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From Flashcardlet big > Previous exam 2009 > Flashcards

Previous exam 2009 Flashcards

1
Q

List the immunnosuppressant medication needed for heart transplant recipients.

A

Induction: IL-2 receptor antagonists (Basilixumab, a monoclonal Ab), polyclonal anti-thymocyte antibodies, OKT3 (murine monoclonal Ab to T cell receptor, not used)

Maintenance: triple cocktail of;, Calcineurin inhibitors (cyclosporine or tacrolimus), anti-metabolite (MMF or azathioprine), glucocorticoids (for first year)

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2
Q

In radial artery harvesting what nerves can be injured

A

Lateral antebrachial cutaneous - damage causes parasthesia/numbness to radial aspect of volar forearm

Superficial branch of radial nerve - damage causes parasthesia/numbness to thumb and dorsum of hand

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3
Q

What are causes of hypoxia after LVAD

A

Undetected or new PFO shunting R to L due to unloaded LV

  1. Pre op echo a must - incl bubble study
  2. Poss tear in IAS
  3. High LVAD flow with MR

Pulmonary V/Q mismatch
Massive PE with PFO

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4
Q

What are predictors of mortality CABG

A
  1. Age >70 2. LV dysfunction 3. Chronic kidney disease 4. Emergent surgery 5. Preop shock 6. DM 7. Preop anemia
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5
Q

What is the literature of the PPM and what are the recommedations

A 
AHA Guidelines: Class I
3rd degree AVB, advanced 2nd degree
Symptomatic Mobitz I or II
Syncope due to bradycardia
Congenital heart block e.g. Long QT
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6
Q

Describe the Nicks procedure

A

Posterior Aortic root enlargement by extending aortotomy through non coronary cusp through aortic annulus. Placement of patch.
Will upsize by 1.

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7
Q

What are the treatment options for A2 prolapse

A
  1. Chordal shortening by implanting into pap muscle
  2. Artificial chords
  3. Chordal transfer from PMVL to AMVL
  4. Alfieri stitch or per cutaneous clip
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8
Q

What are causes of inter-atrial shunt?

A
  1. PFO
  2. Primum ASD
  3. Secundum ASD (most common)
  4. Sinus venosus defect
  5. Unroofed coronary sinus
  6. AVSD
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9
Q

What are the surgical indications of chronic type B dissection

A

Acute treatment is morphine for pain, iv B blocker (labetalol, esmolol) to reduce HR to <60 bpm, diltiazem or verapamil if BB intolerant, add nitroprusside if SBP remains >100.

Surgical indications are 1. Persistent/recurrent pain. 2. Rupture 3. Propagation of the dissection (manifests as pain) 4. Malperfusion 5. Aneurysm expansion

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10
Q

How is the diagnosis of Marfan made? What are the genetic factors?

A

Diagnosis based on Ghent Criteria (2010 revised):
If no family Hx of MFS, any 1 of these is diagnostic;
1. Aortic criterion (Aortic dia Z>=2 or aortic root dissection) AND ectopia lentis
2. Aortic criterion AND FBN1 mutation
3. Aortic criterion AND systemic score >=7
4. Ectopia lentis AND FBN1 mutation
If a positive family history of MFS, any 1 of these is diagnostic;
1. Ectopia lentis 2. Systemic score >=7 3. Aortic criterion

Genetics: autosomal dominant, mutation of Fibrillin-1 (FBN1),

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11
Q

What are surgical options post aortic valve replacement aortic dissection

A

Remove valve and place a valved conduit (Bentall)

Replace ascending aorta keeping valve in place

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12
Q

Describe the pathophysiology of HIT. How would you treat this

A 
HIT 1 (10-20%): slight fall in plts 1-4 d after exposure. No treatment needed
HIT 2 (1-3%): Heparin binds platelets directly causing activation and release of PF4.  PF4 binds heparin forming H-PF4 complex. If prior heparin exposure, IgG to H-PF4 complex forms which bind to platelet Fc receptors. This causes further release of PF4.  Ultimately get a cascade of platelet activation, granule release, and aggregation. Granules release pro coagulant factors (thrombin, V, fibronectin, fibrinogen, vWF) therefore increased thrombin.

Management: stop all heparin, anticoagulants with argatroban or lepirudin to prevent thrombosis, warfarin

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13
Q

Abciximab mechanicm of action and it’s half life?

A

Abciximab = Reopro

Class: anti platelet agent, inhibits glycoprotein IIb/IIIa receptor on platelet surface inhibiting aggregation by interfering with binding of fibrinogen, vWF
Half life 30 mins, renallY excreted

Indications: Primary PCI for STEMI

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14
Q

List 6 echo findings of ischemic (functional) MR

A 
Normal leaflet morphology
Leaflet tethering (tenting height, tenting area)
Dilated annulus
Papillary muscle displacement
LV dilation (sphericity)
LV dysfunction
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15
Q

Causes of Metabolic acidosis in (non cyanotic baby) (low flow shunt)

A 
hypoplastic arch
critical aortic stenosis 
coarctation 
interrupted arch 
subaortic stenosis
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16
Q

Describe mechanism of reperfusion injury

A

Ischemia damages cell membranes incl mitochon, lowers intracell pH. Repercussion leads to Ca++ overload, generation of ROS Mitochon dysfunction due to Ca overload and membrane disruption, uncoupling of ox phos. Ca++ load also causes myocyte contracture when O2 returns. ROS damage membranes. Leukocyte activation due to cytokines release from damaged myocytes. Complement activate. Apoptosis.

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17
Q

Aortic valve sparing surgery complication

A

Aneurysm of root (Remodelling technique) esp Marfans
AI
Bleeding (esp remodelling as larger suture line exposed vs reimplantation)
Correct sizing of graft difficult
Possible kinking of coronary button
Low cardiac output

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18
Q

Aortic valve sparing surgery complications

A
  1. Thromboembolism esp stroke
  2. AI
  3. Pseudoaneurysm
  4. Coronary button aneurysm in MFS
  5. Endocarditis
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19
Q

How can a person be a co-author

A

According to the Uniform Requirements for Manuscripts Submitted to Medical Journals, a credited author should meet the following conditions:

  1. Substantial contribution to conception and design, data acquisition, or analysis and interpretation of data
  2. Drafting the paper or revising it critically for content
  3. Final approval of the published version.
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20
Q

FFR what is it? what is the cut off?

A

Fractional Flow Reserve = ratio of distal coronary pressure to aortic pressure during maximal hyperaemia (adenosine, papaverine). Derived from pressure tracings in coronary cath. Estimates the percent of normal coronary blood flow that would be available to myocardium served by that artery. An index of the physiologic significance of a stenosis. Independent of BP, HR, contractility.
Normal value is 1.0, values <0.75 indicate inducible ischemia, high risk lesion.

21
Q

Benefits of MAZE procedure

A

Designed to block all re-entrant circuits in atria.
Prevents both flutter and fibrillation.
Restores AV synchrony, thus decr risk of stroke
Cut and sew/cryo/RF can all be used
Cut and sew freedom from AF >90% at. 3-5 years

22
Q

Causes of tricuspid valve regurgitation?

A
  1. Secondary to MV disease
  2. IE
  3. Primary pulmonary HTN
  4. RV infarction
  5. Myxomatous degeneration 6. Trauma 7. Appetite suppressant drugs
23
Q

Tricuspid valve endocarditis. What are 3 treatment options

A

TV endocarditis most common in IVDU.

  1. Valve repair
  2. Valve replacement (bio or mech)
  3. Valvectomy
24
Q

What are left coronary artery aneurysm treatment indications?

What are treatment options?

A

Causes: Kawasaki disease, iatrogenic (cath), atherosclerosis (most common), congenital, SLE, Takayasu’s
More common in RCA and Cx

Treatment depends on severity of coexisting CAD-if symptomatic with emboli to distal coronaries surgery is recommended
Treatment: 1. LIMA-LA with ligation or resection of the LCA +- SVG to circ
2. medical mgmnt with anti coagulation and anti platelets
3. Covered stent

25
Q

Describe the shock trial

A

NEJM 1999:341;625
RCT: emerg revasc (balloon/CABG n=152) vs med Tx (n=150) for cardio genie shock 2ary to AMI
No diff 30d mortality (47%vs56%)
Lower 6&12 mo mortality in revasc (50%vs63%, 53% vs 66%)
Biggest benefit age <75

26
Q

What are 5 indications to operate on for aortic valve endocarditis

A 
heart failure 
Fungus or resistant organisms
Annular or aortic abscess/fistula
Recurrent systemic embolization
Persistent sepsis despite abx
Prosthetic valve endocarditis
27
Q

What are indications for pulmonary valve replacement in patient who had an old tetralogy of fallout repair

A 
Pts with symptoms related to chronic PR
Mod/severe RV volume overload
RV dysfunction
Arrhthmias due to RV dilation
Onset of TR
Exercise intolerance
28
Q

What is the natural history of TOF if left untreated

A

Onset of cyanosis, progression of RVH with RV dilation and RV failure. Hypoxia causes seizures. Delayed growth and development, risk of sudden death.
Survival (unrepaired): 75% 1 year, 30% 10 years, 10% 20 years.

29
Q

What are the classes of evidence

A

Classes of Recommendation:
1. Evidence of useful and effective treatment “benefit&raquo_space;> risk” Should be performed”
2. Conflicting evidence
2a “benefit&raquo_space;risk, reasonable to perform”
2b “benefit >=risk, may be considered”
3. Evidence of harm or no benefit

Level of Evidence (size of population studied)
A. Multiple RCT or meta analyses
B. single RCT or non randomized studies
C. Expert opinion, case studies only

30
Q

What are signs of cardiac tamponade

A

Beck’s Triad: elevated JVP, muffled heart sounds, hypotension
Also tachycardia, elevated filling pressures, pulsus paradoxus (>10 mmHg decline in systolic BP with inspiration)

31
Q

Draw and describe the CVP curve

A

CVP equivalent to right atrium. Sequence is “a c x v y”
3 positive waves:
a: atrial contraction
c: closure of tricuspid valve
v: ventricular contraction/passive atrial filling

2 negative waves:

x: atrial diastole
y: atrial emptying

32
Q

A patient is on LVAD what is the cause of an elevated Bilirubin

A

Elevated bilirubin is indicative of RV failure.
This may be due to underlying bi ventricular failure that unmasks RV failure once the LVAD is in place.
May also be due to RV unable to handle increased venous return or to bulging of septum into LV due to reduced LV pressures with resulting poor geometry of RV

33
Q

List 5 criteria for CRT

A 
QRS >= 150 ms
LVEF <= 35%
NYHA class 2-4
Sinus rhythm 
LBBB pattern
34
Q

What is protocol of anticoagulation in pregnant women

A

Warfarin crosses placenta easily. Contraindicated in pregnancy as teratogenic. Vulnerable during weeks 6-9 gestation.

AHA guidelines: STOP WARFARIN between weeks 6-12 and use either monitored UFH or LMWH (Level Ic). UFH appears to be more effective than LMWH. Enoxaparin is NOT recommended in preg women with mechanical valves. Then warfarin can be used up to week 36, or continue UFH/LMWH. Switch to heparin several weeks before delivery. ASA can be added in second and third trimester.

No data on safety of dabigatran in pregnancy.

35
Q

What is the hemodynamic difference between restrictive cardiomyopathy and constrictive pericarditis

A

.

36
Q

What test can you do to differentiate between restrictive cardiomyopathy and constrictive pericarditis?

A

Cardiac catheterization shows square root sign in ventricular diastolic pressure in CP. Also get filling pressure equalization in all 4 chambers in CP.
Echo shows significant resp variation in ventricular filling velocity in CP, minimal in RCM.

CT shows thickened and calcified pericardium in CP. CXR shows calcification in CP.

37
Q

What are the criteria to change the rate of ultra filtration in kids

A

.

38
Q

What are 5 risk factors for development of post op renal failure

A
  1. Age > 70
  2. CHF
  3. Type 1 DM
  4. Preop serum creatinine > 130
  5. Prolonged CPB (> 3h)
39
Q

What are 4 devices/techqniques to improve exposure in the heart for off pump surgery

A

Octopus/starfish
Deep pericardial retraction sutures
Opening right pleura
Tilting or rotating OR table

40
Q

What are the ways to detect ascending aorta atherosclerosis

A
  1. Epiaortic scan
  2. CT
  3. TEE
  4. MRI
  5. Palpation
41
Q

What are 4 indications for ICD post CABG

A
  1. LV dysfunction (LVEF<35%)
  2. More than 40 days post MI
  3. NYHA class I-III (LVEF <30% if NYHA I)
  4. On optimal pharmacological therapy
  5. QRS >120 s (ESC only)
  6. NSVT on Holter (ESC only)

(Based on AHA and ESC guidelines)

42
Q

What are 5 reasons why the mammary artery is optimal conduit

A
  1. Resistant to developing atherosclerosis
  2. Optimal patency >90% at 10 years
  3. Survival advantage when used to LAD (83% vs71% for 3 VD at 10 years)
  4. Produces its own NO and prostacyclin, resistant to vasoconstrictor agents
  5. Good size match to target
43
Q

What is the cardiac involvement in carcinoid syndrome.

A

Carcinoid syndrome is mediated by humoral factors released by carcinoid tumours(serotonin, bradykinin).

Cardiac manifestations are valvular lesions characterized by fibrous deposits on valve cusps, cardiac chambers, and rarely intima of aorta and PA. Termed cardiac plaques. Most often affects the right side as compounds are inactivated in the lungs unless R to L shunt.
Affected valves thickened, retracted, get central TR, possible TS. Signs incl JVD, RV dilation, RV heave, murmurs, ascites, low voltage ECG

44
Q

What are treatment options in a patient with known CAD with a calcified ascending aorta

A
  1. Hybrid revasc = LIMA to LAD, then PCI of 1 or more non-LAD territory coronaries
  2. Bilat IMA grafts, then Y or T graft to other targets
  3. Off pump distals, then circ arrest for proximals to aorta
  4. Clamp-less devices for proximals e.g. Enclose device, PasPort
  5. Peripheral arterial cannulation, fibrillatory arrest for anastomoses
  6. Replace ascending aorta under DHCA and graft to it.
45
Q

Name the types of Endoleaks

A
  1. Leak at graft end
    A - proximal B - distal
  2. Aneurysm sac fills from branch vessel (most common)
  3. Leak through failed graft fabric/graft to graft connection
  4. Porous graft–will reverse with heparin
  5. Endotension - continued expansion of aneurysm without evidence of a leak.
46
Q

What are risk factors for AV disruption following mitral valve surgery

A 
age
small, female 
calcified annulus
oversizing 
aggressive debridement
heart retraction 
re-ops
post op hypertension 
heart distention 
double vavle
47
Q

List the consequences of CMV infection post cardiac transplant

A 
rejection episodes 
mono-type syndrome
pneumonitiis
hepatitis 
gastroenteritiis 
encephalitis
48
Q

Post cardiac transplant develops renal failure. What will you change in terms of medication

A

Change nephrotoxic immunosuppressant agents (Calcineurin inhibitors) to less toxic versions.

D/c anti metabolites (MMF or azathioprine), start anti proliferative such as Sirolimus or Everolimus to allow reduction in doses of
Calcineurin inhibitors.

Or, d/c Calcineurin inhibitors and use Sirolimus/Everolimus + MMF

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