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Adult Cardiac Surgery Board Review > TSRA Clinical Scenarios - Adult Cardiac Surgery > Flashcards

TSRA Clinical Scenarios - Adult Cardiac Surgery Flashcards

1
Q

Heparin dose for CPB?

A

400 units/kg

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2
Q

ACT required for initiation of CPB?

A

400-480

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3
Q

5 min after cross clamp is released when coming off CPB, the heart begins to distend w/o contraction. What is the next move?

A

Two possible problems:
1) valve leak
2) heart is not ejecting
Squeeze the heart. Pace the heart. If this does not resolve quickly, cross clamp again.
Talk to anesthesia and perfusion to see if they can help determine a cause on echo or via labs.

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4
Q

Coming off CPB, you attempt to pace, but have no capture. Leads are well placed. Perfusion says K is 7. UOP is minimal. You cross clamp and vent the heart. How do you manage K?

A

Hemoconcentrate. IV insulin with glucose. Lasix or bicarb can also help.

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5
Q

A patient fibrillates when coming off CPB. How do you defibrillate?

A

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

If distended, manually squeeze the heart and empty with CPB, place vents if needed, then cardiovert.

Vent air, inc perfusion pressures to 75 (coronary perfusion and to flush out embolized air), optimize oxygenation, lytes, and temp. Check Echo for AI.

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6
Q

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

A

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

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7
Q

Explain CPB components.

A

Venous cannulas drain to reservoir by gravity or vacuum, pumped into the oxygenator/heat exchanger, then continues to arterial air filter and to the arterial cannula in the patient.

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8
Q

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

A

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

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9
Q

What is your differential for inadequate venous drainage on CPB?

A

Air lock
Cannula malposition
Add suction
Increase cannula size
Reduce flows if flow is high
Make sure no other avenues of blood flow into the heart - AI needs a vent, azygous vein needs adjustment to snares, L SVC needs snare or cannulation depending on situation (cannula if NO innominate).
Retroperitoneal or peritoneal hemorrhage?

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10
Q

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

A

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.

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11
Q

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

A

Check for rupture of the sinus - inspect inferior aspect of the heart
Check position of cannula
Check if balloon is ruptured

Persistent L SVC

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12
Q

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

A

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

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13
Q

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

A

R coronary ostium is anterior and susceptible to air embolism.
Re-institute CPB w/ high perfusion pressure 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.

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14
Q

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

A

Can clamp vs cold bypass flow

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15
Q

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?

A

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

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16
Q

In a patient w/ CABG w/ open LIMA, what is the problem with antegrade cardioplegia?

A

Antegrade will perfuse the OM and PDA territories, but not the LAD.
Retrograde will perfuse all.

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17
Q

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

A

Retrograde cardioplegia would ensure delivery. Antegrade would likely require direct delivery of cardioplegia.

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18
Q

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

A

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).

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19
Q

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

A

If you perforate the sinus, the posterior heart may be stuck, making dissecting in a bloody field more difficult. On the other dissection on the front end may damage CABGs.

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20
Q

After cross clamping, 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?

A

Aortic insufficiency.

Switch to retrograde cardioplegia and turn on the aortic root vent vs an LV vent to decompress the heart.

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21
Q

How do you ensure adequacy of retrograde cardioplegia catheter delivery?

A

Cessation of electrical and myocardial activity. Appropriate pressure in cannula is around 40 mmHg. Observe flow through coronary veins and arteries. Can also check coronary ostia through aortotomy for backflow. Finally, heart should be cooling.

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22
Q

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

A

Myocardial edema. This is why the balloons on the cannula are not usually 100% occlusive.

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23
Q

Where does a persistent L SCV usually drain?

A

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

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24
Q

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

A

Stop flow. Look for kinks or clamps to r/o obstruction. Ensure pressure monitoring line is connected.
If all above ruled out, concern for dissection. Visualize the root and ask anes to look at aorta.
If dissection, cool with original aorta cannula distal to the clamp and prepare for dissection repair.

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25
Q

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

A

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

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26
Q

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

A

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.

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27
Q

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

A

CPB, clamp, and arrest with antegrade. Repair the hole directly with prolene or a pericardial patch.

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28
Q

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

A

Access - cannula placement
Collateral - clamp, drainage, L SVC, vents/suckers; hypothermia?
Myocardial mass - hypertrophy may require hypothermia

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29
Q

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

A

Innominate vein

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30
Q

Redo mitral w/ innominate vein injury during sternotomy. How do you manage?

A

Pack the area and close the sternum with penetrating towel clamps.
Peripheral CPB. Put pump suckers in the injured field.
Reopen and dissect vein to length for 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.

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31
Q

Redo case. You attempt to dissect SVC for cannulation, but make a large hole before pursestring is in. How do you manage?

A

Tamponade it.
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.
Once controlled, may need primary vs pericardial patch.

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32
Q

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

A

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.

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33
Q

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. How do you manage?

A

Goals: identify injury, cannulate beyond repair.
Venogram if available.
This hx is concerning for iliac vein injury.
If chest is open, can centrally cannulate, otherwise, may need access in contralateral femoral vein.
If the injury is above the iliacs, can use fluoro get wire and cannula above and go on, then open the abdomen and repair the injury.

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34
Q

SVC is ruptured during balloon dilation for SVC syndrome. How do you manage?

A 
Give heparin.
Emergency median sternotomy.
Bicaval cannulate - for the SVC, enter the RA and traverse cannula through injury. 
Empty the heart.
Primary vx pericardial patch closure.
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35
Q

Bicaval cannulation in an old lady, and the IVC tears below the diaphragm. How do you manage?

A

Get venous access and go on CPB.
If possible, traverse the cannula through the injury from above.
Place a Rummel clamp if possible below the injury.
May need patch for tension free repair.

If unable, may need to go on w/ SVC cannula and suckers. Get femoral access.
Can attempt incising the diaphragm through sternotomy to get exposure.
If all else fails, extend sternotomy inferiorly and convert to RUQ subcostal incision.

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36
Q

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

A

Heparin and sternotomy.
CPB and arrest the heart.
Wide patch repair even if small.
Bypass the coronary lesion if during a cath case for coronary disease.

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37
Q

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

A

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.

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38
Q

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

A

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.

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39
Q

What symptoms represent unstable angina?

A

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

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40
Q

What symptoms represent stable ischemic heart disease

A

exertional angina - predictable, improves with rest

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41
Q

What is included in guideline-directed medical therapy?

A

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

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42
Q

What are hemodynamically significant coronary lesions on left heart cath?

A

Left main >50%

non-LM >70%

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43
Q

What FFR is hemodynamically significant? When is FFR used?

A

< 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.

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44
Q

What is the SYNTAX score?

A

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

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45
Q

What are the cutoffs for the SYNTAX score?

A

> 22 is intermediate complexity.
32 is high complexity.
The results of the SYNTAX trial revealed that patients with 3-vessel or L main disease benefited from CABG over PCI.

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46
Q

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

A

Gated cardiac CT

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47
Q

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

A

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.

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48
Q

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

A

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

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49
Q

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

A

1) 3-vessel disease, especially w/ syntax >22 (mod) and low surgical risk.
2) Significant L main disease (50%).
3) Multivessel (>1) w/ proximal LAD disease.

Europe guidelines add:
Multivessel (2+) w/ EF <40.
Multivessel (2+) w/ >10% ischemic territory.

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50
Q

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

A

CABG.

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51
Q

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

A

CABG.

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52
Q

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

A

Concurrent CABG.

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53
Q

What is the ideal graft for the LAD?

A

IMA. Left preferred. Right is second choice.

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54
Q

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

A

BIMA and radial.

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55
Q

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

A

Skeletonized.

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56
Q

Known risks of sternal infection and malunion in cardiac surgery?

A

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

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57
Q

When should CABG patients receive aspirin?

A

Preoperatively is ideal, within 6 hrs postop is fine too.

Continued indefinitely.

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58
Q

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

A

Cancel the case.

Plavix and ticagrelor (Brilinta) need to be stopped for 5 days preop.

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59
Q

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

A

Plavix and ticagrelor (Brilinta) can be stooped 24 hrs to 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.

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60
Q

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

A

reduce incidence and sequela of atrial fibrillation

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61
Q

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

A

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

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62
Q

Which postop CABG patients require ACE or ARB?

A

LVEF <40, HTN, DM, CKD. Unless otherwise contraindicated.

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63
Q

What is the continuous IV insulin target in postop CABG?

A

blood glucose concentration <180

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64
Q

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

A

L Cx or RCA usually if critically stenosed and perfusing LV myocardium - can improve survival and decrease reintervention

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65
Q

RIMA patency is directly related to what?

A

Degree of proximal stenosis of the target vessel. Ie how much competitive flow is there?

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66
Q

When is a radial artery recommended? What is patency of the RA prone to?

A

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.

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67
Q

Who is the ideal patient who gets complete arterial revascularization?

A

<60, with few comorbidities, severe L sided stenosis, and critical R sided stenosis. Skeletonize.

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68
Q

What are inferior leads?

A

II, III, aVF

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69
Q

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

A

Inferior leads: II, III, aVF.

Or posterior findings: reciprocal V1-2.

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70
Q

What EKG changes suggest LV or LAD/LCx territory ischemia?

A

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

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71
Q

What is diagnostic for STEMI?

A

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

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72
Q

What is the diagnostic criteria for NSTEMI?

A 
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.
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73
Q

When can IABP be useful in the setting of MI?

A

refractory shock despite initial medical management; post-infarct VSD; acute papillary muscle rupture

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74
Q

What are contraindications for IABP?

A

Severe AI and PVD precluding placement.

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75
Q

What is the first line reperfusion strategy for STEMI?

A

PCI. Door to balloon time of 90 min.

76
Q

What is the role for CABG in STEMI?

A

Failure of PCI + coronary anatomy suitable + persistent ischemia.
OR MI complication - papillary muscle rupture, post-infarct VSD, LV rupture

77
Q

What coronary disease is left-main equivalent?

A

> 70% in LAD and L Cx

78
Q

A patient presents w/ NSTEMI, stable, meets indication for CABG. How do you manage?

A 
Maximize medical mgmt: heparin, ASA, O2 if needed, IABP if refractory angina or low EF. 
Urgent CABG (plavix should be stopped 24 hrs).
79
Q

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

A

Urgent CABG d/t cardiac arrest. Also for life-threatening arrhythmia d/t ischemic disease.

80
Q

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

A

CABG.

Consider delaying until RV is optimized w/ inotropes, diuretics, or even mechanical support.

81
Q

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

A

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

82
Q

A patient requires CABG and is found to have a porcelain aorta. How does this affect planning?

A

Preop: evaluate groins and axilla w/ CT.
Consider beating heart CABG - may need fluids, pressors, and shunt.
If needed, peripheral cannulation: axillary or femoral.
Try to use all arterials, and Y off the LIMA if needed.
SVG may be anastomosed to innominate, carotid, SCA, R axillary artery, or descending aorta.
Be ready to circ arrest.

83
Q

A CABG patient has porcelain aorta and AI. They are getting AVR. How do you make sure the heart doesn’t distend too much?
How do you do proximal anastomoses?
What uf you cant find a safe place to clamp?

A

LV vent via R SPV or LV apex.
The patient will need ascending aortic replacement in order to place proximal anastomoses.
The patient may need circulatory arrest if you cannot find a safe place to clamp.

84
Q

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

A

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

85
Q

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

A

No touch technique - avoid embolization of debri

86
Q

What is your myocardial protection strategy for redo CABG?

A

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.

87
Q

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)?

A

sequencing vein grafts

88
Q

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?

A

Grafts to that area on TEE should be reconstructed immediately.

89
Q

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

A

End-to-side to patent arterial grafts.

Use RIMA in situ if possible.

90
Q

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

A

Suspect coronary/graft injury.
Heparinize and obtain femoral bypass.
Can attempt repair once injury is exposed vs coronary perfusion catheter.
Complete the operation.

91
Q

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

A

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

92
Q

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

A

EKG - rule out ongoing ischemia and arrhythmia.
Echo diagnostic - color flow Doppler shows size and location of VSD (also valves, R side pressures, PA, tamponade).
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).
LHC - can determine if need for revasc.

93
Q

Post-infarct VSD mortality?

A

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

94
Q

Manage a post-infarct VSD preop.

A

Reduce afterload to decrease L-to-R shunt (nitroprusside).
Maintain cardiac output and perfusion (milrinone).
Increase coronary perfusion pressure.

IABP and inotropes. Milrinone.
ECMO or biventricular support can be used for temporary salvage before more definitive surgery can be performed.

95
Q

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

A

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.

96
Q

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

A

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

97
Q

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

A

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).

98
Q

When is delayed repair for post-infarct VSD acceptable?

A

Severe end-organ damage unable to undergo operative repair.
May need LVAD to improve end organ dysfunction and allow for maturation of the infarcted tissue.
Biventricular assist device may be needed if LVAD worsens R-to-L shunt.

99
Q

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

A

Time in cardiogenic shock

100
Q

Is asymptomatic severe aortic stenosis an indication for surgery?

A

No

101
Q

How can you “unmask” asymptomatic severe aortic stenosis to objectively confirm a patient is without impairment?

A

exercise stress test (treadmill) - positive if symptoms occur, systolic blood pressure falls by more than 10 mm Hg, dysrhythmias occur, or ST segment changes are noted

102
Q

What is the peak gradient in the context for aortic stenosis?

A

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.

103
Q

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

A

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.

104
Q

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

A

Stroke volume index <35% ml/min/m^2.

105
Q

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

A

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

106
Q

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?

A

pseudo-AS

107
Q

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

A

Septal myectomy and possible mitral valve surgery

108
Q

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

A

Cardiac cath to cross the valve and obtain a hemodynamic AV study.

109
Q

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

A

TAVR CT scan - valve morphology (TTE unreliable), AV annulus and LVOT sizing, coronary height and orientation, and sinus height and width sizing.

110
Q

What are the diagnostic criteria for severe AS?

A 
Any of the following: 
- mean AV gradient >40
- peak velocity across AV >4 m/s
- AVA <1 or indexed <0.6
- dimensionless index <0.25 
Always confirm. Always r/o CAD, aneurysm, and MV disease.
111
Q

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

A

Anatomy.
Age and medical conditions affecting long-term prognosis.
Preference.

112
Q

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

A

STS >15%. TAVR shows survival benefit in these patients.

113
Q

Compare likely complications for TAVR vs SAVR.

A

TAVR - ppm.

SAVR - bleeding, re-hospitalization, atrial fibrillation.

114
Q

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

A

Lower reintervention rate in <60 yrs old.

Superior survival at 15 yrs if b/w 50-70 yrs.

115
Q

What complication of a surgical bioprosthetic aortic valve placement will likely reduce benefit from a valve-in-valve procedure?

A

patient-prosthesis mismatch

116
Q

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

A

TAVR is not approved for use in this population.

117
Q

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

A

4.5 cm

118
Q

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

A

Effective orifice area (obtained by sizing valve and finding the corresponding EOA published by the manufacturer)/BSA.

119
Q

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

A

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

120
Q

Is EOAI <0.85 a contraindication for aortic valve surgery?

A

No. In a comorbid elderly patient w/ symptomatic severe AS, a risk of moderate PPM is preferred over cross-clamp time and surgical risk.

121
Q

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

A

Class IIa indication for replacement at time of surgery.

122
Q

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

A 
May just be slow d/t hypertrophy. 
Check crossclamp.
Check drainage. 
Add LV vent in R SPV. 
Open aorta and give direct cardioplegia.
Cool patient.
123
Q

Intraop TEE during AVR for AS shows moderate perivalvular leak. How do you mange?

A

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).

124
Q

What can you do if a patient’s EOAI is <0.85 during AVR for AS, and this is unacceptable?

A

consider root enlargement or total root replacement

125
Q

What can make an asymptomatic severe AS a surgical candidate?

A 
Low gradient w/ <50% EF.
Critical AS (>5m/s velocity).
Severe LVH.
Concomitant cardiac operation.
Severe calcification.
126
Q

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

A

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

127
Q

In workup for AR, a bicuspid valve morphology tells you what about the future procedure?

A

More amenable to repair, especially with more normal sized roots. Jet direction is critical.

128
Q

Which AR patients need a heart cath?

A

Need: significant risk factors for CAD or those older than 40 in whom AVR is considered.

129
Q

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

A

cardiac cath w/ root angiography and measurement of LV pressures

130
Q

Severe AR is defined by what echo/angio parameters?

A 
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+
131
Q

Diagnosis of chronic severe AR requires evidence of what?

A

LV dilation

132
Q

2017 guidelines indications for surgery for chronic AR?

A

symptoms and severe
other cardiac surgery and severe (moderate is IIb)
asymptomatic, severe, and LVEF <50
asymptomatic with severe LV dilation - LVEDD >75mm or ESD >55mm
asymptomatic with LV ESD >65 and normal EF (IIb)

133
Q

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?

A

Prior to bypass, you should be ready for distention - have retrograde cardioplegia access.
Arrest immediately.
Create the aortotomy, then give direct cardioplegia.

134
Q

When trying to establish retrograde cardioplegia for an AR case, you have difficulty, and the position is questionable. What can be done?

A

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

135
Q

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

A

Initiate CPB, clamp, give ostial cardioplegia.

136
Q

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

A

Replacement is safest.

137
Q

During AR surgery, 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?

A

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.

138
Q

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?

A

Use a bovine or autologous pericardial patch to ensure no tension on the suture line.

139
Q

You complete an AVR, but there is periprosthetic regurgitation. What do you do?

A

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.

140
Q

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

A

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

141
Q

In non-surgical candidates w/ AR, what are some of the operative considerations for TAVR?

A

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.

142
Q

Describe the benefits of aortic valve repair in AR surgery?

A

Similar results for AVR w/o need for anticoagulation as opposed to mechanical implants and possibly improved durability compared to bioprosthetics

143
Q

How do stented pericardial aortic valves tend to fail?

A

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

144
Q

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

A

Mechanical valves, though they do limit lifestyle d/t need for anticoagulation, and they limit future TAVR options.

145
Q

What tests should you obtain before a redo AVR?

A

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

146
Q

Compared to TAVR, redo AVR is associated with what risk profile?

A

Lower vascular complications and perivalvular leak.

Higher short-term stroke rate, atrial fib rate, AKI, bleeding.

147
Q

How do you decide b/w valve in valve TAVR vs redo SAVR?

A

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.
Eval for risk of coronary obstruction: coronary height needs to be >10mm.

148
Q

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

A

<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.

149
Q

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?

A

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.

150
Q

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

A

There needs to be a compelling reason to NOT do redo SAVR.

Most current TAVRs are designed for AS, not AI.

151
Q

In what situations should a ViV TAVR be more strongly considered as opposed to a redo AVR?

A

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

152
Q

ViV TAVR self-expanding vs balloon expandable discussion.

A

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

153
Q

For a younger patient at low surgical risk w/ severe structural bioprosthetic aortic valve deterioration, what is the ideal procedure?

A

Redo AVR.

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 concomitant surgical pathology.

154
Q

Discuss cannulation strategy for redo AVR.

A

Be prepared for anything - have preop imaging; axilla, femorals, and legs prepped (vein if coronary injury). Consider placing femoral sheaths (4-5 Fr).
Consider bypass 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.

155
Q

Discuss myocardial protection in a redo AVR w/ AI.

A

Retrograde cardioplegia +/- antegrade and ostial.

LV vent.

156
Q

What are the considerations for the conduction system in redo AVRs?

A

Higher risk of heart block. Make sure you have reliable wires and consider a-wires.

157
Q

Discuss prevention and management of fibrillation during initial dissection of a redo AVR w/ moderate AI.

A

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)

158
Q

Discuss operative plan for redo AVR w/ previous CABG.

A

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
May need to mobilize grafts for aortotomy vs transect and rebypass w/ ligation of the old graft.

159
Q

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?

A

Transect aorta.

160
Q

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

A

Patch.

May need homograft recon if necessary.

161
Q

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

A

Preparation: have legs prepped so vein can be taken.

Look at cath to ensure you are distal to disease during bypass.

162
Q

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

A

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.

163
Q

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

A

Before closing aortotomy, visualize the ostia.

Give retrograde plegia and look for blood return from the os.

164
Q

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

A

In redo settings, the aorta can be less compliant. Use a patch, and try not to “oversize” the aorta.

165
Q

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

A

Likely functional MR 2/2 AS.

Safest: redo SAVR and monitor MR as outpt for need for MitraClip.

166
Q

What critical diagnoses need to be considered in the differential for patients with a failed AVR being considered for re-intervention?

A

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

167
Q

What critical diagnoses need to be considered in the differential for patients with a failed AVR being considered for re-intervention?

A

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

168
Q

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

A

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.

169
Q

Primary mitral regurgitation is generally caused by what?

A

primary leaflet abnormalities - usually result of degenerative disease

170
Q

Secondary MR is generally caused by what?

A

structurally normal valve leaflets are unable to coapt completely - owing to a distortion of either the annulus or the subvalvular apparatus

171
Q

LV dysfunction and secondary MR prognosis compared to either abnormality in isolation?

A

much worse; controversial whether revascularization alone is helpful; controversial whether addressing MR will be of value

172
Q

Carpentier’s Type 1 MR?

A

normal leaflet motion - results from LV enlargement and annular dilation (functional MR)
can also be from perforation in leaflet

173
Q

Carpentier’s Type II MR?

A

leaflet prolapse - can be degenerative, acute papillary rupture after MI

174
Q

Carpentier’s Type IIIa MR?

A

leaflet restriction, systole and diastole - rheumatic

175
Q

Carpentier’s Type IIIb MR?

A

restriction during systole alone - chronic ischemic disease

176
Q

Dilated cardiomyopathy is likely to cause what type of MR?

A

type 1 - normal leaflet motion

pts may have severely depressed LV fct

177
Q

Ischemic MR tends to cause what type of MR?

What is mechanism?

A

type IIIb - systolic restriction
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

178
Q

What is the study of choice to clarify the mechanism of MR?

What is a problem with this study?

A

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

179
Q

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

A

mitral valve REPLACEMENT, chordal sparing - bio valve is probably best since poor prognosis long-term

  • remember GDMT, as this is secondary MR
  • stage D - RVol >60ml, RF >50%, ERO >0.4 cm2
  • 2a evidence
  • either way, 2 yr survival is 20-25% - why bio valve is likely best
180
Q

What is an Alfieri stitch and when is it appropriate?

A

At the time of apical incision such as LVAD for Type I (nl leaflet motion) secondary MR

181
Q

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

A

avoids excess manipulation of heart that predisposes to AV groove dissociation

182
Q

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?

A

LVAD. Consider Alfieri stuure after apical coring.

183
Q

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

A

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.

184
Q

Pt w/ severe symptomatic secondary mitral regurgitation and EF <50%. Pt sx are persistent despite GDMT. What is recommended for mitral valve?

A

Eval for transcatheter edge-to-edge MV repair (2a)

  • LVEF 20-50
  • LVESD <70mm
  • PASP <70 mmHg

If anatomy not good, then consider surgery (2b)

185
Q

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

A

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.

186
Q

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

A

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

Adult Cardiac Surgery Board Review (29 decks)

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