SESATS CTS Adult Cardiac Flashcards
Manage incidentally found pulmonary AVMs
embolize all, even incidentally found (risk of stroke, bleeding)
Pt presents w/ flail chest, pain is controlled, unable to wean from vent. Consider what mgmt?
rib plating
What is Haller index required for pectus surgery?
> 3.5
Compare Nuss and Ravitch.
No difference in pain or cosmetic outcome except that Ravitch is open. Nuss may require removal of strut.
Are PFTs affected by pectus surgery?
Usually no change in PFTs
For penetrating lung trauma requiring intervention, what is ideal surgical procedure?
Tractotomy. Avoid lobectomy and pneumonectomy for BPF.
Solitary fibrous tumor appearance on PET?
Not FDG avid.
Solitary fibrous tumor gross appearance on parietal and visceral pleura?
sessile on the parietal pleura and pedunculated on the visceral pleura
Solitary fibrous tumor microscopy appearance? What appearance is more aggressive?
Spindle cells, considered more aggressive when >4mitoses/HPF are present
Treatment for solitary fibrous tumor?
Excise with negative margin and follow w/ yearly surveillance
How do you monitor ground glass opacities?
Monitor for development of solid component, size >8 mm.
What do you do for GGO that is >8 mm or has solid component?
Can do wedge for pure GGO. Lobectomy and lymph nodes if solid component >5mm. Consider segment +/- LADx if <5mm.
How do you manage a pleural effusion with high ADA?
Pleural biopsy to dx TB effusion. No drainage needed if positive, as these resolve w/o drainage.
How do you image pancoast tumor and decide on approach?
MRI
What treatment do you need before resection of any pancoast tumor?
Induction chemo BEFORE any resection
How do you manage a pancoast tumor adherent to artery or vein?
Can resect and reconstruct artery and vein
What structure, if invaded by pancoast tumor, cannot be resected?
Do not resect if C8 needs sacrificed
What lymph node status precludes pancoast tumor resection?
Do not resect if N2 disease on workup
What FEV1 and DLCO are indications for lung transplant?
FEV1<20 AND either DLCO<20 or homogenous emphysema are indications for lung transplantation; also BODE score >7, pCO2>50, pHTN.
In lung volume reduction surgery, what is the vent strategy?
During single lung ventilation, patients with advanced COPD may develop air trapping and hyperinflation, causing hemodynamic instability. Ventilatory techniques, such as using low tidal volumes (eg, 5 mL/kg), lower respiratory rates, and longer expiratory times (eg, an inspiratory to expiratory ratio of 1:3 or 1:5), can help to prevent this complication. Lowering minute ventilation in this way may lead to alveolar hypoventilation and elevation in the arterial partial pressure of carbon dioxide (PaCO2). Accepting deliberate alveolar hypoventilation to mitigate auto-positive end-expiratory pressure (auto-PEEP) is known as permissive hypercapnic ventilation (PHV). With this technique, the pH is allowed to drop gradually into the range of 7.35 to 7.2.
If the strategies of permissive hypercapnia cause the pH to drop below 7.2, strategies such as a cautious increase in ventilatory rate, suctioning of airway secretions, optimizing muscle relaxation, and administering inhaled bronchodilator therapy, should help to improve alveolar ventilation.
If a patient should develop hyperinflation and hemodynamic instability despite measures to minimize air trapping and auto-PEEP, transient disconnection of the endotracheal tube from the ventilator usually leads to resolution over several seconds.
What are lung volume reduction surgery criteria?
Results of NETT trial for emphysema:
- <75 yrs
- dyspnea w/ max med/pulm rehab
- FEV1 20-45
- DLCO >20
- air trapping: resid vol >150%, TLC >100%
- no smoking for >6 months
- 6 min walk >140m
- no pHTN (PA sys P <45)
- pulm rehab ability 6-10 wks
- CT w/ heterogenous disease focused in the upper lobes.
Which esophageal cancers go straight to esophagectomy?
Straight to esophagectomy in T1b and low risk T2 (<3cm, well-diffx, no LVI); T1a can have EMR or RFA. Chemo on back end if nodes are positive; for any other esophageal cancer, start with induction chemoradiation and re-stage for possibility for resection (complete responders do best).
What is added to esophageal cancer treatment if nodes are positive after resection
Chemo
When is neoadjuvant chemoradiation used in esophagectomy?
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).
Non-small cell chemo strategy - first line?
Pembro is first line agent for advanced non small cell lung cancer with >50% PD-L1 expression.
When to add EGFR TKI for non small cell lung cancer?
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.
A patient is going to undergo septal myectomy (for HCM). What in the history increases risk for postop complete heart block the most?
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.
Pt is s/p CABG and ready for DC. They have small effusions. What should their DC meds include?
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.
Describe ideal configurations for ITAs and radial grafts.
In-situ ITA to LAD. L and R have similar patencies.
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 specifics - 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.
What is basal inferior aneurysm/dyskinesis and why is it important in regard to mitral regurgitation?
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.
How can you tell if your septal myectomy is complete?
What do you do if it is not?
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.
Most common bacteria for infective endocarditis of the tricuspid valve
Staph aureus
Explain the difference in R sided infective endocarditis vs L sided management/tx.
R sided responds well w/ IV abx.
R HF AND severe tricuspid regurgitation; difficult to treat organisms; sustained infection; and vegetations 2cm or > w/ PEs should be considered for surgery.
In addition, patients w/ high risk for recurrence (IVDU) are less ideal candidates for early surgical intervention.
Is valvectomy a good first line option for tricuspid endocarditis?
No. IV abx will usually work. Also, valvectomy w/o replacement is associated w/ poor long-term outcome d/t hepatic dysfunction.
Do postop mitral or tricuspid bioprosthetic patients need anticoag or antiplatelet postop?
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.
What do you give postop mitral or tricuspid bioprosthetic patients if contraindication to anticoag?
Single-dose antiplatelet (ASA).
What do you do with an ischemic heart disease (CAD) pt w/ EF 35-50%?
Class IIa recommendation for CABG over medical or PCI. Significant survival benefit regardless of DM.
If there is a CABG indication for acute ischemic heart disease, what is the timing?
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).
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.
Revise graft. Don’t just try to de-air.
How do you manage a severely stenotic vein graft s/p remote CABG?
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
Which CAD pts do you need to consider carotid disease in?
L main, triple vessel, older than 75.
Do a good history. Get a duplex.
How do you manage a patient who has actively symptomatic carotid and operative/symptomatic coronary artery disease?
Active = within the last 3 months. Perform synchronous carotid endarterectomy and CABG.
How do you manage a patient who has actively symptomatic carotid and medically manageable (over short term) coronary artery disease?
Can start with CEA or carotid stent then staged CABG (6 wks after stent, 2 wks after CEA).
How do you manage a patient who has incidental asymptomatic carotid disease and actively symptomatic coronary artery disease?
CABG, then staged CEA.
What causes mitral regurgitation in patients with ischemic cardiomyopathy?
annular dilation
What to do with MV for patient with significant MV regurgitation undergoing CABG?
repair or replace; prefer repair if possible (ie with a complete and relatively undersized ring)
How do you eval after mitral valve repair (intraop)?
Wean CPB then use TEE to look for anything greater than mild regurgitation.
What to do if inadequate mitral valve repair when eval w/ TEE after weaning CPB intraop?
mitral valve replacement is durable and definitive (don’t try smaller ring or placing edge-edge stitch)
Manage a VSD found after DES placement for ischemic cardiomyopathy
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).
How does VSD after DES for MI usually present?
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.
How do you manage anticoag in patient with mechanical valve undergoing minor procedure with low bleeding risk (cataracts, dental extraction)?
Continue VKAs w/ therapeutic INR. If the procedure is more invasive, it’s ok to temporary interrupt without bridging.
What’s the best way to manage worsening type B dissection despite optimal medical mgmt?
TEVAR (L SCA to celiac)
When do you operate for mitral regurgitation?
Causes insidious LV dysfunction. Early intervention in asymptomatic patients w/ severe MR when there is LV dysfunction (<60% EF) or enlargement (>40 mm).
In others w/ preserved EF and dimension, ok to do surgery if 95% likelihood of repair and mortality <1% (IIa).
Transcath MVr has no role in low-risk primary degen MR.
Manage functional mitral regurg.
FMR is different than primary degenerative MR.
Initial therapy is med therapy. Consider cardiac resynchronization therapy.
Surgery considered after optimization of medical therapy.
Manage acute, decompensated MR secondary to MI and ruptured papillary muscle.
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.
If acute type A dissection is suspected, how do you diagnose?
CT chest/abd. May need pelvis to eval femorals.
Manage uncomplicated type B dissection.
BP control (BB w/ goal HR 60) and serial imaging. Vasodilators can be used as adjunct.
Manage Marfan-related aortopathy
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.
What is ideal bypass in type A w/ dissected R axillary and rupture? How do you obtain neural protection?
CPB prior to sternotomy via femorals since axillary is not available. Antegrade and retrograde are both effective.
Marfan associations.
- 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
Characteristics of Loeys-Dietz syndrome
- aneurysms everywhere, aggressive
- skeletal problems
- craniofacial problems
- cutaneous findings
- pregnancy complications (uterine rupture)
- hx of allergies/inflammatory dz
- GI inflammation (eos esophagitis, IBD)
What is size indication for intervention in a pt w/ connective tissue disorder (eg Marfan) and aortic root pathology?
Diameter 4.5. Perform root replacement.
Remodeling technique is not appropriate strategy for performing valve-sparing root replacement in pts w/ CTD.
In a patient with type B dissection and distal malperfusion, what is the management?
endovascular stent graft
How do you manage an elevated L hemidiaphragm in a patient s/p CABG?
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 dissection too superior.
How does functional ischemic mitral regurgitation occur?
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.
Potential advantages of off-pump CABG (OPCAB)?
Transfusion rates are lower.
Periop mortality, MI rates, stroke, renal failure are comparable.
Does a pt w/ 3v CAD and mildly regurgitant bicuspid valve without root dilation need surgery for the valve?
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.
What is the preferred bypass conduit for 3v CAD?
all arterial
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?
Confirm you’re in true lumen via angiogram or IVUS.
What is blood cardioplegia?
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.