CHF

1. CHF Umer Ahmed, MS III Daniel Mehrhoff, MS III Tazeen Al-Haq, MS III

2. Definitions • Forward Heart Failure – heart unable to maintain adequate cardiac output to meet systemic demands and/ or able to do so only by elevating filling pressure. • Backward Heart Failure – Heart unable to accommodate venous return resulting in vascular congestion (systemic or pulmonary) • Heart Failure can involve left side of heart, right side of heart or both(biventricular failure) • Components of ineffective filling (diastolic dysfunction)and/or emptying-systolic dysfunction • Most cases of HF are associated with poor cardiac output(low-output HF);however HF may not be due to intrinsic cardiac disease,but due to increased demand-HOP

3. Pathophysiology • Primary insults (myocyte loss,overload) -> pump dysfunction, which leads to remodeling (dilation, hypertrophy) and neurohumoral activation->necrosis and apoptosis. • Both pathways result in further damage (re-starting the cycle), edema, tachycardia, vasoconstriction, congestion • Compensatory response to myocardial stress – • increased end-systolic ventricular pressure(pressure overload) e.g. aortic stenosis-> hypertrophy.

4. Pathophysiology Increased end-diastolic ventricular volume (volume overload) e.g. aortic regurgitation ->cardiac dilation Systemic response to ineffective circulating volume results in activation of sympathetic nervous and renin-angiotensin-alsosterone systems which causes -Salt and water retention with intravascular expansion - increased heart rate and myocardial contractility - increased afterload

5. Classification of Heart Failure by Hemodynamic Abnormality Diastolic Heart Function About 30% of heart failure Characterize by impaired LV relaxation The hemodynamic abnormality is an elevated LVEDP – normally it should relax down to around 5-10 mmHg The elevated LVEDP causes increased left atrial and pulmonary capillary pressures

6. Diastolic Heart Failure Fluid is transudated across the pulmonary Capillaries causing intestitial edema and dyspnea Systolic performance is initially normal or hyperdynamic, but later fails. Examples include hypertensive heart disease, HCM, and diabetic cardiomyopathy

7. High Output Systolic Heart Failure Pure forms of systolic heart failure are uncommon and are characterize by: A low LVEDP Normal or hyper dynamic left ventricular function Tachycardia And increased cardiac output

8. High Output Systolic Heart Failure • Occurs with peripheral shunting with large AV fistulas, large hepatic hemangiomas, and Paget’s disease • Occurs with decrease peripheral resistance, as in Gram negative sepsis • Other causes are hyperthyroidism, beriberi, • Carcinoid, anemia and pregnancy • Note: it is either due to a dramatic decrease in after load or an increase in preload. Basically High output heart failure- differs from the usual heart failure in that the heart may pump out its usual amount of blood, but that still may not be enough to meet the body's needs

9. Low Output Systolic Heart Failure The vast majority of systolic failure involves both decreased systolic dysfunction and an elevated LVEDP Decreased forward output causes weakness, fatigue, fluid retention. Note: which leads to increased LVEDP

10. Causes of Low Output Systolic HF • Coronary artery disease – 40% • Dilated cardiomyopathy – 30% • Valvular heart disease – 15% • Hypertensive heart disease – 10% • Restrictive cardiomyopathy - < 1%

11. Pathophysiology of Heart Failure • Decreases Stroke Volume -> Decrease cardiac output – > decrease Renal perfusion –> increase Renin –> increased Angiotensin- >increased Angiotensin II –> increased Sodium retention –> increased water retention –> increased Preload –> increased Ventricular filling pressures –> Exacerbation of heart failure –>

12. Morbidity and Mortality • 50% die with progressive heart failure, 40% of sudden death due to VT/VF • LVEF is closely associated with prognosis! • Other markers of poor outcome include low sodium, high BUN, low potassium, high or low magnesium, high catecholamine levels • Exercise tolerance does not predict outcome

13. Classifications of Heart Failure by Myocardial Abnormality Myocardial Abnormalities Ischemic Hypertensive Dilated Restrictive Hypertrophic

14. Ischemic Cardiomyopathy • Caused by coronary disease • By far the most common cause of heart failure • Characterized on echo by segmental wall motion abnormalities. .

15. Hypertensive Cardiomyopathy • Chronic HTN causes LVH, which increases LV stiffness and elevates LVEDP • Systolic function may be normal, hyperdynamic, or eventually, decreased • Characterized on echo by concentric LVH

16. Dilated Cardiomyopathy • 50% are idiopathic, presumably post viral • Other causes include alcohol, cocaine, inhaled glue, chemotherapy, late hemochromotosis, and selenium and carnitine dificiencies • Characterized on echo by four chamber cardiac enlargement

17. Peripartum Dilated Cardiomyopathy • Occurs from the beginning of the third trimester to six months postpartum • There is predilection of older women in African Americans • About two thirds resolve spontaneously • There is increased risk of occurrence with subsequent pregnancies

18. Dilated Cardiomyopathy and Embolization • About 2% of patients form mural thrombi and can have arterial embolization • Pulmonary emboli can arise from the RV • Anticoagulation is indicated even if no mural thrombi can be detected

19. Restrictive Cardiomyopathy < 1% • Caused by infiltrative diseases, such as amyloid, sarcoid, hemochromotosis, and lipid storage diseases • Presents with left and right heart failure, initially from diastolic dysfunction, but later from systolic failure also. HF from due to restrictive cardiomyopathy usually presents as refractory left and right sided heart failure.

20. Restrictive Cardiomyopathy • Characterized an echo by normal sized ventricles, huge atria, and (in Amyloidosis) by a “sparkling” appearance of the LV myocardium. • The venticles cannot enlarge, because they have already been enlarged.

21. Hypertrophic Cardiomyopathy • There are disordered myocytes in the region of the hypertrophy, especially in the region of the upper ventricular septum • Areas other than the septum can be affected; Asians frequently have an apical form • Occasionally there is a concentric LVH • Sudden death is probably due to ventricular arrhythmias

22. Hypertropic Cardiomyopathy • Hypertrophic cardiomyopathy (HCM) is associated with sudden cardiac death, especially in exercising young people with the familial form • The severity of the LV outflow gradiant is not related to the risk of sudden death • There is no cure except heart transplant .

23. New York Heart Association (NYHA)Functional Classification of Heart Failur • Class I: ordinary physical activity does not cause symptoms of HF • Class II: comfortable at rest, ordinary physical activity results in symptoms • Class III: marked limitation of ordinary activity; less than ordinary physical activity results in symptoms. • Class IV: inability to carry out any physical activity without discomfort; symptoms may be present at rest.

24. Acute Versus Chronic Heart Failure • Acute heart failure is the patient who is entirely well but who suddenly develops a large myocardial infarction or rupture of a cardiac valve. • Chronic heart failure is typically observed in patients with dilated cardiomyopathy or multivalvular heart disease that develops or progresses slowly

25. Acute Versus Chronic Heart Failure • Acute heart failure is usually largely systolic and the sudden reduction in cardiac output often results in systemic hypotension without peripheral edema. • In chronic heart failure, arterial pressure tends to be well maintained until very late in the course, but there is often accumulation of peripheral edema .

26. Backward versus forward heart failure • Forward heart failure-Is the inability of the heart to pump enough blood to meet the needs of the body for oxygen during exercise or at rest. • Backward heart failure-Is the inability of the heart to meet the oxygen needs of the body when heart filling pressures are too high

27. Redistribution of Cardiac Output • Finally, the redistribution of cardiac output is an important compensatory mechanism when cardiac output is reduced. This redistribution is most marked when a patient with HF exercises, but as heart failure advances, redistribution occurs even in the basal state.

28. Demographics • The most expensive medical problem in the US • The most common diagnose in hospitalized elderly patients Note: It is the most expensive medical problem, because in the later stages patient are hospitalized over and over again as the disease progressed with frequent exacerbations and remissions.

29. CHF Diagnosis Tazeen Al-Haq

30. CHF Diagnosis • Four components involved in the diagnosis of CHF • History • Physical • Labs • Imaging

31. History • Classical manifestations of heart failure include • Fatigue • Dyspnea on exertion • Orthopnea • Paroxysmal nocturnal dyspnea • Fluid retention • Older patients with heart failure often present with nonspecific symptoms • Nocturia • Insomnia • Irritability • Anorexia

32. Physical Examination • Left heart failure • Low cardiac output (forward) • Fatigue • Syncope • Systemic hypotension • Cool extremities • Slow capillary refill • Peripheral cyanosis • Pulsus alternans • Mitral regurgitation • S3 aka Kentucky gallop • Occurs at the beginning of diastole after S2 and is lower in pitch than S1 and S2 • Will increase on expiration

33. Pulsus Alternans • Is a physical finding with arterial pulse waveform alternating strong and weak beats • Almost always indicative of left ventricular systolic impairment and also occurs in aortic and mitral valve stenosis, hypertrophic and congestive cardiomyopathy, pericarditis and use of general anesthesia • Carries a poor prognosis • EF is decreased in left ventricular dysfunction which causes an increase in EDV • In the next cycle of systolic phase, the myocardial muscles are stretched more than usual causing an increase in muscle contraction and a stronger systolic pulse

34. Physical Examination • Left heart failure • Venous congestion (backward) • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea • Cough • Crackles

35. Physical Examination • Right heart failure • Low cardiac output (forward) • Can mimic most of the symptoms of forward left heart failure if decreased right ventricle output leads to left ventricle underfilling • Tricuspid regurgitation • S3 (right-sided) • will increase on inspiration

36. Physical Examination • Right Heart failure • Venous congestion (backward) • Peripheral edema • Elevated JVP with abdominal jugular reflex • Kussmaul’s sign • Rise in JVP with inspiration • Usually JVP falls with inspiration due to reduced pressure in the expanding thoracic cavity • Suggests impaired filling of the right ventricle • Hepatomegaly • Pulsatile liver • Signifies severe tricuspid regurgitation or constrictive pericarditis

37. Investigation • Identify and assess precipitating factors and treatable causes of CHF • HEART FAILED • HTN (common) • Endocarditis • Anemia • Rheumatic heart disease and other valvular disease • Thyrotoxicosis • Failure to take meds (very common) • Arrhythmia (common) • Infection/Ischemia/Infarction (common) • Lung problems (PE, pneumonia, COPD) • Endocrine (pheochromocytoma) • Dietary indiscretions (common)

38. Investigations • Blood work • CBC • Electrolytes • BUN and Creatinine • TSH • Ferritin • Cardiac biomarkers • B-type/Brain natriuretic peptide (BNP) • Secreted by ventricles due to LV stretch and wall tension • Sensitive marker of ventricular pressure and volume overload • Higher levels are suggestive of heart failure • Lower levels (<100 pg/mL) is most useful for ruling out heart failure

39. Cardiac Biomarkers • Provide diagnostic and prognostic information • Identify increased risk of mortality in acute coronary syndromes • Troponin I and T • Peak at 1-2 days and remain elevated up to 2 weeks • DDx: MI, CHF, acute pulmonary embolism, myocarditis, chronic renal insufficiency, sepsis, hypovolemia • CK-MB • Peak at 1 day and remain elevated for 3 days • DDx: MI, myocarditis, pericarditis, muscular dystrophy, cardiac defibrillation

40. Investigations • Chest X-Ray • HERB-B • Heart enlargement/Cardiomegaly • Pleural Effusion • Re-distribution (alveolar edema) • Kerley B-lines • Bronchiolar-alveolar cuffing

41. Chest X-Ray

42. Chest X-Ray Cardiomegaly

43. CHF Treatment Umer Ahmed

44. General Principals in the Treatment of CHF • No one simple treatment regimen is suitable for all patients. • The following are a general guideline, but the order of therapy may differ among patients and/or with physician preferences.

45. General Principles in the Treatment of CHF Mild CHF (NYHA Class I to II) • Mild restriction of sodium intake (no-added-salt diet of <4 g sodium) and physical activity (aka Lifestyle Changes). • Start a loop diuretic if volume overload or pulmonary congestion is present. • Use an ACE inhibitor as a first-line agent.

46. General Principles in the Treatment of CHF Mild to Moderate CHF (NYHA Class II to III) • Start a diuretic (loop diuretic) and an ACE inhibitor • Add a β-blocker if moderate disease (class II or III) is present and the response to standard treatment is suboptimal

47. General Principles in the Treatment of CHF Moderate to Severe CHF (NYHA Class III to IV) • Add digoxin (to loop diuretic and ACE inhibitor) • Note that digoxin may be added at any time for the relief of symptoms in patients with systolic dysfunction. (It does not improve mortality.) • In patients with class IV symptoms who are still symptomatic despite the above, adding spironolactone can be helpful.

48. Monitoring a Patient with CHF • Weight—unexplained weight gain can be an early sign of worsening CHF • Clinical manifestations (exercise tolerance is key); peripheral edema • Laboratory values (electrolytes, K, BUN, creatinine levels; serum digoxin, if applicable)

49. Medical Devices • Ventricular assist device (VAD). When your weakened heart needs help pumping blood, surgeons may implant a VAD into your abdomen and attach it to your heart. These mechanical heart pumps can be used either as a "bridge" to heart transplant or as permanent therapy for people who aren't candidates for a transplant.