Presentation is loading. Please wait.

Presentation is loading. Please wait.

Low-Output Heart Failure –Systolic Heart Failure (HFREF): –Decreased Left ventricular ejection fraction –Diastolic Heart Failure (HFPEF): –Elevated Left.

Similar presentations


Presentation on theme: "Low-Output Heart Failure –Systolic Heart Failure (HFREF): –Decreased Left ventricular ejection fraction –Diastolic Heart Failure (HFPEF): –Elevated Left."— Presentation transcript:

1

2 Low-Output Heart Failure –Systolic Heart Failure (HFREF): –Decreased Left ventricular ejection fraction –Diastolic Heart Failure (HFPEF): –Elevated Left and Right ventricular end-diastolic pressures –Normal LVEF High-Output Heart Failure –Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism, beri-beri, carcinoid, anemia –Often have normal cardiac output Right-Ventricular Failure –Seen with pulmonary hypertension, large RV infarctions.

3 Causes of Low-Output Heart Failure Systolic Dysfunction Coronary Artery Disease Idiopathic dilated cardiomyopathy (DCM) »50% idiopathic (at least 25% familial) »9 % myocarditis (viral) »tachycardia, peripartum, hypertension, HIV, connective tissue disease, substance abuse (alcohol), doxorubicin/herceptin Hypertension Valvular Heart Disease Diastolic Dysfunction Hypertension Coronary artery disease Hypertrophic obstructive cardiomyopathy (HCM) Restrictive cardiomyopathy

4 (Mal)adaptation-hemodynamic

5 ( Mal) adaptation-neurohormonal Activation of the sympathetic nervous system –Vasoconstriction/increased afterload –Tolerance –Arhythmogenic

6 Activation of renin-angiotensin system –Na resorption –Vasoconstriction –Apoptosis/fibrosis

7 Antidiuretic hormone Proinflammatory cytokines –TNFalpha –IL-6

8 Clinical Presentation of Heart Failure Due to excess fluid accumulation: –Dyspnea (most sensitive symptom) –Edema –Hepatic congestion –Ascites –Orthopnea, Paroxysmal Nocturnal Dyspnea (PND) Due to reduction in cardiac ouput: –Fatigue (especially with exertion) –Weakness

9 S3 gallop –Low sensitivity, but highly specific Cool, pale, cyanotic extremities –Have sinus tachycardia, diaphoresis and peripheral vasoconstriction Crackles or decreased breath sounds at bases (effusions) on lung exam Elevated jugular venous pressure Lower extremity edema Ascites Hepatomegaly Splenomegaly Displaced PMI Apical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement>

10 Lab Analysis in Heart Failure CBC –Since anemia can exacerbate heart failure Serum electrolytes and creatinine – before starting high dose diuretics Fasting Blood glucose –To evaluate for possible diabetes mellitus Thyroid function tests –Since thyrotoxicosis can result in A. Fib, and hypothyroidism can results in HF. Iron studies –To screen for hereditary hemochromatosis as cause of heart failure. ANA –To evaluate for possible lupus Viral studies –If viral mycocarditis suspected

11 Laboratory Analysis (cont.) BNP –With chronic heart failure, atrial mycotes secrete increase amounts of atrial natriuretic peptide (ANP) and brain natriuretic pepetide (BNP) in response to high atrial and ventricular filling pressures –Usually is > 400 pg/mL in patients with dyspnea due to heart failure.

12 Chest X-ray in Heart Failure Cardiomegaly Cephalization of the pulmonary vessels Kerley B-lines Pleural effusions

13 Cardiomegaly

14 Pulmonary Edema due to Heart Failure

15 Kerley B lines

16 Cardiac Testing in Heart Failure Electrocardiogram: –May show specific cause of heart failure: –Ischemic heart disease –Dilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular block –Amyloidosis: pseudo-infarction pattern –Idiopathic dilated cardiomyopathy: LVH Echocardiogram: –Left ventricular ejection fraction –Structural/valvular abnormalities

17 Further Cardiac Testing in Heart Failure Coronary arteriography –Should be performed in patients presenting with heart failure who have angina or significant ischemia –Reasonable in patients who have chest pain that may or may not be cardiac in origin, in whom cardiac anatomy is not known, and in patients with known or suspected coronary artery disease who do not have angina. –Measure cardiac output, degree of left ventricular dysfunction, and left ventricular end-diastolic pressure.

18 Further testing in Heart Failure Endomyocardial biopsy Not frequently used Amyloidosis, giant-cell myocarditis

19 Classification of Heart Failure ACCF/AHA Stages of HFNYHA Functional Classification A At high risk for HF but without structural heart disease or symptoms of HF. None B Structural heart disease but without signs or symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. C Structural heart disease with prior or current symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. DRefractory HF requiring specialized interventions.

20 Aggravating Factors Medications New heart disease Myocardial ischemia Medications New heart disease Myocardial ischemia Endocarditis Obesity Hypertension Physical activity Dietary excess Endocarditis Obesity Hypertension Physical activity Dietary excess Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism

21 Heart Failure and Myocardial Ischemia Coronary HD is the cause of 2/3 of HF Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia Segmental wall motion abnormalities are not specific if ischemia Angina coronary angio and revascularization Angina coronary angio and revascularization No angina No angina Search for ischemia and viability in all ? Search for ischemia and viability in all ? Coronary angiography in all ? Coronary angiography in all ?

22 VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ ACE-i. Mechanism of Action A.C.E.

23 ACE-I. Clinical Effects Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival

24 Mortality Reduction with ACE-i StudyACE-iClinical Seting CONSENSUSEnalaprilCHF SOLVD treatment EnalaprilCHF AIRERamiprilCHF Vheft-IIEnalaprilCHF TRACETrandolaprilCHF / LVD SAVECaptoprilLVD SMILEZofenoprilHigh risk HOPERamiprilHigh risk

25 Placebo Enalapril Probabiility of Death Probabiility of Death Months p< p< CONSENSUS N Engl J Med 1987;316:1429 CONSENSUS N Engl J Med 1987;316: ACE-i

26 Mortality, % Mortality, % 4 4 SAVE N Engl J Med 1992;327:669 SAVE N Engl J Med 1992;327:669 Years Placebo Captopril 0 0 n=1115 n=1116 p=0.019 ² -19% n = days post AMI EF < mg / day n = days post AMI EF < mg / day Asymptomatic ventricular dysfunction post MI Asymptomatic ventricular dysfunction post MI ACE-i

27 Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < % Selected high risk subgroups Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < % Selected high risk subgroups ACE-i. Indications AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

28 ACE-i. Practical Use Start with very low doseStart with very low dose Increase dose if well toleratedIncrease dose if well tolerated Renal function & serum K + after 1-2 wRenal function & serum K + after 1-2 w Avoid fluid retention / hypovolemia (diuretic use)Avoid fluid retention / hypovolemia (diuretic use) Dose NOT determined by symptomsDose NOT determined by symptoms

29 ACE-i. Dose (mg) InitialMaximum InitialMaximum Captopril 6.25 / 8h 50 / 8h Enalapril 2.5 / 12 h 10 to 20 / 12h Fosinopril 5 to 10 / day 40 / day Lisinopril 2.5 to 5.0 / day 20 to 40 / day Quinapril 10 / 12 h40 / 12 h Ramipril 1.25 to 2.5 / day 10 / day AHA / ACC HF guidelines 2001

30 ACE-I. Adverse Effects Hypotension (1st dose effect) Hypotension (1st dose effect) Worsening renal function Worsening renal function Hyperkalemia Hyperkalemia Cough Cough Angioedema Angioedema Rash, ageusia, neutropenia, … Rash, ageusia, neutropenia, …

31 ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension

32 ß-Adrenergic Blockers Mechanism of action ß-Adrenergic Blockers Mechanism of action Density of ß 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative Density of ß 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative

33 Placebo Carvedilol Months N = 2289 III-IV NYHA COPERNICUS NEJM 2001;344:1651 Survival% ß-Adrenergic Blockers p= % RR

34 Patient stable Patient stable No physical evidence of fluid retention No physical evidence of fluid retention No need for i.v. inotropic drugs No need for i.v. inotropic drugs No contraindications No contraindications In hospital or not In hospital or not ß-Adrenergic Blockers When to start

35 InitialTarget Bisoprolol 1.25 / 24h 10 / 24h Carvedilol / 12h25 / 12h Metoprolol succinnate 12,5-25 / 24h200 / 24h Start Low, Increase Slowly Start Low, Increase Slowly Increase the dose every weeks Increase the dose every weeks ß-Adrenergic Blockers Dose (mg)

36 Hypotension Hypotension Fluid retention / worsening heart failure Fluid retention / worsening heart failure Fatigue Fatigue Bradycardia / heart block Bradycardia / heart block ß-Adrenergic Blockers Adverse Effects

37 ALDOSTERONE Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Collagen depositionFibrosis - myocardium - myocardium - vessels - vessels Spironolactone Edema Arrhythmias Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Aldosterone Inhibitors -

38 Aldactone Placebo Survival months p < Annual Mortality Aldactone 18%; Placebo 23% N = 1663 NYHA III-IV Mean follow-up 2 y RALES NEJM 1999;341:709 Spironolactone

39 Spironolactone. Indications Recent or current symptoms despite ACE-i, diuretics, dig. and  -blockersRecent or current symptoms despite ACE-i, diuretics, dig. and  -blockers AHA / ACC HF guidelines 2001 Recommended in advanced heart failure (III-IV), in addition to ACE-i and diureticsRecommended in advanced heart failure (III-IV), in addition to ACE-i and diuretics HypokalemiaHypokalemia ESC HF guidelines 2001

40 Spironolactone. Practical use Do not use if hyperkalemia, renal insuf.Do not use if hyperkalemia, renal insuf. Monitor serum K + at “frequent intervals”Monitor serum K + at “frequent intervals” Start ACE-i firstStart ACE-i first Start with 25 mg / 24hStart with 25 mg / 24h If K + >5.5 mmol/L, reduce to 25 mg / 48hIf K + >5.5 mmol/L, reduce to 25 mg / 48h If K + is low or stable consider 50 mg / dayIf K + is low or stable consider 50 mg / day New studies in progress New studies in progress

41 RENIN Angiotensinogen Angiotensin I ANGIOTENSIN II Angiotensin I ANGIOTENSIN II ACE Other pathways Vasoconstriction Proliferative Action Proliferative Action Vasodilatation Antiproliferative Action Antiproliferative Action AT1 AT2 AT1 Receptor Blockers AT1 Receptor Blockers RECEPTORS Angiotensin II Receptor Blockers (ARB)

42 Candesartan, Eprosartan, Irbesartan Candesartan, Eprosartan, Irbesartan Losartan, Telmisartan, Valsartan Not indicated with beta blockers Not indicated with beta blockers Indicated in patients intolerant to ACE-I Indicated in patients intolerant to ACE-I Angiotensin II Receptor Blockers (ARB) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

43 Positive Inotropes Digitalis Digitalis Sympathomimetics Sympathomimetics Catecholamines Catecholamines B-adrenergic agonists B-adrenergic agonists Phosphodiesterase inhibitors Phosphodiesterase inhibitors Amrinone, Milrinone, Enoximone Amrinone, Milrinone, Enoximone Calcium sensitizers Calcium sensitizers Levosimendan, Pimobendan Levosimendan, Pimobendan

44 May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF NOT for use as chronic therapy May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF NOT for use as chronic therapy Positive Inotropic Therapy

45 Digitalis. Mechanism of Action Blocks Na + / K + ATPase => Ca + + Inotropic effect Inotropic effect Natriuresis Natriuresis Neurohormonal control Neurohormonal control - Plasma Noradrenaline - Peripheral nervous system activity - RAAS activity - Vagal tone - Normalizes arterial baroreceptors NEJM 1988;318:358

46 Digitalis. Clinical Effects Improve symptoms Modest reduction in hospitalization Does not improve survival Improve symptoms Modest reduction in hospitalization Does not improve survival

47 Digitalis. Indications When no adequate response to When no adequate response to ACE-i + diuretics + beta-blockers ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 AHA / ACC Guidelines 2001 In combination with ACE-i + diuretics In combination with ACE-i + diuretics if persisting symptoms if persisting symptoms ESC Guidelines 2001 ESC Guidelines 2001 AF, to slow AV conduction AF, to slow AV conduction Dose to mg / day

48 Placebo n=3403 Placebo n=3403 Digoxin n=3397 Digoxin n= Mortality % Mortality % DIG N Engl J Med 1997;336:525 DIG N Engl J Med 1997;336:525 Months p = 0.8 Digitalis N=6800 NYHA II-III N=6800 NYHA II-III

49 Diuretics. Indications 1.Symptomatic HF, with fluid retention Edema Edema Dyspnea Dyspnea Lung Rales Lung Rales Jugular distension Jugular distension Hepatomegaly Hepatomegaly Pulmonary edema (Xray) Pulmonary edema (Xray) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

50 Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightStart with variable dose. Titrate to achieve dry weight Monitor serum K + at “frequent intervals”Monitor serum K + at “frequent intervals” Reduce dose when fluid retention is controlledReduce dose when fluid retention is controlled Teach the patient when, how to change doseTeach the patient when, how to change dose Combine to overcome “resistance”Combine to overcome “resistance” Do not use aloneDo not use alone

51 Thiazides, Loop Diuretics. Adverse Effects K +, Mg + ( %) (sudden death ???) K +, Mg + ( %) (sudden death ???) Na + Na + Stimulation of neurohormonal activity Stimulation of neurohormonal activity Hyperuricemia ( %) Hyperuricemia ( %) Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic Sharpe N. Heart failure. Martin Dunitz 2000;43 Kubo SH, et al. Am J Cardiol 1987;60:1322 MRFIT, JAMA 1982;248:1465 Pool Wilson. Heart failure. Churchill Livinston 1997;635

52 Diuretic Resistance Neurohormonal activation Neurohormonal activation Rebound Na + uptake after volume loss Rebound Na + uptake after volume loss Hypertrophy of distal nephron Hypertrophy of distal nephron Reduced tubular secretion (renal failure, NSAIDs) Reduced tubular secretion (renal failure, NSAIDs) Decreased renal perfusion (low output) Decreased renal perfusion (low output) Altered absortion of diuretic Altered absortion of diuretic Noncompliance with drugs Noncompliance with drugs Brater NEJM 1998;339:387 Kramer et al. Am J Med 1999;106:90

53 Managing Resistance to Diuretics Restrict Na + /H 2 O intake (Monitor Natremia) Restrict Na + /H 2 O intake (Monitor Natremia) Increase dose (individual dose, frequency, i.v.) Increase dose (individual dose, frequency, i.v.) Combine: furosemide + thiazide / spiro / metolazone Combine: furosemide + thiazide / spiro / metolazone Dopamine (increase cardiac output) Dopamine (increase cardiac output) Reduce dose of ACE-i Reduce dose of ACE-i Ultrafiltration Ultrafiltration Motwani et al Circulation 1992;86:439

54 Inotropes, long term / intermittent Inotropes, long term / intermittent Antiarrhythmics (except amiodarone) Antiarrhythmics (except amiodarone) Calcium antagonists (except amlodipine) Calcium antagonists (except amlodipine) Non-steroidal antiinflammatory drugs (NSAIDS) Non-steroidal antiinflammatory drugs (NSAIDS) Tricyclic antidepressants Tricyclic antidepressants Corticosteroids Corticosteroids Lithium Lithium Drugs to Avoid (may increase symptoms, mortality) ESC HF guidelines 2001

55 Refractory End-Stage HF Review etiology, treatment & aggrav. factors Review etiology, treatment & aggrav. factors Control fluid retention Control fluid retention Resistance to diuretics Resistance to diuretics Ultrafiltration ? Ultrafiltration ? iv inotropics / vasodilators during decompensation iv inotropics / vasodilators during decompensation Consider resynchronization Consider resynchronization Consider mechanical assist devices Consider mechanical assist devices Consider heart transplantation Consider heart transplantation

56 Cardiac Resynchronization Therapy* in Patients With Severe Systolic Heart Failure For patients who have left ventricular ejection fraction (LVEF) less than or equal to 35%, a QRS duration greater than or equal to 0.12 seconds, and sinus rhythm, cardiac resynchronization therapy (CRT) with or without an ICD is indicated for the treatment of New York Heart Association (NYHA) functional Class III or ambulatory Class IV heart failure symptoms on optimal recommended medical therapy

57 Indications for CRT Therapy

58 Heart Transplant. Indications Refractory cardiogenic shock Refractory cardiogenic shock Documented dependence on IV inotropic support to maintain adequate organ perfusion Documented dependence on IV inotropic support to maintain adequate organ perfusion Peak VO2 < 10 ml / kg / min Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity

59 Ventricular Arrhythmias / Sudden Death Antiarrhythmics ineffective (may increase mortality) Antiarrhythmics ineffective (may increase mortality) Amiodarone do not improve survival  -blockers reduce all cause mortality and SD  -blockers reduce all cause mortality and SD Control ischemia Control ischemia Control electrolyte disturbances Control electrolyte disturbances ICD (Implantable Cardiac Defibrillator) ICD (Implantable Cardiac Defibrillator) In secondary prevention of SD In secondary prevention of SD In sustained, hemodynamic destabilizing VT In sustained, hemodynamic destabilizing VT Ongoing research will establish new indications Ongoing research will establish new indications

60 Device Therapy for Stage C HFrEF (cont.) RecommendationsCORLOE ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤35%, and NYHA class II or III symptoms on chronic GDMT, who are expected to live ≥1 year* IA CRT is indicated for patients who have LVEF ≤35%, sinus rhythm, LBBB with a QRS ≥150 ms I A (NYHA class III/IV) B (NYHA class II) ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤30%, and NYHA class I symptoms while receiving GDMT, who are expected to live ≥1 year* IB CRT can be useful for patients who have LVEF ≤35%, sinus rhythm, a non- LBBB pattern with a QRS ≥150 ms, and NYHA class III/ambulatory class IV symptoms on GDMT. IIaA CRT can be useful for patients who have LVEF ≤35%, sinus rhythm, LBBB with a QRS 120 to 149 ms, and NYHA class II, III or ambulatory IV symptoms on GDMT IIa B CRT can be useful in patients with AF and LVEF ≤35% on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or rate control allows near 100% ventricular pacing with CRT IIaB

61 Diastolic Heart Failure Incorrect diagnosis of HF Incorrect diagnosis of HF Inaccurate measurement of LVEF Inaccurate measurement of LVEF Primary valvular disease Primary valvular disease Restrictive (infiltrative) cardiomyopathies (Amyloidosis…) Restrictive (infiltrative) cardiomyopathies (Amyloidosis…) Pericardial constriction Pericardial constriction Episodic or reversible LV systolic dysfunction Episodic or reversible LV systolic dysfunction Severe hypertension, ischemia Severe hypertension, ischemia High output states: Anemia, thyrotoxicosis, etc High output states: Anemia, thyrotoxicosis, etc Chronic pulmonary disease with right HF Chronic pulmonary disease with right HF Pulmonary hypertension Pulmonary hypertension Atrial myxoma Atrial myxoma LV Hypertrophy LV Hypertrophy Diastolic dysfunction of uncertain origin Diastolic dysfunction of uncertain origin

62 Treatment of HFpEF RecommendationsCORLOE Systolic and diastolic blood pressure should be controlled according to published clinical practice guidelines IB Diuretics should be used for relief of symptoms due to volume overload IC Coronary revascularization for patients with CAD in whom angina or demonstrable myocardial ischemia is present despite GDMT IIa C Management of AF according to published clinical practice guidelines for HFpEF to improve symptomatic HF IIaC Use of beta-blocking agents, ACE inhibitors, and ARBs for hypertension in HFpEF IIaC ARBs might be considered to decrease hospitalizations in HFpEF IIbB Nutritional supplementation is not recommended in HFpEF III: No Benefit C

63 Stages, Phenotypes and Treatment of HF


Download ppt "Low-Output Heart Failure –Systolic Heart Failure (HFREF): –Decreased Left ventricular ejection fraction –Diastolic Heart Failure (HFPEF): –Elevated Left."

Similar presentations


Ads by Google