Transcript Cardiology Review: Heart Failure and Valve Disease April 20, 2007

Cardiology Review:
Heart Failure and Valve Disease
March 17, 2016
Dr. Sharon Chih
Assistant Professor Medicine
University of Ottawa Heart Institute
Outline
• Heart Failure
– Causes
– Clinical features
– Management
• Approach to valve disease
– Mitral stenosis and regurgitation
– Aortic stenosis and regurgitation
Definition: Heart Failure
• Condition where the heart cannot pump an adequate
supply of blood at normal filling pressures to meet the
metabolic needs of the body
• Clinically
– Reduced cardiac output
– Congestion
– Impaired quality of life
– Reduced life expectancy
Distinguish from cardiomyopathy
• Pathologic abnormality of myocardium
resulting in abnormal myocardial structure
- cardiac dilatation and hypertrophy
• All patients with cardiomyopathy do not
have HF
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.
Ischemic heart disease
Valvular disease
Hypertension
Dilated cardiomyopathy
•
•
•
•
•
•
5.
6.
Idiopathic
Myocarditis / pericarditis
Arrhythmias
Thyroid disease
Pregnancy
Toxins (alcohol, chemotherapy)
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
•
•
•
Amyloid
Sarcoidosis
hemochromatosis
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 embolism
Pulmonary HTN
Right ventricular infarction
Parenchymal pulmonary disease
COPD
Interstitial lung disease
Chronic infections
Adult respiratory distress syndrome
Diagnosis of HF
•
•
•
•
Constellation of symptoms and signs
CXR
Echocardiogram
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
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•
•
•
•
S3 gallop
Displaced apex
MR
Pulmonary rales
Loud P2
• Right-Sided
– Symptoms
•
•
•
•
Peripheral edema
Abdominal bloating
Nausea
Anorexia
Signs
•
•
•
•
Elevated JVP
Hepatomegaly
Ascites
Edema
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
• Myocarditis and infectious
endocarditis
Non-cardiogenic pulmonary edema due to changes in capillary permeability
• 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
•
•
•
•
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 doughnutshaped 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
– On CT
• Gravity-dependent
consolidation or ground glass
opacification
cuffing
Alveolar
edema
Kerley B
The Role of the Echo in HF
Diagnosis
• Essential screening tool for all patients
suspected with HF
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Systolic and diastolic performance
Regional wall motion abnormalities
Valvular disease
Pericardial disease
Pulmonary hypertension
Natriuretic Peptides
Schlendorf et al. Curr Treat Options Cardiovasc Med
Natriuretic Peptides - Diagnosis
SO YOUR PATIENT HAS
HEART FAILURE… WHAT
NOW?
The clinical course of heart failure with associated types and
intensities of available therapies
Larry A. Allen et al. Circulation. 2012;125:1928-1952
Copyright © American Heart Association, Inc. All rights reserved.
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
Goals of Therapy
1.
2.
3.
4.
5.
Identify and Treat the Underlying Cause
Eliminate the acute precipitant
Manage HF symptoms
Slow progression of LV disease
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
Heart Failure Management Guidelines
• CCS 2014 focused update: CJC 2015;31:3-16
• ACCF/AHA 2013: JACC 2013;62:e147-239
• ESC 2012: EHJ 2012;33:1787-1847
• ACCF/AHA/HRS focused device update: JACC
2012;60:1297-1313
• HFSA 2010: Journal of Cardiac Failure 2010;16:475-539
• NHF/CSANZ 2011 update: MJA 2011;194:405-9
Overview of Chronic HF
Management
1. Nonpharmacologic
2. Pharmacologic
3. Surgery
4. Devices
5. Heart transplantation
Nonpharmacologic
1.
2.
3.
4.
5.
6.
7.
8.
Physical exercise
Diet
• Na restriction <1500 mg/d
• Fluid restriction: 1-1.5 L/d
• Low saturated fat, high fibre
Smoking cessation
Abstain from alcohol
Vaccinations
• Pneumococcal, influenza
Avoid medications that may exacerbate HF
• NSAIDS, thiazolidinediones, non-dihydropyridine Ca channel
blockers, tyrosine kinase inhibitors, clozapine, TCA
Screen for depression/anxiety
Education
• Indications/adverse effects of medications
• Symptoms to monitor
• Management of fluid retention
• Regular contact with GP/Cardiologist
Pharmacologic
1. Prognostic
• ACEI/ARB
• Beta-blockers
• Mineralcorticoid receptor antagonists
• Hydralazine/Nitrates
• ARNI
2. Reduce hospitalisations/Improve symptoms
• Ivabradine
• Digoxin
3. Other
• Iron
• Antithrombotics
BB
ACE I
sprionolactone
diuretics
ACEI/ARB/Nitrates+Hydralazine
• ACEI for symptomatic and asymptomatic patients EF ≤40%
Class I Recommendation, Level of Evidence A
• ACEI intolerance
• Cough, angioedema: ARBs Class I Recommendation, Level of Evidence A
• Renal failure/↑K+: hydralazine/nitrate Class IIb Recommendation, Evidence
C
• Hydralazine/isosorbide dinitrate recommended in addition to BB/ACEI for
symptomatic HF
• African Americans: Class I Recommendation, Level of Evidence B
• Non African Americans: Class IIa Recommendation, Level of Evidence B
A-HEFT
Taylor et al. NEJM, 2004
•N = 1050 AA, NYHA III-IV
•ACEI + BB
•Hydralazine 37.5-75 mg tds
ISDN 20-40 mg tds
•RRR 43% (NNT = 25)
SOLVD
Exner et al. NEJM, 2001
•Enalapril vs. placebo
•Hospitalisations higher in blacks
•Significant benefit with enalapril
in whites but not blacks
Beta-Blockers
• BB for symptomatic and asymptomatic patients EF ≤40%
Class I Recommendation, Level of Evidence A
• Use BB shown to be effective in trials
• Carvedilol 3.125 – 25 mg bd
• Metoprolol succinate 12.5 – 200 mg od
• Bisoprolol 1.25 – 10 mg od
• Nebivolol 1.25 – 10 mg od
• DO NOT use when patient is WET or in SHOCK
• Wait till acute episode has resolved then initiate
• Start low and go slow - titrate q 2 weeks
• Try NOT to stop…unless WET or in SHOCK
• Reduce dosage if necessary. Avoid abrupt discontinuation
• Reinstate gradually before discharge
Mineralcorticoid Receptor Antagonists
TRIAL
RALES
Pitt et al. NEJM 1999;341:709
EPHESUS
Pitt et al. NEJM 2003;348:1309
EMPHASIS – HF
Zannad et al. NEJM 2011;364:11
MRA
N
Spironolactone 1663
25-50 mg od
NYHA
LVEF
RRR
Mortality
NNT
III-IV
≤35%
30%
9
Eplerenone
25-50 mg od
6632 2wk post MI
+ HF or DM
≤40%
15%
44
Eplerenone
25–50 mg od
2737
≤30%*
24%
33
II
*<35% if QRS >130 ms)
•
MRA for NYHA II-IV patients EF ≤35% despite ACEI/BB
Class I Recommendation, Level of Evidence A
•
Not recommended if Creatinine <220, K < 5.0 mmol/L
•
Monitor creatinine and potassium 1 wk, 4 wk, 3 mnths
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
Valvular Disease
Heart Sounds: A Review
Heart Sounds
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
– Minimally calcified
– No significant MR
– No thrombus
• Surgical repair
• 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 regurgitation
– 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