1. CARDIAC FAILURE Senior-Prof KR Sethuraman. MD

2. Learning objectives and outcomes Define cardiac failure Define cardiac failure State Starling’s law and explain how it applies to cardiac failure State Starling’s law and explain how it applies to cardiac failure Describe the physiological compensatory mechanisms to maintain haemodynamic stability in cardiac failure Describe the physiological compensatory mechanisms to maintain haemodynamic stability in cardiac failure List the causes of cardiac failure List the causes of cardiac failure

3. Learning obj (contd) Compare and contrast the clinical features and causes of right heart failure, left heart failure, congestive cardiac failure, acute heart failure and high-output heart failure Compare and contrast the clinical features and causes of right heart failure, left heart failure, congestive cardiac failure, acute heart failure and high-output heart failure Describe the clinical features of cardiac failure Describe the clinical features of cardiac failure Describe a grading system for cardiac failure Describe a grading system for cardiac failure Define Orthopnoea and paroxysmal nocturnal dyspnoea (PND) Define Orthopnoea and paroxysmal nocturnal dyspnoea (PND)

4. Learning obj (contd) Outline useful investigations to determine diagnosis and prognosis in cardiac failure Outline useful investigations to determine diagnosis and prognosis in cardiac failure Outline the principles of management of cardiac failure Outline the principles of management of cardiac failure

5. Definition: Heart failure is “a state in which the heart cannot provide sufficient cardiac output or blood supply to meet the metabolic needs of the body and its tissues.” Heart failure is “a state in which the heart cannot provide sufficient cardiac output or blood supply to meet the metabolic needs of the body and its tissues.” It is commonly termed congestive heart failure (CHF) since symptoms of increased venous pressure are often prominent It is commonly termed congestive heart failure (CHF) since symptoms of increased venous pressure are often prominent

7. Frank-Starling’s law revisited… “The more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the next systolic contraction (stroke volume). “The more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the next systolic contraction (stroke volume). The force of contraction increases as the ventricles are filled with more blood, due to the effect of an increasing load on single muscle fiber.” The force of contraction increases as the ventricles are filled with more blood, due to the effect of an increasing load on single muscle fiber.”

8. Preload, Congestion & Output: a chart High output High preload congestive failure Low output High preload congestive failure High output Low preload state Low output Low preload state

9. Ae tiology Ae tiology It is a common end point for many diseases of cardiovascular system It is a common end point for many diseases of cardiovascular system It is the end result of diseases that cause It is the end result of diseases that cause -Inappropriate work load -Inappropriate work load - volume or pressure overload -Restricted filling in Diastole -Myocyte loss -Myocyte loss

10. Mechanisms leading to LV Failure Volume over load: Regurgitation of valve Volume over load: Regurgitation of valve ( preload) High output status Pressure overload: Systemic hypertension Pressure overload: Systemic hypertension ( afterload) Outflow obstruction ( afterload) Outflow obstruction Loss of muscles: Post MI, Chronic ischemia Loss of muscles: Post MI, Chronic ischemia Connective tissue diseases Connective tissue diseases Infection, Poisons (alcohol,cobalt,Doxorubicin) Infection, Poisons (alcohol,cobalt,Doxorubicin) Restricted Filling: Pericardial diseases, Restrictive Restricted Filling: Pericardial diseases, Restrictive (“Diastolic Failure”) cardiomyopathy, tachyarrhythmia (“Diastolic Failure”) cardiomyopathy, tachyarrhythmia

11. Hemodynamic changes From a hemodynamic stand point, Heart Failure can be due to systolic dysfunction or diastolic dysfunction From a hemodynamic stand point, Heart Failure can be due to systolic dysfunction or diastolic dysfunction

13. Pathophysiology (revise…) Hemodynamic changes Hemodynamic changes Neurohormonal changes Neurohormonal changes Cellular changes Cellular changes

14. Types of Heart Failure Systolic & Diastolic failure Systolic & Diastolic failure High Output Failure High Output Failure Pregnancy, anemia, thyrotoxicosis, A/V fistula, Beriberi, Pagets disease Pregnancy, anemia, thyrotoxicosis, A/V fistula, Beriberi, Pagets disease Low Output Failure Low Output Failure Acute (sudden & recent onset ; not severity ) Acute (sudden & recent onset ; not severity ) large MI, aortic valve dysfunction--- large MI, aortic valve dysfunction--- Chronic (Long standing >3months) Chronic (Long standing >3months)

15. Types of Heart Failure( cont.) Right vs Left sided heart failure: Right vs Left sided heart failure: Right sided heart failure : Right sided heart failure : Most common cause is left sided failure Most common cause is left sided failure Other causes included : Pulmonary embolisms Other causes included : Pulmonary embolisms Other causes of pulmonary htn. Other causes of pulmonary htn. RV infarction RV infarction MS MS Usually presents with: LL edema, ascites Usually presents with: LL edema, ascites hepatic congestion hepatic congestion cardiac cirrhosis (on the long run) cardiac cirrhosis (on the long run)

16. Neurohormonal changes, Neurohormonal changes, revisited Neuro-Hormonal changes Favorable effects Unfavorable effects  Sympathetic activity  Sympathetic activity  HR,  contractility, vasoconstriction: vasoconstriction:  V return,  filling Arteriolar constriction:  After load :  workload &  O 2 consumption  O 2 consumption  Renin-Angiotensin –  Renin-Angiotensin – Aldosterone Aldosterone Salt & water retention  VR Vasoconstriction:  after load  Vasopressin  Vasopressin Same effect  interleukins &TNF   interleukins &TNF  May have roles in myocyte hypertrophy Apoptosis  Endothelin  Endothelin Vasoconstriction:  VR  After load

17. Symptoms Low cardiac output symptoms (“Forward failure”) Low cardiac output symptoms (“Forward failure”) Easy Fatigability, Dizziness, Fainting, oliguria Breathing difficulties: (Pulmonary venous congestion) Breathing difficulties: (Pulmonary venous congestion) Shortness of Breath, Orthopnea, paroxysmal nocturnal dyspnea Abdominal symptoms: Abdominal symptoms: Anorexia, nausea, abdominal fullness, Rt hypochondrial pain

20. Physical Signs Higher diastolic BP + some fall in systolic BP (“decapitated BP”) e.g., 120/80 changes to 105/85 Higher diastolic BP + some fall in systolic BP (“decapitated BP”) e.g., 120/80 changes to 105/85 Elevated Jugular Venous Pressure Elevated Jugular Venous Pressure Crepitation (end-inspiratory crackles) Crepitation (end-inspiratory crackles) Outwardly displaced & sustained apical impulse Outwardly displaced & sustained apical impulse Third heart sound (“gallop”) Third heart sound (“gallop”) low pitched sound heard during rapid filling of ventricle low pitched sound heard during rapid filling of ventricle

21. Physical signs (cont.) Fourth heart Sound (S 4 ) Fourth heart Sound (S 4 ) - at the end of diastole - at the end of diastole - during atrial systole - during atrial systole Pale, cold & clammy (sweaty) skin

22. Dx of Heart Failure: Framingham Criteria Major Criteria: Major Criteria: Cardiomegaly Cardiomegaly S 3 Gallop S 3 Gallop PND (paroxysmal nocturnal dyspnoea) PND (paroxysmal nocturnal dyspnoea) Acute Pulmonary Edema Acute Pulmonary Edema ↑ JVP or +Hepato-Jugular reflux (not reflex) ↑ JVP or +Hepato-Jugular reflux (not reflex) ↑ pulmonary venous pressure > 16 cm H 2 O ↑ pulmonary venous pressure > 16 cm H 2 O Crackles (=Rales or crepitations) Crackles (=Rales or crepitations)

23. Dx of Heart Failure (cont.) Minor Criteria Minor Criteria Leg edema, Night cough Night cough Dyspnea on exertion Dyspnea on exertion Hepatomegaly Hepatomegaly Pleural effusion Pleural effusion ↓ vital capacity by 1/3 of normal Tachycardia 120 bpm Tachycardia 120 bpm Weight loss 4.5 kg over 5 days management Weight loss 4.5 kg over 5 days management

24. Differential diagnosis Pericardial diseases Pericardial diseases Liver diseases Liver diseases Nephrotic syndrome Nephrotic syndrome Protein losing enteropathy Protein losing enteropathy

25. Chest X-ray Size and shape of heart Size and shape of heart Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema) Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema) Pleural effusion Pleural effusion NORMAL Ac Pulm Oedema

26. Electrocardiogram Evidence of Myocardial Ischemia Evidence of Myocardial Ischemia Old MI or recent MI Old MI or recent MI Evidence of LV/RV Hypertrophy & “strain” Evidence of LV/RV Hypertrophy & “strain” Arrhythmia, esp. Atrial Fibrillation Arrhythmia, esp. Atrial Fibrillation LBBB LBBB

27. Laboratory Findings Anaemia – often as a comorbidity Anaemia – often as a comorbidity Hyperthyroidism - cause or comorbidity Hyperthyroidism - cause or comorbidity Pre-renal uremia due to low-output Pre-renal uremia due to low-output Chronic renal insufficiency, Chronic renal insufficiency, Electrolytes abnormality Electrolytes abnormality

28. Echocardiogram Function of both ventricles in systole & diastole Function of both ventricles in systole & diastole Wall motion abnormality that may signify CAD Wall motion abnormality that may signify CAD Valvular abnormality – stenosis or regurgitation Valvular abnormality – stenosis or regurgitation Intra-cardiac shunts – e.g., Ventricular Septal Defect Intra-cardiac shunts – e.g., Ventricular Septal Defect

29. TREATMENT Correction of reversible causes Correction of reversible causes Ischemia: medications, repair of blocked Coronary arteries Ischemia: medications, repair of blocked Coronary arteries Valvular heart disease: medications, Valve-repair Valvular heart disease: medications, Valve-repair Thyrotoxicosis & other high output status Thyrotoxicosis & other high output status Shunts: closure of the shunt (ASD, VSD, or PDA) Shunts: closure of the shunt (ASD, VSD, or PDA) Arrhythmia: control of Rhythm or the Heart-Rate Arrhythmia: control of Rhythm or the Heart-Rate Atrial fibrillation, Atrial flutter, Atrial fibrillation, Atrial flutter, Medications Medications Avoid negative inotropic agents like Avoid negative inotropic agents like Ca channel blockers, some antiarrhythmics Ca channel blockers, some antiarrhythmics

30. Principles of management Early subclinical LV Failure: beta-blocker helps Early subclinical LV Failure: beta-blocker helps Diet – Salt and fluid restriction Diet – Salt and fluid restriction Diuretics like furosemide Diuretics like furosemide Vaso-Dilators like ACE Inhibitors, Vaso-Dilators like ACE Inhibitors, Digoxin if there is co-existing atrial fibrillation Digoxin if there is co-existing atrial fibrillation Decubitus & O 2 – complete bed rest in propped up position for patients with clinical failure Decubitus & O 2 – complete bed rest in propped up position for patients with clinical failure

31. Thank you

33. Physical signs (cont.) Mechanism of S 3 sudden deceleration of blood Mechanism of S 3 sudden deceleration of blood as elastic limits of the ventricles are as elastic limits of the ventricles are reached reached Vibration of the ventricular wall by blood Vibration of the ventricular wall by blood filling filling Common in children Common in children