Transcript Heart Failiure and Valve disease

Cardiology Review:
Heart Failure and Valve Disease
March 30, 2009
Dr. Lisa Mielniczuk
Assistant Professor Medicine
University of Ottawa Heart Institute
Outline
• Heart Failure
– Causes
– Symptoms
– Treatments
• Approach to valve disease
– Aortic stenosis and regurgitation
– Mitral stenosis and regurgitation
HF Prevalence in Canada
4
Chow C-M et al. Can J Cardiol 2005;21(14):1265-71.
Leadership. Knowledge. Community.
Majority of HF Patients Treated by GPs/FPs
5
Tu K et al. Can J Cardiol 2004;20:282-91.
Leadership. Knowledge. Community.
Why Heart Failure?
Projected number of incident hospitalizations for CHF
patients, using high, medium and low population growth
projections in Canada 1996-2050
HF Cases are on the rise!
Definition
• Condition where the heart cannot pump an
adequate supply of blood at normal filling
pressures to meet the metabolic needs of
the body
• Clinically
– Ventricular dysfunction
– Reduced exercise capacity
– Impaired quality of life
– Shortened life expectancy
Cardiomyopathy
• Characterized by ventricular
– Dilatation
– Hypertrophy
• Frank Starling: CO = SV x HR
• Laplace: Tension = Press x rad/ 2 x thick
Gross Pathologic Findings
• Enlargement of all 4 chambers
• Normal valves with regurgitation
– Enlargement and distortion of the subvalvular
apparatus
• Intracavitary thrombi
Increased contractility
Normal
A
Heart Failure
Hypotension
Stroke volume (cardiac output)
Heart Failure
B
C
Pulmonary congestion
Left ventricular end diastolic pressure (volume)
Classification of Cardiomyopathy
• Multiple ways to consider classification:
– Etiologic
– Systolic vs. Diastolic
– Right vs. Left
– Pathologic
General Causes of HF
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Coronary artery disease
Myocardial infarction
Valve disease
Idiopathic cardiomyopathy
Hypertension
Myocarditis / pericarditis
Arrhythmias
Thyroid disease
Pregnancy
Toxins (alchohol, chemotherapy)
Dilated Cardiomyopathy
• CAD is the most common
cause of systolic
dysfunction
• Idiopathic (50%)
• Familial
• Substance abuse
• What are the other nonischemic causes of a dilated
cardiomyopathy?
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Myocarditis
Infiltrative disease
Peripartum
HIV
Chemotherapy
Electrolyte imbalance
Nutritional: thiamine,scurvy
Mechanisms and Causes of HF
Impaired Contractility
Myocardial infarction
Transient ischemia
Chronic volume overload
MR/AR
Dilated cardiomyopathy
Increased Afterload
AS
Uncontrolled HTN
Systolic Dysfunction
Left Sided HF
Diastolic Dysfunction
Obstruction of LV filling
MS
Pericardial constriction or
tamponade
Impaired ventricular relaxation
LVH
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Transient ischemia
Mechanisms and Causes of HF
Cardiac Causes
Left sided HF
Pulmonary stenosis
Right ventricular infarction
Right Sided HF
Pulmonary Vascular Disease
Pulmonary emobolism
Pulmonary HTN
Right ventricular infarction
Parenchymal pulmonary disease
COPD
Interstitial lung disease
Chronic infections
Adult respiratory distress syndrome
The Heart Failure Continuum
Functional Classification
ACC/AHA STAGES OF
HEART FAILURE
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
NYHA FUNCTIONAL
CLASS
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)
INCREASING SEVERITY OF HEART FAILURE
CLASS IV
•Severe limitation,
may experience
symptoms at rest
Stages of Heart Failure
STAGE A
High risk but no
structural heart disease
•HTN, ASCD
•DM, obesity
•FH
•cardiotoxins
Treat HTN,
lipids
Smoking
cessation
ACE or
ARB if
appropriate
STAGE B
STAGE C
STAGE D
Structural heart
disease but no
symptoms
Current or prior
symptoms HF
Refractory HF
•Previous MI
•LVH, low EF
•Valvular disease
•Structural
disease plus
symptoms
•Marked symptoms
despite maximal meds
•hospitalized
ACE or
ARB
BB
Routine: ACE, BB
and diuretics
Selected: aldo
agents, ARBs, dig,
nitrates
Devices:CRT/ICD
End of life
MCS
transplant
Diagnosis of HF
• Constellation of symptoms and signs
• CXR
• Alternative Methods
– Invasive hemodynamic studies
– Echocardiogram
– Serum BNP testing
Symptoms and Signs of HF
Increased filling pressures
Congestion
Poor Cardiac Output
Poor Perfusion
Evaluating the JVP
• Consensus: <2 cm
above the sternal angle
considred normal and
>4cm ASA is abnormal
• http://cal.fmc.flinders.ed
u.au/gemp/ClinicalSkills
/clinskil/year1/cardio/car
dio04.htm
Congestion
• Left-Sided
– Symptoms
• Dyspnea
• Orthopnea
• Paroxysmal
nocturnal
dyspnea
• Fatigue
– Signs
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S3 gallop
Displaced apex
MR
Pulmonary rales
Loud P2
• Right-Sided
– Symptoms
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Peripheral edema
Abdominal bloating
Nausea
Anorexia
– Signs
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Elevated JVP
Hepatomegaly
Ascites
Edema
Assessing Perfusion
• Symptoms
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Fatigue
Confusion
Dyspnea
sweating
• Signs
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Hypotension
Tachycardia
Cool extremities
Altered mental status
Rising creatinine
Liver enzyme
abnormalities
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.
– Cardiac arrhythmias
– Fluid overload -- for example,
kidney failure.
– Cardiomyopathy
– Obstructing valvular lesions -for example
– Myocarditis and infectious
endocarditis
• Non-cardiogenic pulmonary
edema -- due to changes in
capillary permeability
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Smoke inhalation.
Head trauma
Overwhelming sepsis.
Hypovolemia shock
Acute lung re-expansion
High altitude pulmonary edema
Disseminated intravascular
coagulopathy (DIC)
– Near-drowning
– Overwhelming aspiration
– Acute Respiratory Distress
Syndrome (ARDS)
CXR Findings of Pulmonary
Edema
• cardiogenic pulmonary edema • Non-cardiogenic pulmonary
• Kerley B lines (septal lines)
edema
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– 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
– 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
– On CT
• Gravity-dependent
consolidation or ground glass
opacification
• Air bronchograms are
common
cuffing
Alveolar
edema
Kerley B
Goals of Therapy
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Identify and Treat the Underlying Cause
Eliminate the acute precipitant
Manage HF symptoms
Modulate the neurohormonal response
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
underlying disease
Pharmacotherapy
↓cardiac function
+ inotropes
 wall stress
↓renal/tissue perfusion
vasodilators
Peripheral/pulmonary
edema
BB
Neurohormonal changes
 ANF
 vascular resistance
 norepinephrine
ACE I
diuretics
 aldosterone
sprionolactone
Na/fluid accumulation
 angiotensin II
Management Strategy
Education
Severe symptoms: refer to specialist, ER or HF clinic
Risk
factor
reduction
Fluid/salt
regimen
If EF>40%: treat cause (HTN)
If EF<40%
ACE I +Beta blocker
intolerant
Prescribe ARB
Consider nitrates
Titrate to target doses
If QRS>120, consider CRT
If EF<30% consider ICD
Clinically stable
•Add ARB
NYHA III
•Digoxin or
nitrates
•Combo diuretics
•spironolactone
Continue therapy
Class IIIb-IV
Can J Cardiol 2007; 23
MERIT HF Study
The MERIT-HF Study Group, Lancet 1999; 353:2001
US CARVEDILOL TRIAL
SOLVD-P
Exner, DV, Dries, DL,Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916.
CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429
meta-analysis of five trials involving 12,763 patients
Flather, MD,Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575
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
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SOB at rest
Pulmonary congestion (orthopnea, PND etc)
Pulmonary HTN (RHF)
Hoarseness from laryngeal nerve compression
MS - Examination
• Loud S1
– From high pressure gradient from LA and LV
• Opening snap
– Sudden tensing of chordae and stenotic
leaflets on valve opening
• 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 - Causes
Mitral Annulus
•Annular calcification
Leaflets
•Rheumatic disease
•Endocarditis
•Myxomatous disease
•prolapse
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 les than total LV CO
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Elevation of LA volume
Reduction of forward CO
Volume related stress on LV
Severity depends on:
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Size of orifice during regurge
SVR opposing LV blood flow
LA compliance
Duration of regurgitation
MR – Clinical Presentation
• Chronic
– Fatigue
– If LV contractile dysfunction – heart failure
• Acute
– Pulmonary edema
– hypotension
MR - Examination
• Murmur
– Pansystolic murmur heard at apex
• S3
– Reflects increased volume returning to LV in
early diastole
• LV displacement
– If LV enlargement present
MR - Diagnosis
• CXR
– Pulmonary edema if
acute
– Left atrial and
ventricular dilatation
– Calcification of MV
• Echo
– Identifies structural
cause of MR
– LV /LA size and
function
MR - Treatment
• Acute MR
– Vasodilators and
diuretics
– Reduce the resistance
to forward flow
– Relieve pulmonary
edema
• Chronic
– Operative repair once
symptoms develop or
LV starts to dilate
Aortic Stenosis
• Thickened and
restricted
opening of
aortic valve
• Obstruction to
LV outflow
AS - Causes
• Age related
calcification of
valve
• Rheumatic heart
disease
• Congenital
bicuspid AV
AS - Pathophysiology
• Blood flow across the AV is impeded
• Once AVA reduced by 50%:
– Significant LV pressure needed to drive blood into
aorta
– Results in LV hypertrophy
– Reduced LV compliance
• 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
AF
6 months
AS -Exam
• Murmur
– Late peaking systolic ejection murmur
• Carotid pulse
– Weakend (parvus) and delayed (tardus) due
to LV obstruction
• 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
– Endocarditis prophylaxis
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