochemical n physiological mechanism, increased (increased hemodynamic burden n reduce O2delivery) Fundamental causes Precipitating causes
- 10. Underlying causes • CAD , DM , HPT , VHD , arrythmias, infection n inflamation, conegital , drug induced , idiopathicSystolic heart failure • CAD , DM , HPT , VHD , hyperthropic cardiomyopathy, restrictive cardiomyopathy (amyloidosis) , pericarditisDiastolic heart failure • Acute MR/AR , MI , Myocarditis , arrythmias, drugs induced , sepsisAcute heart failure • Anemia, hyperthyroid, pagets, GN, multiple myoloma, carcinoid syndrome, polychaethemia vera High output heart failure • LVD , CAD , pulmonary HPT , PS , pulmonary embolism , chronic pulmonary disease , neuromuscular dsRight heart failure
- 11. Precipitating causes Recurrent or continued coronary ischaemia Recurrent myocardial infarction Hypokalaemia, hypomagnesaemia, hyperkalaemia Psychotropic drugs-for example, tricyclic antidepressants Digoxin (leading to toxicity) Antiarrhythmic drugs that may be cardiodepressant (negative inotropism) and proarrhythmic
- 12. Left heart failure IHD Systemic HPT Mitral/aortic valve disease Primary disease of myocardium Right heart failure LHF Pulmonary congestion Elevation of pulmonary arterial pressure •Intrinsic disease of lung parenchyma and/ or pulmonary vasculature (cor pulmonale) •Primary pulmonic/ tricuspid valve disease •Congenital-L to R shunt Isolated RHF
- 13. NYHA classification of HF •No limitation in physical activity despite presence of heart disease. This can be suspected only if there is a history of heart disease which is confirmed by investigations - for example, echocardiography Class I: asymptomatic •Slight limitation in physical activity. More strenuous activity causes shortness of breath - for example, walking on steep inclines and several flights of steps. Patients in this group can continue to have an almost normal lifestyle and employment Class II: mild •More marked limitation of activity which interferes with work. Walking on the flat produces symptoms Class III: moderate •Unable to carry out any physical activity without symptoms. Patients are breathless at rest and mostly houseboundClass IV: severe
- 14. Clinical manifestation Left Heart failure Dyspnoea Cough- fluid transudation onto airspace Orthopnoea-increase Venous Return PND Others-cadiomegaly,tachy,s3, fine rales (respiration thru edematous pulmonary alveoli, MR, systolic murmur, AF Right heart failure Systemic and portal venous congestion Hepatosplenomegaly Peripheral edema Pleural effusion Ascites
- 15. Differential diagnosis ARDS Cardiogenic shock COPD MI Pneumonia Pneumothorax Pulmonary edema / embolism Respiratory failure Emphysema
- 16. Framingham Systems major PND , neck vein distyensiom Rales, cardiomegaly S3 gallop, acute PE CVP greater than 16cm H2O Hepatojugular reflux PE, visceral congestion Weight loss 4.5 in 5d minor Bilateral ankle edema Nocturnal cough Dyspnoea on ordinary exertion tachycardia Pleural effusion To diagnose HF = 2major / 1major+2minor
- 17. Investigation • Established baselineFBC , electrolyte(K+) , RFT, LFT • Biomarker for heart failure and reflects the myocyte stretch and exclude other diagnosisBNP • Alveolar oedema, kerley B lines , cardiomegaly, dilated upper lobe vessels , pleural effusionCRX • Indicate the cause • Confirm the presence or absence of LV dysfunctionEcho • Indicate the cause, look sign of ischemia, MI , ventricular hyperthrophyECG
- 18. Management and treatment Acute heart failure Sit upright O2n 100% if no lung disease IV acces and monitor ECG treat arrythmia Ix and dimorphine , frusemide , GTN spray Necessary IX, history and examination Chronic heart failure Stop smoking, eat less salt, optimize weight n nutrition Treat cause (arrhythmia, valve disease) Treat exacerbating factor s(anemia , thyroid disease) Avoid exacerbating factors, NSAIDs • Diuretics- furosemide, spironolactone • ACE inhibitor – angitensin receptor blocker • B-blocker – carvedilol • Digoxin • Vasodilator - hydralazine Drugs
- 19. Complication • Unintentional rapid weight loss (a loss of at least 7.5% of normal weight within 6 months) Cardiac cachexia • Due to poor blood supply Impaired kidney function • Malabsorption • Hepatic congestion and dysfunction GIT • AF, ventricular arrhythmiasArrhythmias • Stroke, peripheral and pulmonary embolism, DVT, Thromboembolism Prognosis Better in asymptomatic left ventricular dysfunction than that in those whose left ventricular dysfunction is symptomatic. NYHA class, left ventricular ejection fraction, and neurohormonal status Dependent on severity, age, and sex, with a poorer prognosis in male patients
- 20. Predictor of poor prognosis High NYHA functional class Reduced left ventricular ejection fraction Raised plasma catecholamine and natriuretic peptide concentrations, Reduced sodium concentration Third heart sound Diabetes mellitus