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Aortic Valve Disease
Cardiology Aortic Valve Disease Lecture
| Question | Answer |
|---|---|
| What are the 3 possible outflow tract obstruction sites for the LV? | Subvalvular obstruction, valvular stenosis, supravalvular stenosis |
| Subvalvular obstruction: when does it occur (2)? | 1) abnormal thickening of the intraventricular septum as seen in hypertrophic cardimyopathy and 2) congenital subaortic membranes in the left ventricular outflow tract |
| Supravalvular stenosis | usually in form of muscular ridge of hypoplasia of the ascending thoracic aorta (congenital) |
| What is the normal structure of the aortic valve? | 3 leaflets: right, left and non-coronary cusps; cross section is ~3-4 cm^2; attach to aortic wall in the sinuses of valsalva |
| What is a commissure? | where the leaflet edges coapt |
| When does the aortic valve open? Close? | When the LV pressure exceeds the central aortic pressure; closses when it falls below central aortic pressure |
| What are the two basic causes of valvular aortic stenosis? | Congenital and Acquired |
| What is the most common presentation and time of presentation of congenital valvular disease? | Unicuspid and bicuspid aortic valves. Individuals with unicuspid aortic valves typically present during infancy and childhood. In contrast, individuals with bicuspid aortic valves tend to present during the 3rd through 5th decades of life. |
| What are the three most common forms of acquire valvular disease? | Rheumatic, calcified degenerative, and systemic disease |
| Rheumatic valvular disease: underlying cause, pathophysiology, comorbidities | Cause: sequelae of the valvulitis associated with acute rheumatic fever. Pathophysiology: marked thickening and restriction of the leaflet margins with commissural fusion. Commonly co-morbid with mitral stenosis (esp. in women) |
| Calcific degenerative valve disease: what do you typically see? What is thought to cause it? | Seen with aging population; abnormal thickening and calcification of the valve leaflets; thought to be product of chronic inflammation + upregulation of neurohormonal mediators (renin-angiotensin system, lipid accumulation, + lymphocytic infiltration) |
| What systemic disease can typically lead to acquired valvular disease? | Rheumatoid arthritis, ankylosing spodylitis, Paget's disease, and onchronosis |
| What hemodynamic changes do you see with worsening aortic stenosis? | Persistent transvalvular pressure gradient (increaseing LV systolic pressure); Central aortic pressure gradient tracing is blunted; chronic elevation of LV pressure-->left ventricular hypertrophy (little change in cavity size)-->decrease in LV compliance |
| What physical exam findings (nonauscultatory) would you see in a patient with aortic stenosis? | PMI: inferolaterally displaced + sustained + presystolic heave; carotid pulse: delayed impulse + "pulsus parvus et tardus" |
| In aortic stenosis, why does the PMI become more inferolaterally displaced? | Due to increased LV hypertrophy |
| In aortic stenosis, why does the apical impulse of the PMI become more prolonged? | Due to prolongation of left ventricular systolic ejection |
| In aortic stenosis, why do you observe a presystolic heave at the PMI? | Due to prominent ATRIAL contraction |
| What is a "pulsus parvus et tardus?" | Low amplitude pulse with delayed upstroke |
| What auscaltory findings would you expect with aortic stenosis (mild)? | Rhomboid shaped systolic ejection murmur best heart at the cardiac base and radiating to the suprasternal notch and LV apex; early systolic ejection sound ("click") |
| What auscaltory findings would you expect with aortic stenosis (worsening)? | Systolic ejection murmur (SEM) becomes later peaking, S2 split narrows (may even become reversed splitting with paradoxical movement with respiration), SEM intensity can decrease with decreaseing stroke volume, S4 sound appears |
| In worsening aortic stenosis, why would you see the systolic ejection murmur peak later? | As the valve orifice narrows, time delay to peak systolic ejection |
| In worsening aortic stenosis, does the S2 split narrow? Why do you see reversed (pardoxical) splitting? | The aortic component of the S2 sound becomes increasingly delayed while P2 is largely unaffected. As A2 becomes more delayed, it can occur after P2, causing a split on expiration. Inspiration moves P2 forward, closing the split. |
| In worsening aortic stenosis, why does the intensity of the SEM decrease? | LV begins to fail, decreasing the stroke volume-->decrease intensity of SEM |
| What causes the S4 to develop in aortic stenosis? | Decreased ventricular compliance (due to increased hypertrophy) |
| What is prognosis for patient with aortic stenosis? | Fairly long latent period; once symptoms develop-->event free survival decreases dramatically |
| What are the cardinal symptoms of aortic stenosis? What are the average survival times after developing these symptoms? | Angina (5 years), syncope (3 years), dyspnea and congestive heart failure (2 years) |
| Why would a patient with sever aortic stenosis develop angina? | Angina caused by mismathc between O2 demand and supply: increased LVEDP and decreased MAP decreases coronary blood flow --> decreased flow to coronary arteries to meet increased O2 demand (due to increased myocardial wall tension)--> angina |
| How would severe aortic stenosis lead to syncope? | Results from cerebral hypoperfusion--exacerbated by physical exertion and brady- or tachy-arrhythmias |
| What are the hemodynamic changes that occur with mild aortic stenosis (in terms of pressure, CO, and systemic blood pressure)? | Gradual increase in left ventricular systolic pressure + transvalvular gradients; in early stages, LVEDP can be high normal or mildly elevated; Cardiac output and systemic blood pressure remain normal |
| What are the hemodynamic changes that occur with worsening aortic stenosis (in terms of pressure, CO, and systemic blood pressure)? | LVEDP rises to maintain output; rise in LV blood pressure transmitted back to pulmonary bed (pulmonary hypertension)-->congestive heart failure. LV systolic dysfunction-->decreased forward flow-->ongoing elevation in pulmonary pressures-->CHF |
| How would you use echocardiography to evaluate aortic stenosis? | Gives info on left ventricular function, valvular anatomy; with doppler: valve gradients, valve area, valvular regurgitation, and pulmonary pressures |
| How + When would you use cardiac catherization to evaluate aortic stenosis? | Using Gorlin formula, can measure cardiac output, systolic ejection time, aortic valve presure gradients, aortic valve area. Used when noninvasive data inconsistent (2nd line); can be used to evaluate coronary anatomy (angiography) |
| What information does and EKG provide to help you evaluate aortic stenosis? | Evaluate LVH, left atrial enlargement, and left axis deviation |
| What findings can be made from a chest x-ray of a person with aortic stenosis (severe)? | cardiomegaly, aortic valve calcification, and dilation of the aorta |
| What is the medical management of aortic stenosis? | Diuretics (decrease intravascular volume); digoxin (enhances myocardial contractility); inotropes (acute management of critically ill); AVOID VASODILATORS (patient may not be able to augment CO appropriately) and neg. IONOTROPES |
| What are the surgical management options of aortic stenosis? | Bioprosthetic or metallic valve replacement (similar risks as other valve replacements); percutaneous ballon valvuloplasty (pediatric use only); percutaenous transcatheter aortic valve implantation (TAVI) if bad replacement candidate |
| Why is percutaneous balloon valvuloplasty not recommended in patients with aortic stenosis (over valve replacement)? | Peri-procedural complication rates ~9% incidence of death or serious complications (aortic regurgitation, myocardial perforation, infarction); at 6 months 50% have recurrent Aortic stenosis |
| What are the acquired causes of aortic regurgitation? | Rheumatic valvular disease (usually w/ mitral valve disease); endocarditis; aortic root disease (ascending thoracic aortic aneurysm + aortic dissection); systemic diseases (rare) |
| How can rheumatic valvular disease lead to aortic regurgitation? | Inflammation of valve leaflets-->chronic fibrosis-->retraction of leaflet tips-->incomplete coaptation-->regurgitation |
| How can endocarditis lead to aortic regurgitation? | Bulky vegetations OR leaflet destruction OR perforation OR complications from perivalvular abscesses |
| How can aortic root dieseases lead to aortic regurgitation? | Ascending thoracic aortic aneurysm: dilation of aortic valve annulus w/ incomplete coaptation of aortic valve leaflets --> chronic hypertension contributes often. Aortic dissection: from retrograde extension of dissection to the aortic valve |
| How can systemic diseases lead to aortic regurgitation? | Rare--associated with connective tissue diseases. Examples: lupus, rheumatoid arthritis, ankylosing spondylitis, vasculitide (e.g. Takayasu's arthritis) |
| What are the common congenital causes of aortic regurgitation? | Bicuspid and quadricuspid aortic valves; sinus of valsalva aneurysms; subaortic membrane; subaortic ventricular septal defect |
| What changes do you see in the hemodynamics of a patient with aortic regurgitation? | Chronic-->LV remodeling in response to chronic volume overload: LVEDV + P increases-->increased LVED wall tension-->eccentric hypertrophy with LV cavity dilation-->cardiomegaly-->LV systolic dysfunction |
| What do you see in patients with chronic severe aortic regurgitation? | Widening of aortic pulse pressure due to 1) increased forward stroke volume (due to high LVEDV) and 2) Rapid diastolic run-off of blood from aorta into LV --> lower than normal end diastolic pressure |
| What do you see in patients with acute severe aortic regurgitation? | Abrupt increase in preload with no compesatory remodeling and dilation of LV --> LV filling pressure increases rapidly --> pulmonary edema. |
| When do you see acute severe aortic regurgitation (causes)? | Ednocarditis, aortic dissection, trauma |
| What changes do we see in left ventricular pressure-volume relationships with Acute and Chronic AR? | Acute: shift along fixed pressure-volume curve (increase in volume-->increase in pressure). Chronic: remodling dampens this effect-->minimal increase in LV pressure until systolic dysfunction occurs-->CHF |
| What physical findings are seen in patients with severe (chronic) aortic regurgitation? | Laterally displaced PMI; Quinke's sign; Corrigan's / water hammer pulse; Deroziez's sign; Hill's sign |
| What is Quincke's sign? | Prominent vascular pulsations which can be seen in the capillary beds of the fingernails (easier if light is shining through the finger bed |
| What is Corrigan's sign/water hammer pulse? | Palpation of the peripheral artery reveals rapid distension and collapse in the contour of the pulse |
| What is Deroziez's sign? | A systolic femoral murmur heard when compressig proximal femoral artery; a diastolic murmur is heard when compressing the distal vessel |
| What is Hill's sign? | >60 mmHg differential in the bracchial and popliteal systolic pressure |
| What are the cardiac auscultation findings with Aortic Regurgitation? | Diastolic murmur (3rd + 4th left intercostal space) augmented at end of expiration with patient leaning forward; DECRESCENDO as flow as Aortic and LV pressures equilibrate. Systolic murmur due to high SV. Austin-flint murmur (low frequency diastolic) |
| What finding indicates the severety of chronic aortic regurgitation? | Duration (NOT intensity) of diastolic murmur |
| How can you tell the difference between a systolic murmur due to aortic regurgitation and one due to aortic stenosis? | Palpate contour of carotid pulse |
| What is an Austin-Flint murmur? | Low frequency diastolic murmur consistent with finding in mitral stenosis but that occurs in the absence of MS. Due to impairment of mitral valve diastolic excursion from torrential flow related to aortic regurgitant jet |
| What findings do you expect in acute aortic regurgitation? | Auscultaroy findings similar to chronic AR, but less impressive. Primary physical findings similar to cardiogenic shock: tachycardia, hypotension, pulmonary edema. Peripheral findings of chronic AR not present usually. |
| What is the prognosis + evaluation of patients with Aortic stenosis? | Long latent period before symptoms; LV dysfunction-->symptom onset rapid. Valve replacement best if prior to onset of symptoms, LV dysfunction, or cardiomegaly |
| How can you evaluate the function of a patient with suspected aortic regurgitation? | EChocardiography (level of regurgitation, LV size, function) recommended every 1-2 yrs if mild AR, 6-12 months if more severe. Excercise testing if diagnosis dubious. Catherterization useful but not necessary. |
| How should you treat asymptomatic patients with AR? | No treatment; follow with serial exams and echos |
| How should you treat patients with with preserved LV systolic function and diastolic hypertension? | Diuretics, Na restrictio, and vasodilator (nifedipine or ACE inhibitors) may help alleviate symptoms and slow progression of disease |
| What are the surgical options for people with AR? | Aortic valve replacement (metallic or prosthetic) before symptoms significant OR LV dilation OR LV systolic dysfunction. Concomitant aortic pathology can be treated with aortic root replacment. Intra aortic ballon pump contraindicated (will worsen AR) |
Created by:
karkis77
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