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Cardiology Review: Heart Failure and Valve Disease April 8, 2013. Dr. Lisa M Mielniczuk Assistant Professor Medicine University of Ottawa Heart Institute. Outline. Heart Failure Causes Symptoms Treatments Cardiomyopathies Approach to valve disease Mitral stenosis and regurgitation - PowerPoint PPT Presentation
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Cardiology Review:Heart Failure and Valve Disease
April 8, 2013
Dr. Lisa M Mielniczuk
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)
Str
oke
volu
me
(ca
rdia
c o
utpu
t)
A
B C
Pulmonary congestion
Hy
po
ten
sio
n
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
What does the MCC want?
• How will you make the diagnosis?– Keep it on your differential of acute/chronic
dyspnea– Look for the signs and symptoms of heart
failure– Recognize the underlying causes of HF– Echo/ chest xray / labs
What does the MCC Want?
• How will you treat?– Acutely: diuretics, identify and remove precipitant– Chronically: beta blocker, ACEI etc.
• When to refer to a specialist?– Persistent or severe symptoms– Poor treatment response– Uncertain diagnosis
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
Aortic Stenosis Causes:
• Valvular– Congenital, acquired calcific, rheumatic
• Subvalvular– Hypertrophic cardiomyopathy
• Supravalvular– Coarctation, congenital
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
What does the MCC want?
• What is your ddx of a patient with a systolic murmur?– Systolic ejection: aortic stenosis (pulmonary
stenosis)– Pansystolic: mitral regurgitation or tricuspid
regurgitation (VSD)
What does the MCC Want?
• How do I know if it is pathologic?– Severity (loud, new)– Other signs of heart dysfunction – Concomitant HF, arrhythmia, ischemia etc.
• What do I do about it?– Echo, ECG, labs– Refer to specialist– Treat HF if an issue– Endocarditis prophylaxis
What does the MCC Want?
• What is the ddx of a diastolic murmur?– Aortic insufficiency– Mitral stenosis– (tricuspid stenosis)
• How do I know if it is pathologic?– Chances are it is
• What do I do about it?– Echo, chest xray, labs– Treat HF– refer
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