A.A.

Gede Budhitresna MD,PhD,FINASIM

WARMADEWA SCHOOL MEDICINE

Heart Failure

The most common reason for

hospitalization in adults >65 years

Heart Failure
Results from any structural or functional abnormality that impairs the ability of the ventricle to eject blood (Systolic Heart Failure) or to fill with blood (Diastolic Heart Failure).

Definition-Heart Failure (HF) Key Concepts

CO = SV x HR-becomes insufficient to meet metabolic needs of body SV- determined by preload, afterload and myocardial contractility EF< 40% (need to understand) Classifications HF Systolic failure- dec. contractility Diastolic failure- dec. filling Mixed

Heart Failure

The Vicious Cycle of Congestive Heart Failure

LV Dysfunction causes Decreased cardiac output

Decreased Blood Pressure and Decreased Renal perfusion

Stimulates the Release of renin, Which allows conversion of Angiotensin to Angiotensin II. Angiotensin II stimulates Aldosterone secretion which causes retention of Na+ and Water, increasing filling pressure

 Main causes Ischemic heart disease, Cardiomyopathy, Hypertension Other causes: Valvular heart disease, Congenital heart disease, Alcohol and drugs, Hyperdynamic circulation (anaemia, thyrotoxicosis, haemochromatosis, Paget's disease), Right heart failure (RV infarct, pulmonary hypertension, pulmonary embolism, cor pulmonale (COPD)), Arrhythmia and Pericardial disease.

 Impaired cardiac contractility as in myocardial infarction and cardiomyopathy Ventricular outflow obstruction (pressure overload) as in hypertension and aortic stenosis Impaired ventricular fillings as in mitral stenosis and constrictive pericarditis Volume overload as in mitral regurgitation

 Infections Arrhythmias Physical, Dietary, Fluid, Environmental, and Emotional Excesses. Myocardial infarction Pulmonary embolism Anemia Thyrotoxicosis and pregnancy Aggravation of hypertension Rheumatic, Viral, and Other Forms of Myocarditis Infective endocarditis

The heart depends on a number of adaptive mechanisms for maintenance of its pumping function: 1- The Frank Starling mechanism (cardiac dilatation) 2- Myocardial hypertrophy 3- Increased release of catecholamines, activation of renin-angiotensin-aldosteron system and other Neurohumoral adjustments N.B.: These effects are compensatory at first, then they are overwhelmed and become pathophysiological

PATHOPHYSIOLOGICAL CHANGES
Ventricular dilatation Myocyte hypertrophy Increased collagen synthesis Altered myosin gene expression Altered sarcoplasmic Ca2+-ATPase density Increased ANP secretion Salt and water retention Sympathetic stimulation Peripheral vasoconstriction

Neurohormonal changes
N/H changes Favorable effect
HR , contractility, vasoconst. V return, filling Salt & water retention VR

Unfavor. effect
Arteriolar constriction After load workload O2 consumption Vasoconstriction after load Same effect

Sympathetic activity

Renin-Angiotensin Aldosterone Vasopressin

Same effect

interleukins &TNF

May have roles in myocyte hypertrophy Vasoconstriction VR

Apoptosis

Endothelin

After load

Types of Heart Failure

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

High-Output Heart Failure

Right-Ventricular Failure

Causes of Low-Output Heart Failure

Systolic Dysfunction
Coronary Artery Disease Idiopathic dilated cardiomyopathy (DCM) 50% idiopathic (at least 25% familial) 9 % mycoarditis (viral) Ischemic heart disease, perpartum, hypertension, HIV, connective tissue disease, substance abuse, doxorubicin Hypertension Valvular Heart Disease

Diastolic Dysfunction

Hypertension Coronary artery disease Hypertrophic obstructive cardiomyopathy (HCM) Restrictive cardiomyopathy

Can You Have RVF Without LVF?

What is this called?
COR PULMONALE

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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

Physical Examination in Heart Failure

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>

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Measuring Jugular Venous Pressure

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

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.

Chest X-ray in Heart Failure

Cardiomegaly Cephalization of the pulmonary vessels Kerley B-lines Pleural effusions

Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc. pressure or volume overload as in Heart failure

American Heart Assn-Media files Animations

Pulmonary vessel congestion

Pulmonary Edema due to Heart Failure

Kerley B lines

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

Further Cardiac Testing in Heart Failure

Exercise Testing
Should be part of initial evaluation of all patients with CHF.

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.

Further testing in Heart Failure

Endomyocardial biopsy
Not frequently used Really only useful in cases such as viral-induced cardiomyopathy

Ventricular remodeling

Heart Failure Classification Systems

New York Heart Association Functional Classification of HF
Classes I to IV

ACC/AHA Stages of HF (newer)

Stages A to D

STAGE
CLASS 1 MILD
CLASS 2 MILD CLASS 3 MODERATE CLASS 4 SEVERE

DISABILITY
No symptoms Can perform ordinary activities without any limitations
Mild symptoms - occasional swelling Somewhat limited in ability to exercise or do other strenuous activities Noticeable limitations in ability to exercise or participate in mildly strenuous activities Comfortable only at rest Unable to do any physical activity without discomfort Some HF symptoms at rest
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Chronic Treatment of Systolic Heart Failure

Correction of systemic factors
Thyroid dysfunction Infections Uncontrolled diabetes Hypertension

Lifestyle modification
Lower salt intake Alcohol cessation Medication compliance

Maximize medications
Discontinue drugs that may contribute to heart failure (NSAIDS, antiarrhythmics, calcium channel blockers)

Order of Therapy
1. 2. 3. 4. 5. 6. Loop diuretics ACE inhibitor (or ARB if not tolerated) Beta blockers Digoxin Hydralazine, Nitrate Potassium sparing diuretics

Diuretics
Loop diuretics
Furosemide, buteminide For Fluid control, and to help relieve symptoms

Potassium-sparing diuretics
Spironolactone, eplerenone Help enhance diuresis Maintain potassium Shown to improve survival in CHF

ACE Inhibitor
Improve survival in patients with all severities of heart failure. Begin therapy low and titrate up as possible:
Enalapril 2.5 mg po BID Captopril 6.25 mg po TID Lisinopril 5 mg po QDaily

If cannot tolerate, may try ARB (angiotensin receptor blocker)

ACE Inhibitors for CCF

Beta Blocker therapy

Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can improve overall and event free survival in NYHA class II to III HF, probably in class IV. Contraindicated:
Heart rate <60 bpm Symptomatic bradycardia Signs of peripheral hypoperfusion COPD, asthma PR interval > 0.24 sec, 2nd or 3rd degree block

Beta blockers in CCF

Hydralazine plus Nitrates

Dosing:
Hydralazine
Started at 25 mg po TID, titrated up to 100 mg po TID

Isosorbide dinitrate
Started at 40 mg po TID/QID

Decreased mortality, lower rates of hospitalization, and improvement in quality of life.

Digoxin
Given to patients with HF to control symptoms such as fatigue, dyspnea, exercise intolerance Shown to significantly reduce hospitalization for heart failure, but no benefit in terms of overall mortality.

DIGOXIN cont.
Cardiac glycosides : Digoxin : Inhibition of Na/K ATPase pump increase intracellular sodium concentration eventually increase cytosolic calcium. It restores the vagal tone and abolishes the sympathetic over activity.

DIGOXIN cont.
Cardiac glycosides : Digoxin Increase the refractoriness of AV node thus decrease ventricular response to atrial rate. Digoxin is used as a first-line drug in patients with congestive heart failure who are in atrial fibrillation.

DIGOXIN cont.
Digoxin : Adverse effects / Precautions : Nausea, vomiting, gynecomastia, visual disturbances and psychosis. Ventricular bigeminy, AV block and bradycardia. Amiodarone and verapamil can increase the plasma concentration of digoxin by inhibiting its excretion.

DIGOXIN cont.
Digoxin toxicity treatment: Toxicity can be treated with higher than normal doses of potassium. Digoxin antibody (digibind) is used specifically to treat life-threatening digoxin overdose.

Other important medication in Heart Failure -- Statins

Statin therapy is recommended in CHF for the secondary prevention of cardiovascular disease. Some studies have shown a possible benefit specifically in HF with statin therapy
Improved LVEF Reversal of ventricular remodeling Reduction in inflammatory markers (CRP, IL-6, TNF-alphaII)

Meds to AVOID in heart failure

NSAIDS
Can cause worsening of preexisting HF

Thiazolidinediones
Include rosiglitazone (Avandia), and pioglitazone (Actos) Cause fluid retention that can exacerbate HF

Metformin
People with HF who take it are at increased risk of potentially lethic lactic acidosis

Implantable CardioverterDefibrillators for HF

Sustained ventricular tachycardia is associated with sudden cardiac death in HF. About one-third of mortality in HF is due to sudden cardiac death. Patients with ischemic or nonischemic cardiomyopathy, NYHA class II to III HF, and LVEF 35% have a significant survival benefit from an implantable cardioverter-defibrillator (ICD) for the primary prevention of SCD.

Left ventricular assist device

Management of Refractory Heart Failure

Inotropic drugs:
Dobutamine, dopamine, milrinone, nitroprusside, nitroglycerin

Mechanical circulatory support:

Intraaortic balloon pump Left ventricular assist device (LVAD)

Cardiac Transplantation
A history of multiple hospitalizations for HF Escalation in the intensity of medical therapy A reproducable peak oxygen consumption with maximal exercise (VO2max) of < 14 mL/kg per min. (normal is 20 mL/kg per min. or more) is relative indication, while a VO2max < 10 mL/kg per min is a stronger indication.

Intraaortic balloon pump

IABP Machine

Acute Decompensated Heart Failure Cardiogenic pulmonary edema is a common and sometimes fatal cause of acute respiratory distress. Characterized by the transudation of excess fluid into the lungs secondary to an increase in left atrial and subsequently pulmonary venous and pulmonary capillary pressures.

Acute Decompensaated Heart Failure (cont.) Causes:

Acute MI
Rupture of chordae tendinae/acute mitral valve insufficiency

Volume Overload
Transfusions, IV fluids Non-compliance with diuretics, diet (high salt intake)

Worsening valvular defect

Aortic stenosis

Decompensated Heart Failure

Symptoms
Severe dyspnea Cough

Clinical Findings
Tachypnea Tachycardia Hypertension/Hypotension Crackles on lung exam Increased JVD S3, S4 or new murmur

Labs/Studies in Acute Decompensated Heart Failure

Chemistry, CBC EKG Chest X-ray May consider cardiac enzymes 2D-Echo

Decompensated Heart Failure

Treatment
Strict Is and Os, daily weights Oxygen, mechanical ventilation if needed Loop diuretics (Lasix!) Morphine Vasodilator therapy (nitroglycerin) Nesiritide (BNP) can help in acute setting, for short term therapy

Heart Failure Complications

Pleural effusion Atrial fibrillation (most common dysrhythmia) Loss of atrial contraction (kick) -reduce CO by 10% to 20% Promotes thrombus/embolus formation inc. risk for stroke Treatment may include cardioversion, antidysrhythmics, and/or anticoagulants

Heart Failure Complications

High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF <35%

HF lead to severe hepatomegaly, especially with RV failure Fibrosis and cirrhosis - develop over time Renal insufficiency or failure

Keys to understanding HF
All organs (liver, lungs, legs, etc.) return blood to heart When heart begins to fail/ weaken> unable to pump blood forward-fluid backs up > Inc. pressure within all organs. Organ response LUNGS: congested > stiffer , inc effort to breathe; fluid starts to escape into alveoli; fluid interferes with O2 exchange, aggravates shortness of breath.

Shortness of breath during exertion, may be early symptoms > progresses > later require extra pillows at night to breathe > experience "P.N.D." or paroxysmal nocturnal dyspnea . Pulmonary edema Legs, ankles, feet- blood from feet and legs > back-up of fluid and pressure in these areas, heart unable to pump blood as promptly as received > inc. fluid within feet and legs causes fluid to "seep" out of blood vessels ; inc. weight

In God we trust, everything else should be based on evidence

(Claude Organ)

THANK YOU

agbudhitresna@yahoo.com