Valvular emerginces
A 67-year-old man presents to
the ED with sudden onset of
chest pain and shortness of
breath. He is 5 days status-post
inferior wall myocardial
infarction. On examination the
patient has pulmonary edema
and a loud holosystolic murmur
heard best at the left lateral
sternal border, with adiation to
the base.
What is the most appropriate
initial management?
2
3
Non of my business , what else? 4
• How Is it an Emergency ?
• How to know ?
• Rheumatic heart Disease
& Infective indocarditis
• Understand ECHO
images
5
• ↑ stroke rate 3.2 times
• ↑ death rate 2.5 times
• Mitral prolapse is the most
common.
• 3% annnual mechanical valve
complications
• systemic embolization from a
prosthetic valve is 1% /yr.
6
7
8
• Innocent (e.g. anemia, thyrotoxicosis,
sepsis, fever, renal failure, and pregnancy)
• New = N T
• Diastolic Murmur = !!??
• Chronic
e.g. Mitral (RHD)  AF, P-HTN , RVF
9
• Stenosis < 2 cm2 (4-6cm2)
• C/O  ↓ exercise, DOE, orthopnea,
RVF Also hoarseness & dysphagia
(Ortner’s Syndrome)
• O/E  small impulse, low sBP, , thin
body habitus, p. cyanosis, and cool
extremities
10
loud S1 , opening snap in early diastole low-pitched
rumbling diastolic apical murmur.
INVESTIGATIONS
ECG , CXR, ECHO
TREATMENT
■ atrial fibrillation.
■ Anticoagulate if systemic embolization
■ Prophylaxis for endocarditis.
■ Cautious diuretic use.
■ Percutaneous balloon/operative repair.
■ Valve replacement is a last resort.
11
severe mitral stenosis  avoid strenuous physical activity
If hemoptysis occurs –> thoracic surgery may be warranted
Valvoplasty 12
COMPLICATIONS
■ Atrial fi brillation
■ pulmonary hemorrhage
■ Pulmonary HTN and Rt HF
■ Systemic emboli
13
14
15
Chronic Acute
C/O
-Often asymptomatic
-Gradual dyspnea on
exertion and fatigue
-Palpitations (AF )
-Abrupt dyspnea, tachypnea,
Cardiogenic shock, Chest pain
-Symptoms of (endocarditis, MI,
trauma )
O/E holosystolic, at the apex
and radiating to the axilla
midsystolic murmur radiates to
the base not the axilla. +
Pulmonary edema
Patients may deteriorate quickly due to
cardiogenic shock or cardiac arrest
16
Chronic Acute
ECG
left atrial and ventricular
hypertrophy.
Atrial fibrillation and P mitrale
- no atrial enlargment
- no LVH
o/e
minimally enlarged left atrium,
pulmonary edema, left ventricular
enlargement
Normal cardiac silhouette,
pulmonary edema
17
18
Chronic Acute
■ Treat CHF & AF
■ Anticoagulate if
systemic embolization
■ Endocarditis
prophylaxis
■ Valve replacement
■ pulmonary edema ttt.
■ Nitroprusside for afterload reduction
(increases forward output by increasing
aortic flow and partially restoring mitral
valve competence as left ventricular size
diminishes)
■ Dobutamine if hypotensive.
■ Intra-aortic balloon pump as bridge to
surgery.
■ Immediate valve replacement.
■ Treat the underlying disease process.
• presents
– with acute episodes of respiratory distress
due to pulmonary edema and
asymptomatic in between attacks
– Pronounced dyspnea may mask angina
that accompanies the ischemia
• Treatment
– Aortic balloon counter pulsation
– Surgery may be warranted if mitral valve rupture
– Evaluate for endocarditis
– Treat atrial fibrillation with heparin, control ventricular
rate with beta blockers and calcium channel blockers
– Keep INR 2-3
19
• Common, specially
young thin females.
• autosomal dominantmainly
• association with anxiety dis.
and ↓BMI.
PATHOPHYSIOLOGY
Myxomatous proliferation of
leaflet → abnormal stretching
of valve leaflets during systole
20
SYMPTOMS
asymptomatic, Atypical chest pain,
Palpitations, Lightheadedness, Dyspnea.
EXAM
■ Early to midsystolic click with high-pitched
late systolic murmur best at left lateral
border
■ standing→ earlier and greater prolapse →
accentuates the click +moves it closer to S1
21
22
TREATMENT
■ asymptomaticNo treatment.
■ Proph. endocarditis if regurgitation or
thickened valve leaflets.
■ β-Blockers may help with atypical
chest pain
DIAGNOSIS
■ ECG: Nonspecific c ST-T wave
changes, (PSVT)
■ CXR: NAD
■ Echo
23
Complications
 Stroke
 Endocarditis
 Tachydysrhythmias (atrial and ventricular)
 PSVT (most common dysrhythmia)
 Increased incidence of WPW, PACs, PVCs
 Ventricular tachycardia (VT) possible
 Sudden death ( Risk factors include syncope/pre-
syncope, inferolateral ST-T changes and thickened or
redundant valve leaflet on TTE).
A 72-year-old woman is brought to the ED
following a syncopal event.
She reports orthopnea and vague,
intermittent chest pain, both present for the
past 6 months.
o/e : BP of 108/84, rales at both lung bases,
a prolonged apical impulse, and a loud
systolic murmur radiating into her neck.
What test will confirm the most likely
diagnosis?
What medication is important to avoid in
this patient?
24
Angina + Syncope + Dyspnea(dCHF)
- >65 years, calcified valve degeneration.
- younger patients congenital bicuspid valve.
- Rheumatic heart disease (less common)
specially if mitral valve diseased.
Pathophysiology
■ LV outflow is obstructed → LVH, ↓ cardiac output,
and eventual dilated cardiomyopathy with
hypertrophy.
■ signs or symptoms if aortic outflow is ↓75% (to < 1
cm).
25
EXAM
■ Narrowed pulse pressure
■ Heaving, prolonged apical impulse
■ Crescendo–decrescendo systolic to the neck
■ CHF symptoms
DIAGNOSIS
■ ECG: LVH with strain, left bundle branch block.
■ CXR: LVH, pulmonary congestion .
■ Echocardiography: Confirms & measures.
26
Angina + Syncope + Dyspnea(dCHF)
Exercise stress testing may provoke dysrhythmias and
is contraindicated.
Aortic valve stenosis 27
Bicuspid aortic valve 28
TREATMENT
■ Treat CHF with gentle diuresis.
■ Rule out ACS in acute presentations.
■ Hydrate gently for hypotension.
Avoid:
■ Preload or afterload reducers (no nitroglycerin)
■ Negative inotropes.
■ Prophylaxis for endocarditis.
■ Definitive treatment is valve replacement.
29
Complications
■ Sudden death from dysrhythmias or acute onset of failure may occur
■ Survival is 2–5 without replacement.
ETIOLOGIES
Acute aortic regurgitation
■ Infective endocarditis
■ Aortic dissection with proximal extension
■ Trauma
■ Prosthetic valve dysfunction
Chronic aortic regurgitation
■ Rheumatic heart disease
■ Bicuspid aortic valve
■ Dilation of the aortic root (Marfan, ankylosing
spondylitis, rheumatoid arthritis)
PATHOPHYSIOLOGY
Acute aortic valve failure → rapid rise in LV
diastolic pressure → acute pulmonary edema
and cardiogenic shock
30
31
Acute Chronic
C/O
-Abrupt onset of dyspnea
-fever(endocarditis)
-Chest pain ( if aortic dissection)
Gradual onset of dyspnea on exertion,
orthopnea, nocturnal dyspnea
EXAM
- Tachycardia, tachypnea
- Pulmonary edema and
cardiovascular collapse
- High-pitched blowing diastolic
murmur heard best at left
sternal border
- Normal pulse pressure
■ Widened pulse pressure (opposite of AS)
■ same diastolic murmur.
■ Austin Flint murmur (mid-diastolic rumble)
■ “Water hammer” pulse
■ Quincke’s sign
■ Duroziez’s murmur
■ De Musset sign
■ Congestive heart failure
32
Acute Chronic
work
- ECG : normal
- CXR: Pulmonary edema.
-ECG: LVH, left atrial enlargement.
- CXR: Congestive heart failure.
TREATMENT
-Standard for pulmonary edema
- Nitroprusside for afterload reduction
- Dobutamine (in addition to
nitroprusside) if hypotensive
- Immediate valve replacement
- Antibiotics: If endocarditis suspected
- Avoid: Intra-aortic balloon pump
■ Nifedipine for asymptomatic AR
■ Afterload reducers, digoxin,
hydralazine, and surgical referral for
elective valve replacement for
symptomatic AR
■ Prophylaxis for endocarditis
33
CAUSES: right ventricular
dilation (pulmonary HTN),
endocarditis, and rheumatic
heart disease.
SYMPTOMS Fatigue,
Dyspnea, Lower extremity
swelling
EXAM: Holosystolic murmur
at left lower sternal border
34
35
DIAGNOSIS
■ ECG: Right atrial and ventricular
enlargement, atrial fi brillation (in the majority
of cases).
■ Echo is confirmatory.
TREATMENT
■ Treat atrial fibrillation.
■ Endocarditis prophylaxis
36
37
38
Complications
●Systemic embolization
●Bleeding
●Valve obstruction due to thrombosis or
pannus.
●Endocarditis
●Structural deterioration, particularly with
bioprosthetic valves
●Paravalvular regurgitation ( leak )
●Hemolytic anemia
●Patient-prosthesis mismatch
● abrupt mechanical valve failure
39
SYMPTOMS/EXAM
■ Vary with location and rapidity of valve
failure
■ Findings of severe anemia (due to hemolysis)
■ Findings consistent with aortic/mitral
regurgitation (acute or chronic)
■ Muted mechanical valve sounds, if
mechanical valve failure
Percutaneous Aortic “Valve in Valve”
Implantation for Severe Aortic Regurgitation in
a Degenerated Bioprosthesis
40
Targeted INR is
- 3.0 - 3.5  mitral valve.
- 2.5 - 3.0  aortic valve.
sudden  acute onset of hypotension, CHF
 Muted mechanical valve sounds
 gradual course discovered on ECHO
TREATMENT
■ Anticoagulation ■ Valve replacement
41
42
43
ETIOLOGIES MURMUR PHYSICAL FINDINGS
AS
Calcific valve
Bicuspid valve
Cresc–dec systolic
Radiating → neck
Paradoxically split S2
Narrowed pulse pressure
Diminished and slow-rising carotid pulse
AR
Endocarditis
Aortic dissection
Blowing diastolic Heard best at
left sternal border
Acute > Pulmonary edema and CV collapse
Chronic > “Water hammer” pulse ,
Quincke’s sign, Duroziez’s murmur, De
Musset sign
MS Rheumatic heart Diastolic Heard best at apex Loud S1
MR
Endocarditis,
ACS
Loud holosystolic Heard best at
apex Radiating → base
Acute : Pulmonary edema and CV collapse
Chronic: LV heave
MP
Unknown, likely
congenital
Late systolic heard best at left
lateral heart border
Early to mid systolic click
■ In a patient with severe mitral stenosis, hypovolemia and tachycardia
are poorly tolerated. “Slow and full” are appropriate goals.
■ In patients with critical aortic stenosis, excessive preload reduction
with vasodilators and diuretics is to be avoided.
■ In patients with acute aortic insufficiency, classic physical findings
may be absent. Medical stabilization entails the cautious use of
vasodilators and diuretics. Intra-aortic balloon counter pulsation is
contraindicated.
■ Complications of prosthetic heart valves range from structural failure
and thrombosis to systemic embolization, hemolysis, and
endocarditis.
■ admission depends on severity of symptoms not presence of
murmur unless aortic stenosis and syncope is suspected.
■ Valvular heart Disease pt. at risk for recurrent cardiovascular event.
4444
45
46

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Valvular emerginces

  • 2. A 67-year-old man presents to the ED with sudden onset of chest pain and shortness of breath. He is 5 days status-post inferior wall myocardial infarction. On examination the patient has pulmonary edema and a loud holosystolic murmur heard best at the left lateral sternal border, with adiation to the base. What is the most appropriate initial management? 2
  • 3. 3
  • 4. Non of my business , what else? 4
  • 5. • How Is it an Emergency ? • How to know ? • Rheumatic heart Disease & Infective indocarditis • Understand ECHO images 5
  • 6. • ↑ stroke rate 3.2 times • ↑ death rate 2.5 times • Mitral prolapse is the most common. • 3% annnual mechanical valve complications • systemic embolization from a prosthetic valve is 1% /yr. 6
  • 7. 7
  • 8. 8
  • 9. • Innocent (e.g. anemia, thyrotoxicosis, sepsis, fever, renal failure, and pregnancy) • New = N T • Diastolic Murmur = !!?? • Chronic e.g. Mitral (RHD)  AF, P-HTN , RVF 9
  • 10. • Stenosis < 2 cm2 (4-6cm2) • C/O  ↓ exercise, DOE, orthopnea, RVF Also hoarseness & dysphagia (Ortner’s Syndrome) • O/E  small impulse, low sBP, , thin body habitus, p. cyanosis, and cool extremities 10 loud S1 , opening snap in early diastole low-pitched rumbling diastolic apical murmur.
  • 11. INVESTIGATIONS ECG , CXR, ECHO TREATMENT ■ atrial fibrillation. ■ Anticoagulate if systemic embolization ■ Prophylaxis for endocarditis. ■ Cautious diuretic use. ■ Percutaneous balloon/operative repair. ■ Valve replacement is a last resort. 11 severe mitral stenosis  avoid strenuous physical activity If hemoptysis occurs –> thoracic surgery may be warranted
  • 13. COMPLICATIONS ■ Atrial fi brillation ■ pulmonary hemorrhage ■ Pulmonary HTN and Rt HF ■ Systemic emboli 13
  • 14. 14
  • 15. 15 Chronic Acute C/O -Often asymptomatic -Gradual dyspnea on exertion and fatigue -Palpitations (AF ) -Abrupt dyspnea, tachypnea, Cardiogenic shock, Chest pain -Symptoms of (endocarditis, MI, trauma ) O/E holosystolic, at the apex and radiating to the axilla midsystolic murmur radiates to the base not the axilla. + Pulmonary edema Patients may deteriorate quickly due to cardiogenic shock or cardiac arrest
  • 16. 16 Chronic Acute ECG left atrial and ventricular hypertrophy. Atrial fibrillation and P mitrale - no atrial enlargment - no LVH o/e minimally enlarged left atrium, pulmonary edema, left ventricular enlargement Normal cardiac silhouette, pulmonary edema
  • 17. 17
  • 18. 18 Chronic Acute ■ Treat CHF & AF ■ Anticoagulate if systemic embolization ■ Endocarditis prophylaxis ■ Valve replacement ■ pulmonary edema ttt. ■ Nitroprusside for afterload reduction (increases forward output by increasing aortic flow and partially restoring mitral valve competence as left ventricular size diminishes) ■ Dobutamine if hypotensive. ■ Intra-aortic balloon pump as bridge to surgery. ■ Immediate valve replacement. ■ Treat the underlying disease process.
  • 19. • presents – with acute episodes of respiratory distress due to pulmonary edema and asymptomatic in between attacks – Pronounced dyspnea may mask angina that accompanies the ischemia • Treatment – Aortic balloon counter pulsation – Surgery may be warranted if mitral valve rupture – Evaluate for endocarditis – Treat atrial fibrillation with heparin, control ventricular rate with beta blockers and calcium channel blockers – Keep INR 2-3 19
  • 20. • Common, specially young thin females. • autosomal dominantmainly • association with anxiety dis. and ↓BMI. PATHOPHYSIOLOGY Myxomatous proliferation of leaflet → abnormal stretching of valve leaflets during systole 20
  • 21. SYMPTOMS asymptomatic, Atypical chest pain, Palpitations, Lightheadedness, Dyspnea. EXAM ■ Early to midsystolic click with high-pitched late systolic murmur best at left lateral border ■ standing→ earlier and greater prolapse → accentuates the click +moves it closer to S1 21
  • 22. 22 TREATMENT ■ asymptomaticNo treatment. ■ Proph. endocarditis if regurgitation or thickened valve leaflets. ■ β-Blockers may help with atypical chest pain DIAGNOSIS ■ ECG: Nonspecific c ST-T wave changes, (PSVT) ■ CXR: NAD ■ Echo
  • 23. 23 Complications  Stroke  Endocarditis  Tachydysrhythmias (atrial and ventricular)  PSVT (most common dysrhythmia)  Increased incidence of WPW, PACs, PVCs  Ventricular tachycardia (VT) possible  Sudden death ( Risk factors include syncope/pre- syncope, inferolateral ST-T changes and thickened or redundant valve leaflet on TTE).
  • 24. A 72-year-old woman is brought to the ED following a syncopal event. She reports orthopnea and vague, intermittent chest pain, both present for the past 6 months. o/e : BP of 108/84, rales at both lung bases, a prolonged apical impulse, and a loud systolic murmur radiating into her neck. What test will confirm the most likely diagnosis? What medication is important to avoid in this patient? 24
  • 25. Angina + Syncope + Dyspnea(dCHF) - >65 years, calcified valve degeneration. - younger patients congenital bicuspid valve. - Rheumatic heart disease (less common) specially if mitral valve diseased. Pathophysiology ■ LV outflow is obstructed → LVH, ↓ cardiac output, and eventual dilated cardiomyopathy with hypertrophy. ■ signs or symptoms if aortic outflow is ↓75% (to < 1 cm). 25
  • 26. EXAM ■ Narrowed pulse pressure ■ Heaving, prolonged apical impulse ■ Crescendo–decrescendo systolic to the neck ■ CHF symptoms DIAGNOSIS ■ ECG: LVH with strain, left bundle branch block. ■ CXR: LVH, pulmonary congestion . ■ Echocardiography: Confirms & measures. 26 Angina + Syncope + Dyspnea(dCHF) Exercise stress testing may provoke dysrhythmias and is contraindicated.
  • 29. TREATMENT ■ Treat CHF with gentle diuresis. ■ Rule out ACS in acute presentations. ■ Hydrate gently for hypotension. Avoid: ■ Preload or afterload reducers (no nitroglycerin) ■ Negative inotropes. ■ Prophylaxis for endocarditis. ■ Definitive treatment is valve replacement. 29 Complications ■ Sudden death from dysrhythmias or acute onset of failure may occur ■ Survival is 2–5 without replacement.
  • 30. ETIOLOGIES Acute aortic regurgitation ■ Infective endocarditis ■ Aortic dissection with proximal extension ■ Trauma ■ Prosthetic valve dysfunction Chronic aortic regurgitation ■ Rheumatic heart disease ■ Bicuspid aortic valve ■ Dilation of the aortic root (Marfan, ankylosing spondylitis, rheumatoid arthritis) PATHOPHYSIOLOGY Acute aortic valve failure → rapid rise in LV diastolic pressure → acute pulmonary edema and cardiogenic shock 30
  • 31. 31 Acute Chronic C/O -Abrupt onset of dyspnea -fever(endocarditis) -Chest pain ( if aortic dissection) Gradual onset of dyspnea on exertion, orthopnea, nocturnal dyspnea EXAM - Tachycardia, tachypnea - Pulmonary edema and cardiovascular collapse - High-pitched blowing diastolic murmur heard best at left sternal border - Normal pulse pressure ■ Widened pulse pressure (opposite of AS) ■ same diastolic murmur. ■ Austin Flint murmur (mid-diastolic rumble) ■ “Water hammer” pulse ■ Quincke’s sign ■ Duroziez’s murmur ■ De Musset sign ■ Congestive heart failure
  • 32. 32 Acute Chronic work - ECG : normal - CXR: Pulmonary edema. -ECG: LVH, left atrial enlargement. - CXR: Congestive heart failure. TREATMENT -Standard for pulmonary edema - Nitroprusside for afterload reduction - Dobutamine (in addition to nitroprusside) if hypotensive - Immediate valve replacement - Antibiotics: If endocarditis suspected - Avoid: Intra-aortic balloon pump ■ Nifedipine for asymptomatic AR ■ Afterload reducers, digoxin, hydralazine, and surgical referral for elective valve replacement for symptomatic AR ■ Prophylaxis for endocarditis
  • 33. 33
  • 34. CAUSES: right ventricular dilation (pulmonary HTN), endocarditis, and rheumatic heart disease. SYMPTOMS Fatigue, Dyspnea, Lower extremity swelling EXAM: Holosystolic murmur at left lower sternal border 34
  • 35. 35 DIAGNOSIS ■ ECG: Right atrial and ventricular enlargement, atrial fi brillation (in the majority of cases). ■ Echo is confirmatory. TREATMENT ■ Treat atrial fibrillation. ■ Endocarditis prophylaxis
  • 36. 36
  • 37. 37
  • 38. 38 Complications ●Systemic embolization ●Bleeding ●Valve obstruction due to thrombosis or pannus. ●Endocarditis ●Structural deterioration, particularly with bioprosthetic valves ●Paravalvular regurgitation ( leak ) ●Hemolytic anemia ●Patient-prosthesis mismatch ● abrupt mechanical valve failure
  • 39. 39 SYMPTOMS/EXAM ■ Vary with location and rapidity of valve failure ■ Findings of severe anemia (due to hemolysis) ■ Findings consistent with aortic/mitral regurgitation (acute or chronic) ■ Muted mechanical valve sounds, if mechanical valve failure
  • 40. Percutaneous Aortic “Valve in Valve” Implantation for Severe Aortic Regurgitation in a Degenerated Bioprosthesis 40
  • 41. Targeted INR is - 3.0 - 3.5  mitral valve. - 2.5 - 3.0  aortic valve. sudden  acute onset of hypotension, CHF  Muted mechanical valve sounds  gradual course discovered on ECHO TREATMENT ■ Anticoagulation ■ Valve replacement 41
  • 42. 42
  • 43. 43 ETIOLOGIES MURMUR PHYSICAL FINDINGS AS Calcific valve Bicuspid valve Cresc–dec systolic Radiating → neck Paradoxically split S2 Narrowed pulse pressure Diminished and slow-rising carotid pulse AR Endocarditis Aortic dissection Blowing diastolic Heard best at left sternal border Acute > Pulmonary edema and CV collapse Chronic > “Water hammer” pulse , Quincke’s sign, Duroziez’s murmur, De Musset sign MS Rheumatic heart Diastolic Heard best at apex Loud S1 MR Endocarditis, ACS Loud holosystolic Heard best at apex Radiating → base Acute : Pulmonary edema and CV collapse Chronic: LV heave MP Unknown, likely congenital Late systolic heard best at left lateral heart border Early to mid systolic click
  • 44. ■ In a patient with severe mitral stenosis, hypovolemia and tachycardia are poorly tolerated. “Slow and full” are appropriate goals. ■ In patients with critical aortic stenosis, excessive preload reduction with vasodilators and diuretics is to be avoided. ■ In patients with acute aortic insufficiency, classic physical findings may be absent. Medical stabilization entails the cautious use of vasodilators and diuretics. Intra-aortic balloon counter pulsation is contraindicated. ■ Complications of prosthetic heart valves range from structural failure and thrombosis to systemic embolization, hemolysis, and endocarditis. ■ admission depends on severity of symptoms not presence of murmur unless aortic stenosis and syncope is suspected. ■ Valvular heart Disease pt. at risk for recurrent cardiovascular event. 4444
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  • 46. 46