heart failure final.. presentation medicine pptx

Medicine

1. HEART FAILURE Ref:DAVIDSON’S PRINCIPLES AND PRACTICE OF MEDICINE Abiya Thomas Adithya S Babu

2. CONTENTS DEFINITION TYPES CAUSES PATHOGENESIS CLINICAL ASSESSMENT COMPLICATIONS INVESTIGATIONS MANAGEMENT

3. HEART FAILURE Definition Heart failure describes the clinical syndrome that develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filling pressure.

4. mild to moderate heart failure = symptoms occur only when the metabolic demand increases during exercise and some other form of stress severe heart failure= symptoms may be present at rest

5. TYPES 1.LEFT HEART FAILURE left ventricular output and left atrial and pulmonary venous pressure Acute MI , Mitral stenosis 2.RIGHT HEART FAILURE right ventricular output and right atrial and systemic venous pressure Chronic lung disease, pulmonary embolism and pulmonary valvular stenosis 3.BIVENTRICULAR HEART FAILURE Both sides of heart are affected IHD or Dilated cardiomyopathy

6. CAUSES OF HEART FAILURE 1.Reduced ventricular contractility- MI , Myocarditis 2.Ventricular outflow obstruction(pressure overload)- . Hypertension, aortic stenosis (LHF);Pulmonary hypertension(RHF) 3.Ventricular inflow obstruction- Mitral stenosis, tricuspid stenosis

7. 4.volume overload- Left ventricular volume overload (mitral or aortic Regurgitation);Ventricular septal defect;Right ventricular volume overload (atrial septal defect);increased metabolic demand (high output)
5.Arrhythmia- Atrial fibrillation;Tachycardia;Complete heart block
6.Diastolic dysfunction- Constrictive pericarditis,Restrictive cardiomyopathy,Left ventricular hypertrophy and fibrosis; Cardiac tamponade .

8. PATHOGENESIS Cardiac output is determined by preload (the volume and pressure of blood in the ventricles at the end of diastole), afterload (the volume and pressure of blood in the ventricles during systole) myocardial contractility

9. PATHOGENESIS Ventricular dysfunction-impaired systolic contraction or diastolic dysfunction- seen in ventricular hypertrophy High output failure-due to large arteriovenous shunt in patients w/o heart disease;or due to high cardiac output Valvular disease-impaired filling of ventricles due to mitral or tricuspid stenosis;aortic and tricuspid stenosis,hypertrophic cardiomyopathy

10. CLINICAL ASSESSMENT Heart failure may develop suddenly as in MI, or gradually as in valvular heart disease.
Compensated heart failure- those with impaired cardiac function, in whom adaptive changes have prevented the development of overt heart failure.
atrial fibrillation or infection may precipitate heart failure in these.
acute heart failure sometimes come along with a decompensating episode, on a background of chronic heart failure-acute-on-chronic heart failure.

11. Clinical assessment of acute heart failure Presents with a sudden onset of dyspnea at rest that progresses to acute respiratory distress, orthopnoea & prostration.
H/o acute MI
patient appears agitated, pale, clammy;
peripheries cool to the touch
pulse –rapid

12. BP usually high.
JVP usually elevated
gallop rhythm, a 3 rd heart sound heard quite early
chest examination- crepitations at lung bases or throughout the lungs.
Expiratory wheeze
potential precipitants- URTI or inappropriate cessation of diuretic medication.

13. Clinical assessment of chronic heart failure Relapsing and remitting course
Periods of stability and episodes of decompensation Low cardiac output- fatigue , listlessness, poor effort tolerance, weakness Periphery – cold ; BP low Oliguria, uremia

14. The clinical picture depends on the nature of underlying heart disease and type of heart failure.

15. COMPLICATIONS Renal failure- Poor renal perfusion and drug therapy Hypokalaemia- Diuretics and RAAS Hyperkalemia -Drug therapy Hyponatremia -Diuretics and water retention

16. Impaired liver function Thromboembolism
Arrhythmia -Electrolyte changes
Sudden death

17. INVESTIGATIONS CHEST XRAY 1.Abnormal distension of the upper lobe pulmonary veins with the
patient in the erect position .

18. 2. KERLEY B LINES -Vascularity of the lung fields becomes more prominent and the right and Ieft pulmonary arteries dilate.
-Interstitial oedema causes thickened interlobular septa and dilated lymphatics. -These are evident as horizontal lines in the costophrenic angles

19. ECHOCARDIOGRAPHY Determine aetiology Detect valvular heart disease Identify patients with benefits from long term treatment UREA, CREATINE, ELECTROLYTE, HB,TFT

20. MANAGEMENT PLAN Management of acute heart failure Medical emergency

21. If the above measures are ineffective then inotropic agents such as dobutamine (2.5-10 ug /kg/min) may be required to augment cardiac output, particularly in hypotensive patients. Insertion of an intra-aortic balloon pump may be beneficial in patients with acute cardiogenic pulmonary oedema and shock.

22. Management of chronic heart failure Aims of treatment
-Increase contractlity
- Optimising preload or decreasing afterload
-Control cardiac rate and rhythm

23. 1. Education

24. 2. Drug treatment

25. a.Diuretics Diuretics promote urinary sodium and water excretion leading to a reduction in blood plasma volume Inturn reduces preload and improves pulmonary and systemic venous congestion.
Also reduce afterload and ventricular volume, leading to a fall in ventricular wall tension and increased cardiac efficiency.

26. In case of severe chronic heart failure with renal impairment, oedema may persist even after loop diuretic therapy so furosemide combined with thiazide diuretic such as bendroflumethiazide is used. K sparing diuretics such as spironolactone and eplerenone is also used in severe HF cases

27. b.ACE INHIBITORS Prevent conversion of angiotensin I to angiotensin II
reduces peripheral vasoconstriction
activation of the sympathetic nervous system and salt and water retention due to aldosterone release as well as preventing the activation of the renin- angiotensin system caused by diuretic therapy.

28. Adverse effects of ACE inhibitors include symptomatic hypotension and impairment of renal function, especially in patients with bilateral renal artery stenosis or those with pre-existing renal disease. Short-acting ACE inhibitors can cause marked falls in BP, particularly in the elderly or when started in the presence of hypotension, hypovolaemia and , hyponatraemia .

29. c.ARB Act by blocking action of angiotensin II on heart , peripheral vasculature and kidney
Adverse effects
Renal dysfunction and Hyperkalemia
similar to ACE INHIBITORS

30. d.Neprilysin inhibitors - a small-molecule inhibitor of neprilysin , which is responsible for breakdown of endogenous diuretics ANP and BNP
-Used in combination with ARB (Valsartan) additional symptomatic and mortality benefit over ACE INHIBITORS -only drug is sacubitril

31. e.Vasodilators When ACE INHIBITORS and ARB contraindicated
Vasodilators nitrates reduce preload
Arterial dilator hydralazine reduce afterload
Limited use

32. f. Beta blockers Beta-blockade helas io_counteract the deleterious effects of enhanced sympathetic stimulation and
reduces the risk of arrhythmias and sudden death.

33. G.IVABRADINE -Act on inward current in SA node reduce HR
-Used when beta blockers and contraindicated or not effective
-Ineffective in atrial fibrillation H.DIGOXIN -control HR
-no effect on long term survival I.AMIODARONE -Potent Anti Arrhythmic drug
-Last option

34. NON PHARMACOLOGICAL TREATMENTS 1. Implantable cardiac defrillators 2. Resynchronisation devices-In conduction delay prolonged depolarization lead to uncoordinated left ventricular contraction 3. Coronary revascularisation -Coronary bypass surgery or percutaneous intervention improve areas of inadequate blood supply 4. Cardiac transplantation In intractable heart failure ,CAD and cardiomyopathy
C/I -Pulmonary vascular disease, congenital heart disease, primary Pulmonary hypertension

35. THANK YOU