Transcript basics Cardiology review Dr. L Mielniczuk2013

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
Increased contractility
Normal
A
Heart Failure
Hypotension
Stroke volume (cardiac output)
Pathophysiology of Heart Failure
B
C
Pulmonary congestion
Left ventricular end diastolic pressure (volume)
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.
2.
3.
4.
5.
Coronary artery disease /
myocardial infarction
Valvular disease
Hypertension
Diabetes
Cardiomyopathy
–
A. DILATED
•
•
•
•
•
•
–
–
Idiopathic
Myocarditis / pericarditis
Arrhythmias
Thyroid disease
Pregnancy
Toxins (alcohol,
chemotherapy)
B. HYPERTROPHIC
C. RESTRICTIVE
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
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 Cardiac Output
Poor Perfusion
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.ed
u.au/gemp/ClinicalSkills
/clinskil/year1/cardio/car
dio04.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?
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
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
underlying 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 ACEI 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
Who needs a bB?
• All HF patients with LVEF 40% (use clinically proven beta-
blocker)
• In stabilized HF patients with NYHA Class IV symptoms
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
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
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
• 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
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
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–
–
–
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 - Causes
MITRAL 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