Congestive Heart Congestive Heart FailureFailure

M Chadi AlraiesM Chadi Alraies

Thursday, January 3, 2008Thursday, January 3, 2008

Essentials of DiagnosisEssentials of Diagnosis LV failure: LV failure:

Exertional dyspnea,Exertional dyspnea, cough, cough, fatigue, fatigue, orthopnea, orthopnea, PND, PND, cardiac cardiac

enlargement, enlargement, rales, rales, gallop rhythm, gallop rhythm, pulmonary venous pulmonary venous

congestion. congestion.

RV failure: RV failure: Elevated venous Elevated venous

pressure,pressure, hepatomegaly, hepatomegaly, dependent edema; dependent edema;

TypesTypes

Systolic heart failureSystolic heart failure Diastolic heart failureDiastolic heart failure High output heart failureHigh output heart failure

Thyrotoxicosis, Thyrotoxicosis, Severe anemia, Severe anemia, Arteriovenous shunting (including Arteriovenous shunting (including

dialysis fistulas), dialysis fistulas), Paget's disease of bone, Paget's disease of bone, Thiamine deficiency (wet beriberi). Thiamine deficiency (wet beriberi).

PathophysiologyPathophysiology

1.1. Contractile state of the Contractile state of the myocardium, myocardium,

2.2. Preload of the ventricle Preload of the ventricle

3.3. Afterload applied to the ventriclesAfterload applied to the ventricles

4.4. Heart rate.Heart rate.

Cardiac contractility Cardiac contractility (pump)(pump)

Coronary artery disease (infarction) Muscle:

Hypertrophy Restrictive cardiomyopathy Myocardial toxins (medications, cocaine,

ETOH) Myocarditis Idiopathic dilated cardiomyopathy

Increased preloadIncreased preload

LVLV Mitral regurgitationMitral regurgitation Aortic regurgitationAortic regurgitation

RVRV ASDASD VSAVSA Post infarction interventricular Post infarction interventricular

perforationperforation

Increased afterloadIncreased afterload

LVLV Aortic stenosisAortic stenosis HTNHTN HOCMHOCM

RVRV Pulmonary HTNPulmonary HTN Pulmonic valve Pulmonic valve

stenosisstenosis Left heat failureLeft heat failure

Conduction systemConduction system

BradycardiaBradycardia TachycardiaTachycardia

Pathophysiology Pathophysiology 1.1. Decreased stroke volumeDecreased stroke volume2.2. Raised end-diastolic volume and pressure Raised end-diastolic volume and pressure 3.3. Ventricular dilation will occur. Ventricular dilation will occur. 4.4. Chronic elevation of diastolic pressures.Chronic elevation of diastolic pressures.5.5. Increased capillary pressure.Increased capillary pressure.6.6. Transudation of fluid with resulting pulmonary or Transudation of fluid with resulting pulmonary or

systemic edema. systemic edema. 7.7. Activation of neural and humoral systems. Activation of neural and humoral systems. 8.8. Increased activity of the sympathetic nervous system.Increased activity of the sympathetic nervous system.9.9. Increased myocardial contractility, heart rate, and Increased myocardial contractility, heart rate, and

venous tone.venous tone.10.10.Increased peripheral vascular resistance.Increased peripheral vascular resistance.11.11.Increased LV afterload, so that excessive sympathetic Increased LV afterload, so that excessive sympathetic

activity may further depress cardiac function.activity may further depress cardiac function.

The renin–angiotensin–aldosterone The renin–angiotensin–aldosterone system system

1.1. Reduction of renal blood flow and Reduction of renal blood flow and glomerular filtration rate.glomerular filtration rate.

2.2. The renin–angiotensin–aldosterone The renin–angiotensin–aldosterone system is activated.system is activated.

3.3. Increase in peripheral vascular Increase in peripheral vascular resistance.resistance.

4.4. Increase in sodium and water Increase in sodium and water retention.retention.

RemodelingRemodeling Left ventricular dysfunction is a progressive Left ventricular dysfunction is a progressive

process. process. Remodeling occurs in association with Remodeling occurs in association with

homeostatic attempts to decrease wall stress homeostatic attempts to decrease wall stress through increases in wall thickness. through increases in wall thickness.

This ultimately results in a change in the This ultimately results in a change in the geometry of the left ventricle such that: geometry of the left ventricle such that: The chamber dilates, The chamber dilates, hypertrophies,hypertrophies, Becomes more spherical.Becomes more spherical.

It precedes the development of symptoms, by It precedes the development of symptoms, by months or even years. months or even years.

The process of remodeling continues after the The process of remodeling continues after the appearance of symptoms and may contribute appearance of symptoms and may contribute importantly to worsening of symptoms despite importantly to worsening of symptoms despite treatment.treatment.

CausesCauses Ischemic cardiomyopathyIschemic cardiomyopathy HTNHTN DCM:DCM:

ETOHETOH Myocarditis (HIV)Myocarditis (HIV) IdiopathicIdiopathic

CardiotoxinsCardiotoxins Infiltrative cardiomyopathy (sarcoidosis, Infiltrative cardiomyopathy (sarcoidosis,

Amyloidosis, hemochromatosis)Amyloidosis, hemochromatosis) Valvular hear disease.Valvular hear disease.

Stages of HFStages of HF

Stages of Heart Failure and Treatment Options for Systolic Heart Failure.

SymptomsSymptoms

LV failure: LV failure: Exertional dyspnea,Exertional dyspnea, Cough, Cough, Fatigue, Fatigue, OrthopneaOrthopnea PNDPND NocturiaNocturia

RV failure: RV failure: RUQ painRUQ pain Loss of appetiteLoss of appetite NauseaNausea Dependent edemaDependent edema

Exacerbations Exacerbations

1.1. Patient noncompliancePatient noncompliance

2.2. Excessive salt and fluid intakeExcessive salt and fluid intake

3.3. ArrhythmiasArrhythmias

4.4. Excessive activityExcessive activity

5.5. Pulmonary emboliPulmonary emboli

6.6. Intercurrent infectionIntercurrent infection

7.7. Progression of the underlying Progression of the underlying disease.disease.

New York Heart Association New York Heart Association classification classification

II IIII IIIIII IVIV Has major limitations:Has major limitations:

Patient reports are highly subjectivePatient reports are highly subjective Symptoms vary from day to day. Symptoms vary from day to day.

Insufficiently sensitive to be useful in Insufficiently sensitive to be useful in predicting outcomes or assessing the predicting outcomes or assessing the results of treatment.results of treatment.

SignsSigns dyspneic dyspneic cachectic or cyanotic cachectic or cyanotic cold extremities and diaphoresiscold extremities and diaphoresis jugular venous jugular venous S3 & S4 gallopS3 & S4 gallop hyperthyroidism and hypothyroidism hyperthyroidism and hypothyroidism crackles at the lung bases crackles at the lung bases Expiratory wheezing and rhonchi Expiratory wheezing and rhonchi bibasilar dullness to percussion bibasilar dullness to percussion hepatic enlargement—tender or nontender hepatic enlargement—tender or nontender Ascites Ascites Peripheral pitting edema Peripheral pitting edema

LabLab

anemia anemia renal insufficiency renal insufficiency hypokalemia hypokalemia HyperkalemiaHyperkalemia HyponatremiaHyponatremia Thyroid functionThyroid function

Brain natriuretic peptideBrain natriuretic peptide A mean of identifying patients with

elevated left ventricular filling pressures. The assessment of this peptide cannot

reliably distinguish patients with systolic from those with diastolic dysfunction.

Aids in differentiating dyspnea due to HF from dyspnea due to other causes in an emergency setting.

The role of brain natriuretic peptide measurement in the identification and management of patients with symptomatic or asymptomatic left ventricular dysfunction remains to be fully clarified.

EKGEKG CXRCXR EchocardiogramEchocardiogram

Size and function of both ventricles and Size and function of both ventricles and atria. atria.

Pericardial effusion.Pericardial effusion. Valvular abnormalitiesValvular abnormalities Intracardiac shuntsIntracardiac shunts Segmental wall motion abnormalities Segmental wall motion abnormalities

(old MI)(old MI) Dilated cardiomyopathy Dilated cardiomyopathy

CARDIAC CARDIAC CATHETERIZATIONCATHETERIZATION

The combination of:The combination of: AnginaAngina Noninvasive evidence of significant Noninvasive evidence of significant

myocardial ischemia.myocardial ischemia. Symptomatic heart failure.Symptomatic heart failure.

TreatmentTreatment

Primary Targets of Treatment in Heart Failure

Pharmacologic Pharmacologic TreatmentTreatment

CORRECTION OF REVERSIBLE CAUSES:CORRECTION OF REVERSIBLE CAUSES: Valvular lesions Myocardial ischemia Uncontrolled hypertension Arrhythmias Alcohol- or drug-induced myocardial

depression Stop Calcium channel blockers,

antiarrhythmic drugs, and NSAID’s

Diuretic therapyDiuretic therapy

Thiazides Thiazides

Hydrochlorothiazide, metolazone, Hydrochlorothiazide, metolazone, chlorthalidone. chlorthalidone.

Block sodium reabsorption in the cortical Block sodium reabsorption in the cortical diluting segment at the terminal portion diluting segment at the terminal portion of the loop of Henle and in the proximal of the loop of Henle and in the proximal portion of the distal convoluted tubule portion of the distal convoluted tubule

Thiazides are ineffective when the GFR Thiazides are ineffective when the GFR falls below 30–40 mL/min.falls below 30–40 mL/min.

Loop diureticsLoop diuretics

Furosemide, bumetanide and Furosemide, bumetanide and torsemide.torsemide.

Rapid onset and a relatively short Rapid onset and a relatively short duration of action duration of action

Two or more doses are preferable to a Two or more doses are preferable to a single larger dose. single larger dose.

Inhibit chloride reabsorption in the Inhibit chloride reabsorption in the ascending limb of the loop of Henle, ascending limb of the loop of Henle, which results in natriuresis, which results in natriuresis, kaliuresis, and metabolic alkalosis. kaliuresis, and metabolic alkalosis.

Potassium sparing Potassium sparing diuresticsdiurestics

Spironolactone, triamterene, and Spironolactone, triamterene, and amiloride amiloride

Spironolactone is a specific inhibitor Spironolactone is a specific inhibitor of aldosterone.of aldosterone.

INHIBITORS OF THE INHIBITORS OF THE RENIN–ANGIOTENSIN–RENIN–ANGIOTENSIN–

ALDOSTERONE ALDOSTERONE SYSTEMSYSTEM

Why ACEI?Why ACEI?

Decrease angiotensin II.Decrease angiotensin II. Vasodilation.Vasodilation. Decreasing sodium retention by Decreasing sodium retention by

reducing aldosterone. reducing aldosterone. Increase bradykinin levels, Increase bradykinin levels,

stimulate the synthesis of stimulate the synthesis of prostaglandinsprostaglandins and and nitric oxidenitric oxide. .

Why ACEI?Why ACEI?

Reduce mortality by approximately Reduce mortality by approximately 20%20%

Prevent hospitalizationsPrevent hospitalizations Increase exercise toleranceIncrease exercise tolerance Reduce symptoms.Reduce symptoms. Indicated for the management of Indicated for the management of

patients with reduced EFs without patients with reduced EFs without symptoms.symptoms.

Dosing ACEIDosing ACEI

ACE inhibitors should be titrated ACE inhibitors should be titrated over a period of 1–3 months.over a period of 1–3 months.

Cr. 3 and K 5.5 acceptable.Cr. 3 and K 5.5 acceptable. Renal dysfunction is more frequent Renal dysfunction is more frequent

in:in: Diabetics, Diabetics, Older patients, Older patients, Low systolic pressures Low systolic pressures

ARB’sARB’s

Candesartan or valsartan, provide Candesartan or valsartan, provide important benefits as an important benefits as an alternativealternative, , and and in additionin addition, to ACE inhibitors in , to ACE inhibitors in chronic heart failure.chronic heart failure.

No effect on bradykinin, No effect on bradykinin, prostaglandins, and nitric oxide.prostaglandins, and nitric oxide.

SpironolactoneSpironolactone

AldosteroneAldosterone mediates: mediates: Myocardial remodeling and fibrosis.Myocardial remodeling and fibrosis. Sodium retention.Sodium retention. Potassium loss.Potassium loss.

spironolactone should be considered spironolactone should be considered as a neurohormonal antagonist.as a neurohormonal antagonist.

Monitor potassium level after 1 and Monitor potassium level after 1 and 4 weeks of therapy.4 weeks of therapy.

BBBB

BBBB chronic elevations of catecholamines and chronic elevations of catecholamines and

sympathetic nervous system activity sympathetic nervous system activity cause progressive myocardial damage, cause progressive myocardial damage, leading to worsening LV function and leading to worsening LV function and dilation.dilation.

stablestable patients (defined as having no patients (defined as having no recent deterioration or evidence of recent deterioration or evidence of volume overload) with volume overload) with mild, moderate, mild, moderate, and even severeand even severe heart failure should be heart failure should be treated with a -blocker unless there is a treated with a -blocker unless there is a noncardiac contraindication. noncardiac contraindication.

BBBB

Ensure that they were free of fluid Ensure that they were free of fluid retention at the time of initiation.retention at the time of initiation.

Initiation must be done gradually.Initiation must be done gradually.

BBBB

Start low and Start low and go slowgo slow

How to monitor BB?How to monitor BB? Patients should be instructed to monitor their Patients should be instructed to monitor their

weights at home.weights at home. report any increase or change in symptoms report any increase or change in symptoms

immediately. immediately. If heart failure worsens, this can usually be If heart failure worsens, this can usually be

managed by increasing diuretic doses and managed by increasing diuretic doses and delaying further increases.delaying further increases.

Carvedilol, because of its -blocking activity, Carvedilol, because of its -blocking activity, may cause dizziness or hypotension. This can may cause dizziness or hypotension. This can usually be managed by reducing the doses of usually be managed by reducing the doses of other vasodilators and by slowing the pace of other vasodilators and by slowing the pace of dose increases.dose increases.

DIGITALIS GLYCOSIDESDIGITALIS GLYCOSIDES

The only orally active positive inotropic The only orally active positive inotropic agents. agents.

Lack the benefits of the neurohormonal Lack the benefits of the neurohormonal antagonists.antagonists.

Efficacy in reducing the symptoms of heart Efficacy in reducing the symptoms of heart failure has been established.failure has been established.

Digoxin should be used for patients who Digoxin should be used for patients who remain symptomatic when taking diuretics remain symptomatic when taking diuretics and ACE inhibitors as well as for patients with and ACE inhibitors as well as for patients with heart failure who are in atrial fibrillation and heart failure who are in atrial fibrillation and require rate control.require rate control.

VasodilatorsVasodilators

Nitrates and HydralazineNitrates and Hydralazine

Use this combination in addition to Use this combination in addition to other effective therapies in African other effective therapies in African Americans with severe heart failure. Americans with severe heart failure.

A-HeFT trial.A-HeFT trial.

IV NitratesIV Nitrates

Used primarily for acute or severely Used primarily for acute or severely decompensated chronic heart decompensated chronic heart failure, especially when failure, especially when accompanied by hypertension or accompanied by hypertension or myocardial ischemia. myocardial ischemia.

NesiritideNesiritide

Recombinant form of human brain Recombinant form of human brain natriuretic peptide, is a potent natriuretic peptide, is a potent vasodilator that reduces ventricular vasodilator that reduces ventricular filling pressures and improves filling pressures and improves cardiac output. cardiac output.

POSITIVE INOTROPIC POSITIVE INOTROPIC AGENTSAGENTS

Dobutamine and milrinone.Dobutamine and milrinone. The role is limited to:The role is limited to:

Patients with symptoms and signs of low CO.Patients with symptoms and signs of low CO. No response to intravenous diuretics. No response to intravenous diuretics. Maintain patients who are awaiting cardiac Maintain patients who are awaiting cardiac

transplantation.transplantation. No benefit in terms of survival, decreasing No benefit in terms of survival, decreasing

length of admission, or preventing length of admission, or preventing readmission—and significantly increased readmission—and significantly increased rates of sustained hypotension and atrial rates of sustained hypotension and atrial fibrillation. fibrillation.

CALCIUM CHANNEL CALCIUM CHANNEL BLOCKERSBLOCKERS

agents should be avoided unless agents should be avoided unless they are being utilized to treat they are being utilized to treat associated angina or hypertension, associated angina or hypertension, and for these indications amlodipine and for these indications amlodipine is the drug of choice.is the drug of choice.

IMPLANTABLE CARDIOVERTER IMPLANTABLE CARDIOVERTER DEFIBRILLATORSDEFIBRILLATORS

Patients with…Patients with… Chronic heart failure and Chronic heart failure and Ischemic or nonischemic Ischemic or nonischemic

cardiomyopathy with an EF 35%.cardiomyopathy with an EF 35%. SCD-HeFT trial.SCD-HeFT trial.

BIVENTRICULAR PACING BIVENTRICULAR PACING (RESYNCHRONIZATION)(RESYNCHRONIZATION)

Patient criteria:Patient criteria:1.1. NYHA class III or IV heart failure, NYHA class III or IV heart failure,

2.2. EF of 35%, and EF of 35%, and

3.3. QRS duration 120 milliseconds. QRS duration 120 milliseconds.

CARDIAC CARDIAC TRANSPLANTATIONTRANSPLANTATION

1-year survival rates exceeding 80–1-year survival rates exceeding 80–90%90%

Primary Targets of Treatment in Heart Failure

ReferencesReferences

CMDT 2007CMDT 2007 ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary

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