Unit 3- Aortic Regurgitation

Unit 3- Aortic Regurgitation

What is the “Method of choice” for evaluation and etiology

Echo and Doppler

Aortic Regurgitation Etiology (4)

• Valve Degeneration

• Infective Endocarditis

• Genetic

• Trauma

AR Etiology: Valve Degeneration

• Calcification

• Fibrosis

AR Etiology: Infective Endocarditis

Leaflet Destruction

AR Etiology: Genetic

Connective Tissue Disorders

(Marfan syndrome, Ehlers Danlos, Loeys-Dietz)

Causes Connective Tissue Disorders to occur (3)

• Dilation

• Aneurysm

• Dissection

Marfan’s syndrome

Effacement of S-T Junction

(giant aortic root and ascending aorta)

AR Etiology: Trauma

• Aortic valve rupture

• Leaflet tear

• Non-coaptation

Likelihood of “physiologic” regurgitation: MR

70 – 80%

Likelihood of “physiologic” regurgitation: TR

80 – 90%

Likelihood of “physiologic” regurgitation: PR

70 – 80%

Likelihood of “physiologic” regurgitation: AR

5%

1.

1.1.7 – 2.2cm

2.

2.0 – 3.7cm

3.

2.0 – 3.6cm

4.

2.0 – 3.4cm

Wall Stress

Force on myocardial fibers that pulls them apart; energy is expended in opposing that force.

Wall Stress Equation or “Law of La Place”

pressure x radius / 2 x thickness

wall stress and O2 demand

Increase; Increase

Wall stress is proportional to:_____ & _____

pressure and radius

Wall stress is inversely proportional to: ______

thickness

Is wall stress GREATER in specimen “A” or “B”?

B

Chronic AR

Progressive LV volume overload

Causes of Chronic AR

congenital, valve degeneration, infections

Acute AR

Sudden, short, severe course

Causes of Acute AR

infective endocarditis, aortic dissection, trauma

Acute AR:

Abrupt LV volume overload in an LV that has not had time to adapt. Excessive preload

Acute rise in , and end diastolic pressure

LVEDP; LA

Acute AR: May lead to: (2)

• Pulmonary edema

• Cardiogenic shock

Pulmonary Edema

Condition where excessive fluid accumulates in the lungs, interfering with gas exchange and breathing.

Cardiogenic Shock

Heart is unable to pump enough blood to meet the body's needs. Typically caused by a severe heart attack (myocardial infarction).

Acute AR: Treatment

Surgical intervention frequently needed

Chronic AR:

• LVE, Increase in LV compliance

• SV includes regurgitant volume

Chronic AR: SV includes regurgitant volume:

• Increases systolic BP --This does help maintain a proper CO.

• Some hypertrophy

• LVED volume can be 3 – 4 times normal, leads to failure

AR Complications

Coronary arteries perfuse myocardium in diastole.

AR Complications:

• LVEDP increase, -symptoms of fatigue, dyspnea

• Angina with normal coronaries arteries

• LVE can result in MR, further volume overload

• LV systolic dysfunction, SV decreases, HR increase, reduction in filling time….

*** Patients can remain asymptomatic until far along in the course.***

Define “BNP”

B-type natriuretic peptide

“BNP”

• Bio marker for heart failure

• Ventricles produce B-type natriuretic peptide (BNP) in response to increased wall stress. BNP protects heart from adverse consequences of overload by increasing natriuresis and diuresis, relaxing vascular smooth muscle, and by counteracting cardiac hypertrophy and fibrosis.

Normal BNP

Less than 100 picograms per milliliter (pg/mL) for adults

Patient presentation:

_______ ________ Murmur;

_______ ________ Pressure

Austin Flint;

Wide Pulse

What is Wide Pulse Pressure?

Large difference of 100 mmHg or more between systolic (top number) and diastolic (bottom number) blood pressures

Wide Pulse Pressure Example: 170/60

difference is 110; 170-60=110 mmHg

Sensitive Tools to Detect AR

Spectral doppler and Color doppler

Diagnosing “AR”

Qualitative & Quantitative parameters

What does the slope (diastolic decay) indicate?

Pressure difference between aorta and LV

The steeper the Decel time the more significant

More regurg=fast pressure equalizes=steep slope

AR peak velocity at least m/sec. -severe

4

What does severe AR do to diastolic function?

produce diastolic dysfunction

Pressure ½ time calculation

Decel time x 0.29

Pressure ½ time also known as what? (2)

P 1/2 t or PHT

PHT: Mild

>500 msec

PHT: Moderate

200-500 msec

PHT: Severe

< 200 msec

Who’s got it bad?

3; steeper and higher PHT

Standard practice to measure waveforms; if pt has an arrhythmia

3; 5

“AR” ON M-Mode; Green Arrow

“Fluttering” with closure line

“AR” ON M-Mode: Abnormal; Green Arrow

Incomplete closure of valve leaflets during diastole

DIASTOLIC FLUTTERING OF THE “AMVL”

Severe AR

Early diastolic closure of the MV results in No “A” wave

Review: How does high LVEDP affect P1/2t in AR?

shortens it

Review: What is Wide Pulse Pressure?

difference between your systolic and diastolic blood pressure; greater than 100 mmHg

Review: A dilated LV will have more/less wall stress?

more

Review: Relationship of wall stress to wall thickness?

inverse

Review: Greater risk of pulmonary edema? Acute or chronic AR?

acute

Review: AR etiology:

degenerative, endocarditis, congenital or genetic connective tissue disorders, trauma

Review: Acute, severe AR may cause abnormal MV M-mode. What does it look like?

fluttering or no A wave

Review: P ½ time less than __________ is SEVERE AR.

200 m/sec