SESATS CTS Adult Cardiac Flashcards

1
Q

Manage incidentally found pulmonary AVMs

A

embolize all, even incidentally found (risk of stroke, bleeding)

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2
Q

Pt presents w/ flail chest, pain is controlled, unable to wean from vent. Consider what mgmt?

A

rib plating

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3
Q

What is Haller index required for pectus surgery?

A

>3.5

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4
Q

Compare Nuss and Ravitch.

A

No difference in pain or cosmetic outcome except that Ravitch is open. Nuss may require removal of strut.

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5
Q

Are PFTs affected by pectus surgery?

A

Usually no change in PFTs

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6
Q

For penetrating lung trauma requiring intervention, what is ideal surgical procedure?

A

Tractotomy. Avoid lobectomy and pneumonectomy - c/b BPF.

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7
Q

Solitary fibrous tumor appearance on PET?
IE is it FDG avid?

A

Not FDG avid.

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8
Q

Solitary fibrous tumor gross appearance on parietal and visceral pleura?

A

sessile on the parietal pleura (chest wall) and pedunculated on the visceral pleura (lung parenchyma)

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9
Q

Solitary fibrous tumor microscopy appearance?
What pathology finding denotes more aggressive tumor?

A

Spindle cells.
More aggressive when >4mitoses/HPF are present.

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10
Q

Treatment for pulmonary solitary fibrous tumor?

A

Multidisciplinary care.
If possible, excise with negative margin and follow w/ yearly surveillance.
- Re-resect if margin positive.
- If cannot re-resect, can give adj radiation.
- If cannot initially resect, can give neoadj radiation.
- If more advanced (extensive local disease or mets), dacarbazine or doxorubicin.

*imaging - well-circumscribed soft tissue masses with a homogenous appearance, enhance w/ contrast
*majority of SFTs have indolent behavior with a very low risk of recurrence or metastasis
*STAT6 is sensitive and specific

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11
Q

What do you monitor for in pts with pulmonary ground glass opacities that have been incidentally found?

A

Monitor for development of solid component, size >8 mm.

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12
Q

What do you do for GGO that is >8 mm or has solid component?

A

Can do wedge, or repeat CT imaging 3 mo, or PET/CT, or other biopsy.

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13
Q

How do you manage a pleural effusion with high ADA?

A

Pleural biopsy to dx TB effusion. No drainage needed if positive, as these resolve w/o drainage.

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14
Q

How do you image pancoast tumor to decide on approach?

A

MRI

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15
Q

What treatment do you need before resection of any pancoast tumor?

A

Concurrent chemoradiation BEFORE any resection.

This is followed by surgical resection if there is no evidence of distant metastases or local progression and postoperative chemotherapy.

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16
Q

How do you manage a pancoast tumor adherent to artery or vein?

A

Can resect and reconstruct artery and vein

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17
Q

What structure, if invaded by pancoast tumor, cannot be resected?

A

Do not resect if C8 needs sacrificed

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18
Q

What lymph node status precludes pancoast tumor resection?

A

Do not resect if N2 disease on workup

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19
Q

What are indications for referral for lung transplant for COPD?

A

Disease is progressive despite smoking cessation, med optimization, pulm rehab, and supplemental O2.
BODE 5 or 6.
FEV1 <25% predicted.

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20
Q

In lung volume reduction surgery, what is the vent strategy?

A

During single lung vent, advanced COPD pts can develop air trapping and hyperinflation, causing hemodynamic instability.

Using low TV (eg, 5 mL/kg), lower RR, and longer E-times (eg, an I:E ratio of 1:3 or 1:5), can help prevent trapping.

Lowering MV in this way may lead to alveolar hypoventilation -> inc PaCO2. This is permissive hypercapnic ventilation (PHV). pH is allowed to drop gradually to 7.35 - 7.2.

If pH drops <7.2, cautious increase in RR, suctioning of airway secretions, optimizing muscle relaxation, and administering inhaled bronchodilator therapy, should help.

If a patient should develop hyperinflation and hemodynamic instability, transient disconnection of the endotracheal tube from the ventilator usually leads to resolution over several seconds.

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21
Q

What are lung volume reduction surgery criteria?

A

Results of NETT trial for emphysema:
DEBILITATED: FEV <45, air trapping (resid vol >150%, TLC >100%).
FAILED: dyspnea w/ max med/pulm rehab, no smoking for >6 mo.
FIT: <75 yrs, DLCO & FEV >20, 6 min walk >140m, pulm rehab ability 6-10 wks.
WILL BENEFIT: min pHTN (PA sys P <45), CT w/ *heterogenous dz focused in the upper lobes

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22
Q

Which esophageal cancers go straight to esophagectomy?
What do lower stage cancers get?
What do all other resectable cancer get?
What if nodes are positive after resection?

A

Straight to esophagectomy in T1b and low risk T2 (<3cm, well-diffx, no LVI).

T1a can have EMR or RFA.

For any other respectable esophageal cancer, start with induction chemoradiation and re-stage for possibility of resection (complete responders do best).

Chemo adjuvant if nodes are positive.

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23
Q

What is added to esophageal cancer treatment if nodes are positive after resection? How do you determine if a 2 or 3 drug regimen should be used?

A

Chemo (fluoropyrimidine based).
If excellent PS, can use 3-drug regimen.
2-drug regimens are usually preferred d/t better sfx profile.

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24
Q

When is neoadjuvant chemoradiation used in esophagectomy?

A

Straight to esophagectomy in T1b and low risk T2; T1a gets EMR or RFA. For any other esophageal cancer, start with induction chemoradiation and re-stage for possibility for resection (complete responders do best).

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25
Q

Non-small cell chemo strategy - first line if PD-L1 >1%?
What if >50%?

A

Platinum based + Pembro is first line agent for advanced non small cell lung cancer with PD-L1 expression 1-49%.

If >50% PD-L1 expression, Pembro alone can be given. Atezolizumab or Cempiplimab-rwlc are options as well.

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26
Q

When to add EGFR TKI for non small cell lung cancer?
Who should it be avoided on?

A

EGFR tyrosine kinase inhibitors (erlotinib) are indicated in patients with actionable EGFR mutations and stage IV disease.

AVOID using EGFR directed therapy as an adjuvant in people who have been resected since these can lose effectiveness within 1-2yrs.
Instead, use platinum based chemo after resection of stage II and stage III disease, and save the EGFR directed therapy for later.

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27
Q

A patient is going to undergo septal myectomy (for HCM). What in the history increases risk for postop complete heart block the most?

A

RBBB.
Overall heart block risk is 2%. Those with previous septal alcohol ablation are at highest risk for RBBB - transmural infarct created by the ablation is in the region of the R bundle.

LBBB should not influence the incidence of complete block.

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28
Q

Pt is s/p CABG and ready for DC. They have small effusions. What should their DC meds include?

A

Beta blockers and statin therapy are tracked by STS database - part of the star ranking. DAPT isn’t specifically tracked, but antiplatelet therapy is.

CABG readmission is often 2/2 volume overload. In a patient with effusions, a discharge diuretic is indicated.

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29
Q

Describe ideal configurations for ITAs and radial grafts.

A

In-situ ITA to LAD. L and R have similar patencies. 2nd ITA to 2nd most important graft - usually lateral wall (circ system).

Radial artery is vulnerable to competitive flow - best in size-matched target w/ high grade stenosis; usually circumflex w/ 70% or R coronary w/ 90%.
Radial graft configurations don’t have evidence of benefit of specific configurations - grafts off an in-situ ITA, free grafts off the aorta, or hoods of the venous grafts have similar patencies. Would avoid a direct radial-aortic anastomosis in cases of a small-friable thick-walled aorta.

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30
Q

What is basal inferior aneurysm/dyskinesis and why is it important in regard to mitral regurgitation?

A

It is a severe form of LV ischemic remodeling that incorporates the mechanistic properties of papillary muscle displacement, leaflet tethering, and annular dilation - all of which affect ischemic MR.

An inferior basal aneurysm may predict recurrent ischemic MR because it integrates both leaflet tethering and LV remodeling measures.

LV end systolic dimension and annuloplasty ring size were also significantly associated with a 1-year recurrence of MR.

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31
Q

How can you tell if your septal myectomy is complete?
What do you do if it is not?

A

Need to know if there is a resolution of the LVOT obstruction - TEE and gradient measurement.
A provoked gradient (holding Valsalva on vent) >25 requires resumption of bypass and additional resection. Ie complete the operation.

Do not just give volume, reduce HR, and remeasure.

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32
Q

How can you tell if your septal myectomy is complete?
What do you do if it is not?

A

Need to know if there is a resolution of the LVOT obstruction - TEE and gradient measurement.
A provoked gradient (holding Valsalva on vent) >25 is bad/incomplete and requires resumption of bypass and additional resection. Ie complete the operation.

Do not just give volume, reduce HR, and remeasure.

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33
Q

Most common bacteria for infective endocarditis of the tricuspid valve

A

Staph aureus

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34
Q

Explain the difference in mangement of R sided infective endocarditis vs L sided endocarditis.

A

R sided responds well w/ IV abx.
R HF AND severe tricuspid regurgitation; difficult to treat organisms; sustained infection; and vegetations 2cm or > w/ recurrent PEs should be considered for surgery.
In addition, patients w/ high risk for recurrence (IVDU) are less ideal candidates for early surgical intervention.

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35
Q

Is valvectomy (ie no replacement) a good first line option for tricuspid endocarditis?

A

No. IV abx will usually work. Also, valvectomy w/o replacement is associated w/ poor long-term outcome d/t hepatic dysfunction.

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36
Q

Do postop mitral or tricuspid bioprosthetic patients need anticoag postop?
What about antiplatelet?

A

VKA (warfarin) for 3mo postop - this is the subacute phase that has inc stroke risk because epithelialization of the sewing ring has not occurred.
Lifelong DAPT shows no benefit and has inc bleeding risk.
ASA lifelong after 3 mo VKA is controversial.

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37
Q

What do you give postop mitral or tricuspid bioprosthetic patients if contraindication to anticoag?

A

Single-dose antiplatelet (ASA).

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38
Q

What intervention do you do with an ischemic heart disease (CAD) pt w/ EF 35-50%?

A

Class IIa recommendation for CABG over medical or PCI. Significant survival benefit regardless of DM.

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39
Q

If there is a CABG indication for acute ischemic heart disease, what is the timing?

A

Not emergent. CABG can convert bland infarct into hemorrhagic infarct and worsen ventricular function.
If non-transmural infarct, then delay for 6 hrs.
If transmural, then delay for 3 days (unless other over-riding indications are present).

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40
Q

Manage new isolated wall motion abnormality in pt on table for CABG w/ nl preop EF. The abnormality is in the distribution of one of the grafts.

A

Revise graft. Don’t just try to de-air.

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41
Q

How do you manage a severely stenotic vein graft s/p remote CABG who is going back to the OR for heart surgery?

A

If patent, the prior graft should be left in place (despite some saying they should be replaced if >5 yrs old). If the previous graft stenosis is severe, it is unlikely to create competitive flow, so should be left in place as well.

A new bypass should be placed for severe stenosis.

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42
Q

Which CAD pts do you need to consider carotid disease in?

A

L main, triple vessel, older than 75.
Do a good history. Get a duplex.

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43
Q

How do you manage a patient who has actively symptomatic carotid and operative/symptomatic coronary artery disease?

A

Active = within the last 3 months. Perform synchronous carotid endarterectomy and CABG.

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44
Q

How do you manage a patient who has actively symptomatic carotid and medically manageable (over short term) coronary artery disease?

A

Can start with CEA or carotid stent then staged CABG (6 wks after stent, 2 wks after CEA).

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45
Q

How do you manage a patient who has incidental asymptomatic carotid disease and actively symptomatic coronary artery disease?

A

CABG, then staged CEA.

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46
Q

What causes mitral regurgitation in patients with ischemic cardiomyopathy?

A

annular dilation vs tethering of the leaflets

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47
Q

What to do with MV for patient with significant MV regurgitation undergoing CABG?

A

repair or replace; prefer repair if possible (ie with a complete and relatively undersized ring)

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48
Q

How do you eval after mitral valve repair (intraop)?

A

Wean CPB then use TEE to look for anything greater than mild regurgitation.

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49
Q

What to do if inadequate mitral valve repair when eval w/ TEE after weaning CPB intraop?

A

mitral valve replacement is durable and definitive (don’t try smaller ring or placing edge-edge stitch)

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50
Q

Manage a VSD found after DES placement for ischemic cardiomyopathy

A

Med mgmt is 90% fatal. Emergent surgery is 45% fatal. Multi organ failure inc mortality to ~70%.
Start with VA-ECMO as a bridge to improve other organs (LVAD does not unload flow to the lungs and RV if acute resp failure).
Catheter devices can close defects <1.5 cm present for 10-14 days (sufficient scarring).

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51
Q

How does VSD after DES for MI usually present?

A

1-2% of MIs.
Most common scenario: after first MI in pt w/ single vessel dz. Antero-apical location (LAD territory).
Psx: CV decompensation 3-7 days after MI (esp if adequate flow is not re-established). Holosystolic murmur. Echo usually shows defect in anterior septum w/ L-R shunt. Take note of size of defect (1.5 cm cutoff for perc repair).

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52
Q

How do you manage anticoag in patient with mechanical valve undergoing minor procedure with low bleeding risk (cataracts, dental extraction)?

A

Continue VKAs w/ therapeutic INR. If the procedure is more invasive, it’s ok to temporary interrupt without bridging.

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53
Q

What’s the best way to manage worsening type B dissection despite optimal medical mgmt?

A

TEVAR (L SCA to celiac)

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54
Q

When do you operate for chronic primary mitral regurgitation?
*acute symptomatic MR gets prompt mitral surgery, preferably repair

A

Causes insidious LV dysfunction.
Severe = VC >0.7, RVol >60 ml, RF >50%, ERO >0.4.

Early intervention in asx pts w/ severe MR when there is LV dysfx (<60% EF) or LV enlargement (>40 mm ESD).
Early intervention with sx.
Or in pts w/ preserved EF and dimension if 95% likelihood of repair and mortality <1% at CVC (IIa).

Transcath MVr has no role in low-risk primary degen MR - only for severe MR w/ symptoms or w/ LV systolic dysfunction AND prohibitive surgical risk.

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55
Q

Manage functional mitral regurg.
What parameters do you need to know?
When to do procedures?
What about ischemic?

A

FMR is different than primary degenerative MR.
Initial therapy is med therapy (GDMT).
Know QRS: consider CRT (QRS >150).
Surgery considered after optimization of medical therapy.

Standard recs for coronary revascularization apply.

Know if NYHA HF sx:
For most w/ severe chronic 2ndary MR with…
1) LVEF ≤50%.
2) NYHA II, III, or IVa HF despite optimum Rx + CRT, as indicated.
3) Appropriate anatomy for TEER.
Tx is TEER.
I.E. TEER is 1st line if no concomitant surgical indication.

For patients with severe ischemic MR UNDERGOING CABG or SAVR, consider MV surgery.
I.E. NO isolated MV surgery for functional MR.

*NO recommendation for surgery for nl EF/fct/dimension WITHOUT symptoms or other indication. Unlike other valve pathologies.

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56
Q

Manage acute, decompensated MR secondary to MI and ruptured papillary muscle.

A

Ruptured papillary muscle is a mechanical complication (as opposed to function).
It is a surgical emergency.
May require IABP at time of cath.
Definitive is urgent MV surgery (chordal-sparing replacement vs repair) and revascularization (assn w/ MI). Repair is preferred for long-term survival, but replacement is sometimes safest.

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57
Q

If acute type A dissection is suspected, how do you diagnose?

A

CT chest/abd. May need pelvis to eval femorals.

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58
Q

Manage uncomplicated type B dissection.

A

BP control (BB w/ goal HR 60) and serial imaging. Vasodilators can be used as adjunct.

Intervention for complicated disease, aneurysm to 5.5.
2b recommendation for intervening in high-risk anatomic features.

Complicated: rupture, branch artery malperfusion, extension of dissection, aortic enlargement, uncontrolled HTN, intractable pain.

High-Risk Imaging Findings:
Maximal aortic diameter >40 mm
False-lumen diameter >20–22 mm
Entry tear >10 mm
Entry tear on lesser curvature
Increase in total aortic diameter of >5 mm between serial imaging studies
Bloody pleural effusion
Imaging-only evidence of malperfusion

High-Risk Clinical Findings:
Refractory hypertension despite >3 different classes of antihypertensive medications at maximal recommended or tolerated doses
Refractory pain persisting >12 h despite maximal recommended or tolerated doses
Need for readmission

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59
Q

Manage Marfan-related aortopathy

A

Replace ascending aorta or root >4.2 (TEE internal diameter) or >4.4 (CT or MRI external diameter).
If maximal cross-section area (sq cm) / patient height (m) is >10, then surgery is tx. Shorter pts have dissection at a smaller size. 15% of Marfan pts have dissection at size <5 cm.

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60
Q

What is ideal CPB strategy in type A w/ dissected R axillary and rupture? How do you obtain neural protection?

A

CPB prior to sternotomy via femorals since axillary is not available. Antegrade (arch) and retrograde (SVC: pictured - modified CPB circuit) neural protection are both effective.

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61
Q

Marfan associations.
What gene? What location?
What does this cause?
Physical manifestations?
Diagnosis?

A
  • fibrillin-1 gene (FBN-1) on 15q21.1
  • incomplete microfibrillar system
  • elastin is disordered and fragmented
  • altered TGF-B d/t issues binding w/ fibrillin
  • diagnosed clinically + fibrillin mutx tests
  • ectopia lentis + aortic root dilation (Z-score >2; need CT scan) OR aortix dillation w/ fibrillin mutation is diagnostic
  • also wrist/thumb sign, pectus deformity, pneumothorax, dural ectasia, scoliosis or kyphosis, MV prolapse
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62
Q

Characteristics of Loeys-Dietz syndrome.
Screening/surveillance for aorta?
Medical mgmt?
Indications for aortic surgery?

A
  • aneurysms everywhere, aggressive
  • skeletal problems
  • craniofacial problems
  • cutaneous findings
  • pregnancy complications (uterine rupture)
  • hx of allergies/inflammatory dz
  • GI inflammation (eos esophagitis, IBD)

Screen root w/ TTE, rpt 6 mo, surveillance yearly if stable.
Screen rest of aorta w/ CT or MRI head to pelvis.
CT or MRI yearly if aneurysm/dissection for surveillance.
Can stretch to 2 yrs if no abnormality.

Treat w/ beta blocker or ARB or both in max tolerated doses.

Tend to have severe vascular disease and nearly all have aortic root aneurysms that lead to aortic dissection. Since aortic dissection has been observed with aortic diameters <50 mm, repair is recommended at smaller diameters than recommended for MFS.

For adult patients with Loeys-Dietz syndrome or a confirmed TGFBR1 or TGFBR2 mutation and an aortic diameter of ≥4.2 cm by echocardiogram (internal diameter) or ≥4.4 to 4.6 cm by CT imaging and/or MRI (external diameter) it is reasonable to consider surgical repair of the aorta.

For young children with prominent craniofacial features of Loeys-Dietz syndrome, prophylactic surgery is indicated if the aortic valve annulus is at least 18 to 20 mm and the aortic diameter exceeds the 99th percentile for age.

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63
Q

What is size indication for intervention in a pt w/ connective tissue disorder (eg Marfan) and aortic root pathology?

What would you say to someone who proposes a remodeling technique?

A

Diameter 4.5. Perform root replacement.

Remodeling technique is not appropriate strategy for performing valve-sparing root replacement in pts w/ CTD.

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64
Q

In a patient with type B dissection and distal malperfusion, what is the management?

A

endovascular stent graft

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65
Q

How do you manage an elevated L hemidiaphragm in a patient s/p CABG?

A

Determine symptoms and atelectasis.
If a lot of atelectasis and volume loss, consider bronch.
If effusion, consider drain.
If diaphragm remains elevated after 6-12 mo of obs, then eval function and consider diaphragmatic plication.
Avoid complication by not carrying IMA dissection too superior.

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66
Q

How does functional ischemic mitral regurgitation occur?

A

LV remodeling and dilation after MI results in tethering of the structurally normal leaflets with subsequent regurgitation. Associated with HF and death.

Repair via chordal sparing mitral valve replacement at the time of CABG (or severe persistent sx w/ nl EF or severe persistent sx w/ lower EF [20-50] who is not TEER candidate).
IE don’t do standalone surgery for these patients if asx and normal EF - just GDMT.

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67
Q

Potential advantages of off-pump CABG (OPCAB)?

A

Transfusion rates are lower.
Periop mortality, MI rates, stroke, renal failure are comparable.

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68
Q

Does a pt w/ 3v CAD and mildly regurgitant bicuspid aortic valve without root dilation need surgery for the valve?

A

No.
The ascending aorta needs to be replaced at the time of concomitant surgery if >4.5 cm.
The pt should be followed regularly if aorta is mildly dilated.
Do valve if moderate AR/AI.

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69
Q

What is the preferred bypass conduit for 3v CAD?

A

all arterial

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70
Q

A patient is s/p TEVAR. He is still acidotic despite good hemodynamics, adequate filling pressures, good heart on echo, and pulses in femorals. What do you do?

A

Confirm you’re in true lumen via angiogram or IVUS.

Ensure no other areas of ischemia that have not reperfused (CTA for SMA/celiac/renals).

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71
Q

What is blood cardioplegia?

A

Adjunct in hypothermic myocardial protection.
O2 dissociation curve is shifted left in hypothermia.
Ie release of oxygen to tissue is dec during hypothermia.
Dissolved oxygen is essential for the efficacy of blood cardioplegia, ie the delivery of O2 for blood cardioplegia is most determined by the dissolved O2 content in blood cardioplegia.

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72
Q

Anomalous origin of the right coronary artery causes ischemia. How do you manage?

A

CABG w/ IMA vs ostioplasty w/ unroofing; the latter is simplest and safest. Open the aorta, find the ostia, and “unroof” it from the inside. Confirm patency. Confirm that you haven’t gone all the way through the aorta.

If injury to the button, can recreate the button with a pericardial patch vs bypass.

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73
Q

Del Nido advantages?

A

Long period of arrest (1L~90min).
Equivalent or non-inferior compared to blood cardioplegia.
May have improved return of spontaneous rhythm/dec need for defibrillation.

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74
Q

Advantages of using BIMAs?

A

Improved patency.
Improved survival.
Of note: preserve radials in pts w/ DM and CKD in case future Cimino is needed.

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75
Q

In a patient with aortic stenosis and hx of CAD, how can you tell if low EF is from the stenosis or the CAD?

A

Dobutamine stress echo.

In pts w/ LV dysfx w/ CAD AND aortic stenosis, the dec SV from the bad LV may depress measured velocities and gradients across a severely stenotic valve - low-flow, low-gradient aortic stenosis.

Dobutamine can improve contractility and inc SV across the aortic valve. If the velocity is > 4m/s and gradient > 40 mm Hg, then low-flow low-gradient aortic stenosis is confirmed.

The echo can also localize obstructive CAD.

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76
Q

Redo sternotomy, and you see bright red blood, suspect aortic injury. How do you manage?

A

Do not attempt primary repair.
Do not attempt to open the sternum. Close it with towel clamps.
Cool rapidly while obtaining femoral cannulation for bypass.
Can also place LV vent via lateral thoracotomy through the apex - protects heart from over-distention, especially if there is aortic insufficiency.

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77
Q

Options to protect the brain in total arch for type A.

A

DHCA
DHCA w/ retrograde cerebral perfusion
DHCA w/ antegrade cerebral perfusion
Moderate hypothermia w/ antegrade

Antegrade appears to be more protective than retrograde

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78
Q

What is the implication of a greater curvature tear in a type A dissection?

A

surgical resection and tx of primary tear remains a major surgical principle in aortic surgery - total arch replacement, with individual re-implantation of the head vessels as the ideal option

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79
Q

What should the stenosis percentage be in a target for radial artery? Left target vs right target?

A

greater than 70% on L and 90% on R; they are sensitive to competitive flow

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80
Q

If a standard heart cath injection (during coronary angio) cannot determine coronary disease quantity, what are other options to obtain this information?

A

determine FFR or IVUS; FFR may be more reliable in small/short stature patients

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81
Q

In a non-trauma, non-ischemic patient, what does the presence of a hemorrhagic pericardial or pleural effusion indicate?

A

likely malignancy

82
Q

Workup for redo CABG

A

CTA chest gated to eval grafts and close structures.
Echo - eval valves and EF.

FFR and IVUS is useful if need to eval for tight lesion on angiography (ie cath shows open graft, but maybe the anastomosis looks tight, and you need to decide if it needs redo).

83
Q

Manage recurrent pericarditis

A

For initial episode, tx is usually ASA or NSAIDs. Response predicts reduced risk of recurrence. Glucocorticoid use is associated w/ inc risk of recurrence.

Colchicine and NSAID combo therapy is beneficial for recurrence.

Last resort is intrapericardial steroids.

84
Q

Post-MI VSD best mortality predictor?

A

in order from most predictive to least: pre-op dialysis need, emergency status, shock, increased age, intra-aortic balloon pump requirement

85
Q

What is the principal concern when using retrograde cardioplegia?

A

Variable drainage of the coronary venous system that prevents uniform cardioplegia delivery to the RV. May benefit from antegrade or topical cooling as adjuncts.
Can miss the middle cardiac vein if too deep or cause injury behind the heart.

Also, edema.

86
Q

Most common venous anomaly when considering bypass and cardioplegia?

A

Persistent L SVC.

87
Q

What should be done in a patient w/ a persistent L SVC if the R atrium is to be opened?

A

Cannulate for venous drainage.
If innominate open, can clamp below the L SCV and allow it to drain into current SVC cannula.

88
Q

Differentiate restrictive cardiomyopathy and pericardial constriction in their presentation.

A

Hx of mediastinal radiation can lead to consideration of both diagnoses.

Respiratory variation of ventricular filling velocity is minimal in restrictive cardiomyopathy (myocardium problem). Constriction patients have high variations (d/t non-compliant pericardium equalizes pressures).

Hemodynamic catheterization can be a very important tool to further distinguish b/w these two entities.
LVEDP equalization is a hallmark of constriction (non-compliant pericardium).
LVEDP > RVEDP w/ pulm HTN is restrictive cardiomyopathy.

89
Q

What is the mechanism of functional mitral regurgitation?

A

Papillary muscle displacement and chordal tethering, which prevents proper leaflet coaptation (Carpentier Type IIIB).

Functional = secondary.
Secondary to primary LV dysfx w/ otherwise normal leaflets/chords.

LV dysfunction may be due to coronary heart disease (CHD) or (nonischemic) cardiomyopathy. By contrast, primary MR is caused by primary abnormality of one or more components of the valve apparatus.

90
Q

LVEF <35% in sinus rhythm
w/ LBBB
w/ QRS >150 ms
w/ NYHA II - IV and CHF sx
on GDMT.

What can you offer to improve systolic fct, sx, and survival?

A

Cardiac resynchronization therapy (CRT) - pacing of the left and right ventricles to restore ventricular synchrony and thus improve left ventricular (LV) systolic function, symptoms of heart failure (HF), and survival for these selected patients with LV systolic dysfunction, and electrocardiographic evidence of dys-synchrony (wide QRS).

91
Q

Results of COAPT trial?

A

Decreased mortality and heart failure readmission w/ catheter-based mitral intervention compared to medical control patients; however, the 29.1% all-cause mortality at 2 years in the treatment group is well above the expected mortality in heart transplant or implantable mechanical circ support.

92
Q

Hemodynamic definition of CTEPH?
IE… PA pressure and PCWP cutoffs?

A

PA pressure >25 mmHg (P HTN).
Pulm cap wedge pressure <15 mmHg (P HTN not from heart).

Clinic psx of dyspnea.
Usually in setting of remote hx of PE, echo w/ R overload.

93
Q

What are the essential components and imaging (3 major) in the CTEPH workup?

A

History.
1) Echo.
2) V/Q scan; can be combined w/ CT w/ perfusion contrast.
3) RHC to assess hemodynamics with PA angiography to confirm presence of CTEPH lesions.

94
Q

Surgical indication for BAV patient planning on getting pregnant in setting of aortic aneurysm?
What about general sporadic aortic root /ascending aneurysm patient planning on getting pregnant?

A

5 cm (cor 1) for both of these populations.

In non-pregnant population, 5 cm can be done for root/ascending as 2a rec at an experienced center with multidisciplinary aortic team, but cutoff is 5.5 in arch and descending.

95
Q

Surgical indication for Turner syndrome patient planning on getting pregnant in setting of aortic aneurysm (root/arch/asc/des)?

A

ASI of 2.5 cm/m2 (cor 1).
In normal population, 3.08 ASI is cutoff (2b).

96
Q

What are absolute indications for L SCA to carotid bypass in TEVAR that covers L SCA?

A

Most patients will not benefit from bypass and undergo unnecessary risk of bleeding and phrenic injury.
Most compelling indications are the brain and the heart:
- posterior cerebral circulation threat (ie is circle of Willis intact; is the posterior cerebellar artery a terminal artery)
- a patent LIMA to LAD graft.

L handed individuals may also not tolerate the relative ischemia well.

97
Q

Manage aortic aneurysm in pregnant woman with Marfan.
What specific pieces of information do you need to make decisions?

A

Determine aneurysm size and ob status.
<40mm root - usually tolerate well.
40-45 and pregnant - monthly eval, consider surgery if there are risk factors (FHx, growth 0.3/yr) (2b).

>45 pre-pregnancy - needs surgical intervention.
>45 or 5mm inc and pregnant - terminate if not viable (<20 wks), or c-section if viable; then do surgery.

Of note, if >40mm w/ progressive dilation - do not vaginally deliver

98
Q

Define heparin resistance

A

Failure to achieve ACT of 480 after 450 iu/kg of heparin are given.

99
Q

How do you treat ATIII deficiency that causes heparin resistance?

A

FFP has ATIII, and giving it can normalize the heparin-ACT dose-response curve. 2u FFP is the standard dose.

AT concentrate can also be given (1000 units). When compared to FFP, it requires less additional heparin; avoids thawing time, transfusion related ALI, viral transmission, and volume.

Can attempt rechecking ACT first, since sampling error is the most common cause for low ACT.

100
Q

LVAD success is predicated on patient optimization. How do you manage a preop patient in acute renal failure (w/ hx of decompensated HF w/ biventricular congestion)?

A

Pulmonary catheter-directed therapy is indicated. Initiate inotropes to treat the heart failure, improve renal perfusion, and assist w/ diuresis.

101
Q

When is an implantable cardioverter defibrillator (ICD) indicated?

A

Check CHF EF condition.
1) EF at or below 35% at 90 days post-revasc in pts w/ NYHA II or III HF.
2) EF below 30% regardless of NYHA class.
There must be an expected meaningful survival of at least 1 year.

Secondary prevention of SCD in pts w/ prior sustained VT/VF (not 2/2 reversible cause or w/in 48 hrs after MI), resuscitated SCD likely 2/2 VT/VF.
Primary prevention in pts w/ inc risk of life-threatening VT/VF.

102
Q

How do you manage new HF patient w/ severe MR w/o primary leaflet pathology and tricuspid regurgitation?

A

Improve the cardiac status - guideline-directed medical therapy. Diagnose and treat the underlying myopathic process. Manage arrhythmias.

If severe, symptomatic MR persists despite maximal guideline-directed therapy, surgical valve repair or replacement can be considered (EF >50).

For secondary MR, surgical correction of MR doesn’t always improve quality of life or sx. Heart transplant or VAD should be considered if EF very low. TEER can be considered as well w/ EF 20-50, favorable anatomy (not too much Ca), LVESD <70, PASP <70.

103
Q

A patient with advanced ischemic cardiomyopathy with Stage D heart failure presents acutely. What therapy has the best 5-year survival?

A

OHT. It is better than LVAD.

Guideline-directed medical therapy is generally first-line, but decompensated pts often can’t tolerate beta-blockers and afterload-reducing agents.

Active ischemia should be addressed if viability can be demonstrated. Post cardiotomy shock will be significant.

104
Q

Oxygen delivery equation?

A
DO2 = CO x CaO2
CaO2 = Hb x SaO2 x 1.34 x [0.003(PaO2)]
105
Q

Blood flow at what rate in L/min/m2 can preserve adequate systemic/cerebral oxygenation (in terms of CPB)?

A

1.9-3.1

106
Q

A patient with history of heart failure presents with edema, elevated filling pressures, low cardiac index, and low mixed venous oxygenation.
What is the diagnosis and initial management?

A

Cardiogenic shock.
Lines and inotropic support initially.
EKG to see if ischemia. Echo.
Probably needs diuresis and maybe dialysis.

107
Q

Guidelines for first-degree relative screening in patients with thoracic aortic disease?

A

Echo.
CTA (or MRA) if abnormality found.

108
Q

Based on the IRAD, what is the most common comorbidity for patients w/ acute aortic dissection?

A

HTN. >80% of pts either have the dx or present w/ it.

109
Q

L atrial mass is resected w/ endocardium. Frozen shows sarcoma. Management?

A

Surgical resection, full thickness w/ patch - may require up to cardiac explantation w/ tumor resection, reconstruction, and auto transplantation.
NO cadaveric transplantation.
Medical/radiation therapies are largely ineffective.
Poor overall prognosis - depends on anatomic location and ability to perform complete resection.

110
Q

Most common L atrial tumors?
Management?

A

Myxomas.
Simple excision.

111
Q

In the context of CPB, how has modified ultrafiltration improved cardiac outcomes in adult cardiac surgery patients?

A

Higher post-bypass hematocrit, decreased blood transfusion, decreased postop bleeding.
Higher mean arterial BP in pediatric cardiac surgery.

Initiated after CPB - leave cannulas, blood aspirated from sideport of aortic into a hemofilter then returned to RA hemoconcentrated.

112
Q

How can zero-balanced ultrafiltration (Z-BUF) help with ESRD in patients requiring CPB for cardiac surgery?

A

Adjunct for management of fluids, hyperkalemia, uremia, and inflammatory mediator toxicity.

113
Q

What are some advantages of vacuum-assisted venous drainage for CPB?

What is the pressure limit?

A

Smaller cannula, elimination of air-lock, decreased priming volume, drier operative field w/ improved venous drainage.
Vacuum must be below 100 mmHg or risk hemolysis.

114
Q

Manage a persistent L SVC (no innominate) during case requiring bicaval bypass?

A

Without innominate, the L SVC has to be cannulated.
If innominate exists, L SVC can be clamped or snared below the innominate with a cannula in the normal SVC position.
L SVC normally becomes ligament of Marshall after development of brachiocephalic vein.

115
Q

Seldinger type aortic cannulation for CPB causes type B dissection confirmed by TEE. How do you manage?

A

Switch the cannula to a short type (dispersion), and confirm flow in the true lumen.
NO femoral cannula (this can actually cause type B dissection).
NO emergency procedure unless malperfusion. Do emergent aortic endograft if there is malperfusion.

116
Q

What are cold agglutinins, how do they affect CPB, and how do you manage?

A

Cold agglutinins - auto-abs that agglutinate RBCs at low temps causing hemagglutination and hemolysis.
Can be precipitated in hypothermia and cold cardioplegia; can kill myocardium.
Manage by using warm blood cardioplegia and systemic normothermia.
If found intra-operatively, change CPB strategy to warm; consider using retrograde warm cardioplegia to remove coronary microemboli.

117
Q

A patient with atrial fibrillation and mitral stenosis is to undergo mitral surgery. What scenario might a CMIV be excluded?
What else can be done?

A

High predictors of recurrence in frail patient - advanced age, long duration of atrial fib, large LA size.
CMIV is unlikely to be successful here.
Ligation of LA appendage carries little risk and can be done quickly, so should be considered. +/- PVIs.

118
Q

In a patient undergoing surgery for atrial fibrillation, what variation in the procedure can impact need for PPM? Who likely will need this variation?

A

Biatrial lesion set is associated with an increased need for PPM (ie biatrial CMIV vs LA CMIV [pic]).

Biatrial set is often preserved for prolonged atrial fibrillation or with R side dz and RA enlargement.

  • SA node dysfunction is the primary indication.
  • If concurrent valvular surgery is performed, AV block can happen as a complication assd w/ AV nodal injury.
119
Q

Current guidelines for stopping plavix before surgery?

A

5-7 days if DES placed over a year ago.
If DES <1 year ago, can stop before 5 days w/ short acting antiplatelet bridge.

Continuing plavix use up to CABG is associated with increased need for reoperation.

ASA should not be stopped. Should be dosed <100 mg.

120
Q

ASA should be initiated within what time period to reduce SVG closure?

A

6 hrs. Usually ok if CT output is <100ml/hr.
No “loading” dose is required.
Benefit to SVG patency lost if initiated >48 hrs postop.

121
Q

Recent ACS or PCI - how long does DAPT need to be given?

A

12 months.
Can also be used in pts s/p CABG w/ IIb recommendation.

122
Q

Abx ppx in most standard cardiac cases?

A

first-gen cephalosporin (ancef) prior to skin incision (within 60 min), not to exceed 48 hrs

123
Q

Abx ppx in pts w/ high-risk for S aureus, receiving a prosthetic valve, or pts getting vascular graft insertion?

A

first-gen cephalosporin and glycopeptide (vancomycin) prior to skin incision (within 60 min), not to exceed 48 hrs

124
Q

Recommendations for timing of surgery for IE and a recent TIA or silent cerebral emboli?

A

Risk of postop neuro compromise is low, so early surgery is recommended.
Without evidence of hemorrhage, ok to proceed.

125
Q

In a patient w/ R sided IE and hx of IVDU, what is the treatment regimen if there are no surgical indications?

A

4-6 wks of abx.
Surgery if persistent bacteremia, difficult to eradicate organism (normally just S aureus), persistent vegetation >20 mm, evidence of R HF.

126
Q

What can be done preop to reduce colonization and possibly reduce postop sternal wound infections?

A

Topical abx for the skin and mupirocin for the nares.

127
Q

For cardiac resynchronization therapy, where do the left ventricular leads need to be placed to be effective?

A

Lateral wall. If not lateral enough, will need placement of new, more lateral leads.
This will help delay need for cardiac transplantation.

Reminder: indications for CRT are worsening sx of HF despite optimal GDT, exercise, diet; decreased EF; electrical abnormalities documented (eg widened QRS).

128
Q

What do the three letters in a pacer stand for?

A
  1. Chamber paced: Atrium, Ventricle, Dual, O for none.
  2. Chamber sensed.
  3. Response to sensing: O-none, Inhibited, Trigger, Dual
  4. programmability and rate modulation: O-none, Programmable, Rate modulation
  5. anti-tachyarrhythmia function: O-none, Shock, Pacing, Dual

Example: DOO - both atria and ventricles paced w/o sensing or inhibition.

129
Q

What is an R on T when a patient has temporary pacing?
How is it prevented?

A

When a patient has PVC with DOO pacing on the PVC T wave, an R on T can occur, which can precipitate ventricular fibrillation.

It can also occur if the sense threshold is too high (ie the pacemaker will not sense the incoming underlying electrical discharge).

Lowering the sensing threshold and using a synchronous mode like DDD or AAI can avoid susceptibility to PVCs (because it would sense the PVC).

AOO, DOO, or VOO are asynchronous pacing settings used if bradycardic and coming off bypass so that the Bovie isn’t sensed (and transmitted) by the pacer.

130
Q

How do you manage an R on T in a patient who codes postop w/ internal temporary pacing wires that were set to DOO?

A

Turn off the pacer, reveal V-fib, external cardiovert w/ 150J. If the patient doesn’t respond x3, open the chest.
If asystole or bradycardia are uncovered after pacer is off, then resume pacing with HR 80-100 at max amplitude.

131
Q

How do you manage an inadvertent endocardial LV lead placement?
Why is this an issue?
Are there endovascular options?
What if no interventional options?

A

Rare. Placing pt at inc risk for thromboembolic events.
Need surgical exposure and removal w/ placement of RV lead.

NO transvenous lead extraction as there is excessive risk of dislodging embolic debris.

Warfarin can be considered in pts who are NOT surgical candidates.

132
Q

Along the posterior annulus of the mitral valve, towards, P1, what are you in danger of injuring when placing stitches?

A

circumflex artery

133
Q

What structure is immediately behind the anterior mitral leaflet?

A

non-coronary cusp of the aortic valve

134
Q

During mitral surgery, if sutures are placed too deep behind the anterior mitral leaflet, how is the complication manifested?

A

LV distention from aortic valve incompetence

135
Q

When does warfarin embryopathy occur?

A

Occurs b/w 6-12 wks gestation (1st trimester) and is dose dependent starting at 5 mg/day.

During the 2nd and 3rd trimester, warfarin is recommended if needed.

Ok to continue during 1st trimester if dose <5 mg.

136
Q

How do you treat coarctation of the aorta?

Where is CoA most often?
Associated anatomic aortic pathology?
Assd cardiac pathology? Rate?
Psx?
Surveillance or follow-up imaging?

A

Transcatheter stent placement or open repair. GDMT for HTN.
Prevent coarctation complications of rupture, heart failure, and intracranial hemorrhage (cerebral aneurysm, consider screening [2b]).

Most often just distal to L SCA.
Aneurysmal segment just distal. Collaterals.
BAV. 50%.
Upper extremity HTN and lower extremity hypotension. Measure BP in both arms and lower extremity.
CT or MRI.

137
Q

How do you manage an infected ICD generator after attempted abx w/ the device exposed?

A

*Know PM status…
Complete device AND lead removal w/ placement of a new system.
If the patient is not pacemaker-dependent, the device can be placed after the wound has healed sufficiently.
If they are pacemaker dependent, may require temporary active fixation leads as a bridge after 3 days of neg blood cx.

138
Q

Patients with family hx of HCM and sudden cardiac death (SCD) require what prophylactic therapy?

A

ICD placement.
Also required in HCM pts w/o fam hx in following scenarios: If pt has prior arrest, spontaneous VT, syncope, LV thickness >3cm, abnormal BP response to exercise.

139
Q

Pts w/ prior MI, NYHA Class 1 HF and EF <30% require what mgmt in regards to HF?
Other indications for this mgmt?

A

ICD therapy in addition to best medical mgmt.
Also for NYHA II and III sx if EF <35%.

140
Q

In a patient undergoing coronary revascularization with moderate aortic regurgitation, what should be done with the aortic valve?

A

AVR at time of surgery (IIa recommendation)

141
Q

Compare TAVR to SAVR

A

TAVR: higher rates of PVL, higher rate of PPM, lower rates of bleeding complications, lower rates of AKI and a-fib

142
Q

Manage an atherosclerotic coronary artery aneurysm in patient undergoing CABG.

A

Benign natural history (unlike Kawasaki related aneurysm). At the time of CABG (if has other indication), large aneurysms should be opened and ligated proximally and distally. Distal bypass also should be done.
If small (<2cm), distal bypass should be enough.

143
Q

During TEVAR for type B dissection, the patient develops a retrograde type A. How do you manage?

A

Aortic arch replacement with sewing of the ascending/arch graft to the stent graft.

144
Q

An adult pt w/ hx of rTOF has pulmonic subvalvular stenosis. How do you manage?

A

Need transfer to congenital institution.
Percutaneous vs open valve.

145
Q

How do you confirm pulmonary valvar stenosis in patient w/ repaired TOF?
First line mgmt?

A

Cardiac MRI.
Perc balloon valvuloplasty is likely first line if confirmed.

146
Q

A patient has severe aortic valve regurgitation and severe mitral regurgitation (central regurg). How do you manage?

A

Aortic valve replacement.
Mitral valve REPAIR is preferred.

147
Q

If retrograde cardioplegia is given, and the heart does not arrest w/ low line pressures, what could be the cause?
How do you manage?

A

Consider persistent L SVC. Can drain into coronary sinus and interfere w/ retrograde cardioplegia.
Occlude the L SVC during cardioplegia or use antegrade.

Other problem could be a perforation, AI, or clamp not on all the way.

148
Q

What is the benefit of retrograde cerebral perfusion during aortic arch surgery?

A

Elimination of air and debris from cerebral circulation.

149
Q

POD1 CABG x3 patient has v-fib. They are cardioverted, then EKG shows ST elevation after cardioversion. Management?

A

IABP and coronary angiography.
V-fib is concerning. If angio shows issues, may need to redo vs stent.

150
Q

S/p mech mitral valve replacement 5 wks ago, pt has valve obstruction w/ thrombus formation. How do you manage?

A

TEE diagnostic - how big?
<5mm w/ min clinical impact - anticoagulation alone.

>5mm - fibrinolysis (IV tPA) or reoperation (risky d/t adhesions).

151
Q

Indications for cardiac resynchronization therapy

A

LVEF ≤35% – on optimal evidence-based med tx for 3 mo after dx, and after dx and tx of any reversible causes of persistent HF (ie MI or tachycardia-induced cardiomyopx).

  • QRS ≥150 ms w/ LBBB & NYHA II-IV HF: CRT (and IHD)
  • QRS ≥150 ms w/ non-LBBB & NYHA III-IV
  • QRS <150 ms w/ LBBB & NYHA II-IV
152
Q

Current AHA guidelines for abx ppx for dental procedures?
Which pts and what abx?

A

Only if involves manipulation of the gingiva or periapical area of the teeth or perforation of the oral mucosa.
In the following conditions: prosthetic material in heart, previous IE, CHD, first 6 mo after procedure, OHT pts w/ valvulopathy.
Amoxicillin 2mg 30-60 min preop.
Keflex/Ancef or clinda if allergic.

153
Q

For the prevention of endocarditis, is abx ppx required prior to GI or GU procedures?

A

No. Not for IE prevention.

154
Q

Mitral valve repair is performed and SAM is discovered coming off bypass. How do you manage?

A

Volume load to expand the LV, beta block to inc diastolic filling time, and reduce inotropes as much as possible.

If SAM persists, attempt to salvage repair (especially if young pt) w/ posterior leaflet sliding plasty (decreases posterior leaflet height and moves coaptation line away from LVOT).

Replace MV if repair not possible.

155
Q

Acute mitral regurgitation with pulmonary edema d/t ruptured chord to posterior leaflet causing flail - management?

A

Emergency mitral valve repair

156
Q

Explain the mechanism of neuroprotection during cardiac arrest, specifically DHCA. How is it confirmed to be adequate?

A

Minimizing cerebral rate of oxygen consumption.
Electrocerebral inactivity on EEG is assd w/ least amount of cerebral activity. There is not a specific temperature or time within a temp.

157
Q

What are the NYHA heart failure classifications?

A

I: No limit on activity. No symptoms out of what would be expected during exercise.

II: Some limitation on activity. Comfortable at rest. Ordinary activity causes fatigue, palpitation, dyspnea.

III: Marked limitation. Comfortable at rest. Less than ordinary activity causes symptoms.

IV: Unable to carry out any activity w/o worsening discomfort. Symptoms at rest.

158
Q

When deciding b/w systemic fibrinolysis versus surgery for prosthetic L side mechanical valve thrombosis, what would favor surgery?
(other than surgical risk, expertise, contraindication to fibrinolysis, other surgical indication, or patient choice)

A

Recurrent thrombosis
NYHA class IV
Large clot (0.8 cm)
LA thrombus
Passible pannus

159
Q

Bioprosthetic valve thrombosis management?

A

TEE or 4D CT can help rule out leaflet thrombosis (2a).

Usually, systemic heparin until INR 3-3.5 then lifelong coumadin/VKA. Look for reduction in transvalvular gradient, improved leaflet motion, and clinical improvement.
(Of note, AHA guidelines only mention VKA as initial treatment)

Surgery is reserved if no response or if in shock - replace valve with mechanical prosthesis.

*Tends to be more common w/ transcatheter alves.

*Mechanical valve thrombosis is often more acute and requires immediate intervention (slow-infusion, low dose fibrinolytic or emergency surgery).

160
Q

Risk of stroke with 30 min of DHCA?

A

7.5%

161
Q

A patient requires cerebral perfusion for DHCA but has an aberrant R SCA off the distal arch. What is the strategy?

A

ACP via direct cannulation of carotids

162
Q

How is ACP normally performed for DHCA?

A

R SCA w/ chimney graft and occlusion of the innominate artery, L carotid, and L SCA with clamps or balloon catheters

163
Q

How do you treat endocarditis caused by HACEK organisms assuming no surgical indication exists?

A

Ceftriaxone or fluoroquinolone for 4-6 wks.

164
Q

How do you treat mild-moderate post-cardiotomy shock?

A

Initiate and escalate inotropic support. If that fails, then mechanical circulatory support should be considered.
Milrinone and dobutamine can be added if not hypotensive or tachycardic.

165
Q

Initiation for CPB is begun, there is low volume in the venous reservoir, flows are low, MAP is low, the RA is collapsed. How do you manage?

A

Add volume to the venous reservoir.
This could be vasodilation as well, but that is unlikely to happen early.
If the RA is decompressed, it is unlikely inadequate drainage (ie placing a second cannula will not help).

166
Q

During ACP, regional cerebral oxygen saturation decreases asymmetrically. How do you manage?

A

Insert another carotid cannula in opposite side.
Can increase flow rates, as long as arterial P isn’t >80.
Retrograde cerebral perfusion can yield uniform cooling, but antegrade studies suggest superior outcomes.

167
Q

A patient has undergone DHCA. What is the maximum temperature gradient when rewarming?
Max temp?
Max rewarm rate?

A

The gradient, measured from the arterial outlet to the venous return temp, should not exceed 10 C to prevent formation of gas emboli.
Max temp should be 37 to prevent cerebral hyperthermia.
The max rewarm rate should be < 0.5 C per min.

168
Q

S/p LVAD, a patient has elevated pulm pressures, elevated CVP, and low cardiac output despite a normal MAP w/ epi. What’s the next best agent to add?

A

RV is the problem.
Add milrinone - PDE inhibitor that prevents cAMP degredation and increases intracell Ca. Inc contractility w/ dec PVR and some dec SVR.

169
Q

Diffuse coagulopathy occurs after DHCA. Pressure, packing, topical agents don’t work. Coag labs are corrected via transfusion of platelets, cryo, and FFP. No surgical bleeding. What’s next?

A

Factor VII at a low-dose - has been shown to dec postop bleeding and postop transfusion

170
Q

What can be given to reduce incidence of peri-operative atrial fibrillation?

A

Beta-blockade reduces risk of POAF, but it does not have any impact on post cardiac surgery stroke, MI, or mortality.

171
Q

In patient with LVAD destination therapy, what should MAP goal be to prevent hemorrhagic stroke?
What should the INR target be?
DAPT helpful?

A

MAP <90
INR 2-3

DAPT has NO proven benefit.

172
Q

What PVR in Woods units should heart transplant likely be excluded?

A

>5, though there is no absolute cutoff.
The reasoning is that healthy donors have RVs untrained for pulm HTN, and are prone to RV failure.

173
Q

What is first-line in tx for patients with peri-op R HF s/p OHT?

A

Catecholamines - epi, isoproterenol, dobutamine.
Selective pulm vasodilators can also be used and are effective at reducing PVR w/o causing systemic vasodilation (infrequently used).
RVAD and ECMO should be considered early if cannot wean off CPB.

174
Q

In acute AR, what happens to LV EDP, pulm venous P, and SV?

A

Inc LVEDP, pulm vein P, and SV.
Ie pressures behind aorta and forward flow from aorta inc.
Dyspnea, pulm edema, and heart failure can ensue.

175
Q

What imaging is often best to evaluate the tricuspid valve?

A

TTE

176
Q

Pt has severe aortic stenosis and moderate tricuspid regurgitation with RV enlargement/dysfunction. She is a low risk surgical pt. What is management?

A

Aortic valve replacement and tricuspid annuloplasty.
Tricuspid regurgitation does not reliably respond to correction of L side defects alone.
Tricuspid REPLACEMENT is likely NOT necessary for functional tricuspid disease.
TAVR is only for high and intermediate risk pts w/ symptomatic severe stenosis.

177
Q

Asymptomatic adult pt s/p TOF as a child now has moderate pulmonic regurgitation. What would create indication to operate?

A

Pulmonic valve replacement if any TWO of following:

  • mild or mod RV dysfunction
  • mild or mod LV dysfunction
  • severe RV dilation
  • elevated RV systolic P >2/3 systemic P
  • progressive reduction in exercise tolerance (should be measured w/ cardiopulm exercise test)
178
Q

An adult has pulmonic regurgitation and stenosis after balloon plasty for stenosis as a toddler. He has no symptoms, exercise capacity is stable, and echo is otherwise normal. What is next step?

A

Serial follow up.

Pulmonic valve replacement would be surgery if indicated.

179
Q

Massive air embolism occurs during a case. How do you manage?

A

Stop perfusion and clamp artery and venous lines.
Remove air in circuit by recirculation.
Trendelenburg.
Deep hypothermia.
Retrograde cerebral perfusion via SVC.
Aspiration of the arch via root vent.

Adjuncts: hyperbaric oxygen, induce coma, steroids.

180
Q

How do you manage a symptomatic descending aortic aneurysm?

A

Urgent or emergent repair - EVAR or open

181
Q

Set up an open repair of DAA.
Procedures to consider before OR?
Intubation?
Lines?
Position?
Incision?

A

Consider spinal drainage day before.
DL ETT.
Central line. Radial AND femoral art lines.
R lateral decub position (L side up).
L posterolateral thoracotomy.
Take down IPL.

182
Q

You are doing an open repair of DAA. During proximal dissection, what structures need to be identified and preserved?

What if the vascular structure cannot be preserved?

A

L SCA and dissect distally. Vagus, recurrent, and phrenic nerves are preserved.

If SCA involved, can do TEVAR w/ coverage then LSCA to L CA bypass if needed (hx of CABG w/ open LIMA, HD via LUE, dominant L VA, aneurysmal L SCA, spinal cord protection if TEVAR is extensive).

183
Q

You are doing an open repair of DAA. During distal dissection, what nonvascular structures need to be avoided?

A

Avoid the thoracic duct (ascends chest through T12 with aorta, mostly in R side inferiorly, crosses to L side at T5, and drains into L IJ or L SCV) and esophagus

184
Q

You are doing an open repair of DAA. What is your cannulation strategy?

A
L IPV (inflow) and descending aorta below the aneurysm (outflow). 
LAA and L femoral artery are alternate sites.
185
Q

You are doing an open repair of DAA. Left heart bypass or simple-cross clamping?

A

Left heart bypass has lower mortality. Add moderate hypothermia (32 C) to maintain organ perfusion, spinal cord perfusion, and myocardial protection.

186
Q

You are doing an open repair of DAA. How do you manage the intercostals?

A

Intercostals above T8 are ligated. T8-L1 can be taken as a patch and incorporated into the proximal graft.

187
Q

For a DAA in pt who cannot tolerate open surgery, an EVAR is chosen. What can you do if the external iliac and common femoral arteries are not suitable access vessels?

A

10 mm dacron graft can be sewn on to the common iliac artery through an open retroperitoneal exposure.

188
Q

During EVAR, what amount of coverage proximally and distally should be achieved to reduce risk of type 1 endoleak?

A

2 cm of uninvolved, non-tapered, healthy aorta coverage
*type 1 - proximal or distal endoleak

189
Q

You do a completion angiogram after an EVAR. What do you do for type II endoleak from intercostals? What about L SCA?

A

Intercostals - usually don’t need intervention.

L SCA - embolization and occlusion of the L SCA origin.
Careful for brain, hand, or previous LIMA CABG malperfusion.

190
Q

You do a completion angiogram after an EVAR. What do you do for type I endoleak found?

A

Balloon molding of the device or extension grafts can be applied.

191
Q

You are doing an open repair of DAA that extends below the renals. How do you manage the visceral vessels?

A

Distal clamp is moved to the infrarenal aorta and visceral aorta is opened.
Can use balloon tipped catheters to perfuse the visceral arteries distally from the arterial line.
Celiac, SMA, and R renals can be patched as one to the graft. The L renal artery can be reimplanted as a separate patch.

Branched surgical grafts can also be used to avoid the aneurysmal aortic patches.

Lumbar arteries are normally ligated, but can be reimplanted if worried about spinal perfusion.

192
Q

Postop from aortic aneurysm surgery, the patient cannot move his legs.
How do you manage?
Other workup? What are you looking for?
How is this prevented?

A

Optimize spinal perfusion w/ MAP >100.

Spinal drain should be checked, and CSF should be <10.
Hgb >10.

CT of head to eval for stroke, and MRI of spine for spinal hematoma.
Check pulses in legs to eval for BLE ischemia.

Intraop - cross-clamp should be <30 mins, hypothermia, LHB, reimplantation of T8-L1.

193
Q

Postop open thoracoabdominal aortic aneurysm surgery, the patient cannot move his legs. How do you manage? Other workup? How is this prevented?

A

Optimize spinal perfusion w/ MAP >100.
Spinal drain should be checked, and CSF should be <10.
Hgb >10.
Check CT of head and MRI of spine to eval for stroke or spinal hematoma. Check pulses in legs to eval for BLE ischemia.

Intraop - cross-clamp should be <30 mins, hypothermia, LHB, reimplantation of T8-L1.

Artery of Adamkiewicz is significant in that it is the only major arterial supply supplying the anterior spinal artery along the lower thoracic, lumbar, and sacral segments of the spinal cord. It lies between T9-T12 (also known as the artery of the lumbar enlargement).

194
Q

Postop open thoracoabdominal aortic aneurysm surgery, a patient has a bloody BM. What do you do? How do you prevent?

A

Rule out bowel ischemia (can also be caused by reperfusion). Consider colonoscopy. The colon is more likely to be ischemic if the IMA (inf mes artery) is covered or affected.
General surgery consult to consider exploration.
Abx to cover GI.
Optimize cardiac output O2 delivery.

Prevent with <30 min of vessel reimplantation time and LHB.

(ACC 2020 in iliac aneurysm contribution to bowel/lower body ischemia)
In a meta-analysis of studies reporting exclusion or preservation of the internal iliac artery, Kouvelos et al found an increased pooled occurrence of buttock claudication in those undergoing unilateral (27%) or bilateral (36%) internal iliac artery exclusion. In a separate meta-analysis, Bosanquet et al found similar rates of buttock claudication, as well as a 10% occurrence of erectile dysfunction in men. Other ischemic events, such as spinal, bowel, and gluteal ischemia, were rare, occurring at a rate of <1%.6 Another consideration in treating aorto-iliac disease is the risk of late intervention from growth of ectatic or aneurysmal iliac arteries. In a retrospective analysis of prospectively collected data, Gibello et al found that in patients with AAA undergoing EVAR, after a mean follow-up of 6.2 years, those with common iliac arteries of ≥18 mm in diameter had a significantly higher rate of type Ib endoleaks (7.2% versus 3.2%; P=0.01) and late reinterventions (19% versus 11.8%; P=0.01), leading to higher odds of composite EVAR failure (OR, 1.8; 95% CI, 1.2–2.7) and need for reintervention (OR, 1.9; 95% CI, 1.15–3.3). Hassen-Khodja et al10 and Sala et al9 found that, after open repair of AAA, common iliac arteries of ≥18 mm in diameter tended to dilate over time, warranting consideration of bifurcated grafting rather than aorto-aortic tube grafting.

195
Q

Postop open thoracoabdominal aortic aneurysm surgery, Cr rises, and UOP drops. What do you do? How do you prevent?

A

Optimize CO. Challenge with diuresis. HD if needed. Renal US can evaluate flow if needed.

Prevent with 30 min reimplantation time, LHB, and hypothermia.

196
Q

Postop EVAR covering L SCA, the patient has a cold L hand w/ paresthesia. What do you do?

A

Carotid - SC bypass or SC transposition.

197
Q

Descrive cET for thoracoabdominal disease.

Why do a conventional elephant trunk technique as opposed to a simple arch with a thoracoabdominal staged surgery?

A

The basic principle of the conventional cET resides in the protrusion of a length of tubing into the downstream descending aorta during the time of arch reconstruction to facilitate further distal aortic procedures.

Briefly, in the first operation, the aortic arch is replaced, and a free-floating extension of the arch prosthesis (elephant trunk) is left behind in the proximal descending aorta.

In the second operation, the prosthetic trunk can be extended to the desired level through an open lateral thoracotomy or with the less invasive release of an endovascular stent graft.

The main advantages of the elephant trunk technique become obvious during the second operation and include (i) reduced dissection and surgical preparation of the distal segment of the arc where nerve, bronchial, gastrointestinal and lymphatic structures may potentially be injured; (ii) a facilitated and shortened clamping time during open thoraco-abdominal aneurysm and (iii) no need to clamp proximally the left subclavian artery (reduced risk of stroke and paraplegia).

198
Q

Describe the FET.
What are its advantages over cET? Disadvantages?

A

FET: (i) total resection of the aortic arch; (ii) preparation of the distal aortic stump with obliteration of the false lumen, use of ~4 or 5 U stitches with pledgets inside and a Teflon felt outside; (iii) advancement of the hybrid system in the descending thoracic aorta over a guidewire that has been retrogradely positioned via the femoral artery into the true lumen; (iv) deployment of the stent graft; (v) suturing of the vascular collar to the distal aorta before or after the origin of the left subclavian artery; (vi) complete reimplantion of the arch vessels and (vii) completion of the proximal anastomosis

Advantages over cET: Allows single-stage treatment, reduces risk of additional distal aortic surgery.
Disadvantages: increased risk of SCI, technically demanding.

199
Q

What if an aneurysm involves both the arch and descending aorta requiring both to be addressed (contained rupture, severe symptoms)?
What are your options?

A

Staged repair: elephant trunk via median sternotomy. Then open descending TAA repair after 2-3 mo of recovery.
This can dec risk of paraplegia.

If must be done as a single stage, and you cannot clamp b/w the L CCA and L SCA, deep hypothermia and circ arrest is required.

200
Q

What operative considerations must be addressed in a pt w/ arch aneurysm and chronic distal descending aortic dissection?

Where do you cannulate?

What do you want to double check after distal anastomosis is done?

Is there anything you do to the distal flap if some vessels are perfused by false lumen?

A

Place arterial cannula in non-dissected femoral artery.
Make sure the T8-L1 intercostals are inspected if they are perfused by the false lumen.
Make sure all visceral arteries are open after distal anastomosis. Distal flap should be fenestrated to ensure true and false lumen are perfused.

201
Q

Descrive cET for thoracoabdominal disease.

Why do a conventional elephant trunk technique as opposed to a simple arch with a thoracoabdominal staged surgery?

A

The basic principle of the conventional cET resides in the protrusion of a length of tubing into the downstream descending aorta during the time of arch reconstruction to facilitate further distal aortic procedures.

Briefly, in the first operation, the aortic arch is replaced, and a free-floating extension of the arch prosthesis (elephant trunk) is left behind in the proximal descending aorta.

In the second operation, the prosthetic trunk can be extended to the desired level through an open lateral thoracotomy or with the less invasive release of an endovascular stent graft.

The main advantages of the elephant trunk technique become obvious during the second operation and include (i) reduced dissection and surgical preparation of the distal segment of the arc where nerve, bronchial, gastrointestinal and lymphatic structures may potentially be injured; (ii) a facilitated and shortened clamping time during open thoraco-abdominal aneurysm and (iii) no need to clamp proximally the left subclavian artery (reduced risk of stroke and paraplegia).