Cardiovascular Diseases pdf - د. جاسم محمد

Forth stage

Medicine

Lec-5

د.جاسم محمد

9/11/2015

Aortic Stenosis

Overview:

• Normal Aortic Valve Area: 3-4 cm

• Symptoms:

Occur when valve area is 1/4th of normal area.

• Types:

 Supravalvular

 Subvalvular

 Valvular

Etiology of Aortic Stenosis

• Congenital (Bi-cusped).

• Rheumatic.

• Degenerative/Calcific.

Patients under 70: >50% have a congenital cause

Patients over 70: 50% due to degenerative

Evaluation of AS:

Cardiac catheterization

Should only be done for a direct measurement if symptom severity

and echo severity don’t match OR prior to replacement when replacement is planned.

Pathophysiology of Aortic Stenosis



A pressure gradient develops between the left ventricle and the aorta. (Increased

afterload)



LV function initially maintained by compensatory pressure hypertrophy

to maintain the cardiac output



When compensatory mechanisms exhausted, LV function declines and pulm.edema

supervenes.

Presentation of Aortic Stenosis:

1. Asymptomatic mild/moderate

2. Syncope: (exertional)

3. Angina: (increased myocardial oxygen demand; demand/supply mismatch)

4. Dyspnea: on exertion due to heart failure (systolic and diastolic)

5. Sudden death

Physical Findings in Aortic Stenosis



Slow rising carotid pulse (pulsus tardus)



Thrusting apex beat (LV pressure overload)



Narrow pulse pressure



Heart sounds- soft and split second heart sound, S4 gallop due to LVH.



Systolic ejection murmur- cresendo-decrescendo character. This peaks later as the

severity of the stenosis increases.



Loudness does NOT tell you anything about severity

Investigations



ECG Left ventricular hypertrophy ,LBBB



Chest X-ray May be normal; sometimes enlarged LV and dilated ascending aorta on

PA view, calcified valve on lateral view.



Echo Calcified valve with restricted opening, hypertrophied LV) Doppler

Measurement of severity of stenosis Detection of associated aortic regurgitation.



Cardiac catheterization Mainly to identify associated coronary artery disease May

be used to measure gradient between LV and aorta.

Management of AS



General- IE prophylaxis in dental procedures with a prosthetic AV or history of

endocarditis.



Medical - limited role since AS is a mechanical problem. Vasodilators are relatively

contraindicated in severe AS



Aortic Balloon Valvotomy- shows little benefit.



Surgical Replacement: Definitive treatment

Simplified Indications for Surgery in Aortic Stenosis



Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)



Any patient with decreasing EF



Any patient undergoing CABG with moderate or severe AS

Aortic Regurgitation

Overview:

Definition:

Leakage of blood into LV during diastole due to ineffective coaptation of the

aortic cusps.

Etiology of Acute AR



Endocarditis



Aortic Dissection

Physical Findings:



Wide pulse pressure



Diastolic murmur



Florid pulmonary edema

Treatment of Acute AR



True Surgical Emergency:



Positive inotrope: (e.g., dopamine, dobutamine)



Vasodilators: (e.g., nitroprusside)



Avoid beta-blockers



Do not even consider a balloon pump

Etiology of Chronic AR



Cusps defects



Congenital -Bicuspid aortic valve



Rheumatic



Infective endocarditis



Aortic root dilatation Marfan.

Pathophysiology of AR



Combined pressure AND volume overload



Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart

failure.

Symptoms



Asymptomatic until 4th or 5th decade



Progressive Symptoms include:



Dyspnea: exertional, orthopnea, and paroxysmal nocturnal dyspnea



Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood

pressure.



Palpitations: due to increased force of contraction.

Signs

 Peripheral signs

• Pulses Large volume or ‘collapsing’ pulse.

• Corrigan pulse

• Increased pulse pressure

• Bounding peripheral pulses

• Capillary pulsation in nail beds: Quincke’s sign Femoral bruit (‘pistol shot’)

• Duroziez’s sign

• Head nodding with pulse: de Musset’s sign.

• Hill’s sign

• JVP may be normal or elevated



Central Signs

• Apex: Hyperdynamic and displaced apical impulse.

• Diastolic thrill.

 Auscultation

•

High pitched, blowing, decrescendo diastolic murmur at LSB, best heard at end-

expiration & leaning forward.

• Austin-Flint murmur indicates severity (mid to late diastolic murmur)

• Systolic murmur related to high flow state

Investigations

• ECG Initially normal, later left ventricular hypertrophy and T-wave inversion

• Chest X-ray Cardiac dilatation, maybe aortic dilatation Features of left heart failure

• Echo Dilated LV Hyperdynamic, LV Doppler detects reflux , Fluttering anterior mitral

leaflet

• Cardiac catheterization (may not be required) , Dilated LV , Aortic regurgitation ,

Dilated aortic root.

Management of AR

• General: IE prophylaxis in dental procedures with a prosthetic AV or history of

endocarditis.

• Medical: Vasodilators (ACEI’s), Nifedipine improve stroke volume and reduce

regurgitation only if pt. symptomatic or HTN.

• Serial Echocardiograms: to monitor progression.

• Surgical Treatment: Definitive Rx

Simplified Indications for Surgical Treatment of AR

• ANY Symptoms at rest or exercise

• Asymptomatic treatment if:

• EF drops below 50% or LV becomes dilated.

Tricuspid Regurgitation

CLASSIFICATION OF TR

PRIMARY: Intrinsic abnormality of the valve apparatus

SECONDARY OR FUNCTIONAL : Caused by RV pressure or volume overload.

Aetiology

Primary

Rheumatic fever

Endocarditis

Ebstein anomaly

Secondry

Right venytricular dilatation

Right ventricular infarction

Pulmonary hypertension

Pathophysiology

primary structural abnormalities of the leaflets and chordae

- secondary to myocardial dysfunction and dilatation.

Symptoms

presents with the signs and symptoms of right-sided heart failure.

The spectrum includes



Tirdness



Jaundice, loss of wt and appetite



ascites



peripheral edema.



Concomitant valve lesion

Signs



Jugular venous distention with a prominent V wave cv .



Atrial fibrillation



RV heave and gallop



Pansystolic murmur ,S3



Ascites, peripheral edema, cachexia, cyanosis, systolic pulsation of liver and jaundice

INVESTIGATION

o Chest radiography



Marked cardiomegaly is evident.



Pulmonary arterial and venous hypertension is common.

o Echocardiography



The right ventricle is dilated.



Paradoxical motion of the ventricular septum ..



Prolapse of the tricuspid valve



Vegetations if endocarditis is present.

o Electrocardiography



Findings are usually nonspecific.



Incomplete right bundle-branch block,

o Cardiac catheterization



Right atrial pressure and RV end-diastolic pressure are elevated.



The use of angiography in this setting is controversial.

Lab Studies:

abnormal liver function and hyperbilirubinemia secondary to liver congestion.

Management



Treatment of failure symptoms.



TR associated with mitral valve disease and pulmonary hypertension ,Severe
regurgitation -- tricuspid annuloplasty.



Damged valve may need TVR

Tricuspid Stenosis



Almost always rheumatic in origin



Usually accompanied by mitral stenosis



The valve leaflets become thickened and sclerotic as the chordae tendineae become
shortened. Right atrial enlargement occurs due to the increased pressure build-up.

Other causes:



Carcinoid heart disease



Congenital tricuspid atresia



Infective endocarditis



Right atrial myxoma

SYMPTOMS



Usually symptoms of associated lesion (mitral) predominates



Features of right side heart failure



abdominal discomfort ,peripheral edema

SIGNS



JVP raised with prominent a wave



Mid diastolic murmur at left lower sternal edge



Right sided heart failure features

INVESTIGATION



ECG



CHEST –X ray



ECHO

TREATMENT



During surgery on other valves,the tricuspid valve either replaced or valvotomy



Ballon valvuloplasty for isolated TS,

Pulmonary Stenosis



Majority of PS is congenital (accounts for 7.6% of CHD)



Rarely due to carcinoid disease,



Mild PS may be asymptomatic



Symptoms include shortness of breath, chest pain, fainting, or exertional syncope,

SIGNS



Systolic thrill



LPH



Ejectiom systolic murmur ,click,wide splitting of S2

INVESTIGATION



ECG RVH



CHEST –Xray poststenotic dilatation



ECHO –DOPPLER

TREATMENT



Mild to moderate no treatment



Sever (gradient more than 50mmHg)



Balloon valvuloplasty or surgical valvotomy

Pulmonary Regurgitation



Common complication after surgical or percutaneous relief of pulmonary stenosis



May occur secondary to a dilated pulmonary valve ring due to pulmonary
hypertension or Marfan's disease



PR occurs rarely as a congenital anomaly



PR leads to progressive right ventricular dilatation, right ventricular dysfunction,

Signs and Symptoms



Symptoms of underlying disease



Early diastolic murmue decrescendo (Graham steel)



Features of pulmonary hypertension

Treatment



Treatment of cause