Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV II > BLONDER > Flashcards

BLONDER Flashcards

1
Q

Most common congenital heart disease at birth

A

VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 types of VSD

A
  1. Infundibular
  2. Membranous
  3. Inlet defect
  4. Muscular vsd
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Infundibular VSD

A

below the aortic and pulmonary valves

leads to aortic regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Membranous VSD

A

deficiency in the membranous septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Inlet defect VSD

A

Downs syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

muscular VSD

A

in the trabecular system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

large VSD clinical presentation

A

usually early presentation with CHF in infancy or Eisenmenger’s in late childhood, early adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Medium VSD clinical presentation

A

either asymptomatic or mild CHF in children, usually gets smaller with growth and may have AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

VSD sound in PE

A

holosystolic, left sternal border, 2-3rd intercostal space, thrill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

tetrology of fallot

A
  1. Right ventricular outflow tract obstruction
  2. Ventral Septal Defect
  3. Aorta overrides VSD
  4. Concentric right ventricular hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Patent foramen ovale

A

a foramen covered by the septum primum but is not sealed shut in 20% of normal subjects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to diagnose an ASD

A

echocardiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Second most common adult congenital abnormality

A

ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of ASD

A

o Atrial arrhythmias (atrial fibrillation)
o Paradoxical embolus- DVT then stroke
o Cerebral Abscess- infection is embolized across ASD to brain
o Right heart failure
o Pulmonary hypertension > Eisenmenger syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Types of ASD

A
  1. Secundum
  2. Primum
  3. Sinus venosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Secundum ASD

A

o Due to defects in the foramen ovalis. Usually not associated with other cardiac defects. More common in females.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Primum ASD

A

o Large. Almost always associated with defects in the AV vales or ventricular septum.
• Right above the ventricles
o AV canal, or endocardial cushion defect is the complete form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Sinus venosus

A

o Often associated with >90% with anomalous pulmonary vein insertion
o 2 types
o Superior sinus venosus- SVC defect
o Inferior sinus venosus- IVC defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

scimitar syndrome

A
  1. Partial anomalous venous return- to the systemic venous drainage, rather than directly to the left atrium
  2. Hypoplasia of a lobe of the right lung
  3. Thoracic aorta > Pulmonary artery collaterals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pathophysiology of ASD

A

• The shunt depends on the size of the defect, the compliance of the right and left ventricles, and the phases of contraction- systole/diastole, atrial ventricular, early or late in phase
o Most shunts starts L to R, but all large shunts have some R to L

• Shunt flow leads to a useless circuit of blood through the defect
o Into the RA, RV, PA, LA, back to RA

• This leads to right heart volume overload, well tolerated for years, but can cause pulmonary hypertension and Eisenmengers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are ASDs associated with?

A

• Usually associated with concomitant pulmonic valve stenosis or Eisenmengers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PE for ASD

A

o RV heave

o Palpable Pulmonary artery at upper LSB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Heart sounds of ASD

A

o Wide fixed split S2
o Increased P2 with pulmonary HTN
o S1 split with increase in Tricupsid component

24
Q

Heart murmurs of ASD

A

o SEM Upper LSB from increased flow

o Early DM, upper LSB from PI secondary to pulmonary HTN

25
Q

Etiology of atrial fibrillation

A
  1. Hypertensive heart disease
  2. CHD
  3. RF in underdeveloped countries
  4. Hyperthyroidism
  5. Genetic (likely most common)
26
Q

Classifications of atrial fibrillation

A
  1. paroxsymal
  2. persistent
  3. long standing persistent
  4. permanent AF
27
Q

Paroxysmal AF

A

AF that terminates spontaneously or with intervention within 7 days of onset. Episodes may recur with variable frequently

28
Q

Persistent AF

A

AF that fails to self-terminate within 7 days. Episodes often require pharmacologic or electrical cardioversion to restore normal sinus rhythm. AF generally progresses.

29
Q

Long standing persistent AF

A

Af that has lasted for more than 12 months

30
Q

Permanent AF

A

patients with persistent AF where a joint decision has been made by the patient and clinician to no longer pursue a rhythm control strategy

31
Q

CHA2DS2-VACc

A

the most useful tool for deciding risk of stroke to determine whether to anti-coagulate
o C- congestive heart failure
o H- hypertension
o A- age > 75 = 2 pts
o D- diabetes mellitus
o S2- stroke, TIA, or thromboemobolus = 2 pts
o V- vascular disease- prior MI, PAD, aortic plaque
o A- age 65-74
o Sex category, female = 1 pt

32
Q

treatment for AF

A

warfarin or other anticoagulant

33
Q

rate control

A

pt is appropriately anti-coagulated and the rate is controlled by AV blockers

34
Q

rhythm control

A

effort is made to anti-coagulate and restore NSR by meds or electrical cardioversion. A TEE may be used to rule out LA thrombus prior to cardioversion.

35
Q

salvo

A

2 in a row

36
Q

Multiform

A

More than one QRS morphology

37
Q

Bigeminy

A

Every second beat is a PVC

38
Q

what determines the severity of PVCs?

A

The severity of LV function determines prognosis, not the frequency or complexity of the PVCs

39
Q

Causes of AV block

A

Causes

  1. Increased vagal tone
  2. Fibrosis and sclerosis of conduction system
  3. IHD
  4. Cardiomyopathy and myocarditis- scarring
  5. Congenital heart disease
  6. Familial AV block
40
Q

The most common cause of LV outflow obstruction

A

Aortic stenosis

41
Q

The most common congenital abnormality of the heart

A

bicupsid aortic valve

42
Q

senile aortic stenosis

A
  • Associated with atherothrombotic degeneration of the AV (trileaflet)
  • Presents in much older patients, likely in their 80-90s
43
Q

Cardinal signs of aortic stenosis

A
  1. Dyspnea upon exertion
  2. Syncope- near syncope, exertional lightheadedness
  3. Angina of effort
44
Q

PE findings of aortic stenosis

A
  • Inspection may find JVD with right heart failure (late finding)
  • There is LVH- non displaced large apex impulse, LV dilation is late
  • A precordial thrill, 3rd interspace, LSB may be felt
  • S1 normal, SEM at base, radiates into neck and onto the clavicles (much easier to hear)
45
Q

Causes of mitral regurgitation

A
  1. Ruptured mitral chordea tendinae due to myxomatous disease, infective endocarditis, trauma, rheumatic heart disease (either acute or chronic) or spontaneous rupture
  2. Papillary muscle rupture due to acute MI or trauma or pap muscle displacement due to ischemia or MI
46
Q

Pathophysiology of mitral regurgitation

A
  • LA compliance is usually normal, causing an immediate and severe reflection of high pressure from the LA to the pulmonary circulation, causing pulmonary edema
  • In chronic MR, the LA dilates and becomes very compliant. There is no time for LA dilation in acute MR
  • Because LV is not dilated, much of the CO is diverted into the LA, causing a decrease in effective CO. → cardiogenic shock
47
Q

clinical presentation of acute mitral regurgitation

A

• Acute severe MR- pulmonary edema and cardiogenic shock → pt is dying
o Fast, thread pulse, hypotension with hypoperfusion (cold), wet lungs (crackles), extreme air hunger and orthopnea
o Usually a murmur of MR, but many pts will have a soft or inaudible murmur due to increase in LA pressure diminishing the noise

48
Q

Etiology of chronic mitral regurgitation

A
  1. Leaflets
  2. Mitral annulus
  3. Chordae tendinae
  4. LA
  5. LV- papillary muscle, regional LV dysfunction at the origin of the muscle
49
Q

Signs and symptoms of chronic mitral regurgitation

A
  • Dyspnea on exertion
  • Fatigue
  • Palpitations- especially with atrial fibrillation
  • CHF decompensation, orthopnea, PND, Functional class III or IV
50
Q

Precordial exam of chronic mitral regurg

A

o Holosystolic murmur, or pan systolic murmur at the apex, radiates in direction of MR jet, anterior or posterior (opposite leaflet)
o Decreased S1, wide split S2 from early A1, occasional S3
o Rapid rising and falling bounding pulse-volume problem like AR

51
Q

Causes of mitral stenosis

A
  • Due to inactive rheumatic heart disease.

* Rarely- mitral annular calcifications- not usually of great significance

52
Q

PE findings in mitral stenosis

A
  • Mitral facies- pink purple cheeks (maxillary from decrease in CO and vasoconstriction)
  • Pulmonary HTN leads to right heart failure with RV enlargement, loud P2, etc
53
Q

Cardiac auscultation in mitral stenosis

A

o Increased S1
o Single S2
o Opening snap, follows S2, severe shortens the A2-OS interval
o Mid diastolic murmur (rumble) heard at apex, with pre systolic accentuation- if in NSR

54
Q

aortic root dilatation

A
  1. Marfans
  2. Dissecting AA
  3. Non dissecting AA
  4. Ankylosing spondylitis
  5. Becet’s syphilis, osteogenesis imperfect, psoriatic arthritis
55
Q

PE in aortic regurgitation

A

bounding pulse, large pressure-pulse and pulse-pressure lead to many signs like Demecet’s Traub’s Quinke pulse
Early diastolic decrescendo murmur, LSB, 4-5th ICS, or RSB in AA

CV II (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions