Transcript Valvular Emergencies

Valvular Emergencies
October 11, 2005
Dr. Kanagala
Introduction

There may be abnormalities of cusps,
chordae, or papillary muscles causing
valvular dysfunction.
 Significant valvular abnormality increases
stroke rate 3.2 times and death rate 2.5
times
Chronic Valve Disease
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There may be decades between onset of
dysfunction and symptoms
 Dilation or hypertrophy may preserve
cardiac function
 Account for around ninety percent of
valvular disease
Acute Valve Disease
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Acute valve disease can result in dramatic
symptoms.
Diagnosing a New Murmur
Consider murmur in context of patient’s
medical condition
 Patient may have normal cardiac anatomy,
but murmurs can be associated with other
disease states.
 Examples include anemia, thyrotoxicosis,
sepsis, fever, renal failure, and pregnancy
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Diagnosing a New Murmur
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A diastolic murmur or new murmur warrants
cardiology referral for evaluation/echo.
 Urgency for accurate diagnosis and referral or
admission depends on severity of symptoms not
presence of murmur unless aortic stenosis and
syncope is suspected. Patient may be at risk for
recurrent cardiovascular event.
Innocent or Physiologic
Murmur

No abnormal symptoms or signs
 Soft, systolic ejection murmur begins after
S1 and ends before S2, and heart sounds are
normal
 Review of symptoms reveals no symptoms
compatible with cardiovascular disease, and
complete physical exam is normal.
Mitral Stenosis
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Most common cause is rheumatic heart
disease
 Progressive stenosis may lead to pulmonary
hypertension causing pulmonary and
tricuspid incompetence
 Most patients develop atrial fibrillation
Clinical Features of Mitral
Stenosis
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Symptoms include: tachycardia, anemia,
pregnancy, infection, emotional upset, Afib, exertional dyspnea, paroxysmal
nocturnal dyspnea, acute pulmonary edema,
hemoptysis, orthopnea, PAC, systemic
emboli and infarction, right sided heart
failure
Clinical Features continued…
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mid-diastolic rumbling murmur with
crescendo toward S2
 With onset of Afib the presystolic
accentuation of the murmur disappears. S1
is loud and followed by a loud opening snap
(high pitched, heard at apex)
Clinical Features continued…
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Apical impulse is small and tapping
 Systolic blood pressure is normal or low
 Signs of pulmonary hypertension include
thin body habitus, peripheral cyanosis, and
cool extremities
Diagnosis

ECG: notched or biphasic P waves and right
axis deviation
 Chest X-ray: straightening of left heart
border, findings of pulmonary congestion
like kerley B lines and increase in vascular
markings
 Confirmed with echocardiography (TEE)
Treatment
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Diuretics for pulmonary congestion
Afib treatment
Anticoagulation if at risk for embolic events
With severe mitral stenosis patients should be
warned to avoid strenuous physical activity
If hemoptysis occurs due to mitral stenosis and
pulmonary hypertension, thoracic surgery may be
warranted
Mitral Incompetence

Causes include MI, MVP syndrome,
rheumatic heart disease, coronary artery
disease, collagen vascular disease
 Inferior MI due to right coronary occlusion
is most common ischemic cause
Acute Mitral Incompetence
Causes

MI
 Mitral valve prolapse syndrome
 Rheumatic heart disease
 Coronary artery disease
 Collagen vascular disease
 Inferior MI due to right coronary occlusion
is the most common cause of ischemic
mitral valve incompetence
Acute Mitral Incompetence

Presents with dyspnea, tachycardia, and
pulmonary edema
 S3 and S4 is usually heard
 Acutely, a harsh apical systolic murmur
starts with S1 and may end before S2
 Patients may deteriorate quickly due to
cardiogenic shock or cardiac arrest
Acute Mitral Incompetence

Intermittent mitral incompetence usually
presents with acute episodes of respiratory
distress due to pulmonary edema and can be
asymptomatic in between attacks
 Pronounced dyspnea may mask angina that
accompanies the ischemia
Chronic Mitral Incompetence
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Late systolic left parasternal lift
 High pitched holosystolic murmur starting
with S1 and may end before S2, heard best
in fifth intercostal space, mid-left thorax,
and radiates to the axilla
 First heart sound is soft and often obscured
by the murmur
 S3 heard and followed by a diastolic rumble
Diagnosis

ECG: acute inferior MI, left atrial
enlargement, LVH, new onset pulmonary
edema
 CXR: minimally enlarged left atrium,
pulmonary edema, left ventricular
enlargement
 Echocardiography is essential. TEE done
once patient is stable
Acute Mitral Incompetence
Treatment

Pulmonary edema: oxygen, diuretics,
nitrates, intubation
 Nitroprusside: increases forward output by
increasing aortic flow and partially restoring
mitral valve competence as left ventricular
size diminishes
 Dobutamine may be required for
hypotensive patients
Mitral Incompetence
Treatment

Aortic balloon counter pulsation
 Surgery may be warranted if mitral valve
rupture
 Evaluate for and treat endocarditis
 Treat atrial fibrillation with heparin, control
ventricular rate with beta blockers and
calcium channel blockers
 Keep INR 2-3
Mitral Valve Prolapse
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Click murmur syndrome
 May be congenital
 Male, age above 45, and the presence of
regurgitation place patient at higher risk for
complications
Mitral Valve Prolapse Clinical
Features
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Most are asymptomatic
Atypical chest pain
Palpitations
Fatigue
Dyspnea unrelated to exertion
Midsystolic click
Second heart sound may be diminshed by late
systolic murmur with crescendos into S2
Mitral Valve Prolapse
Diagnosis
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ECG: usually normal
 Chest X-ray: may be normal, or show
pectus excavatum, straight thoracic spine, or
scoliosis
Treatment of Mitral Valve
Prolapse
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Usually not needed in ED
Beta blockers may be used for patients with
palpitations, chest pain, or anxiety
Suggest avoidence of alcohol, tobacco, and
caffeine to relieve symptoms
Patients with Afib/ risk for embolization: warfarin
with INR of 2-3
Patients with MVP and Afib without mitral
regurg., HTN, heart failure, and above 65 can be
managed with aspirin 160mg qd.
Aortic Stenosis
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Most common cause: degenerative heart
disease/ calcific aortic stenosis
 Most common cause in young adults:
congenital heart disease
 Third most common cause in US, but most
common cause world wide: rheumatic heart
disease
Aortic Stenosis: Clinical
Features
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Classic triad of dyspnea, chest pain, and syncope
 Exercise may induce symptoms
 Dyspnea is typically first symptom, followed by
PND, exertional syncope, and angina
 Atrial Fibrillation is less common than in mitral
disease but 10% of patients have it at time of
surgery
Clinical Features Continued…
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A small amplitude pulse
Slow rate of of increase of carotid pulse
LVH
Paradoxical splitting of S2
S3, S4 present
Classic harsh systolic ejection murmur heard best
at second intercostal space radiating to right
carotid artery
Sudden death
Clinical Features Continued…
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Brachioradial delay
 ECG: LVH, in 10% of patients
LBBB/RBBB
 ChestX-ray: starts out normal, but
eventually LVH and CHF
Treatment of Aortic Stenosis

Pulmonary Edema: oxygen and diuretics
 New onset Afib: heparin and cardioversion
 Limit vigorous activity
 Patients with symptoms secondary to aortic
stenosis such as syncope should be admitted
Aortic Incompetence
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Majority of acute cases due to infective
endocarditis
 Aortic dissection of the root is the second
most common cause
 May be due to trauma
Causes:
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Increased ventricular pressure: elevates
pressure in left ventricle, pulmonary
congestion results
 Appetite suppressant drugs have been
linked to aortic incompetence
Causes:
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Calcific degeneration, Ankylosing spondylitis
Congenital disease, Ehlers-Danlos syndrome
Systemic hypertension, Reiters
Myxomatous proliferation
Rheumatic heart disease
Marfan syndrome
Syphils
Aortic incompetence Clinical
Features…
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Dyspnea
 Acute pulmonary edema with pink, frothy
sputum
 Fever, chills: Endocarditis
 Systemic emboli
 Sinus tach
 Dissection of ascending aorta
Clinical Features Continued…
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Sudden death
 Tachycardia, tachypnea and rales
 High pitched blowing diastolic murmur
heard after S2
 Some may have palpitations
 May have stabbing chest pain, fatigue or
dyspnea
 LV failure
Clinical Features Continued…
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2/3 have no symptoms for up to 20 years despite a
significant lesion
Wide pulse pressure with prominent ventricular
impulse
Water hammer pulse
Accentuated precordial apical thrust
Pulsus biferens
Duroziez sign
Quincke pulse
Aortic Incompetence:
Diagnosis
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Acute: The chest x-ray shows acute
pulmonary edema
 Chronic: The ECG shows LVH and chest xray shows cardiomegally, aortic dilation,
and possibly CHF
 ECHO is crucial
 TEE if aortic dissection suspected
Acute Aortic Incompetence:
Treatment
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Pulmonary Edema: oxygen, intubation
Diuretics and nitrites can be used, but may not be
effective
Nitroprusside plus ionotropic agents can be used
to augment forward flow and reduce LVEDP to
prepare for surgery
Caution when using beta blockers-risk of blocking
compensatory tachycardia
Emergency surgery
Chronic Aortic Incompetence
Treatment:
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Vasodilators like Ace inhibitors or
Nifedipine
Right Sided Valvular Heart
Disease Causes
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Endocarditis in drug users due to organisms such
as S.Aureus-isolated symptomatic tricuspid
pathology
COPD/pulmonary HTN
RV failure with dilation
Rheumatic heart disease
Blunt trauma
Congenital: tetrology of Fallot
Pulmonary valve incompetence
Clinical Features
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Dyspnea, orthopnea: most common
 JVD
 Peripheral edema
 Hepatomegaly
 Splenomegaly
 ascites
Clinical Features
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Tricuspid Valve Incompetence: soft blowing
holosystolic murmur heard along left lower
sternal border
 Tricuspid Valve Stenosis: rumbling
crescendo decrescendo diastolic murmur
that occurs just before S1. It is heard at
lower left sternal border
Diagnosis
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Must obtain Echocardiogram
Treatment
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Address the underlying problem
 diuretics
Prosthetic Valve Disease
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Two groups exist: mechanical non-tissue vs.
bioprostheses using porcine, bovine or human
valves
 Survival is better with mechanical, and bleeding
more common in bioprosthetic valves
 Valves may become stenotic and small amounts of
regurgitations common due to incomplete closure
Complications
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Thrombi on valve
Degeneration of valve
Sutures around valve disrupted
Valve failure
Bleeding/embolism
Endocarditis/ ring abscess
May have increased susceptibility to
hemodynamic compromise from new onset A fib.
Complications
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Lifelong anticoagulation is needed to
decrease risk of thromboembloism and
valve thrombosis
Clinical Features
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Dyspnea
 CHF
 Minor/major embolic events
 Neurologic symptoms: thromboemboli due
to valve thrombi or endocarditis
 Bleeding due to anticoagulation
Clinical Features
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Abnormal heart sounds
 Mechanical model: systolic murmur
 Aortic Bioprosthesis: short midsystolic
murmur
 Mitral Bioprosthesis: loud diastolic murmur
Diagnosis
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Chest x-ray: can help identify change in
position relative to previous films
 CBC, RBC, PT/INR
 If you suspect valve dysfunction-echo
 May need cardiac cath
Treatment
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May need cardiac surgery referral if there is
acute dysfunction
 Treatment of prosthetic acute valvular
dysfuntion due to thrombotic obstruction is
thrombolytic therapy
 Lesser degrees of mechanical valve
obstruction: anticoagulate to INR of 2-3.5
Treatment
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Disposition can be difficult decision if
patient has worsening symptoms- consult
cardiology
Question 1:
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Which of the following are clinical features
of Aortic Incompetence?
A) Water Hammer Pulse
B) Pulsus Biferens
C) Duroziez Sign
D) All of the Above
Question 2:
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T/F The most common cause of Aortic
Stenosis in young adults is congenital heart
disease.
Question 3:
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Causes of Acute Mitral Incompetence
include:
A) MI
B) Mitral Valve Prolapse
C) Rheumatic Heart Disease
D) All of the above
Answers
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1)D
 2)T
 3)D