Valvular_heart_disease_aortic_valve_disease.pdf

Valvular heart disease cardiology

1. Valvular
heart disease
Aortic Valve Diseases
DR. NORA ALSAGHEER

3. Cardiac valves

4. Aortic valve disease

5. Normal Valve FunctionNormal Valve Function

Maintain forward Maintain forward
flow and prevent flow and prevent
reversal of flow.reversal of flow.

Valves open and Valves open and
close in response to close in response to
pressure differences pressure differences
(gradients) between (gradients) between
cardiac chambers.cardiac chambers.

7. Abnormal Valve
Function
Valve Stenosis
Obstruction to valve flow during that phase of the
cardiac cycle when the valve is normally open.
Hemodynamic hallmark -“pressure gradient” ~ flow//
VA
Valve Regurgitation, Insufficiency,
Incompetence
Inadequate valve closure--- back leakage
A single valve can be both stenotic and
regurgitant; but both lesions cannot be severe!!
Combinations of valve lesions can coexist
Single disease process
Different disease processes
One valve lesion may cause another
Certain combinations are particularly burdensome
(AS & MR)

8. Lecture outline
General principles :
Pressure overload and volume overload
Heart murmurs
Aortic valve disease

9. VALVULAR STENOSIS
Pressure in upstream chamber IS HIGHER
than Pressure in downstream chamber
during time of flow (when valve is normally
open).
Hemodynamic abnormality = " PRESSURE
GRADIENT"
 
 
Upstream Down stream
High pressurelow pressure

10. VALVULAR
REGURGITATION
 
 
Upstream Down stream
Volume overload
Retrograde flow of blood "upstream" during time when
valve is normally closed.
Hemodynamic abnormality = "VOLUME OVERLOAD"
 

11. Left Ventricular Hypertrophy
“Pressure and Volume overload”

12. LA
RV
RA
LV
Vena
Cava
Aort
a
Pulm
Arter
y
Pulm
Vein

13. RA
RA
RVLV
Aortic stenosis
LV
Normal

14. LA
RV
RA
LV
Vena
Cava
Aort
a
Pulm
Arter
y
Pulm
Vein
Aortic
Insufficiency

15. RA
RA
RVLV
↑↑LV
Example: Aortic regurgitation

17. LV Volume vs Pressure
Overload
FeatureFeature LVPO (AS)LVPO (AS) LVVO (MR,AI)LVVO (MR,AI)
LV VolumeLV Volume normalnormal Dilated**Dilated**
Wall Wall
thicknessthickness
Conc. LVHConc. LVH Normal to Normal to
slightly slightly
increasedincreased
LV LV
compliancecompliance
““stiff” stiff”
noncompliantnoncompliant
Increased Increased
compliancecompliance
LV diastolic LV diastolic
PrPr
increasedincreased Normal to Normal to
slightly slightly
increasedincreased
LV systolic PrLV systolic PrIncreased**Increased** Normal to Normal to
slightly slightly
increasedincreased
LVEFLVEF normalnormal increasedincreased

18. AI
AS

19. Heart murmurs

20. Produced by turbulent blood flow
Turbulence is mainly determined by velocity of
blood flow across a structure
Timing of murmurs (either systolic, or diastolic)
can give helpful information regarding the valve
lesion

21. Systolic MurmursSystolic Murmurs
Aortic stenosisAortic stenosis
Mitral insufficiencyMitral insufficiency
Mitral valve prolapseMitral valve prolapse
Tricuspid insufficiency Tricuspid insufficiency
Diastolic MurmursDiastolic Murmurs
Aortic insufficiencyAortic insufficiency
Mitral stenosisMitral stenosis
S1 S2 S1
Common Murmurs and
Timing

22. Outline for every valve
lesion
Etiology
Pathphysiology
Symptoms and signs
Natural history
Investigations
Management

23. Aortic Valve Disease:
Etiology

Aortic StenosisAortic Stenosis
Degenerative calcific Degenerative calcific
(senile)(senile)

Congenital – Uni or Congenital – Uni or
bicuspidbicuspid
RheumaticRheumatic

ProstheticProsthetic

Acute Aortic InsufficiencyAcute Aortic Insufficiency
Infective endocarditisInfective endocarditis

Acute Aortic DissectionAcute Aortic Dissection

Marfan’s SyndromeMarfan’s Syndrome

Chest traumaChest trauma
Chronic Aortic InsufficiencyChronic Aortic Insufficiency
Aortic leaflet diseaseAortic leaflet disease
Infective endocarditisInfective endocarditis
RheumaticRheumatic
Bicuspid Aortic valveBicuspid Aortic valve
Prolapse & congenital VSDProlapse & congenital VSD
ProstheticProsthetic
Aortic root diseaseAortic root disease
Aortic aneurysm/dissectionAortic aneurysm/dissection
Marfan’s syndromeMarfan’s syndrome
Connective tissue disordersConnective tissue disorders
SyphilisSyphilis
HTNHTN
Annulo-aortic ectasiaAnnulo-aortic ectasia

24. Aortic
stenosis

25. ANATOMY

26. Etiology
Supra-Valvular
Valvular
- Congenital
- Acquired
Sub-Valvular
- Discreet
- Tubular

27. Etiology
Valvular
Congenital
1. Uni-cusped - Rare
- Ages affected 2-30yrs
2. Bi-cusped - 2% of the population
- More common in males
- Associated with
coarctation
in 6% of patients
- Ages affected 40-50yrs

29. Etiology
 Acquired
1. Rheumatic
- Adhesion and fusion of valve commissures leads to
stiffening of the free borders as well as calcification

2. Degenerative (senile)
- Results from mechanical stress
- Associated with traditional risk factors for
CAD such as HTN, Dyslipidemia and smoking

30. A.Normal Trileaflet AV
B.Congenital AS
C.Rheumatic AS
D.Calcific AS
E.Degenerative AS

31. Pathophysiolog
y

33. Symptoms
Cardinal symptoms:
1. Chest pain
- Occurs due to ↑ O2 demand
(LV hypertrophy) and ↓ O2 delivery
- Is often related to concomitant CAD.
2. Presyncope/Syncope
- Caused by transient ↓ cerebral blood
flow
- May also be related transients VF or AF
3. Dyspnea
- Late manifestation of severe AS

34. Signs
Central Pulse :
- Slow rising , low volume ( Pulsus
Parvus et tardus)
- Coarse systolic vibrations at Carotid artery
(Carotid Shudder)
JVP:
- Prominent a wave
Apex:
- Sustained
- Systolic thrill
- Displaced (late with LV failure)

35. Slow rising pulse
Aortic pulse

36. Signs ( Auscultation)
S2 may be soft and single
Paradoxical splitting of S2 in severe AS
S1 S2
Inspiration
Expiration

37. Signs (Auscultation)
Aortic ejection sound with Bicuspid AV
S4
S1
Ejection
Click S2
S2S4S1

38. Auscultation
S1 S2
Mild-Moderate
S1 S2
Severe

39. Natural history

40. Investigations
ECG
- LAD
- LVH

41. Investigations
CXR
- Aortic Calcification
- Post stenotic dilation of Ascending Aorta
Echocardiography
- Routinely used to diagnose and estimate
the severity of AS
- Peak and mean gradients are measured
- Valve area is measured
Mild AS (area >1.5 cm
2
)
Moderate (area >1.0 to 1.5 cm
2
)
Severe (area <1.0 cm
2
)

44. Management
No place for medical therapy if severe AS is
associated with symptoms.
Surgery is the treatment of choice.
Generally speaking ,if the patient has
symptoms with severe AS Surgery is indicated.

45. Aortic
Regurgitation

46. Etiology

47. Etiology (chronic AR)
Two major causes:
A. Intrinsic structural valve problem
1. Congenital : Bicuspid valve
2. Acquired : - Inflammatory (Rheumatic,
Connective tissue
diseases)
- Infectious (IE)
- Degenerative

48. Etiology( chronic AR)
B. Abnormality of the Ascending Aorta
1. Congenital : Marfans disease
2. Infectious : Syphilis (15-25yr after
infection)
3. Inflammatory : Connective tissue
diseases
(RA, AS, GCA)
4. Idiopathic : progressive dilation
(cystic medial
necrosis)

50. Etiology (Acute AR)
Trauma
Aortic dissection
Infective endocarditis

53. Aortic regurgitation
Excess volume to the LV
↑LV end diastolic pressure
Stretching of Myocardium
↑ wall stress
Eccentric LV hypertrophy
↓ effective Stroke volume
↑ Myocardial O2 demand
(Ischemia)
LV failure
↓ Myocardial O2 supply
(Ischemia)

54. Symptoms
Gradual development of Dyspnea , Orthopnea,
and PND
Angina
Palpitations
With Acute AR , abrupt development of
dyspnea.

55. Signs of Chronic AR
Peripheral signs
- De Musset sign (head movment with pulse)
- Water hammer pulse (abrupt distention and quick
collapse)
- Duroziez sign
- Muller’s sign (systolic pulsation of Uvula)
- Pistol shot/ Traube sign
- Quincke sign
- Hill’s sign (Popliteal pressure at least 20 mmHg
higher than brachial pressure

58. Signs of chronic AR
Wide pulse pressure
Central pulse:
- Large volume pulse
- Bisferines pulse
- Corrigan pulse
JVP may be normal or elevated
Displaced and hyperdynamic apex

59. Auscultation
S2 may be soft or accentuated
S3 indicates severe AI
Ejection click
 High pitched, blowing, decrescendo diastolic
murmur at LSB, best heard at end-expiration &
leaning forward

60. Auscultation
Length of murmur correlates with severity.
In Acute AR diastolic murmur is low pitched
and short.
Austin-Flint murmur indicates severity (mid to
late diastolic murmur)
Systolic murmur related to high flow state
S1 S2 S1

61. Investigations
ECG – LVH, LAD
CXR- may show ↑cardiothoracic ratio, and dilated aorta

62. Investigations
Angiography:
- Would aid in diagnosis and grading of severity
Echocardiography:
- The easiest and fastest way of diagnosing
and grading the severity of AR.
- Detection of the underlying mechanism of AR.

63. AsymptomaticAsymptomatic %/Y%/Y
Normal LV function (~good prognosis)Normal LV function (~good prognosis)
Progression to symptoms or LV dysfunction Progression to symptoms or LV dysfunction < 6< 6
Progression to asymptomatic LV dysfunction Progression to asymptomatic LV dysfunction < 3.5< 3.5
Sudden death Sudden death < 0.2< 0.2
Abnormal LV functionAbnormal LV function
Progression to cardiac symptoms Progression to cardiac symptoms > 25> 25
SymptomaticSymptomatic (Poor prognosis) (Poor prognosis)
Mortality Mortality > 10> 10
Natural history

64. Management
Any patient with severe AR and any of the
following should have aortic valve replacement:
1. Symptomatic patients
2. Patients without symptoms, but with
LV systolic dysfunction (EF<50%), or
marked dilation of the LV.

65. Management
Vasodilator therapy ( ACE I, or CCB’s) for:
1. Patients not candidates for surgery
2. Short term to Improve hemodynamics
3. Treatment of hypertension

68. Tricuspid stenosis