Cardiology Review:Heart Failure and Valve Disease

April 7, 2010

Dr. Nisha D’Mello

Assistant Professor Medicine

University of Ottawa Heart Institute

Outline

• Heart Failure– Causes– Symptoms– Treatments

• Cardiomyopathies• Approach to valve disease

– Mitral stenosis and regurgitation– Aortic stenosis and regurgitation

Define Heart Failure

Definition

• Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body

• HF is a complex syndrome in which abnormal heart function results in – clinical symptoms and signs of

• low cardiac output and/or • pulmonary or systemic congestion

Pathophysiology of Heart Failure

Increased contractility

Normal

Heart Failure

Left ventricular end diastolic pressure (volume)

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Pulmonary congestion

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Cardiomyopathy

• Characterized by ventricular – Dilatation– Hypertrophy

• Frank Starling: CO = SV x HR

• Laplace: Tension = Press x rad/ 2 x thick

WHAT CAUSES HEART FAILURE?

Classification of Heart Failure Causes

• Multiple ways to consider classification:– Etiologic– Systolic vs. Diastolic– Right vs. Left

General Causes of HF

1. Coronary artery disease / myocardial infarction

2. Valvular disease3. Hypertension4. Diabetes5. Cardiomyopathy

– A. DILATED• Idiopathic• Myocarditis / pericarditis• Arrhythmias• Thyroid disease• Pregnancy• Toxins (alcohol,

chemotherapy)– B. HYPERTROPHIC– C. RESTRICTIVE

Mechanisms and Causes of HF

Left Sided HF

Impaired ContractilityMyocardial infarctionTransient ischemiaChronic volume overload

MR/ARDilated cardiomyopathy

Increased AfterloadASUncontrolled HTN

Systolic Dysfunction

Diastolic Dysfunction

Impaired ventricular relaxationLVHHypertrophic cardiomyopathyRestrictive cardiomyopathyTransient ischemia

Obstruction of LV fillingMSPericardial constriction or tamponade

Mechanisms and Causes of HF

Right Sided HF

Cardiac CausesLeft sided HFPulmonary stenosisRight ventricular infarction

Parenchymal pulmonary diseaseCOPDInterstitial lung diseaseChronic infections Adult respiratory distress syndrome

Pulmonary Vascular DiseasePulmonary emobolismPulmonary HTNRight ventricular infarction

The Heart Failure Continuum

poor prognosis

average 1-year mortality rate of 33%

HOW DO YOU DIAGNOSE HEART FAILURE ?

Diagnosis of HF

• Constellation of symptoms and signs

• CXR

• Echocardiogram – MUGA– Serum BNP testing

Symptoms and Signs of HF

Increased filling pressures

Congestion Poor Perfusion

Poor Cardiac Output

Assessing Perfusion

• Symptoms– Fatigue– Confusion– Dyspnea

• Signs– Hypotension– Tachycardia– Cool extremities– Altered mental status– Rising creatinine– Liver enzyme

abnormalities

Congestion

• Left-Sided– Symptoms

• Dyspnea• Orthopnea• Paroxysmal nocturnal

dyspnea

– Signs• S3 gallop• Displaced apex• MR• Pulmonary rales• Loud P2

• Right-Sided– Symptoms

• Peripheral edema• Abdominal bloating• Nausea• Anorexia

Signs• Elevated JVP• Hepatomegaly• Ascites• Edema

Evaluating the JVP

• Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal

• http://cal.fmc.flinders.edu.au/gemp/ClinicalSkills/clinskil/year1/cardio/cardio04.htm

Diagnosis of HF

• Constellation of symptoms and signs

• CXR

• Echocardiogram – MUGA– Serum BNP testing

Pulmonary Edema

• General Considerations

– Increase in the fluid in the lung – Generally, divided into cardiogenic and non-cardiogenic categories.

• Pathophysiology

– Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg)

– Further accumulation occurs in the interstitial tissues of the lungs – Finally, with increasing fluid, the alveoli fill with edema fluid (typically

wedge pressure is 25 mm Hg or more)

Cardiogenic vs. Noncardiogenic pulmonary edema

• Cardiogenic pulmonary edema – Heart failure

• Coronary artery disease with left ventricular failure.

• Cardiomyopathy • Obstructing valvular lesions --

for example– Fluid overload -- for example,

kidney failure.

• Non-cardiogenic pulmonary edema -- due to changes in capillary permeability – LUNG

• Smoke inhalation• Near-drowning • Overwhelming aspiration• Acute Respiratory Distress

Syndrome (ARDS)• Acute lung re-expansion• High altitude pulmonary edema

– CAPILLARY• Overwhelming sepsis • Disseminated intravascular

coagulopathy (DIC)

CXR Findings of Pulmonary Edema

cardiogenic pulmonary edema • Kerley B lines (septal lines)

– Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface

• Pleural effusions – Usually bilateral, frequently the

right side being larger than the left

– If unilateral, more often on the right

• Fluid in the fissures – Thickening of the major or minor

fissure • Peribronchial cuffing

– Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls

• Non-cardiogenic pulmonary edema – Bilateral, peripheral air space

disease with air bronchograms or central bat-wing pattern

– Kerley B lines and pleural effusions are uncommon

– – Typically occurs 48 hours or

more after the initial insult

– Stabilizes at around five days and may take weeks to completely clear

Diagnosis of HF

• Constellation of symptoms and signs

• CXR

• Echocardiogram – MUGA– Serum BNP testing

SO YOUR PATIENT HAS HEART FAILURE… WHAT

NOW?

STAGE A•High risk for developing HF (diabetes, CKD, HTN)•No structural disorder of the heart

STAGE B•Structural disorder of the heart (e.g.. Previous MI)•Not yet developed symptoms of HF

STAGE C•Past or current symptoms of HF•Symptoms associated with underlying structural heart disease

STAGE D•End stage disease•Requires specialized treatment strategies

CLASS I•No symptoms and no limitations in physical activity•No shortness of breath when walking, climbing stairs etc.

CLASS II•Mild symptoms and slight limitation during ordinary physical activity

CLASS III•Marked limitation in activity due to symptoms (fatigue, shortness of breath) with less than ordinary activity (e.g.. Short distances or ADL’s)

CLASS IV•Severe limitation, may experience symptoms at rest

NYHA FUNCTIONAL CLASS

ACC/AHA STAGES OF HEART FAILURE

INCREASING SEVERITY OF HEART FAILURE

Functional Classification

HOW DO YOU TREAT HEART FAILURE?

Goals of Therapy

• 1. Identify and Treat the Underlying Cause– Cardiac cath if necessary

• 2. Eliminate the acute precipitant

• 3. Manage HF symptoms

• 4. Slow progression of LV disease

• 5. Improve long-term survival

Precipitants of HF

• Increased metabolic demands– Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy

• Increased circulating volume– Excessive salt or fluid in diet– Renal failure

• Increased afterload– Hypertension– PE

• Impaired contractility– Negative inotropes– Ischemia

• Failure to take medications

Progression of Progression of underlying diseaseunderlying disease

BB ACE I sprionolactone

diuretics

Management

• 1. Education– Fluid and salt restriction– Daily weights– Avoid precipitants

• 2. Diuretics if volume overloaded• 3. Neurohormonal modulation

– ACE-I– bB– spironolactone

• 4. Devices– CRT– ICD

• 5. Referral for cardiac transplantation

Who needs an ACE-I?

• All HF patients with LVEF <40% should be treated with an ACE-I and a beta-blocker, unless a specific contraindication exists

CONSENSUS Trial . N Engl J Med 1987;316:1429-35. SOLVD Investigators. N Engl J Med 1991;325:293-302. Flather MD et al. Lancet 2000;355:1575-81.

These trials form the basis of ACE-I use in HF with LVEF < 40% and/or post-MI with reduced LVEF and/or HF

• All HF patients with LVEF 40% (use clinically proven beta-blocker)

•In stabilized HF patients with NYHA Class IV symptoms

Who needs a B?

MERIT-HF Study Group. Lancet 1999;353:2001-7. CIBIS II Investigators. Lancet 1999;353:9-13. Packer M et al. Circulation 2002;106:2194-9.

Other Drugs ?

• Nitrates

• Digoxin

• Spironolactone

Management Strategy

Severe symptoms: refer to specialist, ER or HF clinic

If EF>40%: treat cause (HTN)

If EF<40%

ACE I +Beta blocker

Titrate to target doses

NYHA III

Prescribe ARB

Clinically stable

Consider nitrates

Continue therapy

•Add ARB

•Digoxin or nitrates

Class IIIb-IV•Combo diuretics

•spironolactone

Education

Risk factor reduction

Fluid/salt regimen

If EF<30% consider ICD

If QRS>120, consider CRT

intolerant

Can J Cardiol 2007; 23

CARDIOMYOPATHY

Classification of Cardiomyopathy

Dilated Cardiomyopathy

• CAD is the most common cause of systolic dysfunction

• What are the other non-ischemic causes of a dilated cardiomyopathy?

• Idiopathic (50%)• Familial• Substance abuse

• Myocarditis• Infiltrative disease• Peripartum• HIV• Chemotherapy• Electrolyte imbalance• Nutritional: thiamine,scurvy

WHO Definition

• Left and or right ventricular hypertrophy which is usually asymmetric and involves the interventriucular septum

• Inappropriate ventricular hypertrophy without a cardiac or systemic cause

Restrictive CM

• What are some causes of restrictive CM?

• Amyloidosis• Sarcoidosis• Hemochromatosis• Chemotherapy• Endomyocardial

fibrosis

Valvular Disease

Mitral Stenosis

• Restriction and narrowing of mitral valve

• Impairment of left ventricular filling

Mitral Stenosis - Causes

• Rheumatic Fever (>90% cases)– 50% patients will have known history– Average 20 years prior to clinical symptoms

• Congenital stenosis of MV

• Extensive calcification

• endocarditis

MS - Pathophysiology

• LA pressure increases – Increased pulmonary

pressures

• LA dilatation– Atrial fibrillation

• Stagnation of blood in LA– thromboembolism

MS - Clinical Presentation

• Natural history variable• 10 year survival (symptoms)

– 50-60%

• Early onset– Dyspnea and reduced exercise capacity

• Advanced– SOB at rest– Pulmonary congestion (orthopnea, PND etc)– Pulmonary HTN (RHF)– Hoarseness from laryngeal nerve compression

MS - Examination

1. Loud S1– From calcification of mitral valve

2. Opening snap– Sudden tensing of chordae and stenotic leaflets on

valve opening

3. Diastolic murmur– Low frequency– Severity relates to duration

MS - Diagnosis

• ECG– LAE, RVH– Atrial fibrillation

• CXR– LAE, pulmonary vascular

redistribution– Prominent pulmonary

arteries

• Echo– Thickened MV– LAE

MS - Treatment

• Percutaneous balloon valvuloplasty

• Surgical repair

• Antibiotics at time of risk

• Diuretics for vascular congestion

• Decrease HR if AF• anticoagulation

Mitral Regurgitation

• Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole

MR - CausesMITRAL ANNULUS•Annular calcification (MAC)

LEAFLETS•Rheumatic disease•Endocarditis•Myxomatous disease(MVP)

CHORDAE TENDINAE•Rupture•endocarditis

PAPILLARY MUSCLE•Dysfunction (MI or ischemia)

LEFT VENTRICLE•Cavity dilatation

MR - Pathophysiology

• Portion of the LV stroke volume ejected into LA– Forward CO is less than total LV CO

• ↑ LA volume• ↓ forward CO• ↑ Volume in LV subsequently• Severity of MR depends on:

– SVR opposing LV blood flow– LA compliance– Duration of regurgitation– Size of orifice during regurgitation

MR – Clinical Presentation

• Chronic– Fatigue– If LV contractile dysfunction – heart failure

• Acute– Pulmonary edema– hypotension

MR - Examination

1. Murmur– Pansystolic murmur heard at apex

2. S3– Reflects increased volume returning to LV in

early diastole

3. LV displacement– If LV enlargement present

MR - Diagnosis

• CXR– Pulmonary edema if

acute– Left atrial and

ventricular dilatation

• Echo– Identifies structural

cause of MR– LV /LA size and

function

MR - Treatment

• Acute MR– Reduce the resistance

to forward flow (Vasodilators)

– Relieve pulmonary edema (Diuretics)

• Chronic– Operative repair once

symptoms develop or LV starts to dilate

Aortic Stenosis

• Thickened and restricted opening of aortic valve

• Obstruction to LV outflow

Normal Tricuspid Aortic Valve

Aortic Stenosis

Normal Tricuspid Aortic Valve Senile Degenerative / Calcific Aortic Valve

Aortic Stenosis

Normal Tricuspid Aortic Valve Congenital Bicuspid Aortic Valve

Aortic Stenosis

Normal Tricuspid Aortic Valve Rheumatic Aortic Valve

AS - Pathophysiology

• Blood flow across the AV is impeded• Once AVA ↓ 50%:

– Significant LV pressure needed to drive blood into aorta

– Results in LV hypertrophy– ↓ LV compliance (Stiffer LV) =>

Increased end diastolic pressure

AS – Clinical Presentation

• Angina– Imbalance b/w myocardial

oxygen supply and demand

• Syncope– Peripheral vasodilation with

inability to augment CO with exercise

• HF– Increased LAP from high

LVEDP– Contractile dysfunction if

longstanding pressure overload

Symptom Median survival

Angina 5 yrs

Syncope 3 years

HF 2 years

AS -Exam

1. Carotid pulse– Weakend (parvus) and delayed (tardus) due to LV

obstruction

2. Murmur– Late peaking systolic ejection murmur

3. S4

– Atrial contraction into stiff LV

AS - Treatment

• Only effective treatment for severe symptomatic disease is surgical correction

• What if asymptomatic?– 20% of patients will progress over 20 years if

mild disease only

Aortic Regurgitation

AR - Causes

• Abnormalities of valve leaflets– Congenital (bicuspid valves)– Endocarditis– Rheumatic

• Dilatation of aortic root– Aortic aneursym – Aortic dissection– syphilis

AR - Pathophysiology

• Severity of AR– Size of regurgitant orifice– Pressure gradient across valve in diastole– Duration of diastole

• Acute– LV noncompliant– LVEDP rises quickly – pulmonary edema

• Chronic– Chronic volume/pressure overload– Dilates – well compensated

AR – Clinical Manifestations

• SOB on exertion

• Fatigue

• Decreased exercise tolerance

AR - Examination

• Murmur– Blowing diastolic along LSB

• Widened pulse pressure

Name Description

Bisferins Double impulse

Corrigans Marked distention and collapse

deMusset Head bobbing

Duroziez To and fro murmur

Hill Greater popliteal SBP

Muller Uvula pulsations

Quincke Nail bed pulsation

Traube Pistol shot femoral art

AR - Treatment

• Asymptomatic disease progresses very slowly

• Surgery if:– Symptoms– Impaired LV function

• Death occurs within 4 years after angina or 2 years after HF

Summary Slide

• Heart Failure– Understand causes of

systolic and diastolic HF

– Awareness of the presentation of left vs. right HF

– Know treatment priniciples

• Valve Disease– Identify the most

common causes of 4 common valve lesions

– Remember clinical presentations

– Surgery treatment of choice any time symptoms present or LV dysfunction

Cardiology Review:Heart Failure and Valve Disease

April 7, 2010

Dr. Nisha D’Mello

Assistant Professor Medicine

University of Ottawa Heart Institute