Aortic Insufficiency Flashcards

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1
Q

what is the definition of Aortic insufficiency?

A

the retrograde flow of blood from aorta to left ventricle in diastole

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2
Q

What is the incidence of Aortic Insufficiency? occurs with?

A

• Occurrence—with the use of doppler/echo, many cases of mild AI have been identified – up to 10% of elderly persons were found to have some degree of AI in one study. Clinically important AI is far less common. • AI affects males and females equally and incidence is similar across various racial groups.

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3
Q

Aortic insufficiency is caused

A

Aortic Insufficiency (AI) may be caused by 1 disease of either the aortic valve (AV) leaflets or the wall of the aortic root or both.

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4
Q

Valvular etiologies of aortic regurgitation?

A

• Degenerative/calcific • Bicuspid • Endocarditis • Rheumatic fever • Valvulitis (ctd) • Anorectic drugs • Trauma • Myxomatous degeneration • Sinus of valsalva aneurysm • ventricular septal defect

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5
Q

Etiologies of ascending aortic regurgitation?

A

• Degenerative • Dilitation due to HTN, aneurysm • Proximal dissection • Marfan syndrome • Inflammatory (Reiters, Behcet, ankylosing spondilitis, relapsing polychondritis, psoratic arthritis, syphilis, etc) • Giant cell arteritis

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6
Q

Etiologies of Acute Aortic Insufficiency?

A

• Acute aortic Dissection • Infective endocarditis • Trauma • Rheumatic fever • Congenital (eg. Rupture of sinus of valsalva) • Post prosthetic valve surgery

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7
Q

what is the pathophysiology of Aortic insufficiency?

A

The diastolic flow of blood back across the AV increases filling of the left ventricle (LV) and thus an initial volume overload is imposed on the LV. Over time, increased LV size, systolic wall stress, LV afterload and hypertrophy can lead to pressure overload as well. AI may be either chronic or acute.

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8
Q

Pathophysiology of LV enlargement?

A

• LV enlargement –“volume overload” • Rearrangement of myocardial fibers which become longer with new sarcomeres added in series. • Increased LV end diastolic volume with increased stroke volume, wall thickness and eccentric LV hypertrophy. • Early on, the LV is able to increase compliance and compensate for the AI by increased stroke volume. Wall stress and LV end diastolic pressure may be normal. • With time, the ventricle dilates and becomes more spherical as changes in the collagen support system, diminished coronary flow reserve, subendocardial necrosis and fibrosis occur. • Progressive LV systolic dilatation/dysfunction ensues leading to a cycle of decompensation with increased wall stress, decreased compliance, increased afterload and increased LV end diastolic pressure which can cause further decompensation and ultimately the syndrome of heart failure. • Ultimately develop a combination of volume and pressure overload** • Mitral regurgitation may occur from LV dilitation

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9
Q

what happens with acute severe aortic insufficiency?

A

• Large regurgitant volume suddenly imposed on an unprepared left ventricle • LV has very limited ability to acutely enlarge • Effective LV stroke volume is decreased • Rapid increase in LV end diastolic pressure • Tachycardia cannot compensate • Pulmonary hypertension and congestion; decreased cardiac output and potentially hypotension and shock

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10
Q

what are the most common causes of acute aortic insufficiency?

A

a) Aortic dissection b) Infective endocarditis c) Trauma

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11
Q

What is the usual history with a patient with aortic insufficiency?

A

The patient with chronic AI may remain asymptomatic for many years. When symptoms do develop they most commonly are the signs of LV failure: Fatigue *Dyspnea on exertion*

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12
Q

Symptoms of aortic insufficiency?

A

Fatigue *Dyspnea on exertion* Edema Orthopnea PND-paroxysmal nocturnal dyspnea Palpitations & awareness of extra systoles because of the greatly increased LV stroke volume Vasomotor symptoms – flushing, sweating, heat intolerance Angina (20%) – sometimes exertional. May be atypical occurring at rest & nocturnally related to bradycardia. Neck pain due to stretching of carotid sheath Patients with acute AI often have cardiogenic shock with hypotension and pulmonary edema.

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13
Q

Physical exam signs of chronic severe aortic insufficiency?

A

a) Head bobbing with each heart beat (DeMussett’s sign) b) Waterhammer pulses – abrupt distention & quick collapse (Corrigan’s pulse) c) Muller’s sign—systolic pulsation of the uvula d) Traube’s sign – booming systolic & diastolic sounds auscultated over the femoral arteries (“pistol-shot femorals”). e) Duroziez’s sign – systolic murmur auscultated over the femoral artery when it is compressed proximally and a diastolic murmur when it is compressed distally. f) Quinckes’s sign – capillary pulsations of the fingertips or by pressing a slide over the patient’s lip. g) Hill’s sign – popliteal cuff systolic pressure exceeding brachial cuff systolic pressure by more than 60 mm Hg. h) Increased pulse pressure (usually greater than 80 mm Hg) i) Diastolic blood pressure is often reduced—often below 60mm or even less j) Apical impulse is diffuse, hyperdynamic and displaced inferolaterally

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14
Q

the diagnosis of aortic insufficiency is very commonly made how? explain the findings that are normal and what’s abnormal?

A

The diagnosis of aortic insufficiency is very commonly made on the finding of a murmur. a) S1 is usually normal b) S2 is variable c) S3 may be present d) Systolic ejection murmur often heard e) Diastolic murmur*

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15
Q

Explain the diastolic murmur that is seen with aortic insufficiency?

A

Diastolic murmur – high frequency blowing type murmur beginning immediately after A2. Heard best with the diaphragm of the stethoscope while the patient is sitting up, leaning forward with the breath held in end expiration. The severity of AI correlates better with the duration than with the intensity of the murmur. The diastolic murmur is usually maximal at the left 3rd or 4th intercostal space along the left sternal border with AI due to valvular disease. If AI is due to aortic root dilatation however the murmur is often maximal along the right sternal border. A mid to late diastolic apical rumble (Austin-Flint murmur) is common in severe AI due to rapid antegrade flow across a mitral orifice narrowed by the aortic reflux which may cause premature closure of the mitral valve.

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16
Q

What is the presentation of the patient with acute aortic insufficiency?

A

Acute AI – These patients are often gravely ill with cardiovascular collapse evident by tachycardia, hypotension peripheral vasoconstriction, pulmonary edema. The peripheral signs of AI may be minimal or absent. Pulsus alternans may be present. Evidence of pulmonary hypertension with a loud S2, S3, & S4 is often present. The diastolic murmur is lower pitched and shorter than in chronic AI. The Austin-Flint murmur is absent or brief.

17
Q

What are the EKG findings of chronic and acute aortic insufficiency?

A

A. ECG 1. Chronic AI-LAD, LVH. PR prolongation may be present if AI due to inflammatory cause. 2. Acute AI – nonspecific ST-T changes

18
Q

What does the Chest x-ray of aortic insufficiency show?

A

Cardiomegaly with chronic AI, aortic root may be dilated.

19
Q

Cardiac catheterization and Aortogram assess what?

A

Cardiac Catheterization & Aortogram – assesses coronary arteries, all valves, LV function. Aortography quantifies AI & assesses aortic root.

20
Q

MRI and ultra fast CT will likely be used for?

A

MRI and ultrafast CT will likely be useful for quantifying regurgitant volumes and end systolic dimension but are not widely available for this purpose and are expensive.

21
Q

What is the most useful test for aortic insufficiency?

A

Echocardiography/Doppler is the most useful diagnostic test – LV diameters & function assessed, aortic root diameter, fluttering of the anterior mitral leaflet, premature closure of the mitral valve may be detected, vegetations may be identified. Color flow and pulsed Doppler reveal a diastolic jet into the left ventricle and can quantify severity. A large Doppler jet in the left ventricular outflow tract of over 60% of the LVOT with flow reversal in the descending aorta would be pathognomonic of severe AI.

22
Q

Explain the natural history of chronic severe aortic insufficiency?

A

chronic severe aortic insufficiency • In asymptomatic patients with normal LV function, the rate of progression to symptoms and/or LV decompensation is less than 5% per year. Progression to asymptomatic LV dysfunction is less than 2% per year and sudden death is less than 0.2% per year. • For asymptomatic patients with LV systolic dysfunction, the rate of progression to symptoms is greater than 25% per year and the mortality rate once CHF ensues is over 20% per year. • *The rates of symptoms ,death or LV dysfunction in patients with an LV end-systolic dimension (LVESD) greater than 55mm is 19% per year. If LVESD is less than 40mm, the rate is 0%.*

23
Q

What is the treatment for chronic severe asymptomatic patients with severe aortic insufficiency?

A

Asymptomatic patients with severe AI (with preserved LV function) •Instruction in symptoms •Depending on LV size and systolic function, follow clinically q 6-12 months and with serial echocardiograms . •Vasodilator therapy (eg. ace inhibitors, etc.) Long term vasodilator therapy for chronic AI has been disappointing and is reserved for patients with symptoms and/or LVEF <50% who are not candidates for AVR* or who are awaiting AVR. Asymptomatic patients with AI and hypertension or other indication.

24
Q

Treatment of symptomatic severe Aortic insufficiency is?

A

In general, treatment of symptomatic severe AI is a temporizing measure pending valve replacement (or for nonsurgical candidates). • Diuretics, salt restriction, digitalis • Vasodilators (ACE inhibitors, etc.) • Bradyarhythmias and atrial fibrillation are poorly tolerated and should be treated aggressively. • Any acute severe aortic insufficiency should be considered for AVR. –By definition, these people are quite ill and unlikely to do well with medical therapy.

25
Q

Any acute severe aortic insufficiency should be considered for?

A

Any acute severe aortic insufficiency should be considered for AVR. –By definition, these people are quite ill and unlikely to do well with medical therapy.

26
Q

acute Aortic insufficiency risks? administration of what?

A

• Risks of severe acute AI are great and prompt surgical intervention may prevent death due to LV failure • Acute administration of vasodilating agents such as nitroprusside or hydralazine may help increase cardiac output and reduce regurgitant volume • Dobutamine may help increase contractility and decrease afterload

27
Q

surgical intervention for aortic insufficiency?

A

• There is an approx. 3% mortality for AVR in AI – higher if concurrent CABG or other valve surgery. –AVR is indicated in patients with significant symptoms regardless of LV function *. –*AVR is indicated in asymptomatic or symptomatic patients with evidence of LV systolic dysfunction ( LVEF < 0.50) or significant enlargement ((LV end systolic dimension > 50mm or end diastolic dimension >65mm).* – Symptomatic patients with severe LV dysfunction ( EF <0.25) are problematic and have higher surgical mortality and many will not improve post AVR. Nonetheless, given the poor prognosis of these patients, all symptomatic patients should be considered for AVR regardless of LV function . – AVR is indicated in patients with moderate or severe AI needing other cardiac surgery such as CABG, dissection repair, etc.

28
Q

Preoperative Predictors of Poor Postoperative Survival and LV Function with surgery for aortic insufficiency?

A

• LV dysfunction preoperatively • LV enlargement preoperatively • NYHA CHF class III or IV (symptoms with ordinary activity or at rest) • Duration of CHF symptoms longer than 12 months *The moral of the above is that you must plan to intervene before your patient is in trouble.*

29
Q

Compare and contrast aortic and mitral regurgitation?

A