TSRA Clinical Scenarios - Adult Cardiac Surgery

Question 1

Heparin dose for CPB?

Answer 1

400 units/kg

Question 2

ACT required for initiation of CPB?

Answer 2

400-480 (480 is book answer).

Question 3

5 min after cross clamp is released when coming off CPB, the heart begins to distend w/o contraction.
What are the general causes of this situation?
What do you do first?
What if this doesn’t work?

Answer 3

Two possible problems:
1) valve leak
2) heart is not ejecting

Don’t let the myocardium blow upand fall off the Starling curve:
1) Squeeze the heart.
2) Pace the heart.
3) If this does not resolve quickly, cross clamp, go up on bypass, and vent.
4) Talk to anesthesia and perfusion to see if they can help determine a cause on echo or via labs.

Question 4

Coming off CPB, you attempt to pace, but have no capture.
You check the leads - they are well placed.
You change the box and wires - same problem.
You ask perfusion what K is - 7.
You ask anes what UOP is - minimal.

You vent the heart.
How do you manage K?

Answer 4

Calcium.
Use the pump: Hemoconcentrate.
Use anesthesia: IV insulin with glucose. Bicarb and/or lasix if there is UOP.
Be careful of hyperkalemia. You will lose the ability to pace, this pertains to postop as well.

*You have to vent because the heart is not ejecting.
*Perfusion/anesthesia should have been keeping track of the K.

Question 5

A patient fibrillates when coming off CPB.
How do you defibrillate?
What if first couple defib attempts don’t work?

What if distended?

What other adjuncts can be used/what needs to be checked and optimized?

Answer 5

Internal paddles set to 10-20 joules and gradually increased.
If not working, give IV lidocaine 1 mg/kg and IV amiodarone bolus 150 and try again.

If distended, manually squeeze the heart, and get ready to get back on CPB, place vents if needed, then cardiovert.
Optimize and treat air, MI, and AI:

1) Vent air in root.
2) Inc MAP to 75 (coronary perfusion and to flush out embolized air).
3) Optimize O2, lytes, and temp.
4) Check Echo for AI.

Question 6

If heart is distending when coming of CPB, what amount of AI requires consideration for replacement?

Answer 6

AI greater than 1+/moderate-severe requires exploration and replacement of the aortic valve.
Should be higher on differential after a mitral surgery - damage to noncoronary leaflet w/ placement of the mitral stitches.

Squeeze the heart, get back on CPB, put in root vent, put in LV vent. Look at echo to eval, do AVR/r.

Question 7

Explain CPB components. Start with drainage and trace the flow.

Answer 7

Venous cannulas drain to reservoir by gravity or vacuum.
Blood pumped into the oxygenator/heat exchanger.
Continues to arterial air filter.
Then to the arterial cannula and into the patient.

Question 8

Attempt CPB, but perfusionist says high aortic line pressure. What is differential?

Answer 8

Obstruction - kink or clamp
Malposition - in one of the aortic branches
Cannula too small - 21-24 Fr should be adequate (18-20 used at USC)
Aortic dissection - systemic P low w/ abnormal ascending aorta

Question 9

What is your differential and initial troubleshooting for inadequate venous drainage on CPB (ie heart is full)?

What if the heart is empty, but reservoir is empty also?

Answer 9

Try circuit issues first - check for air lock and cannula malposition.
Is there chattering?
If so, reduce flows if flow is high.
If not, may need to increase cannula size or just add suction (ideally, start with a larger cannula).

Make sure no other avenues of blood flow into the heart:
- AI - LV vent
- azygous - adjust snares to exclude
- L SVC - snare or cannulation (canx required if NO innominate)

If heart is empty and so is the reservoir, add volume.
If persistent after replacement, consider retroperitoneal or peritoneal hemorrhage. Do an abdominal exam.

Question 10

Attempting CPB flows, but MAP not rising above 40. Pt has hx of ACE use.

Answer 10

Rule out other problems. Could be vasoplegia.
Give pressors - phenylephrine, norepi, vasopressin. Methylene blue can be used as well.

This can occur postop as well.

Question 11

You place a retrograde cardioplegia line in the coronary sinus, but the measured plegia line pressures are low. How do you troubleshoot?

Answer 11

Check position of cannula - if unable to guide with TEE, convert to bicaval CPB and open RA for direct placement.
Check if balloon is ruptured - replace.
Check for L SVC - behind LAA, where the ligament of marshal is anterior to the pulmonary veins.
Check for rupture of the sinus - inspect inferior aspect of the heart and repair with patch.

Question 12

When giving retrograde cardioplegia, you find a L SVC. How do you manage?

Answer 12

Check if there is an innominate.
Present - can snare below innominate drainage to include L SVC in circuit.
Not present - cannulate the L SVC and add it to venous drainage.

Question 13

Coming off CPB from a mitral surgery. BP drops, ST elevation on EKG, and RV distends. You suspect air in the coronary.
Why does this happen?
How do you manage? What are the adjuncts?

Answer 13

R coronary ostium is anterior and susceptible to air embolism.
Re-institute CPB, empty the heart, and flow w/ high perfusion pressure (MAP 70-75) to help support cardiac fct and push air through coronary into venous circulation.
Add a root vent to prevent further air migration into the coronary arteries.
A needle in the apex of the heart can be added to remove air if too much in the apex.

Question 14

If patient has previous CABG and is requiring CPB, how do you manage an open LIMA?

Answer 14

Consider retrograde plegia.
Can clamp vs cold bypass flow.

Question 15

If patient has open SVGs after CABG and needs CPB, but the grafts are high on the aorta, what is an option to make room for cross clamp?

Answer 15

Axillary cannulation may be needed to make room for an aortic cross clamp.

Question 16

In a redo patient w/ previous CABG w/ open LIMA, what is the problem with antegrade cardioplegia? What are possible solutions?

Answer 16

Antegrade will perfuse the OM and PDA territories (assuming they’re open enough), but not the LAD.
Retrograde will perfuse all. Ideally, the LIMA is found and clamped. If not, the heart needs to be cooled very well, and intermittent retrograde perfusion may need to be given.

Question 17

In the setting of aortic insufficiency, discuss options for CPB.

Answer 17

Question is how to deliver plegia.

Retrograde cardioplegia would ensure delivery.
Antegrade would likely require direct delivery of cardioplegia. If you can get partial arrest from antegrade, you can open the aorta then give direct to ensure good plegia.

Question 18

How could you incompletely deliver cardioplegia if using retrograde cardioplegia assuming no L SCV? What can you do?

Answer 18

Tip of the retrograde cannula is distal to the middle cardiac vein. Direct retrograde insertion can help (bicaval cannulation, snare cavas, and open R atrium).

Question 19

What can make retrograde cardioplegia delivery riskier in a redo operation (previous CABG)?

Answer 19

If you perforate the sinus, the posterior heart may be stuck, making dissecting in a bloody field more difficult.
Also, the anterior/lateral cardiac wall dissections on the front end may damage CABGs.

Question 20

After cross clamping for an AI case, 500 ml of antegrade cardioplegia is delivered, but there is poor distention of the aortic root, incomplete arrest, and LV distention.

What is happening and how do you manage?

Answer 20

Aortic insufficiency
Should not have been a surprise.
Switch to retrograde cardioplegia and turn on the aortic root vent vs an LV vent to decompress the heart.
If there is partial arrest, you can also do direct cardioplegia if operating on the aorta or aortic valve anyway (which is the case here).

Question 21

How do you confirm adequacy of retrograde cardioplegia catheter delivery?
What’s the appropriate pressure for cannula flow?

Answer 21

Confirm: Cessation of electrical and myocardial activity.
Observe flow through coronary veins and arteries. Can also check coronary ostia through aortotomy for backflow (if surgery requires aortotomy).
Finally, heart should be cooling - feel back, front, and lateral.

Appropriate pressure in cannula: ~40 mmHg

Of note, in patients with hypertrophied ventricles, consider retrograde to add additional protection to the subendocardium, which can be difficult to protect with antegrade cardioplegia alone.

Question 22

What is a concern with retrograde cannula placement even if it works well to arrest the heart?

How is the retrograde cannula engineered to reduce this risk?

Answer 22

Myocardial edema.
This is why the balloons on the cannula are not usually 100% occlusive, to allow a popoff valve if pressure gets too high.

Question 23

Where does a persistent L SVC usually drain?

Answer 23

Into the coronary sinus, may partially drain via innominate V.

Question 24

You attempt to infuse antegrade cardioplegia. The perfusionist notes high line pressure. How do you manage?

Answer 24

Stop flow.
Look for kinks or clamps to r/o obstruction. Ensure pressure monitoring line is connected.

If all above ruled out, concern for aortic dissection. Visualize the root and ask anes to look at aorta (TEE).
If dissection, cool with original aorta cannula distal to the clamp, and prepare for dissection repair.

Can give direct cardiolplegia or retrograde.

Question 25

After a cardiac surgery pump case w/ retrograde cardioplegia, the myocardium is slow to regain activity. What should you check?

Answer 25

Check retrograde catheter and/or that the balloon is down, in order to allow for adequate coronary sinus flow.

Question 26

When sewing a CABG, you notice bleeding from the coronary arteriotomy. What does this mean? What do you do?

Answer 26

Arrested **myocardium is getting perfusion**. *Check the cross clamp* and that the *root vent* is on. There could be **collaterals**. If unable to ID cause, monitor for electrical activity, and consider *cold topical saline*, *cooling the patient to mild hypothermia* (32 C), *reducing flows as tolerated*, or *increasing frequency of cardioplegia administration*. Can deliver some *plegia through vein graft* once suturing complete.

Question 27

How do you manage a perforation of the coronary sinus after placement of a retrograde cardioplegia catheter?

Answer 27

CPB, clamp, and arrest with antegrade if possible or direct if retrograde was because of inability to do antegrade. If very simple, repair the hole directly with Prolene (won't work on boards), or use a pericardial patch.

Question 28

What are the three broad categories for etiology of persistent electrocardial activity (problem with initiating plegia in CPB)?

Answer 28

Access - plegia cannula placement, kinking Collateral - clamp not across, drainage poor, L SVC, vents/suckers; hypothermia? Myocardial mass - hypertrophy may require more plegia or more hypothermia

Question 29

Redo sternotomy, and there is a significant amount of dark blood from the sternomanubrial jct. What was injured?

Answer 29

Innominate vein.

Question 30

Redo mitral w/ innominate vein injury during sternotomy. How do you manage? How do you get on bypass? What are some options if first surgical attempt at the injury fails? What can be done if more exposure needed?

Answer 30

Pack the area and close the sternum with penetrating towel clamps. (Remember that the vein may be stuck, so opening further will only tear it). Peripheral CPB. Put pump suckers in the injured field. Reopen and dissect vein length for assessment and attempt at closure w/o tension. Primary vs pericardial patch repair. If cannot repair, divide and oversew. If too lateral, may need trapdoor to expose - above clavicle and at 3rd rib space.

Question 31

Redo case. You attempt to dissect SVC for cannulation, but make a large hole before pursestring is in. How do you manage? What is the first step? How do you cannulate? How do you clear field? How do you manage an azygous contributing to bleed?

Answer 31

Tamponade it or J clamp vs vascular clamps. Attempt IVC and aortic cannulation for CPB. Need vacuum venous drainage to prevent air lock. Pump suckers near SVC to clear the field. May be possible to cannulate through the injury. Consider placing pump sucker into azygous vs ligating azygous if you can't see. May need to dissect more proximal and place a Rummel tourniquet vs vascular clamps. Once controlled, may need primary repair vs pericardial patch. Be prepared for phrenic nerve injury with all the dissection around the SVC.

Question 32

You are called to cath lab during a lead extraction after the patient arrested w/ hypotension. What injury is likely? IE what structure? How do you manage?

Answer 32

Venous injury, often in the SVC. Cannulate the groins and start CPB vs open to relieve tamponade and compress SVC while achieving CPB. Open and decompress the heart. Identify the injury, dissect proximal and distal, control it, and repair primarily vs w/ patch.

Question 33

A redo cardiac surgery patient is femorally cannulated with difficulty during the venous cannulation. The venous line has return, but the patient continues to become hypotensive after CPB is started. What should be your suspicion? How do you diagnose? Does management change if chest is open? What if the injury is high?

Answer 33

Femoral venous injury - could be retroperitoneal (likely iliac) or intra-abdominal. Goals: identify injury, cannulate beyond repair. Venogram if available. Chest is open: can centrally cannulate, otherwise, may need access in contralateral femoral vein. Injury is above iliacs: use fluoro to get wire and cannula above and go on, then open the abdomen and repair the injury.

Question 34

SVC is ruptured during balloon dilation for SVC syndrome. How do you manage? What's your cannulation strategy?

Answer 34

Give heparin. Emergency median sternotomy. Bicaval cannulate - for the SVC, enter the RA and traverse cannula through injury - will have to use a malleable cannula, not a right angle. Empty the heart. Primary pericardial patch closure.

Question 35

You're trying to get bicaval cannulation in an old lady, and the IVC tears low near the diaphragm. How do you manage? What are your goals? How do you get more exposure?

Answer 35

Initial goals: get venous access and go on CPB. If possible, traverse the IVC cannula through the injury from above. May need a malleable cannula for this. Next goal: get control below the injury or reduce blood flow to the injury. Try to place a Rummel clamp below the injury. If unable - SVC cannula for everything above, suckers to control bleeding in the pericardial well. Get femoral vein to control bleeding from below. Be careful with distance of femoral cannula is to not worsen the injury. Can attempt incising the diaphragm through sternotomy to get exposure. If unable - extend sternotomy inferiorly and convert to RUQ subcostal incision.

Question 36

Cath lab creates an RV puncture and places a pericardial drain w/ bloody drainage. Manage.

Answer 36

Sternotomy. A trauma surgeon answer is pledgeted horizontal mattress sutures. Safe cardiac surgery answer: Heparin, CPB, and arrest the heart with **wide patch repair**. **Bypass the coronary lesion** if during a cath case for coronary disease.

Question 37

There is a small R PA injury noticed after an aortic surgery when coming off bypass. Manage.

Answer 37

If small, a figure of 8 will fix. If large or uncontrolled, go back on bypass (if you had axillary, can do end to end of previous graft). Decompress the heart, and the PA will decompress. Mobilize the R PA. May need pericardial patch.

Question 38

You puncture the opposite side of the aorta during arterial cannulation. Manage.

Answer 38

May need circulatory arrest. Can cool with the existing cannula if forward flow is okay. May need to establish axillary access. Small aortotomy and local repair.

Question 39

What symptoms represent unstable angina?

Answer 39

chest pain at rest, exertional angina not relieved by rest, and new onset of chest pain

Question 40

What symptoms represent stable ischemic heart disease

Answer 40

exertional angina - predictable, improves with rest

Question 41

What is included in CAD guideline-directed medical therapy?

Answer 41

lifestyle modification, statin therapy (LDL goal 70-100), beta-blockade, aspirin, and ACE inhibition (if LV dysfunction, DM, or CKD)

Question 42

What are hemodynamically significant coronary lesions on left heart cath?

Answer 42

Left main >50% non-LM >70%

Question 43

What FFR is hemodynamically significant? When is FFR used?

Answer 43

< 0.80. Determines hemodynamic significance of the cumulative effect of proximal stenosis. Used to guide revasc in angiographically intermediate coronary stenosis in patients w/ stable angina.

Question 44

What is the SYNTAX score?

Answer 44

16 segments in the coronary tree. Lesions in this tree are scored. The sum of these scores is the overall SYNTAX score.

Question 45

What are the cutoffs for the SYNTAX score in terms of complexity? What was the main implication of the SYNTAX trial?

Answer 45

>22 is intermediate complexity. >32 is high complexity. Both groups show benefit from CABG. The results of the SYNTAX trial specifically revealed that patients with 3-vessel (70%) or L main (50%) disease benefited from CABG over PCI.

Question 46

What is a non-invasive option for imaging the coronary arteries?

Answer 46

Gated cardiac CT

Question 47

What did a secondary analysis of the STITCH trial reveal concerning myocardial viability studies?

Answer 47

They are obtained in preop CABG pts w/ EF <35%. They can predict an improvement in EF postoperatively, but this did not translate into a survival benefit. IE it should not be used as a way to rule out low EF patients for CABG over medical therapy.

Question 48

How do you decide who needs coronary revascularization in patients with stable ischemic heart disease?

Answer 48

Activity limiting symptoms despite maximal medical therapy. Active patients who want PCI for better QoL compared to med therapy. Anatomy with proven survival benefit.

Question 49

After deciding on revascularization, how do you decide who needs CABG?

Answer 49

1) 3v dz, especially w/ syntax >22 (mod) and low surgical risk. 2) Significant LM disease (50%). 3) 2v dz w/ prox LAD, or mod/high complexity anatomy, or DM. 4) If well preserved LVEF, low complexity coronary anatomy, and no DM - CABG still reasonable. 5) 1 vessel dz pts for whom CABG reasonable - large amount of potentially ischemic myocardium in the LAD distribution, those who are not candidates for long-term DAPT, or those who have failed prior PCI. Patients with ischemic cardiac arrest and anatomically complex disease may also be considered for CABG. ***I.E. PCI for pts w/ single-vessel dz w/o large ischemic area in LAD distribution and who can take DAPT, or those w/ two-vessel disease in RCA and L Cx w/o DM.*** Europe guidelines add: Multivessel (2+) w/ EF <40. Multivessel (2+) w/ >10% ischemic territory.

Question 50

Management of significant CAD in 1 vessel w/ refractory angina despite medical therapy and PCI.

Answer 50

CABG.

Question 51

Management of significant CAD in 1 vessel after sudden cardiac arrest from ischemic ventricular arrhythmia.

Answer 51

CABG.

Question 52

Management of CAD at 50% in 1 vessel in patients undergoing valve or aortic surgery?

Answer 52

Concurrent CABG.

Question 53

What is the ideal graft for the LAD?

Answer 53

IMA. Left preferred because of length and ability to avoid midline more (redo surgery). Right is second choice.

Question 54

In a patient undergoing CABG for 3 vessels without excessive risk of sternal complications or other organ failure, what are the ideal graft conduit choices?

Answer 54

BIMA and radial.

Question 55

What can be done technically to reduce the risk of sternal complications in a patient getting BIMA grafts?

Answer 55

Skeletonized.

Question 56

Known risks factors for sternal infection and malunion in cardiac surgery?

Answer 56

Nonelective procedure, age, uncontrolled DM (HbA1c >7), BMI >40, female, COPD, preop hospitalization >3 days, smoking, immunosuppression regimen, radiation mediastinal injury

Question 57

When should CABG patients receive aspirin?

Answer 57

Preoperatively when they discover CAD is ideal. Within 6 hrs postop after CABG. Continued indefinitely.

Question 58

A patient comes in for elective CABG but has not stopped taking plavix. What do you do?

Answer 58

Cancel the case. Plavix and ticagrelor (Brilinta) need to be stopped ideally for 5 days preop, and at least for 24 hrs in more urgent settings (per AHA guidelines). Aspirin, on the other hand, should be continued up to the day of CABG and resumed after.

Question 59

A patient requires an urgent CABG but is taking plavix. What do you do?

Answer 59

Ideally, P2Y12 inh should be stopped 5 days preop. In an urgent setting, holding for 24 hrs preop will reduce major bleeding. Short acting IV antiplatelets (eptifibatide [Integrillin] or tirofiban [Aggrastat]; both gpIIb/IIIa inh) should stopped 2-4 hrs preop. Abciximab (reopro) should be stopped 12 hrs preop.

Question 60

Why are beta blockers reinstituted after CABG (as long as no contraindications)?

Answer 60

Reduce incidence and sequela of atrial fibrillation; of note, preoperative beta blockade does not seem to help. Of note, in pts w/ SIHD and nl LVEF, routine chronic beta blockers are NOT beneficial in reducing CV events after complete revascularization (3: no benefit).

Question 61

What is the target lab value for statin therapy in patients undergoing CABG?

Answer 61

reduce LDL <100 and achieve at least 30% dec in LDL

Question 62

Which postop CABG patients require ACE or ARB?

Answer 62

LVEF <40, HTN, DM, CKD unless otherwise contraindicated. Almost all of them. Cardiology team can start this as outpatient.

Question 63

What is the continuous IV insulin target in postop CABG?

Answer 63

blood glucose concentration <180

Question 64

When anatomically and clinically suitable, what is the RIMA often used for?

Answer 64

L Cx or RCA if critically stenosed and perfusing LV myocardium (R dominant) - can improve survival and decrease reintervention. RIMA is biologically equivalent to the LIMA. BIMA > SIMA in obs studies. >2 arterial grafts may provide additional late mortality compared with 2 arterial grafts.

Question 65

IMA patency is directly related to what physical parameter in the target vessel?

Answer 65

Degree of proximal stenosis of the target vessel. Ie how much competitive flow is there? Ie outflow. Though it should be considered, this information does not really affect whether you choose to use the graft. It may affect your target - ie targeting a more stenosed distal target to improve patency.

Question 66

What lesions should a radial artery be used for? What is patency of the RA prone to? What specific postop medication improves patency?

Answer 66

Prone to spasm in periop period and sensitive to competitive flow. Only use for L side lesions >70% (severe) or R side lesions >90% (critical) - same for gastroepiploic arteries. Give ca channel blocker postop. Total arterial bypass is ideal. >2 arterial grafts shows improved outcomes over 2 arterial grafts. Best practice: - objectively assess palmar and ulnar arteries - subocclusive stenosis should be targets - avoid after transradial cath - avoid in CKD pts w/ likely progression to HD - oral Ca channel blocker x1 yr - avoid BL radial artery procedures in CAD pts

Question 67

Who is the ideal patient who benefits most from complete arterial revascularization?

Answer 67

<60, with few comorbidities (no DM, ESRD), severe L sided stenosis, and critical (90%) R sided stenosis (radials work better here). Skeletonize.

Question 68

What are inferior leads?

Answer 68

II, III, aVF

Question 69

What EKG findings suggests RV or RCA ischemia (or L dominant PDA disease)?

Answer 69

Inferior leads: II, III, aVF. Or posterior findings: reciprocal V1-2.

Question 70

What EKG changes suggest LV or LAD/LCx territory ischemia? There are 3 associated territories, what are they, and what leads indicate each?

Answer 70

Anteroseptal: V1-V2. Anteroapical: V3-4. Anterolateral: V5-6, I, aVL.

Question 71

What is diagnostic for STEMI?

Answer 71

Angina symptoms for 20 min w/ ST elevation 2+mm in 2 contiguous leads or new LBBB. Greater risk for transmural ischemia.

Question 72

What is the diagnostic criteria for NSTEMI?

Answer 72

Angina symptoms >10 mins. Elevated cardiac biomarkers. ST elevation of 0.5-1mm - or ST depression >0.5 mm - or T wave inversion >1mm More likely to have subendocardial ischemia.

Question 73

When can IABP be useful in the setting of MI (3 situations listed)?

Answer 73

Refractory shock despite med mgmt. Post-infarct VSD. Acute papillary muscle rupture w/ MR. Often as a very temporary bridge. If the heart’s viability is significantly in question, then an impella may be a better choice as long as the RV works. If biventricular failure, then ECMO would probably be a better choice (may still need Impella or IABP or pressors to empty/vent LV).

Question 74

What are contraindications for IABP?

Answer 74

Severe AI or PVD w/ resultant prohibitive anatomy (femoral or iliac artery occlusion) preclude placement.

Question 75

What is the first line reperfusion strategy for STEMI? Timing? When might CABG be the right answer in STEMI?

Answer 75

**PCI**. Goal door to balloon time of **90 min**. CABG (5%) ok if... * unsuccessful or complicated PCI (1% of PCIs) * instability after PCI (place IABP) * mechanical compx (LV or septal rupture; fix rupture + CABG) * no longer acute, stabilized * LM or severe mvCAD, esp w/ dec LVEF or DM IE failed or complicated PCI, mechanically complicated MI, or if stable/stabilized w/o s/s of ongoing ischemia clinically or by EKG -> CABG should be strongly considered as the primary reperfusion strategy, especially with beneficial anatomy or DM.

Question 76

What is the role for CABG in STEMI?

Answer 76

Failure of PCI + anatomy suitable + persistent ischemia and large infarct. OR MI complication - papillary muscle rupture, post-infarct VSD, LV rupture -> emergency OR for fix of the rupture and revascularization vs emergency ECMO and try to recover organ fct over 4-5 days before going to OR if too unstable. Emergency CABG should NOT be performed after failed PCI in the absence of ischemia or a large area of at risk myocardium. Also contraindicated in no-reflow states or poor distal targets. (3: Harm)

Question 77

A patient is stabbed in the heart, and trauma takes the pt to the OR where they do a sternotomy and oversew an injury. 36 hrs later, the patient has improved and is stable. An EKG was obtained for some PVCs shows STEMI. Cath shows a ligated LAD. Should PCI be performed?

Answer 77

The key is the timing from the event. **No**. In asx pts w/ STEMI and totally occluded infarct artery **>24 hrs after onset and w/o evidence of severe ischemia, PCI should not be performed**. (3: No benefit) If ongoing ischemia, acute severe HF, or life-threatening arrhythmia, PCI can be of benefit despite time delay. (2a)

Question 78

What coronary disease is left-main equivalent?

Answer 78

>70% in LAD and L Cx

Question 79

A patient presents w/ NSTEMI, stable, meets indication for CABG. How do you manage? IE What's the med mgmt? Timing? What if they ask to go home?

Answer 79

Maximize medical mgmt: heparin, ASA, O2 if needed, IABP if refractory angina or low EF. Urgent CABG (plavix should be stopped 24 hrs). The patient should not be DC home.

Question 80

A patient is resuscitated from witnessed cardiac arrest. Coronary angiography shows 3V disease. What's the revascularization strategy?

Answer 80

PCI of the INFARCT artery (NOT non-culprit lesions - 3:harm). THEN assess if cardiogenic shock. THEN assess for area of infarction. - If stable w/ low complexity - PCI of non-culprit arteries. - If cardiogenic shock - DON'T revasc non-culprit arteries. DEFER this... and determine at-risk myocardium. Non-culprit supplies large area of myocardium? No -> GDMT and heart team discussion. Yes -> Complex/multivessel? - No -> staged PCI. - Yes -> heart team: GDMT w/ staged PCIs vs CABG

Question 81

Manage pt w/ inferior infarction and RV involvement. PCI failed.

Answer 81

CABG during hospital stay. Consider delaying until RV is optimized w/ inotropes, diuretics, or even mechanical support. If this option is chosen, you need to see quick improvement. If improvement, delay until organ system function improves, and patient stabilizes on support. This is the window.

Question 82

A patient presents w/ NSTEMI. PCI fails. They have ongoing ischemia, hemodynamic compromise, and there is substantial myocardium at risk. They are otherwise appropriate for any intervention. Is emergency CABG reasonable?

Answer 82

Yes (2a). Retrospective reviews note reduced mortality in an emergency approach. If on DAPT, use a heart team approach. If in shock, may benefit from MCS before CABG. Need to see quick improvement. Keep MCS until organ systems recover and hemodynamics improve, then promptly go to OR.

Question 83

A patient w/ previous coronary stent undergoes CABG. How do you manage this vessel?

Answer 83

If it is wide open, no reason to bypass as it will likely fail 2/2 competitive flow.

Question 84

A patient requires CABG and is found to have a porcelain aorta. How does this affect planning? Preop eval? Cannulation? Grafts? Proximal placement if vein grafts? Thoughts on clamping?

Answer 84

*The question is how to cannulate, clamp, place proximals.* Preop: evaluate groins and axilla w/ CT. Consider beating heart CABG - need fluids, pressors, shunt. If needed, peripheral cannulation: axillary or femoral. Try to use all arterials, and Y off the IMAs if needed. Where to place proximals? SVG may be anastomosed to innominate, carotid, SCA, R axillary artery, or descending aorta. Be ready to circ arrest.

Question 85

A CABG patient has porcelain aorta and severe AI. They need AVR. How do you make sure the heart doesn't distend too much? How do you do proximal SVG anastomoses? What if you can't find a safe place to clamp?

Answer 85

LV vent via R SPV or LV apex will help prevent distention. The risk here is stroke from LV vent placement before clamp, but the risk from clamping the ascending aorta is higher. Axillary CPB can help raise your clamp if needed or for other cannula sites. For aortic cannula and root vent, can try for a soft spot on root with intra-op US. Retrograde arrest w/ eventual direct ostial vs graft plegia. The patient may need ascending aortic replacement in order to place proximal anastomoses. May need circulatory arrest if you cannot find a safe place to clamp.

Question 86

Redo CABG has higher risk than primary revascularization w/ mortality of 7-11% mostly 2/2 what disease? What causes this?

Answer 86

perioperative MI - can be 2/2 incomplete revascularization, atheromatous emboli, damaged grafts, hypoperfusion through new grafts, or early graft occlusion

Question 87

In a redo CABG, what is the general principle in regard to handling previous venous bypass grafts?

Answer 87

No touch technique - avoid embolization of debri

Question 88

What is your myocardial protection strategy for redo CABG?

Answer 88

Antegrade alone may not protect areas supplied by patent pedicled IMAs and may dislodge debri in SVG. **Retrograde** allows washout of coronary debris and access to myocardial areas of occluded arterial grafts. Clamping of patent arterial grafts ensures uniform cooling. Do NOT do difficult dissection of open LIMA-LAD if risk injuring it. Consider cooling pt to 28-30 if keeping LIMA patent, and give multiple rounds of plegia.

Question 89

During redo CABG, what strategy can be utilized in order to minimize the number of proximal anastomoses (ie the proximal sites on aorta are limited d/t prior grafts)?

Answer 89

Sequencing vein grafts. Can also put grafts on innominate or subclavian if needed.

Question 90

During redo CABG, patient fails to wean from bypass. Doppler is done once all other causes ruled out, and poor flow is found with associated regional abnormality on TEE. What do you do?

Answer 90

Grafts to that area on TEE should be reconstructed immediately.

Question 91

During redo CABG, there is no room on the aorta for proximal anastomoses. What options are there?

Answer 91

End-to-side to patent arterial grafts. Use RIMA in situ if possible. Can also place grafts on innominate artery.

Question 92

During redo CABG sternotomy, there is bright red blood encountered before sternum is completely open. There are EKG changes. What happened? What do you do?

Answer 92

Hints are the blood color and EKG changes - Suspect **coronary/graft injury**. Possibly aorta/innominate as well. Heparinize and obtain femoral bypass (there’s still too much dissecting to do to just attempt opening for central bypass). Can attempt repair once injury is exposed vs coronary perfusion catheter. Complete the operation.

Question 93

During REDO CABG, you are trying to dissect the LIMA-LAD proximally, and you injure it. There are hemodynamic, EKG, and wall motion abnormalities. How do you manage?

Answer 93

Get on bypass. Clamp and arrest the heart. Try to repair the injured mammary, but safest would be to harvest a SVG and bypass. Before dissection of the mammary, you need to be ready to clamp and arrest - heparinized w/ high ACT, cannulated, dissected ascending aorta.

Question 94

What are the important diagnostic studies for post-infarct VSD?

Answer 94

**1. EKG** - rule out ongoing ischemia and arrhythmia. **2. Echo** *diagnostic* - color flow Doppler shows size and location of VSD (also valves, R side pressures, PA, tamponade). **3. RHC** - *step-up in oxygenation* b/w RA and PA is diagnostic >9%; can also see elevated pulm-to-systemic flow ratio (1.4:1 to 8:1). **4. LHC** - can determine if need for *revasc*.

Question 95

Post-infarct VSD mortality?

Answer 95

Poor - 25% within 24 hrs, increasing with time up to 97% in 1 year. This is an indication for urgent surgery.

Question 96

Manage a post-infarct VSD preop. What are your hemodynamic goals and what meds or methods do you use to achieve them?

Answer 96

Reduce afterload to decrease L-to-R shunt (nitroprusside). Maintain cardiac output and perfusion (milrinone). Increase coronary perfusion pressure. IABP and inotropes. ECMO or biventricular support can be used for temporary salvage before more definitive surgery can be performed.

Question 97

How do you do an anterior septal rupture repair (pt w/ post-infarct VSD)?

Answer 97

No PA catheter. Conduit harvest if needed. Bicaval cannulation. Antegrade cardioplegia. LV vent in R SPV. Cool to 25 C. LV transinfarct incision and infarctectomy including septum. Patch with horizontal mattress sutures, felt strip, and Dacron patch. Deair, wean CPB, TEE to assess residual VSD/shunt/LV fct/MR. +/- IABP.

Question 98

How do you do apical VSD repair (postinfarct VSD)?

Answer 98

Bicaval cannulation. R SPV LV vent. Root vent. Incision through infarcted apex. Debride necrotic tissue (may include LV, RV, septum). Reapproximate w/ interrupted mattress through felt (use felt b/w each layer).

Question 99

How do you do posteroinferior VSD repair (postinfarct VSD)?

Answer 99

CPB and arrest. The heart needs to be retracted (like for PDA bypass). LV transinfarct incision w/ 1 cm of space lateral to PDA. Debride necrotic tissue. Inspect mitral for papillary infarct. Inspect posterior septum - can re-approximate using double layer buttress. Large defects require patch (must be tension free).

Question 100

When is delayed repair for post-infarct VSD acceptable?

Answer 100

Situation: pt w/ recoverable end-organ damage 2/2 to low-flow state that's been corrected. May benefit from Impella or IABP to improve dysfunction and allow for maturation of the infarcted tissue. Biventricular assist device may be needed if Impella worsens R-to-L shunt and unable to balance. Can also improve forward flow and decrease afterload on LV with Impella/IABP while using ECMO to decrease load on RV and oxygenate blood to bypass the VSD.

Question 101

What is the greatest predictor of post-operative mortality in pts w/ postinfarct VSD?

Answer 101

Time in cardiogenic shock

Question 102

Is asymptomatic severe aortic stenosis an indication for AVR replacement (TAVI or SAVR)? Discuss this.

Answer 102

Usually, not on its own. Surgical indications severe asx plus... low EF (<50 or <60 x3 studies), other cardiac surgery, Vmax >5, BNP 3x nl, rapid progression. *Severe = Vm >4, delta Pmean >40, AVA 0.6 or less, SVI <35, EF <50 w/ DSE creating Vmax >4.* *If intervention required, transfemoral TAVI should be considered in following settings: 1) STS-PROM >8%, or 4-8 w/o high-risk anatomic features. 2) Age >80 w/ life expectancy >10 yrs (65-80 should have discussion TAVI vs SAVR; <65 w/ life expectancy >20 yrs should have SAVR) ALSO: transfemoral feasible, trileaflet valve, absence of high-risk feaures, survival >12 mo w/ acceptable QoL*

Question 103

How can you "unmask" asymptomatic severe (>4 Vm) aortic stenosis to objectively confirm a patient is without impairment?

Answer 103

exercise stress test (treadmill) - positive if… - Symptoms. - SBP dec by >10 mm Hg. - Dysrhythmias. - ST changes.

Question 104

What is the peak gradient equation (in the context of aortic stenosis)? How is it directly obtained/measured (as opposed to calculated as above)?

Answer 104

Peak gradient = 4(velocity)^2. Maximum gradient present when central aortic pressure is subtracted from LV systolic pressure. Obtained by echo w/ continuous wave doppler. Or during LHC.

Question 105

In what scenario may a patient with severe aortic stenosis have a low gradient?

Answer 105

In a patient with low cardiac output. Velocity, and thus gradient (4[velocity]^2), is affected by CO. This is a low gradient/low flow AS. Get a dobutamine stress echo to confirm.

Question 106

How can a low flow/low gradient AS be confirmed in a patient w/ normal EF (>50)?

Answer 106

**Stroke volume index** <35% ml/min/m^2 - valve area indexed to body size. Must be measured when patient is **normotensive (systolic <140).** The echo will show AVA characteristic of AS (AVA <1 or indexed <0.6), but with normal hemodynamic measurements Vmax <4 or mean delta P <40 mm Hg (AKA pressure gradient). The LV will be small w/ thick walls, diastolic dysfunction, and EF >50%.

Question 107

How can a low flow/low gradient AS be confirmed if the patient has a low EF (<50%)?

Answer 107

Dobutamine stress echo - if gradient increases while AVA remains the same, AS is confirmed.

Question 108

If low flow/low gradient AS is suspected in a patient w/ low EF (<50%), and dobutamine stress echo shows NO change in gradient w/ AVA increase >0.3cm^2 (or if AVA reaches 1cm^2), what is the diagnosis?

Answer 108

pseudo-AS

Question 109

In the workup of AS, a significant subvalvular gradient and asymmetric septal hypertrophy is found, what treatment may be required?

Answer 109

Septal myectomy and possible mitral valve surgery

Question 110

If the diagnosis of AS is uncertain by echo, including dobutamine stress testing, what else can be done to evaluate the gradient?

Answer 110

Cardiac cath to cross the valve and obtain a hemodynamic AV study. Can directly measure gradients.

Question 111

In a potential TAVR candidate for AS, what imaging needs to be obtained?

Answer 111

TAVR CT scan - valve morphology (TTE unreliable), AV annulus and LVOT sizing, coronary height and orientation, and sinus height and width sizing. Should also eval the aorta/iliacs/femorals for access and passage of the TAVR.

Question 112

What are the diagnostic criteria for severe AS? What else should you rule out?

Answer 112

Either of the following: - mean AV gradient > or = 40 mm Hg - peak velocity across AV > or = 4 m/s These are characteristic, but not required - AVA <1 or indexed <0.6 - dimensionless index <0.25 Always confirm. Always r/o CAD, aneurysm, and MV disease.

Question 113

How do you decide on SAVR vs TAVR for severe symptomatic AS?

Answer 113

Guidelines say you can choose either, but considerations are as follows: Anatomy (coronary height, valve shape, femoral/other access site size and anatomy). Age and medical conditions affecting long-term prognosis. Preference. It was previously trending that in principle, you should rule out TAVR as an option (anatomy etc) unless there are other indications for surgical intervention. The pendulum is swinging the other way. **Stage B** (Vmax 3-3.9) w/ **other heart surgery** indication gets **SAVR**. **Stage C** (Vmax 4) w/ **exercise stress test** showing **dec BP or dec exercise capx**, or high severity (**Vmax 5**, **BNP 3x nl**, **rapid progression**) + **low surgical risk** gets **SAVR**.

Question 114

What STS risk score is prohibitive for SAVR for symptomatic severe AS?

Answer 114

STS >8%. TAVR shows survival benefit in these patients. Also: 2 or more frailty measures would favor TAVI. Remember that life expectancy with acceptable quality of life >1 yr is also a requirement in addition to acceptable valve/vascular anatomy.

Question 115

What are the likely complications for TAVR vs SAVR?

Answer 115

TAVR - perivalvular leak, heart block requiring permanent pacemaker, access injuries. SAVR - bleeding, re-hospitalization, atrial fibrillation.

Question 116

What are the benefits of a mechanical aortic valve compared to bioprosthetic?

Answer 116

Lower reintervention rate in <60 yrs old. Superior survival at 15 yrs if b/w 50-70 yrs.

Question 117

What complication of a surgical bioprosthetic aortic valve placement will likely reduce benefit from a valve-in-valve procedure? The context would be a healthy female patient electing for a bio valve, and their root is relatively small.

Answer 117

**patient-prosthesis mismatch** This is why doing a root enlargement at the primary operation is important, even if the initial bioprosthetic valve will meet the current patient needs. It may be wise to plan for the ViV if the patient is expected to outlast the current valve.

Question 118

An AS patient undergoes TAVR CT showing bicuspid aortic valve. The valve is functional, and the patient is low risk. Discuss TAVR use.

Answer 118

TAVR historically not approved for use in this population. But new data is showing comparable outcomes of TAVR is similar to SAVR in BAV AS patients. Surgery remains first-line for AS BAV patients, but TAVR with the latest prostheses may be a safe alternative in patients with increased risk for surgery after meticulous workup of AV anatomy.

Question 119

A patient w/ surgical, severe AS and intermediate surgical risk has an associated ascending aortic aneurysm. At what size is there a strong indication for aorta surgery?

Answer 119

4.5 cm

Question 120

What is the EOA and why is it useful for aortic valve placement?

Answer 120

Effective orifice area (obtained by sizing valve and finding the corresponding EOA published by the manufacturer)/BSA. Used to predict patient-prosthesis mismatch.

Question 121

An aortic valve's EOAI is < 0.85. What does this mean?

Answer 121

Predictive of PPM. 0.65-0.85 is predictive of moderate PPM. <0.65 is severe.

Question 122

Is EOAI <0.85 a contraindication for aortic valve surgery?

Answer 122

No. In a comorbid elderly patient w/ symptomatic severe AS, a risk of moderate PPM is preferred over cross-clamp time and surgical risk (ie TAVR w/ small EOAI is ok). Should try to do an AV annular enlargement if at all possible in a surgically fit patient.

Question 123

During workup for CABG, moderate AS is found. How do you manage?

Answer 123

Class IIb indication for replacement at time of surgery.

Question 124

You are doing surgery for AS, but the heart is not arresting well. How do you manage? What do you have to rule out?

Answer 124

Make sure the heart isn’t blowing up. Check crossclamp. Check drainage. May just be slow d/t hypertrophy. Add LV vent in R SPV. Open aorta and give direct cardioplegia. Can also do retrograde plegia. Cool patient. May need higher dose of cardioplegia.

Question 125

Intraop TEE during AVR for AS shows moderate perivalvular leak. How do you manage? What are you looking for? If having to completely redo, what do you need to make sure of on reattempt?

Answer 125

Clamp, arrest, open aorta, and reassess. If visible defect, place a stitch. If not, remove valve and start over. Ensure decalcification of entire annulus (retained Ca can lead to improper seating). May need to reconstruct with pericardium.

Question 126

What can you do if a patient's EOAI is <0.65 during AVR for AS, and the patient is a good surgical candidate with an active lifestlye?

Answer 126

Higher risk for patient-prosthesis mismatch. Consider root enlargement or total root replacement (Bentall). Other option is a Ross. Can also bail and do bio-Bentall, but this is less ideal and is more of a bailout if the root goes poorly.

Question 127

What can make an asymptomatic severe AS more of a SAVR candidate (higher grade of recommendation) as opposed to TAVR?

Answer 127

Low gradient w/ <50% EF. Critical AS (>5m/s velocity). Severe LVH. Concomitant cardiac operation. Severe calcification.

Question 128

A patient with aortic regurgitation gets an echo. What are you looking for?

Answer 128

Confirm diagnosis and severity, assess for etiology, valve morphology, LV assessments, aortic root size.

Question 129

In workup for AR, you find a bicuspid valve with prolapse leaflets and minimal calcification. What does this tell you what about the expected procedure? What is often an associated pathology?

Answer 129

More amenable to repair, especially with more normal sized roots and without calcification. The root is often affected (ie association w/ ascending aortic aneurysm and dissection), but a valve-sparing root replacement with valve repair is very effective in this population. Jet direction is critical. Of 85 valve-sparing root replacements for bicuspid aortic valve aneurysm disease, 99 percent were free of more than moderate AR at eight years.

Question 130

Which AR patients need a heart cath?

Answer 130

Need: - significant risk factors for CAD - older than 40 in whom AVR is considered It may be good to assess RV/pulm HTN as well.

Question 131

In workup of AR, what test can be done to confirm diagnosis if echo is inconclusive or discordant w/ physical findings?

Answer 131

LHC w/ root angiography and measurement of LV pressures

Question 132

Severe AR is defined by what echo/angio parameters?

Answer 132

jet width >65% of LVOT vena contracta >0.6 cm holodiastolic flow reversal in the prox abdominal aorta regurgitant volume >60 ml/beat regurgitant fraction >50% effective regurgitant orifice >0.3 cm2 angio grade 3+ or 4+

Question 133

Diagnosis of chronic severe AR requires evidence of what?

Answer 133

LV dilation. Be more cautious in these patients. The heart is weakening, so be prepared to support (IABP, ECMO, Impella; pressors). The R heart may also be weak, and there could be pulm HTN to deal with.

Question 134

Guideline indications for surgery for chronic AR?

Answer 134

Symptoms AND severe. ASYMPTOMATIC, SEVERE, AND: Other cardiac surgery (I; mod AR is IIb). LVEF <55 (no other cause identified). Severe LV dilation - LVESD >50 mm (can’t squeeze) or indexed LVESD >25 (IIa). LVEDD >65 (overfill) and nl EF (IIb). Progressive decline in LVEF on 3 studies despite EF >55. *of note, for chronic AR, there is no operating on asymptomatic nl EF patients w/o other evidence of dysfunction (LVESD, LVEDD, progression) *all patients should get BP tx for goal systolic <140. *nonop patients should get GDMT including ACEi/ARB. *TAVI is not for SAVR candidates in AR (III: harm)

Question 135

You are doing surgery in a patient w/ AR. CPB is initiated, and the heart continues to eject, and begins to distend. What do you do?

Answer 135

Prior to bypass, you should be ready for distention - have retrograde cardioplegia access. Arrest immediately after clamping. Create the aortotomy, then give direct cardioplegia. If arrest doesn't happen quickly, this is also the bail out.

Question 136

When trying to establish retrograde cardioplegia for an AR case, you have difficulty, and the position is questionable. What can be done? Assuming you've attempted using posterior palpation and TEE guidance.

Answer 136

Bicaval cannulation. Make room for the cross clamp, and ID the aortotomy site. Initiate CPB. Snare the SVC/IVC. Make a R atriotomy and place direct retrograde catheter for cardioplegia (just past opening to ensure middle vein gets plegia). Clamp, aortotomy, then give direct cardioplegia. Place LV vent.

Question 137

During AR case, what if you injure the coronary sinus and/or retrograde cardioplegia becomes unreliable?

Answer 137

Initiate CPB, clamp, give ostial cardioplegia.

Question 138

During AR case, TEE and direct visualization shows a prolapse of the R cusp. What are the surgical options?

Answer 138

Replacement is safest (as opposed to repair). "Although advances are occurring in primary aortic valve repair, this approach is not yet generalizable, and durability is not known." "...given the complexities of patient selection and surgical techniques, such surgeries should be performed at a Comprehensive Valve Center." AHA 2022 Valve Guidelines

Question 139

During AV surgery for severe AR, a patient fibrillates and arrests while cannulating the RA. The heart dilates, and defibrillation fails. He is unable to be converted back to sinus. What do you do?

Answer 139

Institute CPB, empty the heart, and defibrillate again. If unable to empty the heart d/t severe AI, cross clamp and open the aorta. Decompress the heart with a sucker through the aortic valve and localize the coronary ostia to give antegrade cardioplegia w/ an ostial cannula.

Question 140

You complete an AVR, but are unable to close the aortotomy d/t the large prosthesis putting tension on the aortotomy suture line. What do you do?

Answer 140

Use a bovine or autologous pericardial patch to ensure no tension on the suture line. This can be avoided by not making the aortotomy incision too low and not trying to oversize the valve. Just do a root enlargement.

Question 141

You complete an AVR, but there is periprosthetic regurgitation. What do you do? What does a leak around the non-coronary sinus imply?

Answer 141

Do a good diagnostic evaluation with TEE - quantify and localize the leak, differentiate between prosthetic vs periprosthetic. You may have to remove the prosthetic to fix the problem. Leaks from the non-coronary sinus are most amenable to direct suture repair.

Question 142

Symptomatic **acute** aortic regurgitation should be taken care of expeditiously. Why?

Answer 142

The ventricle has not had time to develop any adaptation to overcome the increased volume which can lead to rapid deterioration.

Question 143

In non-surgical candidates w/ AR being considered for TAVR, discuss the following: Compared to AS disease... native valve characteristics in AR that would affect choice of TAVR self-expanding vs balloon expanding valve? What is the mortality difference b/w TAVR for AR vs AS?

Answer 143

The lack of calcification and larger annulus size may mean a self-expanding prosthesis would be more successful. The 30-day mortality for TAVR for AR is higher compared to TAVR for AS.

Question 144

Describe the benefits of aortic valve repair in AR surgery?

Answer 144

Similar results for AVR w/o need for anticoagulation as opposed to mechanical implants and possibly improved durability compared to bioprosthetics. **AHA guidelines**: "Although advances are occurring in primary aortic valve repair, this approach is not yet generalizable, and durability is not known." "Surgical repair of the aortic valve may be feasible in selected patients, depending on valve and aortic root anatomy and tissue characteristics. Published data suggest that valve repair can be performed safely and effectively by surgeons with training and experience in these techniques. However, given the complexities of patient selection and surgical techniques, such surgeries should be performed at a Comprehensive Valve Center."

Question 145

How do stented pericardial aortic valves tend to fail?

Answer 145

By aortic stenosis of the biologic prosthesis, but tend to last longer than porcine valve.

Question 146

What type of aortic valve is generally favored in younger (<55) patients?

Answer 146

Mechanical valves, though they do limit lifestyle d/t need for anticoagulation, and they limit future TAVR options. Ideally, <50 gets a Ross.

Question 147

What tests should you obtain before a redo AVR?

Answer 147

Echo (consider TEE if concern for endocarditis). Coronary imaging. CTA C/A/P to eval for transcatheter options, root size, SJ width, coronary heights; access options. Carotid duplex PFTs if hx of pulm disease Vein mapping if previous CABG Prev op note: when, what was last valve, other procedures (root enlargement, ascending aorta), CABG conduits and if crossing midline

Question 148

Compared to TAVR, redo AVR is associated with what risk profile? Ie compare risks of specific complications.

Answer 148

Redo AVR has… Lower vascular complications and perivalvular leak. Higher short-term stroke rate, atrial fib rate, AKI, bleeding.

Question 149

How do you decide b/w valve in valve TAVR vs redo SAVR? Pros of ViV TAVR? Contraindications?

Answer 149

Early complication rates are lower for ViV TAVR. Durability is unknown. Endocarditis is a contraindication. Mechanical valves preclude TAVR. Eval for risk of patient-prosthesis mismatch: What were the gradients postop? If they are high, the original valve may already be small => redo SAVR +/- root enlargement. If they are nonoperative, then the patient will have to tolerate some PPM. Eval for risk of coronary obstruction: coronary height needs to be >10mm.

Question 150

In considering valve-in-valve TAVR, what would be considered a small in place prosthetic valve?

Answer 150

<23 mm may require the smallest TAVR inside or require fracturing of the surgical valve via high pressure balloon dilation. At <23 mm, there should be a compelling reason not to do redo SAVR. Similar issues: narrow STJ, small root. **when performing bio SAVR, try to get at least a 23 valve in as to not eliminate future ViV option. This may be a reason in itself to do a root enlargement, and even with an ok EOAI, a small valve does not allow for much exercise.

Question 151

In terms of a valve-in-valve TAVR, what measurement/diameter must be known in terms of the TAVR placement? How can this number be confirmed?

Answer 151

The internal diameter of the previous surgical valve. Look up product guide to find the internal diameter, and confirm w/ CTA or TEE. When evaluating for SAVR, the external diameter of the valve matters as it must fit in place of the native valve annulus.

Question 152

A previous AVR fails d/t AI (as opposed to AS). What are the considerations for procedural management (TAVR vs SAVR)?

Answer 152

There needs to be a compelling reason to NOT do redo SAVR. Most current TAVRs are designed for AS, not AI.

Question 153

What cardiac surgery history and medical history should cause a stronger consideration for ViV TAVR as opposed to a redo AVR? What about imaging findings?

Answer 153

Prior CABG w/ LIMA (esp if near sternum). HFrEF, >75-80 yrs, poor condition, renal failure. Calcified ascending aorta.

Question 154

ViV TAVR self-expanding vs balloon expandable discussion. Self-expanding pros (2). Self-expanding con (1). How is this con decreased in this specific setting?

Answer 154

Self-expanding: Better gradients (important since valve area is being reduced more d/t ViV). Less traumatic in setting of calcified aorta. Do not require rapid pacing (important if HF/sick ventricle 2/2 recurrent AS). Higher pacemaker risk (somewhat mitigated in ViV by previous valve "protecting" conduction system when compared to first time).

Question 155

For a healthy 65yr patient at low surgical risk w/ severe structural bioprosthetic aortic valve deterioration, what is the ideal procedure? What aortic valve and aortic root characteristics would make this patient more likely to benefit from the above answer?

Answer 155

Redo AVR (as opposed to ViV TAVR). Especially if AR. Especially if small valve (<23 mm), narrow STJ, or small root. *Clue would be if initial postop gradients from previous SAVR are high*. Especially if high risk for coronary obstruction (eg surgical valve has leaflets outside the frame, effaced sinuses, low coronary height [<10 mm]). Especially if other concomitant surgical pathology.

Question 156

Discuss cannulation strategy for redo AVR.

Answer 156

Be prepared for anything - have preop imaging; axilla, groins, and legs prepped (vein if coronary injury). Consider placing femoral sheaths (4-5 Fr). Consider CPB prior to opening in following situations - aorta close to sternum, high PA pressures w/ RV close to sternum, critical bypass grafts under sternum, calcified aorta. Otherwise, with careful dissection, can do central cannulation.

Question 157

Discuss myocardial protection in a redo AVR w/ AI.

Answer 157

Can arrest initially w/ retrograde cardioplegia then open aorta and deliver the rest as ostial plegia to ensure good protection. Can try arresting antegrade, but it's difficult to estimate how much is truly going down coronaries vs going into LV.

Question 158

What are the considerations for the conduction system in redo AVRs (inc risk for what, and should consider what to prevent complications)? Where is the conduction system in relation to the aortic valve?

Answer 158

Higher risk of heart block. Make sure you have reliable wires, and consider a-wires. Near the underside of the R/non commissure.

Question 159

Discuss prevention and management of VF during initial dissection of a redo AVR w/ moderate AI. What causes this? What preventative measures can you take? What if the patient continues to be unstable or the heart distends in the incompletely dissected heart? What if the heart distends?

Answer 159

Can be caused by CPB w/ an incompetent valve or bovie near the LV during dissection (keep cautery <45). Have external pads, so you can shock prior to heart being dissected out (100-200 joules). Having heart dissected out before CPB allows you to shock w/ paddles in case of fib during CPB. Instability - cannulate and go on pump immediately. Heart distends - LV vent (ideally R SPV; LV apex if exposed; or clamp aorta and aortotomy w/ ostial plegia)

Question 160

Discuss operative plan for redo AVR w/ previous CABG.

Answer 160

Need preop cardiac cath and study of previous op note. LIMA patent - frequent plegia and cool to 30 vs clamp LIMA (must be easy dissection, don't risk injury) - Can clamp across all tissue w/ vascular clamp. - If dissecting LIMA, be ready to clamp and arrest because injury will require immediate CPB and plegia. Usually bad idea. May need to mobilize grafts for aortotomy vs transect and rebypass w/ ligation of the old graft.

Question 161

During redo AVR, you are unable to access the root and get exposure of the valve via aortotomy, what can be done next for exposure?

Answer 161

Transect aorta.

Question 162

During redo AVR, you tear the aorta/outflow tract when removing the old valve. How do you fix this?

Answer 162

Patch. May need homograft recon if extensive - Bentall.

Question 163

During redo AVR, you injure R coronary ostia while removing the valve. How do you manage?

Answer 163

Preparation: have legs prepped for any root case so vein can be taken. Look at cath to ensure you are distal to disease during bypass.

Question 164

Coming off bypass from redo AVR, and there is RV dysfunction. Assessment and plan?

Answer 164

Always assume regional functional issues are coronary problems. Rule out air in the coronary system. Assume new valve obstructed R coronary ostia - go back on pump, and graft R coronary system. DO NOT reopen aorta and redo valve. You should have made sure you could see coronary ostia before closing aortotomy.

Question 165

How can you be sure coronary ostia are open after redo AVR?

Answer 165

Before closing aortotomy, visualize the ostia. Can place R angle into them. Give retrograde plegia and look for blood return from the os.

Question 166

After redo AVR, you cannot close the aortotomy d/t tension on the aorta.

Answer 166

In redo settings, the aorta can be less compliant, struts can affect the closure, and a second closure line further reduces aortic tissue. Use a patch, and try not to oversize the aortic valve.

Question 167

77yr pt w/ mechanical AVR has failed w/ AS to the point of requiring intervention, and there is MR. CKD. Assessment and plan?

Answer 167

Likely functional MR 2/2 AS. The principle is that the culprit lesion is the AS. In this difficult patient, it's best to think of the safest option... Safest: redo SAVR and monitor MR as outpt for need for Mitra Clip.

Question 168

What critical diagnoses need to be considered in the differential for patients with a failed bio AVR being considered for re-intervention (possible ViV TAVR vs SAVR considerations)?

Answer 168

PPM - look for evidence of high gradients postop => may need enlargement and SAVR over ViV TAVR Endocarditis - echo and cultures in right clinical setting => no ViV TAVR for IE

Question 169

In terms of valve sizing, what info can be obtained before AVR to ensure no PPM?

Answer 169

Check BSA and CTA. If the required size is unlikely to fit the patient's anatomy, be prepared for a root enlargement. EOA (obtained via manufacturer) of valve / BSA should be > 0.80 to prevent PPM.

Question 170

Primary mitral regurgitation is generally caused by what?

Answer 170

primary leaflet abnormalities - usually result of degenerative disease

Question 171

Secondary MR is generally caused by what?

Answer 171

structurally normal valve leaflets are unable to coapt completely - owing to a distortion of either the annulus or the subvalvular apparatus can be from ischemic cardiomyopathy or other causes of dilated cardiomyopathy

Question 172

LV dysfunction and secondary MR prognosis compared to either abnormality in isolation? Is revascularization or addressing MR of value?

Answer 172

much worse; controversial whether revascularization alone is helpful; controversial whether addressing MR will be of value, but data seems to suggest that it does help

Question 173

Carpentier's Type 1 MR?

Answer 173

normal leaflet motion - results from LV enlargement and annular dilation (functional or secondary MR; 2/2 ICM or other dilated cardiomyopathy) can also be from perforation in leaflet

Question 174

Carpentier's Type II MR?

Answer 174

leaflet prolapse - can be degenerative, acute papillary rupture after MI 1) normal 2) too much 3) not enough

Question 175

Carpentier's Type IIIa MR?

Answer 175

leaflet restriction, systole and diastole - rheumatic

Question 176

Carpentier's Type IIIb MR?

Answer 176

restriction during systole alone - chronic ischemic disease

Question 177

Dilated cardiomyopathy is likely to cause what type of MR?

Answer 177

type 1 - normal leaflet motion pts may have severely depressed LV fct

Question 178

Ischemic MR tends to cause what type of MR? What is mechanism?

Answer 178

Type IIIb - systolic restriction of leaflets. Chronic ischemia can cause asymmetric ventricular remodeling => mostly affects inferior and lateral LV wall => disruption of the subvalvular apparatus => downward and lateral (apical) displacement of the PM papillary muscle => leaflet tethering. Also Type I - more pronounced derangement of the annulus in the P2-P3 region resulting from infarction of the posterior wall of the ventricle

Question 179

What is the study of choice to clarify the mechanism and anatomy of MR? What is a problem with this study?

Answer 179

TEE - however, MR severity may be lower intraoperatively d/t anes and ventricular unloading

Question 180

At the time of CABG for severe ischemic MR, what is the preferred surgery for the mitral valve?

Answer 180

Chordal-sparing MV REPLACEMENT - bio valve is probably best since poor prognosis long-term. RCT showed no difference in survival at 2 years, however, the rate of recurrence of mod-severe MR was higher in the repair group. *remember GDMT, as this is secondary MR *stage D - RVol >60ml, RF >50%, ERO >0.4 cm2 *2b COR *either way, 2 yr survival is 20-25% - why bio valve is likely best

Question 181

What is an Alfieri stitch and when is it appropriate? Any technical considerations depending on disease process? What about valve orifice size concern?

Answer 181

At the time of apical incision such as LVAD for Type I (nl leaflet motion) secondary MR. Or for Type II prolapsed leaflet in a sick patient that cannot tolerate a longer repair. It should be rarely used. The repair can be applied to cases of posterior, anterior, or bileaflet prolapse, and involves suturing the free margin of the prolapsed leaflet segment to that of the opposing leaflet segment using a figure-of-eight stitch or continuous running suture, effectively creating a double orifice mitral valve. The depth of leaflet tissue incorporated into the suture line depends on the degree of leaflet redundancy. Larger bites (>1 cm) should be used in Barlow disease, giving strength to the repair but also decreasing leaflet height to prevent systolic anterior motion. For thin leaflets, mattress sutures reinforced with pericardial pledgets may be placed for additional support. Hegar dilators may be used to ensure that the resulting total valve orifice area is at least 2.5 cm2, thus avoiding iatrogenic mitral stenosis.

Question 182

In CABG MVR, why do you do distal anastomoses first before valve?

Answer 182

avoids excess manipulation of heart that predisposes to AV groove dissociation

Question 183

An old pt w/ diffuse CAD and poor targets has dilated cardiomyopathy w/ secondary severe MR and EF of 15%. What should you plan for?

Answer 183

LVAD. Consider Alfieri suture after apical coring.

Question 184

A patient who requires CABG is found to have **moderate** ischemic MR. What do you do for the MR?

Answer 184

Nothing. Concomitant MVr resulted in longer OR time, longer hospitalization, higher rates of a-fib, higher rates of stroke. MitraClip may be better option down the road. **Severe** seconadary MR in the setting of CABG should get repair (2a).

Question 185

Pt w/ severe symptomatic **secondary** mitral regurgitation and EF <50%. Pt sx are persistent despite GDMT. What is recommended for mitral valve? If surgery, discuss repair vs replacement.

Answer 185

Eval for transcatheter edge-to-edge MV repair (TEER) (2a): - LVEF 20-49% - LVESD < or = 70 mm - PASP < or = 70 mmHg If anatomy not good, then consider surgery (2b). If undergoing CABG, fix the MR at the same time (2a). Everyone gets GDMT w/ HF specialist (1). If > or = 50% EF w/ severe persistent sx, do surgery (2b). In an RCT of mitral valve repair versus mitral valve replacement in patients with severe ischemic MR, there was no difference between repair and mitral valve replacement in survival rate or LV remodeling at 2 years. However, the rate of recurrence of moderate or severe MR over 2 years was higher in the repair group than in the replacement group, leading to a higher incidence of HF and repeat hospitalization. The lack of apparent benefit of valve repair over valve replacement in secondary MR versus primary MR, with less durable repairs in secondary MR, highlights that primary and secondary MR are 2 different diseases. (2020 ACC/AHA).

Question 186

What is often the mechanism for acute mitral regurgitation 2-7 days after MI? How do you manage?

Answer 186

Single blood supply to posteromedial papillary muscle - either RCA or L Cx depending on dominance. Anterolateral has dual blood supply (LAD and L Cx). Acute inferior STEMI -> Papillary muscle rupture -> flail leaflet -> apical holosystolic murmur, pulmonary edema -> dyspnea. DO NOT increase afterload or cause volume overload. Give milrinone for inotropy and nitroprusside for vasodilation. IABP should be considered. ECMO may be needed. Surgery: mitral replacement w/ chordal preservation. ## Footnote *Papillary muscle/blood supply/mitral commissure mnemonic: The PDA is posterior and medial. The LAD is anterior, and the LCX is lateral.*

Question 187

How does the jet in primary mitral regurgitation predict leaflet affected?

Answer 187

anterior directed jet is from posterior leaflet prolapse and vice versa; when planning repair, need to know if pt can tolerate second pump run if repair fails

Question 188

Vena contracta for severe mitral regurgitation?

Answer 188

0.7 cm

Question 189

Regurgitant volume for severe MR?

Answer 189

60 ml

Question 190

Regurgitant fraction for severe MR?

Answer 190

50%

Question 191

Central jet (percentage of LA or characteristics) for severe MR?

Answer 191

40% LA or holosystolic eccentric jet

Question 192

In primary mitral regurgitation, which patients should get an operation? Do they have to have severe findings?

Answer 192

This is for PRIMARY MR. There are two conditions. They have to be SEVERE AND have either... - symptoms - this includes EF <30% IF REPAIR can be done. - systolic dysfx: EF <60 (but >30), ESD >40 - new PAH (PA MAP >20, PVR >3 Wood units) - new AF - inc LV size or dec in LV fct x3 studies. OR a center of excellence. Surgery is favored if LA >50mm and/or PAH mild (30-50 systolic). ***These parameters should be adjusted if REPAIR CANNOT be done.

Question 193

If doing a mitral valve repair, what is a necessary adjunct to reinforce most repair techniques?

Answer 193

Ring or band annuloplasty

Question 194

During mitral repair, what is at risk when placing stitches near posteromedial commissure?

Answer 194

Near right trigone - conduction tissue

Question 195

During mitral repair, what is at risk if you place deep stitches at the anterior leaflet while moving from the right to left trigone?

Answer 195

Aortic valve (L/non commissure) - look for aortic insufficiency that wasn't there preop.

Question 196

During mitral repair, what is at risk if you place deep sutures at P1?

Answer 196

Circumflex artery - look for WMA on the lateral wall. Avoid by angling the needle toward the ventricle (away from the atrium).

Question 197

While doing a mitral repair, what is at risk if placing deep retraction stitches outside the annulus of the P3 scallop?

Answer 197

Coronary sinus

Question 198

What is likely the ideal repair in patients w/ mitral regurg 2/2 mitral valve prolapse 2/2 fibroelastic deficiency?

Answer 198

In fibroelastic deficiency, there is a paucity of tissue. Neochords are often the best repair, or a very limited triangular resection. Either way, you need more information from the TEE - where the prolapse is, what the jet looks like, chords and papillaries.

Question 199

In MVR w/ Barlow's valve, what is often the best repair?

Answer 199

There is excess tissue in almost all scallops. Perform quadrangular resection w/ sliding plasty. (B) in picture***

Question 200

A pt with PRIMARY severe MR (vena contracta >0.7 cm, regurg volume >60, regurg fraction >50%, ERO >40%), presents to your clinic. She is asx w/ normal EF (>60%). When does she get surgery? What do you tell the surgeon who wants to do a MV replacement for primary MR? What are options for secondary MR?

Answer 200

Any of the following: - Mortality <1% AND >95% of successful and durable repair - Develops sx - Progressive inc LV size OR dec in LVEF >3 studies - LV ESD >40 - EF drops <60 ***DO NOT do REPLACEMENT if leaflet pathology < 1/2 posterior leaflet (3: harm). If severely symptomatic, and not surgical candidate, TEER is reasonable (life expectancy >1 yr, anatomy reasonable). *2020 AHA **If this was secondary MR, she would be offered GDMT first. If sx continue, then MV surgery (2b). TEER could be offered for: - Severe w/ EF <50 and failed GDMT (EF >20, LVESD <70, PASP <70). 2a. Surgery for severe secondary MR: - With CABG. 2a. - MR 2/2 atrial dilation w/ EF >50 and persistent sx. 2b. - EF <50 w/ persistent sx. 2b. Chordal-sparing mitral valve replacement in CAD w/ severe secondary MR w/ EF <50.

Question 201

56F w/ hx of systolic heart murmur presents to ED w/ worse dyspnea and hemoptysis. She was doing intense physical work when she experienced severe precordial chest pain. She is tachycardic w/ elevated JVP. She has a pansystolic murmur. CXR shows BL pleural effusions. What happened? What are risk factors? What is tx?

Answer 201

Exercise induced acute chordal rupture resulting in severe MR w/ heart failure. The hx of murmur suggests an underlying structural problem - MVP puts pts at inc risk for rupture. Other predisposing factors: rheumatic heart disease and infectious disease. Blunt chest trauma is a rare cause. OR for urgent mitral valve repair. We know this is likely mitral d/t the acute overload presentation in the setting of a systolic murmur. AS is the only other systolic murmur like this, and acute native AS isn’t really a thing.

Question 202

In MR, acute chordal rupture from degenerative etiology needs to be differentiated from papillary muscle rupture d/t ischemia. Why?

Answer 202

The treatment is different. Ruptured chords from degenerative etiology is a primary mitral regurgitation and should get a mitral valve repair. Papillary muscle rupture from ischemic etiology is a mitral regurgitation in an "acute on chronic" setting that may warrant replacement if there is a "secondary mitral regurgitation" component from dilation and may also need a CABG. You may be seeing heart failure symptom exacerbation in the setting of newly diagnosed chronic secondary mitral regurgitation.

Question 203

59M admitted w/ very acute and severe SoB w/ systolic murmur. CXR shows effusions BL w/ R lung opacification and leukocytosis. EKG and troponin normal. What study should be done next? What do you think it will show?

Answer 203

Get echo - can show severe MR 2/2 flail leaflet (AS would be less acute). Do NOT misdiagnose PNA and start abx. The murmur means you need to determine if this is MR, or pt will decompensate.

Question 204

For MV approach, when might L atriotomy be best approach? How is it done?

Answer 204

Most common approach. Incision of choice for robotic and mini-thoracotomy. Approach via R side through Sondergaard's groove (Waterston's). Superiorly, extend incision behind SVC. Inferiorly extend incision behind IVC.

Question 205

For MV approach, when might vertical transseptal be best approach? How is this done? Any advantages? Any disadvantages?

Answer 205

Feasible w/ large LA in setting of chronic MR. Via fossa ovalis. Advantages: Reduces risk of PPM and easier to closed compared to extended superior transseptal approach. Disadvantages: Two suture lines, and you have to look for ASD on TEE after surgery.

Question 206

For MV approach, when might extended superior transseptal (Guiraudon) be best approach? How is this done? Disadvantages? Any advantages?

Answer 206

Situation is when you're in a redo case and can't access Sondergaard. You attempt a vertical transseptal, but there isn't enough exposure because LA isn't large. Vertical transseptal incision is extended superiorly onto the dome of the LA through the limbus of the fossa ovalis. Risk of damaging SA nodal artery (increased risk of PPM). May provide better exposure for a deep chest anatomy/wide AP diameter. Approach of choice in the setting of previous AVR or aortic root placement. Can be easily extended and connected with an aortotomy incision for a Commando operation (endocarditis and radiation). Very good visualization.

Question 207

For MV approach, when might horizontal transseptal (Dubost) be best approach? Any advantages/disadvantages?

Answer 207

Uncommon. Can be considered in the setting of a hostile anatomy b/w the aortic root and LA dome (presence of calcified aortic homograft). Difficult closure, risk of narrowing R superior pulmonary vein, risk of transseptal incision progressing/tearing AV node -> high risk of PPM.

Question 208

For MV approach, when might transaortic be best approach? How is this done? Any advantages?

Answer 208

MV can be seen through an aortotomy after aortic valve resection. Aortotomy can be extended onto the dome of the LA. Useful in in endocarditis when both aortic and mitral valves need to be replaced (transaortic Commando). Exposure can be challenging, in which case the L atriotomy can be connected to an extended transseptal incision.

Question 209

For MV approach, when might left atrial appendage be best approach? How is this done? Any advantages?

Answer 209

Very uncommon. Left thoracotomy. Alternative approach after multiple previous re-operations via R side.

Question 210

For MV approach, when might transventricular be best approach? When is this done?

Answer 210

If entering the LV for another reason (ventricular aneurysmectomy or LVAD).

Question 211

Your patient is being evaluated for a mitral repair. They have a previous AVR complicated by a postop bleed requiring takeback then mediastinitis and sternal wound infection eventually requiring flap closure. How would you approach the mitral? How do you get on bypass? How do you arrest?

Answer 211

R anterolateral thoracotomy via 4th intercostal space centered at the anterior axillary line. Cannulate through femorals. Fibrillatory arrest under moderate hypothermia (requires competent AV). Endoballoon (requires competent AV).

Question 212

A patient s/p mitral repair surgery is coming off pump. The patient becomes hypotensive, and 3+ MR is noted with encroachment of the anterior leaflet onto the LVOT. What is the diagnosis and management? What would the effect of nipride be in this setting (eg before coming off pump, anesthesia tries to "make room for volume")? What else could make this worse?

Answer 212

The patient has SAM. Wait for volume and consider adding beta-blocker to ensure not simply underfilled. Then aim to reduce the POSTERIOR leaflet height - folding valvuloplasty, revise triangular repair to quadrangular w/ sliding annuloplasty. Place a larger ring. If all fails, replace the valve. If the patient is too frail to replace, do an Alfieri stitch. Nipride would accentuate the problem by underfilling the ventricle thus increasing ventricular systolic contraction. Inotropic support and reduced afterload could make things worse.

Question 213

Describe the pathophysiology of SAM after mitral surgery?

Answer 213

Mitral surgery changes the line of coaptation to displace it more anteriorly towards the LVOT. The Venturi effect causes the anterior leaflet to get sucked into the LVOT during systole. At the same time, the posterior leaflet prolapses towards the atrium, creating an anteriorly directed jet. SAM thus causes both mitral regurgitation and LVOT gradient.

Question 214

What increases the risk of SAM in mitral surgery? - posterior leaflet height - hyperdynamic ventricle - anterior leaflet relative size - aorto mitral plane angle - coapt to septum distance - IVS thickness - ring characteristics

Answer 214

Posterior leaflet is >1.5 cm in height after repair (ie it is tall). Small hyperdynamic ventricle. Ring is UNDERsized too much - causes line of coaptation to bulge anteriorly. AL:PL ratio <1.3 Aorto-mitral plane angle <120 degrees (pic - the closer to 90 degrees, the more the anterior leaflet is pulled into LVOT). Coapt/septum distance <25 mm IVS thickness >15 mm Anterior displacement of prosthetic ring.

Question 215

After MV replacement, bright red blood is welling up behind the heart after the cross clamp is released? What is the likely diagnosis? How could it have been prevented? What is the cause? What is the management?

Answer 215

**AV dissociation after mitral valve replacement/ AV groove disruption.** **Remember that this area sees the highest pressure in the body. You should've preserved the posterior leaflet and its subvalvular apparatus or been more careful with calcium debridement or reconstructed the posterior annulus after debridement.** Can happens up to hours after the procedure and is signaled by massive intrapericardial hemorrhage. Rupture occurs in the LV near the AV groove posteriorly. Tends to occur in women w/ small LVs. The cause is technical: - **too much traction on the annulus** during excision of the valve or insertion of the prosthesis - lifting the heart after valve replacement, tearing the annulus - stitching through the posterior AV groove - perforation from papillary muscle excision - perforation of the AV groove during calcium debridement Management: go back on pump and re-arrest. Open the LA. Remove the prosthesis. **Pericardial patch to recreate the annulus**. Reimplant the valve in the newly created rim. - if caused during repair, replace the valve and use the PL to buttress the patch repair and reduce tension on the suture

Question 216

Coming off pump from mitral surgery, ST changes are noted along the lateral leads (V5-V6) and the patient becomes hypotensive. What happened? What is the management?

Answer 216

Differential includes postcardiotomy syndrome and cardiogenic shock from reperfusion or poor protection. Most likely is damage to the circumflex from a bite near the anterolateral commissure or posterior leaflet annulus. Management: back on pump, harvest vein, bypass to distal OM.

Question 217

During mitral surgery, the left atrium is opened, and there is blood. You cannot see anything. What is your checklist?

Answer 217

Make sure there is a working vent/floppy sucker in the RSPV. Check the aortic cross clamp - ensure it is all the way across and occluding flow. Explore the septum for an ASD - can be evaluated from LA, but may require RA incision to repair. Increase drainage. If still issues, can cool more and decrease flow accordingly. Does the patient have AVMs?

Question 218

A patient has an indication for re-operative mitral valve replacement. What workup should be considered?

Answer 218

EKG - rule out AF CXR - count sternal wires CT - assess distance b/w sternum and RV/aorta/innominate vein, aortic Ca CTA gated - if hx CABG, know course and distance of vessels CT abd/pelvis - assess femorals, CPB strat Preop TEE - mitral path (especially re-repair) Cath - figure out CAD RHC - if LV or RV dysfunction Carotid duplex - older, vasc dz, coronary dz, neuro sx PFTs - if COPD ***Op note - what was done to valve, valve manufacturer/size/material if replacement prev, how was it exposed

Question 219

Can a mitral valve be re-repaired?

Answer 219

Yes. Re-repair is associated with lower mortality compared to replacement at reoperation. Severe calcification (leaflets, annulus, subvalvular apparatus) and extensive leaflet destruction (e.g., endocarditis) can prevent re-repairability. You will not be faulted for replacement in redo setting.

Question 220

How close is the circumflex to the PL mitral annulus? When would you suspect injury?

Answer 220

2-4 mm. Suspect injury: high-dose pressors when weaning. Pressor requirement persists. TTE shows lateral wall motion abnormality. EKG correlates w/ V5-V6 or 1 and AVL. * Right leads, V1-V2: Interventricular septum and right ventricle. Anterior leads, V3-V4: Anterior wall of the Left ventricle. Low lateral leads V5-V6: Low lateral wall. High lateral leads I and AVL: High lateral wall. Inferior leads II, III and AVF: Inferior wall.

Question 221

Redo mitral surgery is unable to be weaned from CPB w/o V-pacing. Monitor shows complete dissociation between atria and ventricles. What is diagnosis? What happened?

Answer 221

Complete heart block 2/2 AV node damage 2/2 deep/wide posteromedial mitral commissure stitch during MVR or ring annuloplasty.

Question 222

What are the differences between early and late prosthetic valve endocarditis in terms of timing, causative bacteria, and mortality?

Answer 222

Early: within 2 mo, Staph, higher mortality Late: Strep, lower mortality

Question 223

Discuss the difference in pathophys/anatomy of bio vs mechanical valve infection causing insufficiency.

Answer 223

Mechanical valve: infection localized to sewing ring -> abscess and dehiscence. Bio: infection in leaflets -> vegetations, leaflet perforation

Question 224

A pt is undergoing redo bio MVR. She asks if she will need a 3rd reoperation. What do you say? ie What do the stats show?

Answer 224

Freedom from reoperation at 15 yrs is 80% w/ bio valves in mitral position.

Question 225

What are the hemodynamic differences in bio mitral vs aortic valves in terms of their degeneration? Are there other considerations in bio valve choice for young patients?

Answer 225

Mitral valves are exposed to increased hemodynamic stress during systole, so deteriorate faster. Valve design has improved, and transcatheter valve-in-valve is an option to avoid re-operation.

Question 226

During MV replacement, what is the ideal management of the chords and leaflets?

Answer 226

Try to spare them - improved outcomes. But do not compromise outflow.

Question 227

Define severe symptomatic mitral stenosis. What are measurements/echo findings? What are associated symptoms?

Answer 227

Severe findings: Mitral valve area ≤1.5 cm2 - Diastolic pressure half-time ≥150 ms - Severe LA enlargement - Elevated PASP >50 mm Hg Symptoms: - Decreased exercise tolerance - Exertional dyspnea Diastolic pressure half time = time it takes for the initial maximal pressure gradient across the valve to fall by 50% during diastole

Question 228

How do you manage the anticoagulation in a pregnant woman with a mechanical valve? How is the VKA risk profile? What if anything else can or should be used?

Answer 228

Maintain therapeutic anticoag w/ frequent monitoring. VKA has lowest maternal complications but highest likelihood of miscarriage, fetal death, and congenital abnormalities (esp 1st trimester and at dose >5). Use LMWH instead to target anti-Xa 0.8 - 1.2. Switch to UFH 6 hrs before delivery. If urgent delivery needed, reverse VKA and do C-section. (3:Harm - Must use anti-Xa for LMWH monitoring, dabigatran cannot be used, DOACs have not been assessed and shouldn't be used).

Question 229

A pregnant woman with mechanical prosthetic valves undergoes an embolic event. What workup should they undergo? How should they have been counseled pre-pregnancy?

Answer 229

TEE. Same goes if there is a prosthetic valve obstruction. Pre-pregnancy: Should have gotten echo, seen cardiologist w/ expertise in pregnant VHD patients. Mechanical VHD pregnant pts in particular should be at a tertiary-care center w/ MDT. They should be told that pregnancy is high-risk, and that there is no anticoagulation strategy consistently safe for the mother and baby. Women should receive therapeutic anticoag w/ frequent monitoring during pregnancy. If they cannot maintain therapeutic levels, they should be counseled against pregnancy.

Question 230

A pregnant women w/ severe valve regurgitation has NYHA class III or IV HF symptoms (stage D) refractory to medical therapy. What can be offered? What if they don't have HF symptoms?

Answer 230

Valve surgery (2a). In pregnant pts w/ severe disease w/o severe and refractory HF symptoms (at rest or with min activity), valve surgeries should NOT be performed (3:harm). If she had severe valve disease before pregnancy, she should have had this taken care of.

Question 231

A pregnant female with severe AS has NYHA class III or IV symptoms. What should be done?

Answer 231

valve intervention is reasonable AS = mean gradient 40, V max 4, AVA <1

Question 232

A pregnant female presents with new symptoms from known severe mitral stenosis. What should you do? What should they have had done before pregnancy? Do women who are considering pregnancy have different indications for intervention?

Answer 232

They should get TTE, be seen at a center w/ expertise, and consider exercise testing if asymptomatic and suspicious. Meds to consider are beta-blockers, diuretics. DO NOT give ACEi or ARBs. Intervention has standard indications. Prefer bio valves. Best management would have been to counsel a pt of childbearing age that they should have their MS treated first. *** MS = valve area <1.5 or diastolic PHT >150 (speed at which the LV fills in diastole based on the slope of the change in gradient) 1st: medical therapy. 2nd: PMBV.

Question 233

A pt w/ rheumatic mitral stenosis has severe (<1.5 cm) findings but is asymptomatic. What workup do they need? What are you looking for? What are you trying to rule out with above workup? What should they have done?

Answer 233

Figure out PASP and if AF. So get TTE, TEE, LHC/RHC. If PASP >50 mm Hg or New AF -> Ensure no clot, valve pliable and not much MR (<2+) -> PMBC (perc mitral balloon commissurotomy) at CVC.

Question 234

A pt w/ rheumatic mitral stenosis has severe (<1.5 cm) findings. What are the best options for treatment?

Answer 234

Commissurotomy - either percutaneous or open.

Question 235

What is the population of patients with rheumatic MS that should get SURGICAL (as opposed to percutaneous) commissurotomy?

Answer 235

Severe (<1.5 cm MVA) + Symptomatic (dyspnea on exertion/dec exercise tol) + Not candidate for PMBC (valve not pliable [Wilkin's score >9], clot, >2 MR) + Surgical candidate.

Question 236

In an MS patient undergoing open surgical approach, what leaflet characteristics might show better results with mitral replacement?

Answer 236

severe valvular **thickening** and subvalvular **fibrosis** with leaflet **tethering**

Question 237

Which rheumatic MS patients should get intervention if they are asymptomatic.

Answer 237

Severe findings (<1.5 cm MVA) + PMBC candidate (pliable valve, no clot, <2+ MR) + New onset AF OR PASP >50 mm Hg.

Question 238

Is someone with progressive MS (>1.5 cm MVA) a candidate for MV intervention? What are their options?

Answer 238

Yes. IF... Exertional symptoms. Confirmed: Stress test shows hemodynamically significant MS. PMBC candidate: pliable valve, no clot, <2+ MR. ONLY PMBC offered.

Question 239

A patient has severe MS and has severe symptoms. The junior fellow wants to do surgery. What should you tell them?

Answer 239

There needs to be a reason not to do PMBC. Figure out if... valve is not pliable, clot is present, or MR is >2+. Then they have to be surgical candidate.

Question 240

A patient with symptomatic severe MS is being evaluated for intervention and is found to have moderate to severe TR. Which approach for intervention may be most favorable?

Answer 240

open surgical to include a tricuspid repair

Question 241

A patient with severe symptomatic mitral stenosis also has AS, TVR, and CAD that requires surgery. What is the conduct of this operation?

Answer 241

Bicaval CPB. LV vent. Consider retrograde plegia. Distal coronaries. Aortic valve is excised - break it down. MVR - don't oversize - ensure AV won't be small. AVR. Proximal coronaries. Unclamp but stay on CPB w/ total bicaval. TVr - can be done w/o clamp. Wean CPB.

Question 242

How do you manage mitral annular calcification when considering surgery for mitral stenosis?

Answer 242

Usually old, frail, debilitated patients. DELAY intervention until severely limiting symptoms unable to be managed w/ diuresis and HR control. Some catheter-based strategies are being developed. Surgery may require radical debridement of the annulus down to pericardial fat, reconstruction with pericardial patch that saddles/sandwiches the annulus, then valve placement with sutures from LV to patch to LA to sewing ring. High risk for AV groove disruption, block, and coronaryr injury.

Question 243

A mitral valve surgery is completed, and the cross clamp is removed. The heart is beating, but the LV distends. What should be done to evaluate? What is the likely diagnosis? What should be done if this diagnosis is confirmed?

Answer 243

TEE. Aortic insufficiency 2/2 anterior annular mitral stitches in the non-coronary or L cusp. Rearrest, open the aorta and LEFT atrium, and remove suture or redo the mitral surgery. Repair the aortic cusp or replace it.

Question 244

How can you cause conduction block during mitral surgery?

Answer 244

Sutures too deep near the posterior leaflet near the PM commissure - bundle of His.

Question 245

After mitral surgery, what would cause increased gradients across the LVOT? What do you do?

Answer 245

Prosthesis problem: high-profile mechanical valve, large stented bio valve posts (should be arranged such that the post is not at the LVOT), poorly seated valves. Could also be SAM - if you keep the anterior leaflet, it can crowd into the LVOT. Either way… Diagnose on TEE, and may need to replace the valve w/ lower profile.

Question 246

What is a risk in mitral surgery if you leave the anterior leaflet unresected in a patient with septal hypertrophy? What do you do?

Answer 246

SAM. Stop inotropes, load, add betablocker, and add vasopressors - inc afterload and preload while reducing contractility (you can attempt these maneuvers for SAM after mitral surgery, but not after a myectomy for HOCM). You may need to do an aortotomy and do a transaortic excision of the offending subaortic mitral tissue +/- myectomy.

Question 247

After mitral replacement, there is perivalvular leak on postop echo. What info do you need? How do you manage?

Answer 247

Small leaks stop after protamine. Significant leaks require reimplantation or repair.

Question 248

What are important, specific postoperative hemodynamic and clinical parameters after MVR for MS?

Answer 248

Respiratory status - Many patients require aggressive diuresis. Optimizing CO2 and O2 also contributes to optimized PA pressures and avoidance of R heart failure. Pulmonary pressures - Inotropy and pulmonary vasodilation may be required. "High and dry."

Question 249

What is the INR goal for mechanical MVR?

Answer 249

2.5-3.5. This is higher than AC goal for atrial fibrillation, so it still increases risk in patients already on AC.

Question 250

What complication will occur in mitral surgery if there is aggressive debridement or retraction/lifting of the heart? How do you prevent this?

Answer 250

AV groove disruption/rupture. Prevent by minimizing retraction, preserving the posterior leaflet and its subvalvular apparatus, and using increased caution during debridement in pts w/ annular calcification.

Question 251

What are the three principal goals of surgical intervention for AF?

Answer 251

1) **conduction block** of all micro and macro re-entrant circuits 2) reestablishment or maintenance of electrical **AV synchrony** 3) restoration of **atrial mechanical function** in order to improve diastolic filling (no re-entry circuits, good AV synchrony, good atrial kick)

Question 252

When can stand alone surgery be done for AF?

Answer 252

Symptomatic AF. Refractory to class I/III AADs and/or catheter-based therapy (class IIA, level of evidence [LOE] B-R). According to The Society of Thoracic Surgeons (STS) 2017 Clinical Practice Guidelines for the Surgical Treatment of Atrial Fibrillation, primary stand-alone SA is a reasonable procedure.

Question 253

During Cox Maze, you are dissecting the transverse sinus when you see dark blood beginning to pool. What is the likely injury?

Answer 253

R PA.

Question 254

A patient with ascending aorta aneurysm is undergoing aortic valve or CABG surgery. What is cutoff to add aorta intervention?

Answer 254

4.5 cm end-diastolic diameter.

Question 255

A pt w/ mitral regurg and atrial fibrillation undergoes mitral repair and Cox Maze IV w/ LAA. 2 wks postop, she has palpitations w/ a-flutter in 160s. What is happening?

Answer 255

Peri-mitral flutter. Failure to interrupt conduction across the "LA isthmus" allows for this. It is the most common mode of failure of surgery for AF. LA isthmus (MV isthmus) - linear lesion connecting the box to the mitral annulus.

Question 256

A pt has peri-mitral flutter after mitral repair w/ CMIV and LAA ligation. What is the cause and what can be done?

Answer 256

Conduction across the LA isthmus d/t incomplete lesion line involving the MV annulus. EP can do catheter intervention to complete the ablation line.

Question 257

For AF, a large macro-reentrant circuit develops just above the mitral valve annulus. Which lesions must be completed in regards to preventing ongoing flutter (peri-mitral flutter)?

Answer 257

Mitral line (prevent conduction across the atrial myocardium, AKA LA isthmus) from the "box" to mitral valve. Coronary sinus lesion (prevent conduction across the coronary sinus; collapse the CS during cryoablation so a circumferential lesion can be assured; should connect to the level of the mitral annulus). Place both lesions in the same plane. Transmural ablation (epicardium and endocardium) is key.

Question 258

While performing CMIV, you notice a cryolesion across the pericardial surface of the RA. What complication can you expect?

Answer 258

**Hemidiaphragm paralysis** from damage to the **R phrenic**. This is usually temporary. Make sure the handle of the probe is not in contact with the phrenics (R or L).

Question 259

What are the principles of ensuring a CMIV doesn't fail?

Answer 259

A single break in the line can preserve a macro reentry circuit. These waves will find the weakness. Lesions should be uniformly transmural and contiguous. Ensure minimal tissue folding. Clean the tips of the clamp. Multiple burns per line.

Question 260

In CMIV surgery, can char on the RFA clamp affect outcome?

Answer 260

Yes. The RF clamp relies on perfect contact b/w the tissue and electrodes. Char isolates and disrupts this contact, which can affect tissue from heating, breaking the line, and allowing macro-reentrant circuits through. It is recommended to clean the clamp after every 3 ablations.

Question 261

What is the ligament of marshall? What is its importance in AF/CMIV?

Answer 261

It's an epicardial vestigial fold that marks the location of the embryologic LEFT SVC. It contains the nerve, vein of Marshall, and muscle tracts. It is located on the epicardium between the left atrial appendage and the left pulmonary veins. The corresponding endocardial structure is the LA ridge. It is a source of paroxysmal AF. It helps to dissect it out to get better atrial clip during CMIV. Watch out for L Cx.

Question 262

In CMIV procedure, you cannulate, place the pt on bypass, and place an LV vent. You are exposing the L heart for LPV isolation. You divide the ligament of Marshall, then notice a device protruding through the LAA. What happened?

Answer 262

Rare. You may have compromised the position of the LV vent by accidentally entering the LA. It is still necessary to divide the LoM to access behind the L pulmonary antrum for L PV isolation. Close the defect. Finish the case.

Question 263

You perform a CMIV w/ LAA clip placement. TEE shows a small pouch with clot in the appendage. What happened?

Answer 263

The clip was not placed at the base of the appendage. It should be placed under direct visualization, otherwise a small pouch can be a source of thrombus.

Question 264

In CMIV, what is an alternative to LAA clip? What are some risks with this?

Answer 264

LAA amputation. This will **not remove macro-reentry circuits** at the base. If this is done, you must anchor the **base to the PV isolation box**. Can cause **bleeding** through the suture line or from tributaries at the AV groove near the coronary sinus.

Question 265

During CMIV procedure, after securing Atriclip or amputation of the LAA, the patient is noted to have EKG changes with T wave inversions in the lateral leads. What are you concerned about?

Answer 265

Injury to L circumflex coronary artery causing MI at the time of LAA isolation. This occurs if the LAA orifice is unusually low (normally at level of frenulum b/w L PV several cm away from MV annulus), and the L Cx is unusually high (normally in the AV groove slightly below the coronary sinus).

Question 266

During CMIV, after completion of the RA appendage line, you come off CP bypass and notice the pt in complete heart block. What happened?

Answer 266

Damage to the AV node - cryoprobe too posterior. Damage to the SA node - prevent by placing the final RA lesion from the distal end of the vertical atriotomy to the tip of the RA appendage. Go as far laterally and posteriorly as possible to avoid the pacemaker complex (anterior and medial). Sinus node dysfunction was higher with biatrial lesion sets than left atrial only (40% vs 11.5%). | RFA directed up SVC as far lateral/posterior as possible to avoid SA.

Question 267

What patients may be candidates for a stand alone CMIV?

Answer 267

In patients who meet all 3: - failed or are intolerant to antiarrhythmic drug therapy - failed catheter ablation in the EP laboratory - feasible minimally invasive approach It is reasonable to attempt this procedure. Principle: failed other options and can get min invasive.

Question 268

A patient w/ MR requiring open surgery (TV is nl) has AF as well. Discuss the evidence for PVI (L side only) vs full CMIV.

Answer 268

In a series of 305 patients, there was an equal efficacy of a left-only approach, but a higher pacemaker implantation in those who underwent a biatrial lesion set. Both of these findings were confirmed on a meta-analysis of 2225 patients from 10 studies. The equivalent sinus restoration is supported by a randomized subgroup analysis of mitral valve patients that compared patients undergoing biatrial Mazes with pulmonary vein isolation alone. There is an increased risk of recurrent AF with PVI only.

Question 269

A patient w/ MR requiring open surgery (TV is nl) has AF as well. Discuss the evidence for PVI (L side only) vs full CMIV.

Answer 269

In a series of 305 patients, there was an **equal efficacy of a left-only approach, but a higher pacemaker implantation in those who underwent a biatrial lesion set**. Both of these findings were confirmed on a meta-analysis of 2225 patients from 10 studies. The equivalent sinus restoration is supported by a randomized subgroup analysis of mitral valve patients that compared patients undergoing biatrial Mazes with pulmonary vein isolation alone. However, in a 2008 analysis of 1723 patients, **absence of a biatrial lesion set was a predictor of failure at 48 months.** This finding was also supported by a 2006 meta-analysis of 5885 patients in 69 studies. It is currently unknown which patients do better with a biatrial set. Overall, many surgeons suggest **PVI alone for pts w/ comorbidities who cannot tolerate a lengthier operation (especially if it is an isolated mitral) and full CMIV for those with persistent or recurrent AF**.

Question 270

A patient is undergoing minimally invasive pulmonary vein isolation (PVI), but thrombus is discovered on TEE. What should you do?

Answer 270

Convert to open. *STS E Book: For patients with left atrial clot found on Preop TEE for stand-alone surgical ablation, a trial of anticoagulation therapy is reasonable, with the persistence of thrombus in spite of therapeutic anticoagulation indicating the need for a classic CM procedure in patients who are fit for surgery.

Question 271

A patient s/p Cox Maze decades ago cannot develop sinus tachycardia during exercise. What happened?

Answer 271

One should avoid placing an ablation line through the "sinus tachycardia line" at the right atrium. This can lead to an inability to generate an appropriate response to normal exercise. This was a common complication with CMI (30%).

Question 272

Where is Bachmann's bundle (CMIV surgery)?

Answer 272

Medial and superior to the roof lesion - transecting this will delay the arrival of a sinus impulse from the RA to the LA.

Question 273

What is the "flutter line" and "isthmus lesion"? Why should it be avoided during CMIV surgery?

Answer 273

It is across the cavo-tricuspid isthmus (CTI) - damage results in the inability to develop appropriate bradycardia when asleep. That said, in patients with cavotricuspid isthmus (CTI)-dependent atrial flutter, ablation along the CTI may be necessary (pic).

Question 274

Define severe TR? What will symptoms be?

Answer 274

Vena contracta width ≥0.7 cm. Central jet ≥50% RA. Regurgitant volume ≥45 mL. ERO ≥0.40 cm2. Dense continuous wave signal with triangular shape. Hepatic vein systolic flow reversal. These pts develop dilated RV and RA w/ elevated RA with “c-V” wave. Symptoms include dyspnea on exertion, fatigue, ascites, edema.

Question 275

Which patients with progressive TR (stage B) can get surgical intervention?

Answer 275

3 Requirements: * Stage B: Central jet <50% RA, Vena contracta width <0.7 cm, ERO <0.40 cm2, Regurgitant volume <45 mL. * MUST BE during **L side valve** procedure. * AND have **annular dilation >4.0 cm** OR **prior RHF**. TV surgery for this pt has a 2a indication.

Question 276

What are indications for surgery for severe TR? Differences in recommendations b/w primary and secondary?

Answer 276

Only level 1 indication is during L side valve surgery. If RHF (symptomatic; stage D): - primary TR has 2a indication. - secondary TR surgery if: poor GDMT response AND annular dilation WITHOUT inc PAP (2a). - prior L side valve surgery WITHOUT PH or severe RV dysfx has 2b indication. If asymptomatic (stage C): primary TR w/ progressive RV dilation or sys dysfx has 2b indication. Severe TR: Central jet ≥50% RA, Vena contracta width ≥0.7 cm, ERO ≥0.40 cm2, Regurgitant volume ≥45 mL, Dense continuous wave signal with triangular shape, Hepatic vein systolic flow reversal.

Question 277

During TV surgery, where will the AV node be?

Answer 277

Triangle of Koch

Question 278

In which direction does the tricuspid annulus dilate?

Answer 278

Septal is fixed. Will dilate posteriorly more than anteriorly.

Question 279

How should the tricuspid valve be addressed if taking to the OR for a L valve? IE what is the order of the surgery?

Answer 279

Do L side lesions first. Tricuspid can be addressed with the heart beating (PFO must be closed before unclamping).

Question 280

Describe a tricuspid ring annuloplasty.

Answer 280

Interrupted mattress sutures with a gap a Koch's triangle (1cm from anteroseptal commissure to midpoint on septal leaflet).

Question 281

During tricuspid annuloplasty, what can be injured when placing sutures near the anteropostero commisure?

Answer 281

RCA.

Question 282

How do you select ring size for tricuspid annuloplasty?

Answer 282

Measure the septal leaflet and surface area of leaflet tissue arising from the anterior papillary muscle. Usually 30-32 mm for female, or 32-34 mm for male.

Question 283

What are the major principles for tricuspid replacement?

Answer 283

Preserve native leaflets, similar to mitral (unless infected). When placing sutures near the AV node, place them through the septal leaflet instead. Don't place sutures too deep at the anteroposterior commissure.

Question 284

Principles of the surgery for tricuspid endocarditis: Can you simply excise vegetations? What are the decision making points? Do you have to replace the TV if it is resected (ie IVDU)?

Answer 284

If not extensive damage, can excise vegetations to healthy tissue. Close gaps primarily or with a patch. Consider annuloplasty if valve incompetence is in question. Replace the valve if extensive destruction. 2-stage replacement can be considered in IVDU with normal RV fct and PAP (fallen out of favor).

Question 285

Benefits of tricuspid bioprosthesis over mechanical? How does it compare to L side bio valves? All other things being equal, which would you choose (bio vs mech tricuspid) if you expect heart block?

Answer 285

Bio - No anticoagulation. Bio - Less structural valve deterioration than those in mitral position. BIo - Does not limit transvalvular PM leads in the future, so better choice if expecting heart block. *Be careful placing Swan postop.

Question 286

When coming off pump following TV replacement, the RV dilates, CVP is high, and PAP decreases. How do you manage?

Answer 286

First, make sure the patient is safe - consider full bypass if you're not off and adding support from anes side. Rule out metabolic issues and air emboli - labs and eval ST elevation to see if improving. TEE for assessment. Eval RVOT for obstruction: eg, anterior leaflet tissue billowing -> central portion can be excised while maintaining chordal attachments. Eval for ST changes from RCA occlusion (inferior leads; caused w/ deep stitch at ant/post commissure) -> bypass RCA w/ vein. Make sure there's a Swan-Ganz that's surgeon directed after this procedure (cannot do if mechanical). If above ruled out, and pt has RHF, may not be able to come off. Transition to ECMO. You would expect CVP and PA pressures to go up some because the "popoff" that TR creates is now gone, and the RV is having to push all blood through the pulmonary system.

Question 287

Manage RV dysfunction postop TV repair?

Answer 287

Similar principles to other RV failure: Improve hypoxia and decrease hypercarbia. Decrease pressure in lungs. Support contractility/inotropy w/ Epi, increase lusitropy (and inotropy) w/ Milrinone. Restrict fluids. Diurese. Can add nitric to vent or HFNC to unload PA more w/ less systemic effects than milrinone. Can use IABP to unload even more and improve RCA perfusion. If absolutely needed, can place a R Impella, RA/PA Oxy-RVAD, or VA ECMO.

Question 288

When should an isolated tricuspid valve be done in a reoperative patient?

Answer 288

Principle: valve has to be bad, but pt can't be too sick. * Stage D (Central jet ≥50% RA, Vena contracta width ≥0.7 cm, ERO ≥0.40 cm2, Regurgitant volume ≥45 mL, dense continuous wave signal with triangular shape, Hepatic vein systolic flow reversal; AND RHF symptoms). * No severe PH or severe RV systolic dysfunction. | 2b rec from 2020 ACC/AHA

Question 289

Coming off CPB from TV surgery, the patient has complete heart block. What happened? What do you do?

Answer 289

Sutures near the anteroseptal-septal commissure can easily damage the AV node. Radial force from a prosthetic valve (or dual prosthetics in the MV and TV position). 2 sets of V pacing wires would not be overkill; in addition to external pacing pads before eventual PPM placement.

Question 290

What are options for pacemaker placement after tricuspid surgery?

Answer 290

Endocardial - percutaneous into atrium, then coronary sinus. - if unable to get into coronary sinus, can traverse repaired valve. Epicardial - avoids foreign object through repair/replacement. Only option for mechanical valve.

Question 291

Pt w/ TV endocarditis (+ cultures, and vegetations) has previous PPM, and has an indication for mitral surgery. How do you handle the pacer leads?

Answer 291

Remove the initial wires in setting of bacteremia and endocarditis. New epicardial leads on the RV can be placed (tunneled through the L intercostal space away from the mammary and out to a subcutaneous pocket). Transvenous atrial wires can be placed later if needed or if bacterial burden is too high on initial surgery. "Optimal therapy for cardiac device IE combines complete device extraction and a prolonged course of parenteral antibiotics with complete device and lead removal, even if evidence for infection appears to be limited to the generator pocket site." 2020 Guidelines

Question 292

In carcinoid valvular disease, what is the gross appearance and management of an affected TV?

Answer 292

Grossly, you will see white fibrous tissue deposits/plaques on the endocardium of valve cusps on the ventricular side, causing adherence to the RV wall. TV replacement required. Check pulmonic valve - may need to be replaced as well. L heart valves are not affected d/t inactivation by MAO as it passes through the lungs. ## Footnote A, TV in systole. B, Severe TR. C, Continuous wave Doppler w/ severe TR and TS. D, 3D en face of the TV. E, 3D ventricular view of the TV. F, Surgical findings.

Question 293

What's the best study for tricuspid valve?

Answer 293

Preoperative TTE. This is where you will make your decisions.

Question 294

Before performing TV repair with a beating heart, what anatomic pathology must be ruled out?

Answer 294

PFO. Otherwise air gets into the L side.

Question 295

A patient who is undergoing left side valve surgery gets a LHC preop. What is your cut off to bypass a lesion? What about LM lesions?

Answer 295

70% any lesion. 50% LM. *2021 ACC/AHA/SCAI Guidelines Limited data are available comparing CABG for intermediate CAD (stenosis, 40%–69%) in patients undergoing other cardiac surgery. Observational studies comparing patients undergoing AVR with and without CABG for intermediate CAD suggest that the addition of CABG may reduce ischemic events. Patients with intermediate CAD may benefit from physiological testing with iFR or FFR to guide decision-making.

Question 296

You are coming off bypass from an AVR CABG w/ a 2 hr cross-clamp time. CI is 1.7. What do you do to assess? What do you do if no technical problems?

Answer 296

Look at the heart and the EKG. TEE to eval for MWAs. Assess grafts with flow probe. Determine if there were issues with cardioplegia - if all above ruled out, it could be cardiogenic shock from poor protection. Rest the heart on full flow with the heart completely decompressed for 10-15 min. May require IABP if chemical support doesn't cut it. If the pt worsens over the next 12 hrs, consider catheterization to assess grafts.

Question 297

Sequence of surgery for CABG/MVR/AVR in pt w/ AF?

Answer 297

Distals, aortotomy w/ AV resection, CMIV, MVR, AVR, proximals.

Question 298

You are finishing an AVR/MVR when TEE shows lateral WMA. What happened? What do you do?

Answer 298

You've injured the circumflex likely during the placement of posterior leaflet mitral valve sutures. Re-heparinize and go back on bypass. Take vein, and bypass the circumflex. Keep in mind that you have a new mitral that could be easily dislodged, or you could cause an AV groove disruption when exposing the lateral wall. You cannot just remove the stitch. You've ligated the circumflex and caused irreperable damage.

Question 299

What complications could oversizing the mitral valve cause?

Answer 299

LV rupture when the heart is contracting after coming off CPB. Higher risk of block requiring PPM. If concurrent with AVR, then oversizing MV can cause downsizing of the aortic valve -> pt prosthesis mismatch.

Question 300

A patient has severe AS and severe MR. He is induced and subsequently arrests. What happened? What do you do?

Answer 300

SVR drops, venous return decreasing, coronary flow decreases, ventricles fail. The incidence of arrest on induction is higher for combined pathology than for isolated severe AS. Secure the airway. Ventilate. Begin CPR/ACLS. Heparinize. Prep/drape/scrub. Emergency sternotomy and quick cannulation. Initiate CPB. Proceed with AVR/MVR. If truly worrisome preop, consider awake line placement, and prep and drape before induction w/ sheaths in the groin and a sternal saw working.

Question 301

What important structure is behind p2-p3 of the mitral valve?

Answer 301

Circumflex artery

Question 302

After an AVR/MVR, you are coming off bypass and see bright red blood coming from behind the heart. What do you do? (What do you NOT do?) What increases risk for this complication?

Answer 302

Do NOT lift the heart. This is likely AVG disruption. Go back on bypass first, then repair - depending on location, can do an internal patch repair, external primary repair with pledgets or strips. Risks: extensive annular decalcification near the posterior leaflet, use of an oversized prosthesis, or excessive traction on the left ventricle

Question 303

What is the conduct of an AVR/MVR?

Answer 303

Open aorta, excise leaflets and debride annulus, explore mitral and *do NOT oversize if requiring replacement (size aortic valve at the same time to determine if adequate AV prosthetic will fit), replace mitral, re-size aortic valve, replace aortic valve. *If mitral is oversized before you fit AV, you may end up with prosthesis mismatch.

Question 304

During AVR/MVR, what structure is near mitral lateral A3 and the membranous septum of the aortic valve near the R and non-coronary cusps?

Answer 304

Conduction system. Don't oversize valves - can compress this system. Place A and V wires on all double L valve cases. PPM risk is 5% for single valve. It's 15% for >1 valve.

Question 305

A pt undergoes AVR/MVR. You come off bypass, and TEE shows the following, with increased gradient across the LVOT. What happened?

Answer 305

MV strut is directed into the LVOT. Re-replacement of the valve should be done. This is more likely with bioprosthetic valves. These valves usually have markings for their struts that allow the surgeon to orient the valve in such a way that the space between the struts is over the LVOT.

Question 306

In pt with significant multivessel CAD and significant carotid disease, how do you decide which to approach first?

Answer 306

Most symptomatic should go first with a 4-6 waiting period before second surgery. If both are symptomatic, can do synchronous procedure.

Question 307

After a combined CEA and CABG, the patient has neuro deficits associated with operative CEA. What do you do?

Answer 307

If immediately postop, would get bedside ultrasound evaluation of flow and return to the OR if flap or technical problem is found. If out of PACU, would get head CT and carotid duplex.

Question 308

After a combined CEA and CABG, the pt develops a large neck hematoma with tracheal deviation. What do you do?

Answer 308

If time permits, the patient should go to the OR, prep and drape FIRST. Then intubate, then reopen. If not, open at bedside and be ready to hold pressure while you get to OR and intubate.

Question 309

What are the major Duke criteria for endocarditis?

Answer 309

Major: microbio (atypical requires time b/w 2+ cxs or 3/4+ cxs); endocardial involvement (new regurg, abscess, vegetation, dehiscence of prosthetic). Positive is 2 major, 1 major and 3 minor, or 5 minor.

Question 310

What are the MINOR Duke Criteria? Are there minor echocardiographic criteria?

Answer 310

Predisposition – Intravenous drug use or presence of a predisposing heart condition (prosthetic heart valve or a valve lesion associated with significant regurgitation or turbulence of blood flow). Fever – Temperature ≥38.0°C (100.4°F). Vascular phenomena – Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, or Janeway lesions. Immunologic phenomena – Glomerulonephritis, Osler nodes, Roth spots, or rheumatoid factor. Microbiologic evidence – Positive blood cultures that do not meet major criteria, OR serologic evidence of active infection with organism consistent with IE. *There are no echocardiographic minor criteria.

Question 311

How can the diagnosis of infective endocarditis be rejected (4 scenarios)?

Answer 311

A firm alternate diagnosis is made. Resolution of clinical manifestations occurs after ≤4 days of antibiotic therapy. No pathological evidence of infective endocarditis is found at surgery or autopsy after antibiotic therapy for four days or less. Clinical criteria for possible or definite infective endocarditis is not met.

Question 312

What are the positive echocardiographic findings for infective endocarditis? (and thus fulfill a major Duke criteria)

Answer 312

-Vegetation (oscillating intracardiac mass on a valve or on supporting structures, in the path of regurgitant jets, or on implanted material, in the absence of an alternative anatomic explanation). -Abscess. -New partial dehiscence of prosthetic valve. -New valvular regurgitation. | Other major: 2 (+) blood cxs of typical organisms from separate sites

Question 313

What are the principles of empiric antibiotic therapy in suspected infective endocarditis?

Answer 313

For patients with suspected IE who present WITHOUT acute symptoms, empiric therapy is NOT always necessary, and can be deferred until blood culture results are available, particularly since accurate microbiologic diagnosis is a critical first step in planning the treatment strategy. For acutely ill patients with signs and symptoms strongly suggestive of IE, empiric therapy may be necessary. Such empiric therapy should be administered only after at least two (preferably three) sets of blood cultures have been obtained from separate venipunctures and ideally spaced over 30 to 60 minutes.

Question 314

What should empiric antibiotic therapy cover in IE?

Answer 314

In general, empiric therapy should cover staphylococci (methicillin-susceptible and methicillin-resistant), streptococci, and enterococci. Not necessary to use empiric abx if pt is not in septic shock or high risk. Start after cultures x3 obtained (VHD pts should not get empiric abx after fever if no cultures sent - COR 3:Harm) Those assd w/ drug use should be referred for addiction treatment (COR 1).

Question 315

When should a TTE or TEE be repeated during treatment course of infective endocarditis?

Answer 315

Clinical indications for repeat TTE and/or TEE include new murmur, embolic complications, new or progressive heart failure, and development of atrioventricular block. In addition, patients with persistent fever or persistent bacteremia (eg, longer than five to seven days) warrant repeat echocardiography to evaluate for abscess.

Question 316

What is the role for ASA or antithrombotic therapy for infective endocarditis (preop)?

Answer 316

neither anticoagulant therapy nor aspirin reduces the risk of embolism in patients with IE; remember that pts w/ IE are also at increased risk for bleeding complications (particularly intracerebral) 2020 ACC/AHA: in patients who are taking VKA at time of IE dx, consider stopping (2b)

Question 317

In pts w/ VHD, what atrial fibrillation pts require anticoagulation no matter the CHA2DS2-VASc score?

Answer 317

rheumatic mitral stenosis or mechanical valves (2020 ACC/AHA Guidelines)

Question 318

What IE pts need to be screened with dental evaluation?

Answer 318

IE due to common oral organisms. All active sources of oral infection should be eradicated.

Question 319

What further screening is needed if IE is due to group D streptococci?

Answer 319

colonoscopy is warranted - association w/ cancer

Question 320

When should IE on R side valves receive surgery?

Answer 320

Indications for surgery in R NVE include: - very large vegx (≥20 mm) - recurrent septic pulmonary emboli - highly resistant organisms - persistent bacteremia

Question 321

When should early valve surgery be performed for L side IE?

Answer 321

* Heart failure (HF) symptoms - benefits of surgery appear to be greatest among patients with severe valve dysfunction causing HF, surgery should be undertaken as soon as **signs and symptoms of HF** appear and before hemodynamic instability occurs. * Complicated infection - **paravalvular** extension of infection with development of **annular** or **aortic abscess**, destructive **penetrating lesion** (eg, **fistula**), and/or **heart block** * Difficult-to-treat pathogens - include **fungi** and multidrug-resistant organisms (eg, **Pseudomonas aeruginosa**, **S. aureus** [yes, even S aureus], and **vancomycin-resistant Enterococcus**). * Persistent infection - bacteremia or fever lasting **>5 days** (not 7) after initiation of appropriate antibiotic therapy.* | 2020 Valve Guidelines consulted - level 1 recs

Question 322

For neuro symptoms associated with IE (in pt w/ indication for surgery), should surgery be delayed?

Answer 322

Depends on how severe and what kind of stroke. No delay: silent microembolism, transient ischemic attack, cerebral abscess, or ischemic stroke with no hemorrhagic conversion and without severe neurological impairment or decreased level of consciousness. For patients with major ischemic stroke (ie, with severe neurologic deficit or altered consciousness), or intracranial hemorrhage, many would delay surgery for ≥4 weeks.

Question 323

In the setting of active infection in a pt w/ IE and a surgical indication, is repair or replacement preferred?

Answer 323

Valve REPAIR is preferable to valve replacement when feasible; valve replacement is associated with a small risk of infection of prosthetic materials. Valve repair may be possible when a leaflet perforation occurs in the absence of extensive leaflet destruction or annular involvement. Also, there is no increased reinfection risk b/w mechanical and bioprosthetic valve installed after IE.

Question 324

How does a prosthetic valve affect the decision for surgery for IE (PVE)?

Answer 324

Early surgery for prosthetic valve endocarditis is indicated for IE complications **SIMILAR** to native valve endocarditis (eg, HF due to prosthetic valve dysfunction, paravalvular regurgitation, or intracardiac fistula; annular abscess, difficult-to-treat pathogen, persistent infection). If presistent fever w/o bacteremia or new murmer, get **TEE** to help dx PVE. If too much shadowing, **CT cardiac** is less affected by the shadowing of mechanical valves. If still trouble diagnosing (infection tends to be at annulus and won't show leaflet abnormality as much as NVE does; ie fewer vegetations), and no other sources found, get **FDG PET/CT** to eval the heart valve. If no other source of persistent bacteremia (relapsing infections), heart valve infection must be presumed. PVE has higher mortality and post-tx HF-related disability compared to NVE. S aureus is most common pathogen for PVE (23%). Mortality is as high as 70%.

Question 325

You are doing preop work for AV IE and find an annular abscess at the R/non-con commissure. What do you do in the OR? What complications should you watch for?

Answer 325

Completely unroof the abscess and debride grossly infected tissue. Patch the defect w/ autologous or bovine pericardium. Involvement of a large part of the annulus may require replacement w/ homograft/xenograft (muscular portion may fill in tissue defect after extensive debridement). The R/non-con is the site of the membranous septum, so **VSD** can occur w/ aggressive debridement. R/non-con is also near the conduction system, so inc risk for **conduction disturbance and PPM need**.

Question 326

You are doing surgery for IE on mitral valve. Only a part of P2 is involved. What should be done?

Answer 326

Excise and repair. Avoiding placement of prosthesis is preferred in an infected setting.

Question 327

You are doing surgery for IE on mitral valve. The entire posterior annulus is involved with abscess. What should you do?

Answer 327

Careful debridement of all tissue. If enough tissue remaining, reinforce the posterior annulus w/ interrupted figure of 8 sutures from LA to LV, creating a fold of tissue which can be used to secure the prosthetic valve. If not enough tissue, may need pericardial reconstruction. Be careful of the coronary sinus, circumflex, and bundle of His.

Question 328

Common causes of culture negative endocarditis?

Answer 328

Most common: giving abx before getting cultures. HACEK: Hameophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella. Also fungal organisms. Consult ID.

Question 329

Discuss the timing for intervention in L side endocarditis in patient with stroke.

Answer 329

Depends on patient risk factors and whether it is embolic or hemorrhagic. Controversial timing. For hemorrhagic stroke, most agree that operation should be delayed. The duration requires judgment and balancing risks of cardiac vs neurologic complications. Reasonable to delay 3 to 4 weeks after the stroke. If there is a significant decline in cardiac function, recurrent stroke/systemic embolism, or persistent sepsis, a delay of less than 4 weeks may be necessary. With embolic CVA in the absence of bleeding, an operation may be safe in 3 to 5 days.

Question 330

Describe management for R side valve endocarditis. First line? Most common pathogens? Indications for surgery? Other workup?

Answer 330

Initial tx is abx. S aureus 70%. Strep and enterococci are next most common. Surgery indications: (get TEE in all, get cardiac CT if possible abscess) - 2cm vegetation - recurrent PE - highly resistant organism (MDR enterococci, P aeruginosa, fungi, other MDR GNB, MRSA [not MSSA], Brucella) - RHF 2/2 severe TR - heart block - paravalvular abscess

Question 331

What is the INR goal for tricuspid mechanical valve? (no additional risk factors, not high-risk valve)

Answer 331

3.0. Same as mitral. Ball-in-cage and tilting disc valves (other than Medtronic) require 3.5 in the mitral or tricuspid position.

Question 332

A non-adherent IVDU patient has second recurrence of tricuspid endocarditis with a surgical indication. What other options are there?

Answer 332

Valve excision without replacement - if pulmonary pressures and pulmonary vascular resistance are not elevated and good RV and LV fct Guideline recs include addiction specialist referral and consultation about long-term prognosis for refraining from actions that increase the risk of reinfection before repeat surgical intervention (1).

Question 333

Describe considerations in management for prosthetic valve endocarditis.

Answer 333

Need to know timing and if complicated... Is it early or late? <2 mo after surgery is often aggressive (staph) and requires intervention within 1-2 weeks. If late PVE (>2 mo; strep), treat like native valve endocarditis. Is there valve dehiscence or paravalvular leak? Requires intervention within 24-48 hrs.

Question 334

A pt w/ AV endocarditis and paravalvular abscess requires a homograft. The pt is in complete heart block after weaning from CPB. What is the ideal management?

Answer 334

permanent epicardial atrial and ventricular epicardial pacing leads are less likely to become infected than transvalvular leads

Question 335

You do an emergency ED thoracotomy for a pt who was stabbed. You place pledgeted sutures. Coming off CPB, there is localized wall motion abnormality and corresponding ST elevation. What do you do?

Answer 335

Probably coronary artery injury. Use vein and bypass the injured coronary. Next time, identify the coronary vessels, and place horizontal mattress pledgeted sutures that exclude the artery.

Question 336

A patient is stabbed in the chest and taken to the OR. After sternotomy, you find a RA injury. How do you manage?

Answer 336

Clamp the RA and sew. No need for CPB. Eval the heart with TEE and ensure no ASD/VSD/valvular damage.

Question 337

You discover a large ventricular injury in penetrating trauma. How do you manage?

Answer 337

Larger defects may require a patch. Otherwise pledgeted horizontal mattress sutures often work. Make sure septal injury and valve injury are ruled out with echo if dealing with large defects or multiple chamber defects.

Question 338

There is penetrating chest injury to the coronary sinus in a sick trauma patient. How do you manage?

Answer 338

Ligate it. Patch can be considered if the patient and heart are not friable.

Question 339

When can you ligate a traumatic coronary injury?

Answer 339

If it is distal, and there is not reversible ventricular dysfunction.

Question 340

What is the major mechanical force (pathology) that leads to aortic dissection? Other factors?

Answer 340

Hypertension. Other risk factors: connective tissue disease, fam hx of aneurysm or dissection, aortic valve dz, pregnancy, recent open or catheter aortic manipulation, stimulants.

Question 341

Where are you likely to find the dissection tear in type A?

Answer 341

right anterior aspect of ascending aorta, spiraling around the arch into the descending

Question 342

What are the causes of mortality in typa A aortic dissection?

Answer 342

aortic rupture, pericardial tamponade, acute AI and CHF, acute MI, stroke

Question 343

What is the ideal study for a type A dissection?

Answer 343

CT angio from neck through femoral vessels, EKG-gated

Question 344

What study can be done to diagnose type A aortic dissection in an unstable patient?

Answer 344

If the patient is unstable and not-responsive to medical management, they are unlikely to tolerate a CT scan. If suspicion for TAAD (hx of aneurysm, pulse deficit, neuro deficit, severe pain, sudden onset of painl; hx of Marfan, fam hx, aortic valve dz, recent aortic procedure; XR w/ mediastinal widening, tracheal or NG deviation to the R), get TEE on-table in OR or ED. TTE can also be done at bedside, though TEE is preferred.

Question 345

What is your exam and workup for possible type A dissection?

Answer 345

Vascular history. Palpate pulses x4 extremities and carotids. BP in BUE to eval diff. Neuro exam. EKG, **D-dimer (<500 ng/ml makes TAAD unlikely)**, CBC, lytes, LDH, cardiac markers, coags, type/cross. CXR - widened mediastinum, single side effusion CTA EKG gated vs MRA. TEE if cross sectional imaging contraindicated or not available.

Question 346

What d-dimer level makes type A dissection less likely?

Answer 346

<500 ng/dL

Question 347

What are the initial goals of management for type A dissection?

Answer 347

Access and monitoring. HR <60 and BP 100-120 systolic. Esmolol w/ loading dose 250-500 mcg/kg, then 25-50 mcg/kg/min. Can add nitroprusside at 0.25-0.50 mcg/kg/min if esmolol controls HR, but BP needs control. Pain control. Foley.

Question 348

What are the cannulation strategies for a type A dissection undergoing surgery?

Answer 348

Ensure good CT review to know where dissection is and isn't. Know what extent of dissection is to know how much of arch needs to be done. R axillary artery w/ graft. Direct cannulation of ascending aorta: Seldinger w/ TEE guidance vs samurai. Femoral artery. Venous cannulation: usually dual stage, but bicaval can be done if retrograde cerebral perfusion needed.

Question 349

CTA shows type A aortic dissection with arch vessel involvement. What surgery should be done?

Answer 349

Hemiarch is often sufficient to completely resect the tear and exclude the false lumen to re-establish arch vessel perfusion. If the actual TEAR involves the arch vessels (not just the dissection), the arch may need to be replaced.

Question 350

In type A dissection what would necessitate more extensive ARCH surgery?

Answer 350

Arch rupture. >5.5 cm arch aneurysm. Tear involves arch.

Question 351

In type A dissection, what are the options if the aortic root is involved?

Answer 351

Bentall, David.

Question 352

Type A dissection found in pt under 40 yrs. What should you evaluate for? Why?

Answer 352

CTD - Marfan, Loeys-Dietz, Turner (female). If CTD is known or suspected, the ENTIRE ROOT should be replaced.

Question 353

In type A dissection w/ CTD, future reinterventions are most frequently due to failure to do what?

Answer 353

failure to replace the whole root, failure to replace the entire ascending aorta, or aneurysm of the aortic wall at the coronary artery button

Question 354

How do you manage intramural hematoma in the ascending aorta? How do you diagnose an IMH?

Answer 354

Treat like ascending dissection. CT IMH hallmarks: absence of intimal tear, absence of false lumen flow (differentiates from penetrating aortic ulcer).

Question 355

In type A dissection, how do you manage dissection of coronary ostia? Which his more commonly involved L or R ostia? What do you do if only the ostia are involved? What if the dissection tears into the coronary vessel itself?

Answer 355

RCA is more frequent than left, but both need to be evaluated. May need retrograde cardioplegia. If only ostia - mobilize the buttons and reapproximate the dissected layers. If the coronary vessel is dissected - bypass or interposition with GSV.

Question 356

A type A dissection patient is going on bypass via central cannulation. The femoral arterial line monitor shows a decrease in pressure. What happened? What do you do?

Answer 356

False lumen compression. It’s possible that either the femoral art line OR the arterial bypass cannula is in the false lumen. Check a radial pressure. If it's normal, then the femoral is either malperfused (possibly re-entry tear) or the femoral line is in the false lumen. Either way, it's unreliable. If radial pressure is dampened too, then check the TEE, but plan to recannulate. Due to re-entry tears, distal flow dynamics can change with changes in flow. Look for this to happen on initiation of CPB, cross clamping, or after circ arrest.

Question 357

In a type A dissection, SMA occlusion is found. How do you manage?

Answer 357

Often, re-establishing true lumen flow at the type A will be enough. If there is a question about bowel integrity, then do a laparotomy and assess. Stenting, fenestration, or bypass may be needed.

Question 358

A patient with type A becomes comatose after decerebrate posturing (preop). What do you do?

Answer 358

Patients with dense neurological deficits, have an extremely poor prognosis. It may be best not to offer surgery. In those with less severe neuro deficits, even paraplegia, surgical repair is warranted, all else being equal.

Question 359

If there is ileofemoral malperfusion during a type A dissection, what should be considered for intervention? What if the pulse has been lost for a few hours?

Answer 359

Ax-fem or fem-fem bypass. If no flow for 6 hrs, may require ppx fasciotomies (including operative time), especially if there is outflow/venous compromise, unless you can perform careful and frequent serial exams, including compartment pressure evaluation with a trigger for fasciotomy at delta pressure <30 (ie compartment less than 30 mmHg below diastolic blood pressure)

Question 360

How do you manage a chronic type A aortic dissection?

Answer 360

Defined as >90 days. Scenario is a CT done for another reason with the patient remembering an episode of severe tearing back pain a few months ago. Surgery is indicated for complications or symptoms, eccentric expansion, rapid expansion, or aortic insufficiency, **aortic diameter of 5.5 cm**. Get an echo, a good physical exam, including BUE and lower extremity BP, and a good review of symptoms, including myocardial ischemia symptoms.

Question 361

A patient s/p type A dissection repair shows distal false lumen perfusion. What are they at risk for? How do you manage?

Answer 361

Risk: Aneurysmal dilation and rupture. Mgmt: strict BP control to <120 systolic. CT surveillance at 1, 3, 6, and 12 months is recommended. Yearly after this. 70% will be free from reoperation at 10 years. Echo to eval the aortic valve at some point is warranted.

Question 362

How do you manage a type B dissection?

Answer 362

1) Medical. BP and HR control (impulse control). Usually esmolol drip w/ nitroprusside if needed. Malperfusion treated as needed. 2) Look for complicated disease or high-risk anatomical features that would push for intervention.

Question 363

You are starting a CABG, and the arterial cannula is placed. There is high line pressure, and the aorta develops an enlarged purple hematoma. What happened? How do you confirm?

Answer 363

This is an aortic dissection. Adventitial hematoma could be the cause, but the high line pressure makes this dx less likely. Confirm w/ TEE.

Question 364

How will an iatrogenic (intraop) ascending aortic dissection manifest? What should you assess?

Answer 364

Increase in line pressure after arterial cannula placement. Purple hematoma involving the ascending aorta. MAPs drop. TEE to confirm via a flap in the ascending aorta. Eval EKG for ST changes. Eval pericardial well for blood.

Question 365

Manage an iatrogenic ascending aortic dissection.

Answer 365

Stop perfusing through the cannula. Treat hypotension w/ volume and pressors. Hypotension, if it occurs, in this setting is likely 2/2 myocardial ischemia or acute AI - use TEE to eval both, but either way you're opening the aorta and looking. There is no tamponade w/ the pericardium open, and rupture should be visualized. Cannulate the axillary or femoral artery. Clamp higher, evaluate coronaries, aortic valve, previous clamp site. Find tear. Hopefully it is contained within ascending aorta. Replace if so. If not, may need arch surgery or at least a hemiarch.

Question 366

During surgery, you cause an iatrogenic ascending aortic dissection. The LV begins to distend. What does this mean?

Answer 366

Aortic valve incompetence. Place an LV vent or open the aorta.

Question 367

You are replacing the descending thoracic aorta for a type B. During systemic cooling, the LV distends, and VF occurs. What do you do to decompress?

Answer 367

Decompress via the L SPV or LV apex.

Question 368

How can aortic dissection occur at the end of the case? What do you do?

Answer 368

Removal of the cross clamp under pressure. Make sure "flows way down" before removing clamp. If this occurs, re-heparinize, and obtain axillary or femoral cannulation.

Question 369

How do you manage acute AI in the setting of iatrogenic ascending aortic dissection?

Answer 369

Evaluate the leaflets. If they are intact, repair the aortic dissection and resuspend the aortic valves as long as anatomy allows you to realign the center of coaptation. Reevaluate the valve w/ TEE before leaving the OR. ## Footnote Teflon felt is placed between the dissected layers of media and adventitia to form a reinforced “neomedia” that can withstand suture placement. Valve resuspension is completed by reattaching the commissural posts to the aortic wall at the appropriate height using horizontal mattress 4-0 polypropylene suture.

Question 370

S/p CABG, a pt develops signs of MI and hemodynamic instability in the ICU. What is your workup?

Answer 370

EKG to eval for ST changes in specific anatomy. CXR to eval for bleeding. TTE to eval for WMA and possibly dissection. If likely coronary problem, proceed to angio. If likely aortic dissection, get gated CTA if stable or TEE in OR.

Question 371

You are attempting a mini-thoracotomy cardiac surgery requiring bypass. You cannulate the femoral, but resistance is noted. What is the next step, and what are you worried about? What if the dx is confirmed?

Answer 371

If concerned, can do an angio to eval for dissection. If type B dissection is confirmed, check TEE to eval for ascending. Abort the procedure, do CTA to confirm extent. Medically manage for 4-6 wks and return to OR later. Cannulate a different site.

Question 372

What are the indications for repairing a TAA?

Answer 372

Symptomatic aneurysm (defined at 4 cm). Ruptured. (1) End-diastolic diameter 5.5 cm (1). 5.0 cm by experienced surgeon in a Multidisciplinary Aortic Team (2a). Aortic size index 3.08 cm/m2 or AHI 3.21 cm/m (2b). Aortic area over height ratio 10 cm2/m (2a). If undergoing AV surgery or CABG, then EDD 4.5 cm (2a). If cardiac surgery for other reason, then 5 cm is indication (2b). If getting surveillance, expansion ≥0.5cm/y or ≥0.3 cm/y x2 yrs (1). If bicuspid aortic valve, 5 cm (4.5 cm if SAVR indication) (2a). Genetic factors also affect size cutoffs (image).

Question 373

How does bicuspid aortic valve affect indication for surgical repair in aortic root aneurysm? What about AS or AR? Any changes in indication for intervention?

Answer 373

Similar indications for ascending aortic aneurysm in tricuspid aortic valve pts (5.5 w/o additional risk factors, 5 for increased risk or high-volume centers, 4.5 if other cardiac surgery indication). No changes for AS/AR. Standard recommendations for aortic valve intervention apply to patients with bicuspid aortic valve.

Question 374

In pt w/ aortic root aneurysm requiring surgery, how do you manage the valve operatively?

Answer 374

If valve is normal, a valve sparing procedure can be performed - David. If <40 yrs old, consider Ross. ## Footnote Aortic Reimplantation. The aortic root is dissected as low as possible, at the root insertion into ventricular muscle. The pathologic aortic root is transected, and the coronary buttons are harvested (A). The alignment examination is completed using 3 traction sutures placed at each commissure (B). A Dacron graft is appropriately sized and the native aortic valve is reimplanted directly into the graft (C). The coronary buttons are reattached and the graft is secured to the ascending aorta (D).

Question 375

You finish replacing the aortic root and are deairing. There is 11mm ST elevation in the inferior leads (II, III, AVF). How do you manage? How do you prevent this?

Answer 375

Possibly air - vent, flow higher, support w/ inotropy as long as it's improving. If no improvement, consider **technical problem with the RCA button**. The change in orientation can cause kinking, stretching, or compression. Bypass the RCA unless you can reimplant it higher. Prevent this by sizing and placing the button with the heart engorged. Can also manifest as difficulty coming off bypass, new WMA, arrhythmias, new EKG changes, or unexplained RV failure. DDx is poor myocardial protection, air embolism, protamine reaction.

Question 376

You do a valve sparing root replacement and are coming off bypass. There is 3+ AI. What do you do?

Answer 376

Go back on, resect the valve, and replace it.

Question 377

When coming off CPB after root surgery, there is persistent blood coming from behind the proximal anastomosis. What happened?

Answer 377

Probably bleeding from the root vs LCA suture line. Pack it and use topical agents. Stop the rest of the bleeding in the surgical field. If the bleeding persists, you may need to go back on CPB and place the stitch after the heart is arrested and emptied. If the pt cannot tolerate another pump run, pack the chest open, resuscitate, and go back. This is a difficult suture to place once the patient is off CPB. You can injure the LA dome. Prevent it by taking your time on the posterior portion of the aortic anastomosis.

Question 378

How do you follow aortic root patients after replacement?

Answer 378

BP control and anticoag mgmt (if valve surgery done). Postop CT is needed to assess growth of non-replaced aorta and to eval for aneurysm formation.

Question 379

How are pts w/ aortic root dilation that don't meet surgical criteria treated?

Answer 379

Control HTN. Optimize lipid profile. Smoking cessation. Reduce risk factors for atherosclerosis. All should have an echo (1) and cross-sectional imaging (2a) at time of diagnosis. All should have follow up imagine (echo or cross-sectional) in 6-12 mo, then q6-24 mo (2a).

Question 380

You are doing a redo aortic root replacement, but cannot safely dissect the tissue around the aortic root posteriorly. What are your options?

Answer 380

The implication is the coronary arteries will be difficult/dangerous to mobilize. Cabrol technique - coronary reimplantation by placing an interposition tube graft to the open coronary ostium then doing a side-to-side anastomosis to the main aortic graft. Hemi-Cabrol - direct implantation of the RC button (usually easer to mobilize) and reimplantion of LC artery w/ interposition graft b/w the LC ostium and aortic graft.

Question 381

Diameter indication for surgical repair of sporadic ascending/root aortic aneurysm?

Answer 381

5.5 cm. 5 for Marfan, Ehler-Danlos, or with experienced surgeons.

Question 382

Diameter indication for surgical repair of sporadic aortic arch aneurysm?

Answer 382

5.5 cm. There isn't a 5.0 or 4.5 caveat here, unlike ascending aneurysms.

Question 383

Diameter indication for surgical repair of Marfan associated ascending aortic aneurysm? Anything else to consider?

Answer 383

Need to know if risk factors for aortic complications - FHx of dissection, progressive aortic regurgitation, rapid expansion (increase by 0.5 cm or more per year). - no risk factors: 5 cm - risk factors: 4.5 cm *these cutoffs include TAA assd w/ following: familial thoracic aortic aneurysm/dissection, Turner syndrome, and other non-BAV congenital conditions. It is unclear when to intervene for EDS; some suggest surgery for acute events only.

Question 384

For those with rapid expansion of an ascending TAA, what is considered "rapid," and when should intervention be done?

Answer 384

Rapid: increase by 0.5 cm or more per year. 0.3 cm in 2 years.

Question 385

Diameter indication for surgical repair of Loeys-Dietz ascending aortic aneurysm?

Answer 385

Need to know if risk factors for aortic complications - FHx of dissection, progressive aortic regurgitation, rapid expansion (increase by 0.5 cm or more per year). For LDS, additional risk factors include female sex and TGFBR2 mutations. - none: 4.5 cm - risk factors present: 4 cm

Question 386

Diameter indication for surgical repair of sporadic ascending aortic aneurysm associated w/ bicuspid aortic valve?

Answer 386

Same as for standard ascending. Need to know if risk factors for aortic complications - FHx of dissection, progressive aortic regurgitation, rapid expansion (increase by 0.5 cm or more per year). - none: 5.5 cm - risk factors for TAAD present (2a) or low surgical risk (2b) AND done by experienced surgeon as part of a multidisciplinary aortic team: 5 cm - severe AI or AS (ie needing a SAVR; 2a): 4.5 cm ## Footnote Risk factors for aortc dissection: FHx of aortic dissection, growth rate 0.3 cm/y, coarctation, "root phenotype" aortopathy

Question 387

In a patient undergoing cardiac surgery for another reason, at what diameter should you add intervention for an ascending aortic aneurysm?

Answer 387

4.5 cm if SAVR and done w/ exp surgeon and multidisciplinary team (2a). 5 cm for everyone else (ie not multidisciplinary team, not experienced [2a], or not SAVR [2b]) ## Footnote 2022 ACC/AHA

Question 388

What is the law of laplace and how does it apply to TAA?

Answer 388

tension = pressure x radius These aneurysms will continue to dilate, though smaller sized aneurysms can stay stable over a long period. >6 cm have significant increase in mortality. Repair usually indicated at 5.5 cm if asymptomatic. Can be smaller depending on other conditions/risk factors.

Question 389

Characteristics of Loeys-Dietz syndrome?

Answer 389

Mutation in TGF-B receptor. Hypertelorism, bifid uvula, arterial tortuosity. Aneurysms.

Question 390

Characteristics of Ehlers-Danlose syndrome

Answer 390

Autosomal disorder of COL3a1 gene for type III collagen. No formal aneurysm guidelines as surgery is very high risk. Often present w/ arterial rupture.

Question 391

What infection is assd w/ TAA? How do you manage? | "Infectious aortitis" has supplanted "mycotic aneurysm."

Answer 391

Most often S aureus, Pneumococcus, E coli, and Salmonella. Syphilis - infection destroys muscular and elastic fibers of the media layer. Which was once common, is now rare. Fungal and TB related may arise in immunocompromised pts. ++++++++++++++++++ Surgery is preferred (1) over TEVAR/EVAR, though it can be considered in select patients (2b) - rupture (2a), fistula, HD instability, bridging/hybrid approach plan. Prolonged abx course of 6 wks w/ lifelong suppression if not amenable to open or endo repair (2b).

Question 392

In a patient with previous ascending aortic dissection, what chronic aortic disease process may present later?

Answer 392

Aneurysm. The uncorrected portion (arch, root, buttons) of the aorta tends to continue to dilate. It is often at a faster growth rate with a higher risk of spontaneous rupture.

Question 393

What workup do you want in an ascending TAA pt for possible surgery?

Answer 393

CTA or MRA - extent of aneurysm, include carotids; look at root and arch; include abd/pelvis if considering femoral cannulation; look at proximity to sternum. Echo - eval valves, cardiac function. Cardiac cath - eval coronary vessel disease. PFTs - if smoker w/ COPD; helps determine risk. CBC, CMP, Coags, T/C.

Question 394

What are the cannulation considerations in an ascending aortic aneurysm surgery?

Answer 394

Cannulate and clamp **higher** than what needs to be replaced. Can do central if there's room for cannula, clamp, and sutures. If no room, can do **axillary**.

Question 395

During ascending TAA repair, what can happen if you anastomose an aortic graft that is too long? How do you perform anastomosis?

Answer 395

It can kink when the heart fills. Distal first. Use felt on aorta if tissues are bad. Move clamp on to graft to eval for hemostasis. Proximal anastomosis. Place root vent in graft prior to cross clamp removal and turn off vents while suturing to help deair. Postop BP control. DC w/ beta-block, ARB, and statin.

Question 396

Planning for ascending TAA repair. What if you cannot clamp the ascending aorta with an adequate sewing cuff?

Answer 396

May need circ arrest.

Question 397

You are doing an ascending TAA repair. You fill the heart, and the graft kinks. What do you do?

Answer 397

Can attempt to plicate the lesser curve, but may need to cross clamp, arrest, excise excess graft, and sew graft to graft.

Question 398

You start an ascending TAA repair, but the LV distends once commencing bypass. What is happening?

Answer 398

Significant aortic insufficiency may be present. This should be expected based on preop eval. Clamp and arrest w/ retrograde. Decompress with antegrade vent. If one is not in place, transect the aorta, and deliver direct coronary cardioplegia. Replace the valve.

Question 399

You are starting surgery for ascending TAA, and during the sternotomy, there is a large rush of blood. You think the aorta ruptured. What do you do?

Answer 399

Give heparin. CLOSE the sternum w/ towel clamps. Tell anesthesia. Get blood in the room. Get perfusion ready for cannulation. Get femoral access in case you need to cannulate there. Open the sternum and place manual pressure on the hole. Get on bypass. Use lots of suctions. Cool. Clamp the aorta above the rupture. Open it and arrest the heartw/ direct plegia. Place an LV vent and retrograde sinus cannula if needed. If aneurysm at high risk preop, may be better to axillary/femorally cannulate and be on bypass first. If risk very high, may even cool to 18 degrees for circ arrest before sternotomy.

Question 400

What are the size cutoffs for intervention in patients with an arch aneurysm compared to ascending aneurysm?

Answer 400

The same for the cutoff for sporadic disease. Ascending aorta has caveats for centers of excellence for 5.0 cm cutoff.

Question 401

What are the options for aneurysmal arch repair, and what does the choice depend upon?

Answer 401

Hemiarch, total arch, elephant trunk. Decision depends on distal extent of aneurysm.

Question 402

For the different types of aneurysmal aortic arch repair, what cannulation strategy will work for almost any situation?

Answer 402

R axillary artery; unclutters the field and allows for selective ACP

Question 403

How can you achieve brain perfusion for an uncomplicated hemiarch for arch aneurysm? What if the repair is more complicated or extensive?

Answer 403

retrograde via SVC usually works; antegrade brain protection may be needed for more extensive repair; these methods extend the safe period (ie lower mortality/stroke) for circulatory arrest, selective ACP is just as safe as bilateral ACP; selective ACP extends the safe time more than retrograde CP. ## Footnote Guidelines specifically state one method has not been shown to be inherently better than another.

Question 404

How do you initiate antegrade brain perfusion (arch aneurysm repair)?

Answer 404

Ax cut down. Sternotomy and dissect out head vessels and innominate vein. Cannulate and initiate CPB. Start cooling - cool to 18-20, or until EEG silent, or for preset 30-60 mins. Trendelenberg. Give pentobarbital and mannitol. Turn off CPB - don't need to drain all the blood. Clamp venous. Stop vent. Clamp the R innominate, and initiate antegrade brain perfusion: 500 ml/min (10-15 ml/kg) w/ mean pressure 40-60 mmHg and good backflow through L CCA. Can clamp the L SCA and L CCA here as well. If not good flow/backflow, place a perfusion catheter up L CCA and Y into the antegrade perfusion circuit at similar rate. Do distal portion of surgery. Reclamp. Reinitiate CPB. Rewarm. Do proximal.

Question 405

When do you need a total arch repair for arch aneurysm? Size criteria has been met, the question is asking for the anatomic reason for needing a total arch vs a hemiarch.

Answer 405

When aneurysm extend into the mid/distal arch (past L CCA).

Question 406

When doing a total arch repair for aortic arch aneurysm, how do you decide to manage the head vessels?

Answer 406

If they are aneurysmal, they may need reconstruction. If not, can be fashioned to the graft as an island.

Question 407

What is the safe time period for circulatory arrest at 18 degrees?

Answer 407

The relatively safe time period for circulatory arrest at 18°C is 25 to 30 minutes.

Question 408

When do you add an elephant trunk to aneurysmal arch repair?

Answer 408

When the distal arch or isthmus is involved. Only if a seal can be created. If not, conventional approach should be done.

Question 409

On preop imaging for an aneurysmal arch surgery (total arch), an aberrant LVA is found. How does this change the surgery?

Answer 409

Duplex eval of the RVA to ensure patency and antegrade flow. Eval for intact circle of willis. If RVA is ok, LVA can be temporarily occluded, and reimplanted during patient rewarming (into L CCA, SVG to aorta, tube graft). <2mm LVA w/ patent RVA can be ligated.

Question 410

A pt w/ aneurysmal arch and descending aorta aneurysm psx w/ chest pain and imaging concerning for contained early rupture (periaortic density). How do you manage?

Answer 410

Normally you would want elephant trunk, but this isn't possible because a distal seal would not occur until the completion elephant trunk. Do hemi-clamshell incision extended into the L 4th ICS and do full arch and descending aorta surgery.

Question 411

A very elderly patients presents with surgical ascending aneurysm and 4.5 cm proximal arch. Does age affect the extent of surgical resection?

Answer 411

Elderly patients do not tolerate circulatory arrest as well as younger patients. Cannulate the R axillary artery (or go high on the aorta), and do a hemiarch.

Question 412

A patient with known descending TAA comes in with pain, what is the management?

Answer 412

Repair. ALL symptomatic TAAs should be repaired (ruptured, dissected, pain)

Question 413

For descending TAA, what are the asymptomatic indications for repair?

Answer 413

For most average-sized adults: Diameter of >5.5 cm. Of note, there isn't a 5 cm caveat for centers of excellence/experienced surgeons (as opposed to root/ascending). Patients with high surgical risk (eg, STS Predicted Risk of Mortality [PROM] score >8%, frailty score index >2, two compromised organ systems): Diameter ≥6 to 7 cm. Genetically mediated conditions: (syndromic or nonsyndromic), a smaller diameter is suggested as an indicator for repair. The specific threshold diameter depends on the condition. Smaller patients: including many women, a diameter >2x diameter of the nonaneurysmal aorta or the aortic size index can be used.

Question 414

What rate of expansion for TAAs is an indication for repair?

Answer 414

Asymptomatic TAA with rapid expansion ≥5 mm per year (or 3 mm x2 yrs) for aneurysms <5 cm in diameter

Question 415

What are LVOT gradients found on echo for HCM? For diagnosis and treatment cutoff.

Answer 415

Basal resting gradient: >30 mmHg Provocative gradients (stress valsalva or amyl nitrite): >30 Intervention is considered when gradient is >50

Question 416

What are you looking for on echo if suspecting HOCM?

Answer 416

Level and degree of LVOT obsx. Degree of SAM of mitral valve. If cavitary hypertrophy is diffuse (HOCM) or asymmetric/focal (assn AS or HTN). Gradients: **>30 for dx**, **>50 for intervention**. Septum: **15mm for HOCM**, **30mm assd w/ SCD**. Chamber size and fct: athletic hearts can be 13-15mm LV thickness but have normal relaxation and chamber dilation.

Question 417

What can the EKG show in HOCM?

Answer 417

LV strain pattern, large T-wave in precordial leads, frequent PVCs

Question 418

When would you do an exercise echo for HOCM? What are you looking for?

Answer 418

Some do it for all - risk stratification and assessment for LVOT gradient. Look for: Development of symptoms. LVOT gradient increase. Failure of BP to increase (as it should w/ exercise). Arrhythmia. ST depression. Mitral regurgitation.

Question 419

For HOCM treatment, what are the pertinent decision-making points?

Answer 419

Obstructive physiology. If non-obstructive, no surgery. Need EF to determine meds. If obstructive physiology, need to know of heart failure symptoms or angina. At this point, medical mgmt is still first line. Persistence of symptoms despite medical management will prompt surgical evaluation. The options are surgery (for those who can tolerate) vs alcohol ablation. DDD pacing is an option for non-surgical patients.

Question 420

A patient w/ HOCM and obstructive features has persistent symptoms despite medical management. He is a poor surgical candidate. What other options are there?

Answer 420

Alcohol ablation

Question 421

A patient w/ HOCM and obstructive features has persistent symptoms despite medical management. He is a poor surgical candidate and coronary anatomy is not accessible percutaneously. What other options are there?

Answer 421

DDD pacing - reduces the LVOT gradient and SAM, as well as improving MR and NYHA class https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9225325/

Question 422

You are preparing for a septal myectomy in a HOCM pt. The TEE demonstrates moderate mitral regurgitation. What do you do?

Answer 422

Differentiate between **primary MR** or **SAM**. Ask about the relationship between the PML and AML in terms of height, excess tissue, or chordae. If the PML height is excessive, may need to do repair (sliding valvuloplasty). This should be anticipated preoperatively because a surgeon uncomfortable in this may end up doing a mitral replacement or canceling the case.

Question 423

POD2 after septal myectomy for HOCM, a patient has a harsh systolic murmur and increasing oxygen requirements. PA systolic pressure is increased. What is your differential? What is the workup?

Answer 423

If the patient got diuretics, vasodilators, or went into AF, then LV preload will decrease which could precipitate the recurrence of **SAM and MR** and could explain a similar presentation. **VSD** is rare, but should be on the differential, and this is the description. Get an echo to confirm. PA cath will also show step up in oxygen sat b/w proximal and distal ports. Go back to OR, get TEE, and **repair the VSD w/ pericardium**.

Question 424

How should you treat acute hypotension for HOCM? What specifically should be avoided?

Answer 424

Vasoconstriction (phenylephrine and vasopressin). Positive inotropy, vasodilators, and diuresis should be avoided - can precipitate MR and SAM.

Question 425

Will septal myectomy affect SAM and MR in HOCM?

Answer 425

It will usually correct these pathologies (SAM causes the MR) when there is no other concomitant mitral pathology (ie as long as it’s not primary MR).

Question 426

Describe AF management perioperative for HOCM.

Answer 426

Aggressive as it gets. AF reduces LV preload and can induce recurrent MR or SAM. Cardiovert. Beta block. Give fluid. Give vasopressors (phenylephrine). Psx: harsh systolic murmur after HOCM surgery. You notice AF. Differential would be MR from SAM vs VSD.

Question 427

Describe simply the classic technique for myectomy for HOCM?

Answer 427

11 blade incision below the **nadir of the RCA** and resect **3 cm** length of sub aortic muscle. This can be extended for 7cm to the apex if it is true HOCM.

Question 428

What is the role of genetic testing in family members of HOCM patients?

Answer 428

Not used for establishing diagnosis, but only for screening. May predict progression or complications of HOCM. Counseling patients with HCM regarding the potential for genetic transmission of HCM is one of the cornerstones of care. Screening first-degree family members of patients with HCM, using either genetic testing or an imaging/electrocardiographic surveillance protocol, can begin at any age and can be influenced by specifics of the patient/family history and family preference. As screening recommendations for family members hinge on the pathogenicity of any detected variants, the reported pathogenicity should be reconfirmed every 2 to 3 years.

Question 429

A patient undergoing workup for AVR for severe symptomatic AS is found to have sub-valvular hypertrophy. What should be done?

Answer 429

If TEE or cath document non-valvular LVOT w/ subvalvular gradients and normal valve leaflets, septal myectomy can be performed to improve symptoms of heart failure. Pay attention to TEE when coming off bypass to ensure complete myectomy is done and see if no AS.

Question 430

How do you use an echo to eval cardiac tumors? What are you looking for?

Answer 430

Often diagnostic. Need to use it to eval size, extent, mobility, stalk, degree of obstruction, chamber and wall involvement, and proximity to valvular/electrical structures.

Question 431

What does cross sectional imaging (CT and MRI) help evaluate in workup of cardiac tumors?

Answer 431

Tumor burden, wall penetration, relation to extracardiac structures. Can help eval consistency of mass.

Question 432

What extremity findings might a patient w/ cardiac tumor have? What does it mean?

Answer 432

Digital necrosis 2/2 distal embolization.

Question 433

A patient has a LA myxoma. What could cause pulm HTN and obstructive heart failure?

Answer 433

Tumor causes diastolic mitral orifice inflow obstruction.

Question 434

What is the surgical goal for patients w/ LA myxoma?

Answer 434

Complete excision w/ a 5mm circumferential atrial septal excision with the stalk.

Question 435

If using an LV vent for excision of an LA myxoma, what are the considerations?

Answer 435

Ideally should vent through aortic root. RSPV vent risks tumor embolization.

Question 436

Describe excision of a LA myxoma?

Answer 436

Bicaval CPB w/ snares. Antegrade cardioplegia. Don't manipulate heart until clamped. **LV vent through aortic root** (not R SPV). Open **RIGHT atrium**. Visualize tumor stalk on septum, incise 5mm to this and excise the tumor through the septum w/ a 5mm margin. Inspect for any residual tumor and damage to the mitral valve. Use garbage suction here. Close septum with **patch**. Bi-atrial approach may be necessary. Higher risk of arrhythmia.

Question 437

What if during surgery for LA myxoma excision, the patient arrests on induction? What happened? What do you do?

Answer 437

Loss of *vasomotor tone -> dec *preload -> tumor obstruction of *MV inflow. ACLS. Intubate and give *catecholamines. Immediate sternotomy, heparin, CPB w/ dual stage via RA vs SVC only vs peripheral.

Question 438

What if when coming off bypass for LA myxoma excision, the patient has an ASD on TEE?

Answer 438

Assess size and location. Unless the leak is tiny, go back on bi-caval CPB, find the hole, and fix it (this is why primary closure is not recommended; use a patch).

Question 439

A RA tumor is causing obstructive symptoms, ascites, and hepatomegaly. What are your considerations, workup, and management?

Answer 439

Preop assessment of tumor w/ *TEE and *CT/MRI or possibly venography eval the extent and plan for CPB. Depending on extent, the patient may require bypass via the *R IJ or and/or *femoral.

Question 440

What structure must be preserved on the SVC if a surgery requires RA incision extension for an RA tumor?

Answer 440

SA node. Make sure to go laterally. In addition, protect the the tricuspid valve and AV node.

Question 441

A cardiac tumor is high in the SVC and has embolized to the PA. What is your cannulation strategy and operative conduct?

Answer 441

Central aortic and peripheral venous - femoral and R IJ. CVL access through contralateral SCV. Mobilize the SVC high, possibly above the azygous. Clamp, antegrade, snare. R SPV vent can be used if no L side involvement. Incise RA and extend high and lateral to avoid SA node. Inspect RA, RV, TV, and RVOT. Separate incision can be used on PA to remove embolus.

Question 442

A R side cardiac tumor has embolized to the PA. Intraop it is very distal. What can you do?

Answer 442

Brief period of hypothermic arrest may facilitate full removal of the tumor burden from the distal PA.

Question 443

How do you approach ventricular myxomas?

Answer 443

Often actually extension from atria below the AV valve. Can approach via the outflow tract or the AV valve. If you can do a good inspection, a ventriculotomy is often avoided.

Question 444

You are doing surgery for a myxoma involving the ventricle, and you find that base of the papillary muscle or the chordae of the mitral valve is involved. How do you proceed?

Answer 444

Repair or replacement of the valve will be necessary.

Question 445

Small pedunculated mobile density is attached to the aortic valve and is seen during preop echo for CABG. No signs or risk factors for endocarditis. Normal dental exam. What is it?

Answer 445

Take note of the exclusionary history and physical taken. This is likely a *papillary fibroelastoma. Benign and found incidentally. *Excise them d/t their *embolic potential. The stalk is usually very small and can be excised *flush with the leaflet without incurring any leaflet damage. Arise from valvular endocardium.

Question 446

What are the principles of the approach to cardiac tumor excision?

Answer 446

Carefully planned *CPB. Prevention of embolization by *avoiding manipulation before cross clamping and carefully evaluating chambers before closing. Operative exposure usually through RA, but possibly LA, rarely ventriculotomy. Septum should be closed w/ *tension free patch.

Question 447

A cancer pt presents with shortness of breath, sinus tachycardia, and hypoxia w/ a clear CXR. What should you be suspicious of?

Answer 447

PE

Question 448

What is the diagnostic test of choice for a PE?

Answer 448

CT PA

Question 449

What is Virchow's triad? What are specific examples of each point?

Answer 449

Venous stasis: immobility (intubated, spinal injury), bedrest Endothelial injury: surgery, trauma, access procedures Hypercoagulable state: malignancy, thrombophilia, oral contraceptives, hx of thrombosis

Question 450

What are some signs of right heart strain on echo (PE pt)?

Answer 450

dilation, septal flattening

Question 451

What is the benefit of pulmonary angiography for PE?

Answer 451

eval for clot extent and location

Question 452

What designates a PE as high-risk? How does this change management? What's the risk of death?

Answer 452

Hemodynamic compromise (shock/hypotension), RV dysfunction. Tx w/ heparin and thrombolysis vs embolectomy (as opposed to heparin alone). Risk of imminent death is 10%, 30-day risk is 30%.

Question 453

Absolute contraindications to systemic thrombolytic therapy in acute PE?

Answer 453

Intracranial neoplasm, <2 mo intracranial or spinal surgery/trauma, hx of hemorrhagic stroke, active bleeding, bleeding diathesis (thrombocytopenia), nonhemorrhagic stroke w/in 3 mo.

Question 454

A pt w/ PE has RV strain but has contraindication to thrombolysis (CNS neoplasm, hemorrhagic stroke, recent spine trauma/surgery, etc). What options are there? What if the patient has significant hemodynamic compromise, poor oxygenation, and is a poor surgical candidate?

Answer 454

Catheter-embolectomy vs surgical-embolectomy. If CV and/or resp unstable, consider ECMO.

Question 455

What is the danger to the RV in the setting of PE requiring ECMO?

Answer 455

It does not unload the RV. The RV is still pumping some blood against a clot, so there can be myocardial injury until the clot burden is removed.

Question 456

What is the mortality and 1 yr survival for prompt surgical embolectomy in PE pts w/ large clot burden and contraindication to thrombolysis?

Answer 456

Operative mortality is 6%. 1-year survival is 86%. According to 47 pt series by Leacche et al.

Question 457

You take a PE pt w/ HD compromise, large clot, and thrombolysis contraindication to the OR. What do you look for on TEE?

Answer 457

RA and RV for clot in transit. PFO/ASD. PA for extent of clot.

Question 458

The first step in the management of CTEPH?

Answer 458

initiation of anticoagulant therapy, provided the patient is not at a high risk of bleeding, continued indefinitely

Question 459

A patient w/ CTEPH has a high bleeding risk, so there is hesitancy towards anticoagulation. What can be done?

Answer 459

inferior vena cava filter until the bleeding risk is resolved and adequate anticoagulation can be provided

Question 460

In order to assess the hemodynamic impairment from CTEPH, what should be done?

Answer 460

examine pulmonary artery catheterization (PAC) data: hemodynamic abnormalities at rest that almost invariably warrant surgery (eg, PVR of 240 to 1200 dynes-sec/cm-5 [3 to 15 Wood units] with the majority falling into the range of 600 to 1000 dynes-sec/cm-5 [7.5 to 12.5 Wood units]) for patients without a substantial increase in pulmonary hemodynamics with exercise, the benefits of PTE are less clear - can consider PTE when the patient’s exercise intolerance and quality of life dissatisfaction is of sufficient magnitude that the patient is willing to accept the risk of surgery

Question 461

How do you determine if chronic thromboemboli is accessible for surgery (CTEPH surgery)? What study is the gold standard? What if the pt has RV failure?

Answer 461

Proximally location in **main, lobar, or segmental** pulmonary arteries - amenable to surgical removal. **Digital subtraction pulmonary angiography (DSPA)** is considered the gold standard in defining the extent and location of the thromboembolic obstruction In pts with profound RV failure and shock, the risk of DSPA may be prohibitive - do **CTPA or MRI PA** instead.

Question 462

72 hrs after a CTEPH pt undergoes PTE, he has diffuse opacity in RML and RLL lobes. What happened? What do you do?

Answer 462

reperfusion syndrome (8-10%); mainly supportive tx w/ vent and pressors prn diurese and wean FiO2 resolves in 7-10 days

Question 463

A 67M w/ thymoma s/p thymectomy and radiation returns w/ fatigue dyspnea and edema. What is your differential and a possible workup? What would you predict imaging to show?

Answer 463

**Chronic radx pericarditis**, CHF, restrictive cardiomyopathy, recurrence. CXR to eval for **pericardial calcification** or effusions. CT or MRI may show **thickened or calcified pericardium**. EKG is nonspecific w/ ST-T changes. Echo may show **constrictive physiology - bowing of interventricular septum w/ inspiration**, thickened pericardium. Possible cath.

Question 464

What would the echo and cardiac cath show in constrictive pericarditis?

Answer 464

Echo - **bowing of interventricular septum** to the left **w/ inspiration** (instead of the RV expanding out w/ inc preload, it has to expand into the LV) Cath - square root sign, RV end diastolic P > 1/3 RV systolic P, **equalization of pressures across the atria during diastole, and equalization of ventricular pressures during diastole** (except during inspiration).

Question 465

What are some distinguishing features of restrictive disease as opposed to constrictive disease?

Answer 465

Small or normal sized heart, reduced LV fct, pulmonary and hepatic congestion, BNP may be elevated (unlike in constrictive disease)

Question 466

If diagnosis is in doubt for restrictive CM vs constrictive pericarditis after CXR, CT, echo, cath, and labs, what else can be done?

Answer 466

Endomyocardial biopsy or diagnostic surgical exploration with inspection of the pericardium.

Question 467

How do you treat constrictive pericarditis?

Answer 467

surgery - pericardial stripping

Question 468

What are the goals of pericardial stripping for constrictive pericarditis (anatomically)? What are your CPB considerations?

Answer 468

excise pericardium from phrenic to phrenic, down to diaphragm, and around the AV groove to the entrance of the caval/pulmonary veins posteriorly - CPB is usually needed for at least the left side structures - there may be a lack of surgical planes, which can lead to significant blood loss and damage to coronaries or venous structures (may want groins exposed, would wait to give heparin until aorta is exposed)

Question 469

While doing posterior dissection during pericardial stripping for constrictive pericarditis, what structure do you have to be wary when moving along the AV groove posteriorly?

Answer 469

esophagus - can palpate the TEE probe to stay clear

Question 470

A patient has a history of lymphoma c/b constrictive pericarditis. In the OR, you find large implants not visible on preop imaging. How do you proceed?

Answer 470

Send samples for frozen. If malignancy is found, abort and refer to an oncologist.

Question 471

A patient is undergoing pericardial stripping after constrictive pericarditis was dx after his CABG. You injure a bypass vessel in the OR. What do you do?

Answer 471

CPB Check for HD changes and EKG Repair, interpose, or re-bypass completely.

Question 472

If your descending type B dissection open repair is more proximal near the arch, where would you make the thoracotomy? What if more distal access is required?

Answer 472

3rd or 4th space 7th space if distal access needed

Question 473

What would be considered a "complicated" type B dissection? Are these more common than uncomplicated? Why is this category important?

Answer 473

Persistent pain, malperfusion (spinal, visceral, extremity), impending rupture, life-threatening complications (very general category...). Most Type B dissections are uncomplicated. Complicated dissections usually require surgical or endovascular intervention.

Question 474

During your type B open repair of the descending thoracic aorta, where would you encounter the L RLN?

Answer 474

near the ligamentum and along the posterior proximal neck of the aorta

Question 475

During your type B open repair of the descending thoracic aorta, how do you manage the phrenic and vagus nerves on the transverse arch?

Answer 475

dissect them free from the transverse arch

Question 476

During your type B open repair of the descending thoracic aorta, what is the benefit of staying above T7?

Answer 476

prevent the need for re-implantation of the intercostal arteries and reduce risk of spinal ischemia and thus paraplegia

Question 477

How do you manage the **dynamic** and **static** branch malperfusion in the context of type B aorta repair?

Answer 477

Dynamic malperfusion should be improved after the repair. Static malperfusion usually requires percutaneous balloon septal fenestration and uncovered stent by IR.

Question 478

How do you manage paraplegia after a type B aorta repair?

Answer 478

Lumbar drain. Ideally ICP less than 10. Do not drain >20ml/hr d/t risk for SDH. MAP support to 80-90 w/ fluids, phenylephrine, or vasopressin to improve spinal cord perfusion pressure. No steroids.

Question 479

What are your considerations for a cannulation strategy for type B dissection that is very proximal right off L SCA?

Answer 479

Will likely need circ arrest for the proximal portion. May need to reimplant the L SCA separately (do this preop in a nonurgent setting, consult vascular surgery). R ax cannulation is ideal.

Question 480

CABG patient gets type A after aortic cannulation confirmed on TEE. You are trying to place a retrograde catheter for plegia, but are unable to after multiple attempts. How do you ensure retrograde plegia placement?

Answer 480

Go bicaval, open the atrium, and place the retrograde cannula directly.

Question 481

CABG patient gets type A after aortic cannulation confirmed on TEE. What do you do? What are the operative steps?

Answer 481

1) Stop CPB. Leave cannula in, you don't want to have a bleeding problem. 2) Volume and pressors as needed - can use venous line if you've placed one, just make sure it's deaired. 3) Alternate cannulation - axillary, femoral, percutaneous through ascending aorta confirmed with TEE. 4) Now remove the first cannula, assess proximal/distal extent, assess for rupture, AI (LV distention), MI. 5) Retrograde coronary sinus plegia. LV vent in R SPV. 6) Start cooling to 18. If heart distends and fibrillates, clamp and arrest. 7) Clamp, arrest retrograde, and vent the root via aortotomy. If AI, do proximal work on valve. 9) Circ arrest, brain perfusion. 10) Hemiarch. 11) Deair, resume full flow. 12) Proximal aorta anastomosis, add root vent. 13) Distal and proximal anastomoses for CABG.

Question 482

You are doing a CABG and begin arterial cannulation for CPB. When would you suspect type A dissection? How do you confirm?

Answer 482

Hematoma through the aorta visually. MAP drops. Line pressure is high. Confirm with TEE. Epiaortic US also works. You will see a flap. Determine proximal and distal extent.

Question 483

After CABG, an IABP is placed. In the ICU, heart function recovers, but the leg loses a pulse. The patient is stable. What do you do?

Answer 483

Remove the IABP. If the leg is still without a pulse, check a duplex and CTA to include the chest, abdomen, pelvis, and runoff. If a type B is found, go to the OR emergently for EVAR and possibly fem-fem bypass.