Congenitals, VSD, TET o' FAllot, Infective Endo - Blonder SRS Flashcards Preview

Cardiovascular II Exam 3 > Congenitals, VSD, TET o' FAllot, Infective Endo - Blonder SRS > Flashcards

Flashcards in Congenitals, VSD, TET o' FAllot, Infective Endo - Blonder SRS Deck (44):
1

What is an ASD?

An open communication between the atria via a defect in the intra-atrial septum.

2

In 20 percent of patients the foramen ovale is not covered by what?

The septum primum.  If this does not cover the foramen ovale then patient has patent foramen ovale.

3

What is the primary diagnostic tool used for identifying a PFO?

Echocardiography

4

What direction is the shunting in an ASD or PFO?

Transient Right to Left shunting occurs in most patients during the onset of ventricular contraction.  This explains the neurologic events in non-cyanotic patients (such as stroke).

5

How do patients tolerate right sided volume overload?

Quite well, for years.  Pressure and resistance overloads are NOT well tolerated though.

6

What is afterload primarily due to?

Resistance from arterioles

7

What is the second most common adult congenital anomaly after bicuspid AV?

ASD - most common diagnosed in adults

But, VSD is most common absolute.

8

Patients with ASD are typically asymptomatic until aldulthood.  What are 5 complications that are associated with this structural defect?

  1. Atrial arrhythmias
  2. Paradoxical Embolus
  3. Cerebral Abcess
  4. Right Heart Failure
  5. Pulmonary HTN ---> Eisenmenger Syndrome

 

9

What are the types of ASD?

  1. Secundum ASD
  2. Primum ASD
  3. Sinus Venosus ASD
  4. Scimitar Syndrome (he didn't cover this one, but I guess know that it exists)

10

What is the most common type of ASD? Who is it most common in? What is the associated defect?

 

Lastly, what are the other cardiac defects associated with this condition?

Secundum ASD is 70% of ASD's and is more common in females. 

It arises due to a defect in the foramen ovalis.

It is NOT associated with other cardiac defects... typically.

11

Primum ASD's are 15 to 20% of ASD's and are large defects.  What is this defect nearly always associated with?

What are the "complete" forms?

Are these patients symptomatic?

Almost always associated with defects in the AV valves or ventricular septum.  (generally leads to insufficiency)

AV canal or endocardial cushion defect is the complete form.

Hell yeah these patients are symptomatic.

12

Sinus venosus ASD occur high in the atrium, what are these often (more than 90%) associated with?

What are the two types and what are their root defects?

Associated with Anomolous pulmonary vein insertion.

1. Superior sinus venosus defect - SVC defect

2. Inferior sinus venosus defect - IVC defect

 

13

Shunt flow leads to a useless circuit of blood through the defect.  This flow may be trivial or as much as 8:1.  (more likely 2:1 or 5:1)

This leads to right heart volume overload.  What is the long term consequence of this?

Though well tolerated for years this can cause pulmonary HTN and Eisenmengers.

14

What is the natural history of an ASD?

If less than 8mm, usually asymptomatic.

Larger lesions tend to grow with age.

 

15

What is the likely course of a patient with ASD and a shunt flow greater than 2:1?

Will become symptomatic and require surgical repair by age 40

16

As mentioned previously clinical manifestations of ASD can include arrhythmias.  Which ones though?

 

Atrial arrhythmias

- 20% atrial fibrillation or flutter (increases with advancing age)

17

Apart from the arrhythmias, what are the other associated manifestations of ASD?

Embolic events - stroke, paradoxical stroke, systemic emboli

Migraine cephalgia

PHTN

Eisenmenger

Cyanosis

18

What shunt ratio is needed for Eisenmenger syndrome to develop?

greater than 2.5:1

19

On physical exam what would you find for an ASD upon palpation?

RV heave

Palpable PA at upper LSB

20

What are the heart sounds you would find if an ASD is present?

  1. Wide fixed split S2
  2. Increased P2 with pulmonary HTN
  3. S1 split with increase in tricuspid component
  4. SEM (systolic Ejection Murmur) upper LSB from PI secondary to pHTN

21

What are the four types of VSD?

  1. Infundibular
  2. Membranous
  3. Inlet Defect
  4. Muscular

 

22

Infundibular VSD occurs below the aortic and pulmonic valves.  What does this lead to?

Leads to progressive aortic regurgitation, the hallmark of this condition apparently.

23

What is a conoventricular VSD a deficiency of?

The membranous septum.  This is an alternative name for a membranous VSD.

24

What is the direction and severity of a VSD determined by?

Functional size and the ratio of pulmonary to systemic vascular resistance.

25

Small or restrictive VSD have an orifice diameter less than or equal to 25% of the aortic annulus diameter.  This creates a small L to right shunt with no LV volume overload and no pulmonary hypertension.  What can be caused by this?

Flow impact derived endocarditis in the right ventricle 

26

At what VSD size do you see mild to moderate volume overload of the PA, LA and LV?

Does this size defect lead to pHTN?

Moderate sized defect, between 25% and 75% the size of the aortic annulus.  

This does not cause pulmonary HTN

27

What happens to patients with large VSD's greater than 75% the diameter of the aortic annulus?

Moderate to large left to right shunts with LV volume overload.

If uncorrected, leads to PHTN with pulmonary arterial obstructive disease.

28

Large VSD leading to progressive PHTN leads to right ventricular pressures approaching that of systemic pressure.  What does this lead to?

Leads to Eisenmenger syndrome, which when coupled with VSD is called eisenmenger complex.

Reversal of shunt with Right to left flow, will cause hypoxemia and cyanosis.

 

29

The clinical manifestation of small VSD is typically asymptomatic.  What are the clinical presentations of...

Moderate sized defect?

Large VSD?

1. Moderate: either asymptomatic or mild CHF in children, usually gets smaller with growth and may have AR (aortic regurg I assume)

2. Large: Usually early presentation with CHF in infancy or Eisenmenger's in late childhood/early adulthood.

30

What would you expect to find on PE of a patient with VSD?

Large holosystolic murmur at LSB, 2nd or 3rd ICS with a thrill.

31

What is the test of choice for identifying a VSD?

What options are best for complex lesions?

Echo - test of choice

CT/MRI excellent for complex lesions

32

What are the four features of tetralogy of fallot?

1. RVOT obstruction (pulmonic stenosis)

2. VSD

3. Aorta overrides IVS

4. Concentric RVH

**TQ alert**

33

What determines the need for medical intervention in TOF?

The degree of RVOT obstruction

34

How does infective endocarditis typically present these days?

Acutely, rather than subacutely as in the pre-antibiotic age.

35

What are some key items to flesh out in a possible case of infective endocarditis?

Indwelling prosthetic devices such as: IV catheters, Orthopedic hardware, cardiac devices, Insulin pumps.

IV drug use/abuse

36

It can be difficult to distinguish tricuspid and mitral regurgitation.  What tips did Dr. Blonder have on this topic?

1. Location

2. Inhalation will increase the volume of a tricuspid regurgitation and have no impact on mitral.

3. JVD will be present in tricuspid but not in mitral.

 

37

PE of the infective endocarditis patient should focus on new regurgitant murmurs and CHR.  What are the "stigmata" of endocarditis?

Are these signs for acute or subacute?

  1. Janeway lesions - hemorrhages on palms and soles
  2. Osler nodules - painful nodules in the digit pulp and the proximal fingers
  3. Roth spots - Oval hemorrhages in the eye
  4. Petechial hemorrhage

 

These signs are for subacute only.  Will be absent in acute cases.

38

What is the criteria used for identifying infective endocarditis?

Modified duke criteria

39

What are the "major" criterion for the Duke criteria?

  1. Blood culture positive for a characteristic organism
  2. Echocardiographic findings including valve-related or implant related mass or abcess, or partial seperation of a valve.
  3. New valvular regurgitation

 

40

What are some components of the minor criteria for the Duke criterion?

There's a shit load...

Vascular lesions including petechiae, subungual/splinter hemorrhages, emboli, septic infacts, mycotic aneurysm, intracranial hemorrhage, janeway lesions.

Immunologic phenomena including glomerulonephritis, Osler nodes, Roth spots, rheumatiod factor

Microbiologic evidence including single culture showing uncharacteristic organism

Echocardiographic findings consitent with but not diagnostic of endocarditis including worsening or changing of a preexisting murmur.

41

What are the pathological criteria for diagnosis of IE?

Microorganisms, demonstrated by culture of histo, in a vegitation, embolus from a vegetation or intracardiac abcess.

Histologic confirmation of active endocarditis in vegetation of intracardiac abcess.

42

Diagnosis by the Duke guidelines requires either pathologic OR clinical criteria.  If clinical criteria are uses then what combinations equals IE?

  1. 2 major
  2. 1 major plus three minor
  3. 5 minor

43

What are the typical organisms that cause IE?  

Which is most common?

  1. Strep Viridans - most common
  2. Strep Gallolyticus (bovis)
  3. HACEK group
  4. Staph aureus
  5. Comunity aquired enterococci

44

What considerations must be... considered when obtaining blood cultures for IE diagnosis?

  1. Obtain prior to initation of antibiotics if possible.
  2. At least three sets of cultures
  3. Obtain at seperate sites and not from catheter (unless absolutely necessry)