Previous exam 2009 Flashcards
List the immunnosuppressant medication needed for heart transplant recipients.
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)
Post cardiac transplant develops renal failure. What will you change in terms of medication
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
In radial artery harvesting what nerves can be injured
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
What are causes of hypoxia after LVAD
Undetected or new PFO shunting R to L due to unloaded LV
- Pre op echo a must - incl bubble study
- Poss tear in IAS
- High LVAD flow with MR
Pulmonary V/Q mismatch
Massive PE with PFO
What are predictors of mortality CABG
- Age >70 2. LV dysfunction 3. Chronic kidney disease 4. Emergent surgery 5. Preop shock 6. DM 7. Preop anemia
What is the literature of the PPM and what are the recommedations
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
Describe the Nicks procedure
Posterior Aortic root enlargement by extending aortotomy through non coronary cusp through aortic annulus. Placement of patch.
Will upsize by 1.
What are the treatment options for A2 prolapse
- Chordal shortening by implanting into pap muscle
- Artificial chords
- Chordal transfer from PMVL to AMVL
- Alfieri stitch or per cutaneous clip
What are causes of inter-atrial shunt?
- PFO
- Primum ASD
- Secundum ASD (most common)
- Sinus venosus defect
- Unroofed coronary sinus
- AVSD
What are the surgical indications of chronic type B dissection
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
How is the diagnosis of Marfan made? What are the genetic factors?
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),
What are surgical options post aortic valve replacement aortic dissection
Remove valve and place a valved conduit (Bentall)
Replace ascending aorta keeping valve in place
Describe the pathophysiology of HIT. How would you treat this
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
Abciximab mechanicm of action and it’s half life?
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
List 6 echo findings of ischemic (functional) MR
Normal leaflet morphology Leaflet tethering (tenting height, tenting area) Dilated annulus Papillary muscle displacement LV dilation (sphericity) LV dysfunction
Causes of Metabolic acidosis in (non cyanotic baby) (low flow shunt)
hypoplastic arch critical aortic stenosis coarctation interrupted arch subaortic stenosis
Describe mechanism of reperfusion injury
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.
Aortic valve sparing surgery complication
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
Aortic valve sparing surgery complications
- Thromboembolism esp stroke
- AI
- Pseudoaneurysm
- Coronary button aneurysm in MFS
- Endocarditis
