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ECOS III Final > Cardiac DSA > Flashcards

Cardiac DSA Flashcards

1
Q

What is the etiology for aortic stenosis?

A

Age related calcific degeneration of a normal valve (generally age <70) or a bicuspid aortic valve
Rhuematic dz

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2
Q

What is the clinical presentation for aortic stenosis?

A

Angina, syncope, HF

Parvus et tardus (diminsed caortid upstroke, weak pulse, typically in late or severe AS)

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3
Q

What heart sounds are heard with aortic stenosis?

A

Harsh crescendo-decrescendo systolic murmur
Best heard at the 2nd right intercostal with radiation to the carotid
The more severe the stenosis, the longer duration of the murmur and the more likely it peaks later in systole

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4
Q

What is the etiology for aortic regurgitation?

A 
Aortic root problems (e.g. dilation due to age-related degeneration, HTN, ankylosing spondylitis, syphilis, dissection, Marfans)
Valve problems (e.g. bicuspid aortic valve, endocarditis, rheumatic)
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5
Q

What is the clinical presentation for aortic regurgitation?

A

Dyspnea, PND, orthopnea, palpitations when lying down, wide pulse pressure, bounding pulse

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6
Q

What heart sound is associated aortic regurgitation?

A

Diastolic blowing decrescendo murmur

Beast heard at apex/left sternal border

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7
Q

What is the etiology for mitral stenosis?

A

Rheumatic fever, mitral annular calcification (e.g. in the setting of CKD), congenital

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8
Q

What is the clinical presentation for mitral stenosis?

A

Dyspnea, hemoptysis, Afib, risk of emboli

Dilated LA can compress the recurrent laryngeal nerve and cause hoarseness (severe cases)

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9
Q

What heart sounds are associated with mitral stenosis?

A

Opening snap, low pitched diastolic rumble and loud S1

Best heard at the apex when the pt is in the left lateral decubitus position

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10
Q

What is the etiology for acute mitral regurgitation?

A

Endocarditis, MI with papillary muscle rupture, chordae tendineae rupture

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11
Q

What is the etiology for chronic mitral regurgitation?

A
  1. Primary problem with valve: mitral valve prolapse (MVP, i.e. prolapse due to myxomatous degeneration), rheumatic carditis, prior endocarditis, Marfans, carcinoid (rare)
  2. Secondary dilation of MV annulus (e.g. dilated cardiomyopathy)
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12
Q

What is the clinical presentation for mitral regurgitation?

A

Acutely may cause flash pulmonary edema, shock and death

Chronically may cause pulmonary edema (DOE, PND, orthopnea), RHF

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13
Q

What heart sounds are associated with mitral regurgitation?

A

Holosystolic murmur

Best heard at the apex radiating to the axilla, back or clavicle

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14
Q

What is the etiology for tricuspid regurgitation?

A

Either due to primary valve problem e.g. rheumatic, Ebstein anomaly, carcinoid, endocarditis or
Secondary to elevated RV pressures (e.g. pulmonary HTN, LV failure, restrictive cardiomyopathy)

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15
Q

What is the clinical presentation for tricuspid regurgitation?

A

Murmur like MR but louder with inspiration

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16
Q

Which congenital heart diseases are associated with late cyanosis with L to R shunt?

A

ASD, PFO, VSD, PDA, CoA

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17
Q

What is the etiology for atrial septal defects?

A

Defect in the middle (ostum secundum, MC) or lower (ostum premum which occurs in down syndrome) part of atrial septum

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18
Q

What is the clinical presentation for ASD?

A

small defects are often asymptomatic
large ASDs are typically detected/closed childhood; if not its may become symptomatic by middle age, causing exercise intolerance, dyspnea and fatigue

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19
Q

What are the complications associated with ASD?

A

Pulmonary HTN, Eisenmenger syndrome, RHF, Afib, stroke with paradoxical emboli

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20
Q

What heart sounds are heard with ASD?

A

Loud S1, wide flexed split S2

More pulmonic flow = mild systolic ejection murmur, diastolic rumble across the tricuspid valve

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21
Q

What is the etiology for patent foramen ovale?

A

An atrial opening that usually closes at brith

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22
Q

What is the clinical presentation for PFO?

A

common and usually benign but always consider when a pt <60 presents with TIA or stroke

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23
Q

What is the etiology for VSD?

A

defect in the muscular or membranous portion of the ventricular septum

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24
Q

What are the associations for VSD?

A

fetal alcohol syndrome, down syndrome

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25
Q

What is the clinical presentation for VSD?

A

most large VSDs are detected and closed in childhood

if not patients may become symptomatic with eventual pulmonary HTN and right to left shunting

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26
Q

What heart sounds are heard with VSD?

A

Harsh blowing holosystolic murmur with thrill, loudest at the left third intercostal space with handgrip (smaller defect = louder murmur)

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27
Q

What is the etiology for patent ductus arterioles?

A

Persistent communication between the aorta and pulmonary A

Associated with congenital rubella, prematurity

28
Q

What is the clinical presentation for PDA?

A

Depends on the size
Small PDAs are usually asymptomatic
Moderate PDAs cause Eisenmenger syndrome if not dx
Large PDAs cause infantile heart failure

29
Q

What heart sounds are heard with PDA?

A

Machine like murmur best heard at the left 2nd intercostal space
Wide pulse pressure and bounding peripheral pulse

30
Q

What are the signs of pulmonary HTN?

A

Syncope, atrial and ventricular arrhytmias, cyanosis

Late findings include R and L HF sx

31
Q

What is the presentation of children with Eisenmenger syndrome?

A

cyanosis, fatigue, and sx of RHF

32
Q

What is the presentation for adults with Eisenmenger syndrome?

A

Develops secondary to pulmonary vascular obstructive changes
Cyanosis, clubbing, an increased RV impulse, a narrowly split S2 with a loud P2 component and a soft or absent VSD murmur
Systolic murmur of tricuspid insufficiency at the LLSB, a high frequency early diastolic murmur of pulmonary insufficiency or an S3 at the LLSB
Associated JVD and hepatomegaly indicating right sided filling pressures

33
Q

What is the etiology for Coarctation of the aorta?

A

Infantile: LE cyanosis with weak pulses; associated with Turner’s syndrome
Adult: can also be acquired due to inflammation of the aorta (e.g. Takayasu’s)

34
Q

What is the clinical presentation for coarctation of the aorta?

A

upper extremity HTN, low/unobtainable LE BP, and diminished/delayed femoral pulse, rib notching on CXR

35
Q

Are diastolic murmurs always pathologic?

A

yes

36
Q

Inspiration causes which murmurs to be louder?

A

R heart murmurs

37
Q

Expiration causes which murmurs to be louder?

A

L heart murmurs

38
Q

Which murmurs increase with standing/valsalva?

A

Murmurs associated with MVP and hypertrophic cardiomyopathy

39
Q

Which murmurs increase with hand grip (increased SVR)?

A

Increases with murmurs associated with AR, MR, VSD

40
Q

Which murmurs decrease with hand grip (increased SVR)?

A

Murmur associated HCM

41
Q

Which murmurs are systolic?

A

AS, MR, TR, VSD, ASD and HCM

42
Q

Which murmurs are diastolic?

A

AR, MS and TS

43
Q

What is splitting of S1 associated with?

A

A feature of Ebstein anomaly which is associated with right bundle branch block

44
Q

What are the two components of S1?

A

The mitral component (M1) precedes the carotid pulse upstroke and the tricuspid component (T1) occurs later

45
Q

What are the two components of S2?

A

aortic (A2) and pulmonary (P2) valve

46
Q

What are the major determinants of A2 intensity (and therefore major determinants of S2)?

A

Aortic pressure (a major determinant of the velocity of valve closure)
Relative proximity of the aorta to the chest wall
Size of the aortic root
Mobility and structural integrity of the aortic valve

47
Q

What determines the intensity of P2?

A

Pulmonary arterial pressure particularly diastolic pressure
Size of the pulmonary artery
Mobility and structural integrity of the pulmonary valve

48
Q

When is an increased P2 intensity suggested?

A

when it is louder over the 2nd interspace or when there is transmission to the cardiac apex

49
Q

What can lead to increased intensity of A2?

A

Systemic HTN
Coarctation of the aorta
Ascending aortic aneurysm
When the aortic root is relatively anterior and closer to the anterior chest wall as in metrology of fallout and transposition of the great arteries

50
Q

What can cause increased P2 intensity?

A

Pulmonary arterial HTN of any etiology (MC)
Idiopathic pulmonary artery dilation
ASD
MR

51
Q

What can cause decreased intensity of A2?

A

Conditions that affect the mobility and integrity of the aortic valve
Severe aortic regurgitation (AR) or stenosis
Hypotension

52
Q

What can lead to decreased intensity of P2?

A

Conditions that affect the mobility and integrity of the pulmonary valve
Pulmonary stenosis and regurgitation
Significant RV outflow obstruction associated with a soft and delayed P2
The low pulmonary artery pressures also play a role in attenuating P2

53
Q

What can cause wide splitting S2?

A

Electromechanical delay of the RV

  • RBBB, artificial pacing from the LV and wolf-parkinson-white (WPW) syndrome with LV pre-excitation
  • Premature beats and an idioventricular rhythm of LV origin (QRS complex of RBBB morphology) are also associated with wide splitting
54
Q

What are some hemodynamic causes of wide splitting of S2?

A
  • Increased resistance to RV ejection and prolongation of RV ejection time
  • Isolated reduction of the LV ejection time (examples include severe MR when forward SV decreases with increases in regurgitant volume)
55
Q

What can cause fixed splitting of S2?

A

ASD

Can also occur with RV failure, RV outflow obstruction, pulmonary HTN, and primary RV dysfunction

56
Q

What can cause reversed (paradoxical) splitting of S2?

A

Electromechanical delay such as LBBB

Artificial RV pacing, pre-excitation of the RV (WPW syndrome) and premature beats of RV origin

57
Q

Which hemodynamic factors can cause reversed (paradoxical) splitting of S2?

A

Markedly prolonged LV ejection time
Fixed outflow obstruction as in pts with aortic valve stenosis
Myocardial dysfunction, ischemia or in pts with long standing severe AR

58
Q

What is S3?

A

Ventricular gallop
Early diastolic sound, listen with bell
Turbulent flow of blood hitting an overfilled ventricle
Differential dx: can be normal in its age <35 or in pregnancy
otherwise specific sign of decompensated HF

59
Q

What is S4?

A

Atrial gallop/kick
Late diastolic sound, listen with diaphragm
Atrium pushing blood against a stiff ventricle
Differential dx: always consider pathologic in its >40
May be common in athletes
Associated with ventricular hypertrophy (secondary to HTN) and heart failure

60
Q

What are the surgical considerations for aortic stenosis?

A

Surgery is recommended for pts <65 years or with a life expectancy of >20 years
Transcatheter AVR is recommended for all pts >80 years
Either surgical AVR or transcatheter AVR can be considered for all pts between 65 and 80 years
But younger pts will tolerate valvuloplasty much more than older pts – therefore not recommended in older pts with the advent of TVAR

61
Q

When is surgery done for aortic regurgitation?

A

for sx, EF <50%, LV end systolic dimension >50mm, or LV end diastolic dimension >65mm
all determined by echocardiography

62
Q

What are the tx options for mitral stenosis?

A

Valve replacement when pulmonary edema, a decline in exercise capacity or any evidence of pulmonary HTN occurs

63
Q

When is surgery indicated for chronic mitral regurgitation?

A

For sx or when the LV EF is <60% or the echocardiographic LV end systolic dimension is >4cm
Also in its who have a progressive increase in LV size or decline in LVEF

64
Q

What is indicated for pts with mitral prolapse and severe mitral regurgitation?

A

Earlier surgery if mitral repair can be performed successfully with a high degree of certainty

65
Q

What are tx options for tricuspid regurgitation?

A

Generally well managed with diuretics
Aldosterone antagonists if ascites also present
Treat underlying cause

66
Q

what is the tx for congenital heart dz?

A

surgical repair

ECOS III Final (14 decks)

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