SESATS CTS Adult Cardiac and Thoracic 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 despite pain mgmt. Consider what mgmt?
rib plating for flail chest with respiratory failure is the only indication for rib fracture fixation for which good quality evidence is available
other accepted indications:
- impending/active resp failure in the setting of painful, movable ribs refractory to pain mgmt
- chest wall deformity
- failure to wean from vent not related to pulm contusion
- “on the way out fixation” - found significantly displaced fx found at thoracotomy for other indication
- ongoing chest wall instability or pain d/t nonunion/malunion of rib fx
What is Haller index required for pectus surgery?
>3.5
Compare Nuss and Ravitch.
According to surveys, no difference in pain or cosmetic outcome except that Ravitch is open. Nuss may require removal of strut.
Some surgeons choose Nuss for smaller, focal defects and Ravitch for larger deformities.
Some say that Nuss bars have more discomfort for longer period d/t the ongoing pressure of the bar, while Ravitch procedures only have perioperative pain.
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 - c/b BPF.
Solitary fibrous tumor appearance on PET?
IE is it FDG avid?
Not FDG avid.
Solitary fibrous tumor gross appearance on parietal and visceral pleura?
sessile on the parietal pleura (chest wall) and pedunculated on the visceral pleura (lung parenchyma)
Solitary fibrous tumor microscopy appearance?
What pathology finding denotes more aggressive tumor?
Spindle cells.
More aggressive when >4mitoses/HPF are present.
Treatment for pulmonary solitary fibrous tumor?
What if locally advanced?
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
What do you monitor for in pts with pulmonary ground glass opacities that have been incidentally found?
Monitor for development of solid component, size >8 mm. At this point, consider biopsy.
What do you do for GGO that is >6 mm?
Whatif it has solid component >6mm?
Solitary, pure ground glass nodules ≥6 mm can get repeat CT scans at 6-12 mo then every 2 yrs x2 (5 yrs total) as long as stable. Watch for growth or solid development.
If there is a solid component ≥6 mm, can do repeat CT imaging 3-6 mo (then annual x5 yrs if stable), or PET/CT, or biopsy after multidisciplinary evaluation.
How do you manage a pleural effusion with high ADA
(>40 units/L)?
No drainage needed if positive, as these resolve w/o drainage and standard active anti-TB therapy. Drain if pt is sx from effusion.
Dx thoracentesis if TB suspected but cannot dx via sputum or other studies, or if other etiology of effusion suspected.
Biopsy if <40 ADA, but effusion is otherwise not diagnostic, and TB suspicion is still there. Send for AFB smear, culture, and histopath (would show caseating granulomas or acid-fast bacilli).
How do you image pancoast tumor to decide on approach?
BONUS: How do they present? Dx? Rest of workup? General mgmt?
MRI w/ contrast of the spine, thoracic inlet. Decide on posterior (Paulson - around the scapula) VS anterior transcervical (L-shape from mandible to sternal notch to inferior clavicle), best for tumors involving the SC vessels).
Psx: Shoulder pain - most common initial symptom 2/2 brachial plexus invasion or local extension. Can be shooting through the ulnar distribution that eventually results in weakness with atrophy of intrinsic hand muscles.
Horner syndrome - ptosis, miosis, enophthalmos, anhidrosis. This can be preceded by ipsilateral flushing/sweating.
Up to 25% may eventually develop spinal cord compression causing paraplegia (intervertebral foramina).
Dx: ultimately provided by core needly biopsy. VATS if unsuccessful. Usually NSCLC.
W/u: These are at least T3. Eval for periop therapy (PD-L1, EGFR, ALK). PFTs. Bronch. Mediastinal lymph node eval (EBUS). Brain MRI w/ contrast. PET CT.
Mgmt: (N2 disease is ruled out) Preop concurrent chemoradiation, surgery, adjuvant systemic therapy (chemo + other mgmt depending on biomarker status) with 2 more cycles of RT.
What treatment do you need before resection of any pancoast tumor?
Concurrent chemoradiation BEFORE any resection.
- nonsquamous: carboplatin (or cisplatin), pemetrexed, thoracic RT vs paclitaxel, carboplatin, RT vs cisplatin, etoposide, RT
- squamous: paclitaxel, carboplatin, concurrent thoracic RT vs cisplatin, etoposide and RT.
This is followed by surgical resection if there is no evidence of distant metastases or local progression and postoperative chemotherapy. Then adjuvant chemo + other treatment depending on biomarker status.
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 to be sacrificed
What lymph node status precludes pancoast tumor resection?
Do not resect if N2 disease on workup
What are indications for referral for lung transplant for COPD?
Disease is progressive despite smoking cessation, med optimization, pulm rehab, and supplemental O2.
BODE 5 or 6.
FEV1 <25% predicted.
In lung volume reduction surgery, what is the vent strategy?
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.
What are lung volume reduction surgery criteria?
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
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?
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.
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?
Chemo (fluoropyrimidine based).
If excellent PS, can use 3-drug regimen.
2-drug regimens are usually preferred d/t better sfx profile.
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 if PD-L1 >1%?
What if >50%?
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.
When to add EGFR TKI for non small cell lung cancer?
Who should it be avoided on?
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. 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.
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 requires resumption of bypass and additional resection. Ie complete the operation.
Do not just give volume, reduce HR, and remeasure.
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 mangement of R sided infective endocarditis vs L sided endocarditis.
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.
Is valvectomy (ie no replacement) 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 postop?
What about antiplatelet?
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 intervention 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 (STEMI or NSTEMI), what is the timing?
In general - Not emergent unless the patient is unstable. CABG can convert bland infarct into hemorrhagic infarct and worsen ventricular function.
The 2 indications for emergent CABG for STEMI:
* No PCI available and the patient is in cardiogenic shock/hemodynamic instability (1).
* PCI is not feasible/successful, ongoing ischemia, and there is a large are at risk (IIA). If stabilized, delay for around 3 days (unless other over-riding indications are present). Don’t discharge.
If non-transmural infarct (NSTEMI), delay for at least 6 hrs and complete before discharge… Unless:
* Cardiogenic shock, refractory angina, or hemodynamic instability (immediate invasive revasc [1]).
* High-risk w/ GRACE >140 (invasive strategy within 24 hrs [2a]).
* If NSTEMI patient fails PCI w/ ongoing ischemia/hemodynamic compromise, or threatened occlusion of an artery w/ substantial myocardium at risk, can do emergency CABG (2a).
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 who is going back to the OR for heart surgery?
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.
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 vs tethering of the leaflets
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 (1.5 cm cutoff for perc repair).
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 chronic primary mitral regurgitation?
*acute symptomatic MR gets prompt mitral surgery, preferably repair
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 any of following:
LV dysfx (<60% EF).
LV enlargement (>40 mm ESD).
Symptoms.
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.
Manage functional mitral regurg.
What parameters do you need to know?
When to do procedures?
What about ischemic?
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.
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?
What would be second line if there is a question on initial study?
What if there is a severe contrast allergy?
- 1st line: gated CT with arterial contrast. Chest and abdomen. Would also add pelvis to eval femorals for access.
- 2nd line: TEE. TEE is preferred over TTE - higher sensitivity and better anatomic resolution. TEE can be done in ED or in OR with plan to proceed with surgery if dissection found.
- 3rd line: MRI. Not readily available, requires more advanced interpretation, longer wait time, more difficulty with intervention in scanner. Often used as follow-up in patients with diagnostic uncertainty.
- Contrast allergy: TEE (TTE less preferred). MRI can also be used in the acute setting for a stable patient w/ contraindication to iodinated contrast.
2022 ACC/AHA Guidelines
Manage uncomplicated type B dissection.
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
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 CPB strategy 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 (arch) and retrograde (SVC: pictured - modified CPB circuit) neural protection are both effective.
Marfan associations.
What gene? What location?
What does this cause?
Physical manifestations?
Diagnosis?
- 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.
Screening/surveillance for aorta?
Medical mgmt?
Indications for aortic surgery?
- 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.
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?
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 IMA 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 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.
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 aortic 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.
Do valve if moderate AR/AI.
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.
Ensure no other areas of ischemia that have not reperfused (CTA for SMA/celiac/renals).
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.
Anomalous origin of the right coronary artery causes ischemia. How do you manage?
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.
Del Nido advantages?
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.
Advantages of using BIMAs?
Improved patency.
Improved survival.
Of note: preserve radials in pts w/ DM and CKD in case future Cimino is needed.
In a patient with aortic stenosis and hx of CAD, how can you tell if low EF is from the stenosis or the CAD?
Dobutamine stress echo.
In pts w/ LV dysfx w/ CAD AND AS, 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.
Redo sternotomy, and you see bright red blood, suspect aortic injury. How do you manage?
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.
Options to protect the brain in total arch for type A.
DHCA
DHCA w/ retrograde cerebral perfusion
DHCA w/ antegrade cerebral perfusion
Moderate hypothermia w/ antegrade
Antegrade appears to be more protective than retrograde
What is the implication of a greater curvature tear in a type A dissection?
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
What should the stenosis percentage be in a target for radial artery? Left target vs right target?
greater than 70% on L and 90% on R; they are sensitive to competitive flow
If a standard heart cath injection (during coronary angio) cannot determine coronary disease quantity, what are other options to obtain this information?
determine FFR or IVUS; FFR may be more reliable in small/short stature patients
In a patient undergoing surgery for atrial fibrillation, what variation in the procedure can impact need for PPM? Who likely will need this variation?
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.
How is ACP normally performed for DHCA?
R SCA w/ chimney graft and occlusion of the innominate artery, L carotid, and L SCA with clamps or balloon catheters
Massive air embolism occurs during a case. How do you manage?
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.
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?
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).
You are doing an open repair of DAA. What is your cannulation strategy?
L IPV (inflow) and descending aorta below the aneurysm (outflow). LAA and L femoral artery are alternate sites.
You are doing an open repair of DAA. Left heart bypass or simple-cross clamping?
Left heart bypass has lower mortality. Add moderate hypothermia (32 C) to maintain organ perfusion, spinal cord perfusion, and myocardial protection.
You are doing an open repair of DAA that extends below the renals. How do you manage the visceral vessels?
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.
