S2: Ch1 Cv 2-8

Front 1

455. Nonbacterial thrombotic endocarditis (marantic endocarditis)?

Back 1

a. Associated w/debilitating illnesses such as metastatic cancer (found in up to 20% of cancer pts)
b. Sterile deposits of fibrin and platelets form along the closure line of cardiac valve leaflets.
c. Vegetations can embolize to the brain or periphery.
d. Although the use of heparin may be appropriate, no studies have confirmed its efficacy.

Front 2

456. Nonbacterial Verrucous endocarditis (Libman-Sacks endocarditis)?

Back 2

a. Typically involves the aortic valves in individuals w/SLE
b. Characterized by the formation of small warty vegetations on BOTH SIDES of the valve
c. May present w/regurgitant murmurs.
d. Rarely gives rise to infective endocarditis, but can be a source of systemic embolization.
e. Tx underlying SLE and anticoagulate.

Front 3

457. When should you expect endocarditis?

Back 3

a. In a pt w/a new heart murmur and unexplained fever.

Front 4

458. What imaging is best for diagnosing infective endocarditis?

Back 4

a. Transesophageal echo (TEE) is better than transthoracic echo in the diagnosis of endocarditis.

Front 5

459. How serious is infective endocarditis?

Back 5

a. It is almost always fatal if left untreated.

Front 6

460. Endocarditis prophylaxis?

Back 6

a. Amoxicillin is indicated for pts w/known valvular heart disease or prosthetic valves who are about to undergo oral surgery or GI/GU surgery.

Front 7

461. Atrial Septal Defect (ASD)-Ostium secundum vs. ostium primum vs. Sinus venosus?

Back 7

a. Ostium secundum (most common-80% of cases)-occurs in central portion of interatrial septum.
b. Ostium primum- Occurs low in septum
c. Sinus venosus defects-occurs high in septums

Front 8

462. Pathophys resulting from ASD?

Back 8

a. Oxygenated blood from the LA passes into the RA, increasing right heart output and thus pulmonary blood flow.
b. Leads to increased work of right side of heart: As shunt size increases, RA and RV dilatation occurs w/pulmonary-to-systemic ratios >1.5:1.0.
c. Pulmonary HTN is a serious sequelae, but is rare in ASD.

Front 9

463. Clinical course of ASD?

Back 9

a. Pts are usually asymptomatic until middle age (around 40).
b. Thereafter, sx may begin and include exercise intolerance, dyspnea on exertion, and fatigue.
c. If mild, pts can live a normal lifespan.

Front 10

464. Clinical features of ASD?

Back 10

a. Mild systolic ejection murmur at pulmonary area secondary to increased pulmonary blood flow.
b. Wide, fixed splitting of S2.
c. Diastolic flow “rumble” murmur across tricuspid valve area secondary to increased blood flow.
d. In advanced disease, signs of RVF may be seen.

Front 11

465. Diagnosis of ASD (44)?

Back 11

a. TEE is diagnostic (better than transthoracic echo)
b. CXR: large pulmonary arteries; increased pulmonary markings (vascularity)
c. ECG: right bundle branch block and right axial deviation; atrial abnormalities can also be seen (fibrillation, flutter).

Front 12

466. Complications of ASD?

Back 12

a. Pulmonary HTN-does not occur before 20 yrs of age, but is a common finding in pts over 40.
b. Eisenmenger’s disease
c. Right heart failure
d. Atrial arrhythmias, especially AFib
e. Stroke can result from paradoxical emboli or AFib.

Front 13

467. Tx of ASD?

Back 13

a. Surgical repair when pulmonary-to-systemic blood flow ratio is greater than 1:5:1 or 2:1 if pt is symptomatic.

Front 14

468. Most common congenital cardiac malformation?

Back 14

a. VSD

Front 15

469. Ventricular Septal Defect pathophys?

Back 15

a. Blood flows from the LV (high pressure) into the RV (low pressure) through as hole, resulting in increased pulmonary blood flow. As long as the pulmonary vascular resistance (PVR) is lower than the systemic vascular resistance (SVR), the shunt is left to right.
b. If the PVR increases above the SVR, the shunt reverses.
c. Large defects eventually lead to pulmonary HTN, whereas small defects do not change pulmonary vascular hemodynamics.

Front 16

470. Symptoms of VSD?

Back 16

a. A small shunt produces no symptoms. Many of these close spontaneously.
b. A large shunt w/o elevated PVR (and thus left-to-right shunt) gives rise to CHF, growth failure, and recurrent lower respiratory infections.
c. A large shunt w/a very high PVR (Eisenmenger’s reaction) gives rise to SOB, dyspnea on exertion, chest pain, and cyanosis.

Front 17

471. Eisenmenger’s disease?

Back 17

a. A late complication seen in a minority of pts, in which irreversible pulmonary HTN leads to reversal of shunt, heart failure, and cyanosis.

Front 18

472. Signs of VSD?

Back 18

a. Harsh, blowing holosystolic murmur w/thrill
i. At 4th left interspace.
ii. The smaller the effect, the louder the holosystolic murmur.
b. Sternal lift (RV enlargement)
c. As PVR increases, the pulmonary component of S2 increases in intensity.
d. Aortic regurg may be seen in some pts.

Front 19

473. What decreases the murmur of VSD?

Back 19

a. Valsalva and handgrip.

Front 20

474. Diagnosis of VSD?

Back 20

a. ECG: Biventricular hypertrophy predominates when PVR is high.
b. CXR:
i. Enlargement of the pulmonary artery.
ii. Enlargement of cardiac silhouette: As PVR increases (and L-to-R shunt decreases), heart size decreases, but pulmonary artery size increases.
c. Echo shows the septal defect.

Front 21

475. Complications of VSD?

Back 21

a. Endocarditis
b. Progressive aortic regurg
c. Heart failure
d. Pulmonary HTN and shunt reversal (Eisenmenger’s).

Front 22

476. Tx of VSD?

Back 22

a. Endocarditis prophylaxis is important.
b. Surgical repair is indicated if the pulmonary flow to systemic flow ratio is greater than 1:5:1 or 2:1.
c. For the asymptomatic pt w/a small defect, surgery is not indicated.

Front 23

477. Coarctation of the Aorta?

Back 23

a. Narrowing/constriction of aorta, usually at origin of left subclavian artery near ligamentum arteriosum, which leads to obstruction between the proximal and distal aorta, and thus to increased left ventricular afterload.

Front 24

478. Clinical

Back 24

a. HTN in upper extremities w/hypotension in lower extremities
b. Well-developed upper body w/underdeveloped lower half.
c. Midsystolic murmur heard best over the back.

Front 25

479. Symptoms of Coarctation of aorta?

Back 25

a. HA
b. Cold extremities
c. Claudication w/exercise and Leg fatigue

Front 26

480. Diagnosis of Coarctation of aorta?

Back 26

a. ECG shows LVH
b. CXR:
1. Notching of Ribs!
2. “Figure 3” appearance due to indentation of aorta at site of coarctation, w/dilatation before and after stenosis.

Front 27

481. Complications of Coarctation of aorta?

Back 27

a. Severe HTN
i. Rupture of cerebral aneurysms
ii. Infective endocarditis
iii. Aortic dissection.

Front 28

482. Tx of Coarctation of aorta?

Back 28

a. Standard tx: Surgical decompression.
b. Percutaneous balloon aortoplasty is also an option in selected cases.

Front 29

483. What may coarc of aorta be associated w/in women!?!

Back 29

a. Turner’s syndrome.

Front 30

484. Patent Ductus Arteriosus (PDA) characteristics?

Back 30

a. Communication between aorta and pulmonary artery that persists after birth.
b. Becomes a Left-to-right shunt in life outside the womb if it remains patent (blood flow from aorta into pulmonary artery).