TSRA Clinical Scenarios - Adult Cardiac Surgery Flashcards
Heparin dose for CPB?
400 units/kg
ACT required for initiation of CPB?
400-480 (480 is book answer).
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?
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.
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?
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.
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?
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.
If heart is distending when coming of CPB, what amount of AI requires consideration for replacement?
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.
Explain CPB components. Start with drainage and trace the flow.
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.
Attempt CPB, but perfusionist says high aortic line pressure. What is differential?
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
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?
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.
Attempting CPB flows, but MAP not rising above 40. Pt has hx of ACE use.
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.
You place a retrograde cardioplegia line in the coronary sinus, but the measured plegia line pressures are low. How do you troubleshoot?
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.
When giving retrograde cardioplegia, you find a L SVC. How do you manage?
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.
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?
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.
If patient has previous CABG and is requiring CPB, how do you manage an open LIMA?
Consider retrograde plegia.
Can clamp vs cold bypass flow.
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?
Axillary cannulation may be needed to make room for an aortic cross clamp.
In a redo patient w/ previous CABG w/ open LIMA, what is the problem with antegrade cardioplegia? What are possible solutions?
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.
In the setting of aortic insufficiency, discuss options for CPB.
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.
How could you incompletely deliver cardioplegia if using retrograde cardioplegia assuming no L SCV? What can you do?
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).
What can make retrograde cardioplegia delivery riskier in a redo operation (previous CABG)?
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.
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?
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).
How do you confirm adequacy of retrograde cardioplegia catheter delivery?
What’s the appropriate pressure for cannula flow?
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.
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?
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.
Where does a persistent L SVC usually drain?
Into the coronary sinus, may partially drain via innominate V.
You attempt to infuse antegrade cardioplegia. The perfusionist notes high line pressure. How do you manage?
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.
After a cardiac surgery pump case w/ retrograde cardioplegia, the myocardium is slow to regain activity. What should you check?
Check retrograde catheter and/or that the balloon is down, in order to allow for adequate coronary sinus flow.
When sewing a CABG, you notice bleeding from the coronary arteriotomy.
What does this mean?
What do you do?
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.
How do you manage a perforation of the coronary sinus after placement of a retrograde cardioplegia catheter?
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.
What are the three broad categories for etiology of persistent electrocardial activity (problem with initiating plegia in CPB)?
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
Redo sternotomy, and there is a significant amount of dark blood from the sternomanubrial jct. What was injured?
Innominate vein.
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?
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.
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?
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.
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?
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.
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?
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.
SVC is ruptured during balloon dilation for SVC syndrome. How do you manage?
What’s your cannulation strategy?
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.
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?
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.
Cath lab creates an RV puncture and places a pericardial drain w/ bloody drainage. Manage.
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.
There is a small R PA injury noticed after an aortic surgery when coming off bypass. Manage.
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.
You puncture the opposite side of the aorta during arterial cannulation. Manage.
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.
What symptoms represent unstable angina?
chest pain at rest, exertional angina not relieved by rest, and new onset of chest pain
What symptoms represent stable ischemic heart disease
exertional angina - predictable, improves with rest
What is included in CAD guideline-directed medical therapy?
lifestyle modification, statin therapy (LDL goal 70-100), beta-blockade, aspirin, and ACE inhibition (if LV dysfunction, DM, or CKD)
What are hemodynamically significant coronary lesions on left heart cath?
Left main >50%
non-LM >70%
What FFR is hemodynamically significant? When is FFR used?
< 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.
What is the SYNTAX score?
16 segments in the coronary tree.
Lesions in this tree are scored.
The sum of these scores is the overall SYNTAX score.
What are the cutoffs for the SYNTAX score in terms of complexity?
What was the main implication of the SYNTAX trial?
> 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.
What is a non-invasive option for imaging the coronary arteries?
Gated cardiac CT
What did a secondary analysis of the STITCH trial reveal concerning myocardial viability studies?
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.
How do you decide who needs coronary revascularization in patients with stable ischemic heart disease?
Activity limiting symptoms despite maximal medical therapy.
Active patients who want PCI for better QoL compared to med therapy.
Anatomy with proven survival benefit.
After deciding on revascularization, how do you decide who needs CABG?
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.
Management of significant CAD in 1 vessel w/ refractory angina despite medical therapy and PCI.
CABG.
Management of significant CAD in 1 vessel after sudden cardiac arrest from ischemic ventricular arrhythmia.
CABG.
Management of CAD at 50% in 1 vessel in patients undergoing valve or aortic surgery?
Concurrent CABG.
What is the ideal graft for the LAD?
IMA. Left preferred because of length and ability to avoid midline more (redo surgery).
Right is second choice.
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?
BIMA and radial.
What can be done technically to reduce the risk of sternal complications in a patient getting BIMA grafts?
Skeletonized.
Known risks factors for sternal infection and malunion in cardiac surgery?
Nonelective procedure, age, uncontrolled DM (HbA1c >7), BMI >40, female, COPD, preop hospitalization >3 days, smoking, immunosuppression regimen, radiation mediastinal injury
When should CABG patients receive aspirin?
Preoperatively when they discover CAD is ideal.
Within 6 hrs postop after CABG.
Continued indefinitely.
A patient comes in for elective CABG but has not stopped taking plavix. What do you do?
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.
A patient requires an urgent CABG but is taking plavix.
What do you do?
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.
Why are beta blockers reinstituted after CABG (as long as no contraindications)?
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).
What is the target lab value for statin therapy in patients undergoing CABG?
reduce LDL <100 and achieve at least 30% dec in LDL
Which postop CABG patients require ACE or ARB?
LVEF <40, HTN, DM, CKD unless otherwise contraindicated.
Almost all of them.
Cardiology team can start this as outpatient.
What is the continuous IV insulin target in postop CABG?
blood glucose concentration <180
When anatomically and clinically suitable, what is the RIMA often used for?
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.
IMA patency is directly related to what physical parameter in the target vessel?
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.
What lesions should a radial artery be used for?
What is patency of the RA prone to?
What specific postop medication improves patency?
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
Who is the ideal patient who benefits most from complete arterial revascularization?
<60, with few comorbidities (no DM, ESRD), severe L sided stenosis, and critical (90%) R sided stenosis (radials work better here).
Skeletonize.
What are inferior leads?
II, III, aVF
What EKG findings suggests RV or RCA ischemia (or L dominant PDA disease)?
Inferior leads: II, III, aVF.
Or posterior findings: reciprocal V1-2.
What EKG changes suggest LV or LAD/LCx territory ischemia?
There are 3 associated territories, what are they, and what leads indicate each?
Anteroseptal: V1-V2.
Anteroapical: V3-4.
Anterolateral: V5-6, I, aVL.
What is diagnostic for STEMI?
Angina symptoms for 20 min w/ ST elevation 2+mm in 2 contiguous leads or new LBBB. Greater risk for transmural ischemia.
What is the diagnostic criteria for NSTEMI?
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.
When can IABP be useful in the setting of MI (3 situations listed)?
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).
What are contraindications for IABP?
Severe AI or PVD w/ resultant prohibitive anatomy (femoral or iliac artery occlusion) preclude placement.
What is the first line reperfusion strategy for STEMI?
Timing?
When might CABG be the right answer in STEMI?
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.
What is the role for CABG in STEMI?
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)
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?
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)
What coronary disease is left-main equivalent?
> 70% in LAD and L Cx
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?
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.
A patient is resuscitated from witnessed cardiac arrest. Coronary angiography shows 3V disease. What’s the revascularization strategy?
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
Manage pt w/ inferior infarction and RV involvement. PCI failed.
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.
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?
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.
A patient w/ previous coronary stent undergoes CABG. How do you manage this vessel?
If it is wide open, no reason to bypass as it will likely fail 2/2 competitive flow.
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?
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.
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?
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.
Redo CABG has higher risk than primary revascularization w/ mortality of 7-11% mostly 2/2 what disease?
What causes this?
perioperative MI - can be 2/2 incomplete revascularization, atheromatous emboli, damaged grafts, hypoperfusion through new grafts, or early graft occlusion
In a redo CABG, what is the general principle in regard to handling previous venous bypass grafts?
No touch technique - avoid embolization of debri
What is your myocardial protection strategy for redo CABG?
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.
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)?
Sequencing vein grafts.
Can also put grafts on innominate or subclavian if needed.
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?
Grafts to that area on TEE should be reconstructed immediately.
During redo CABG, there is no room on the aorta for proximal anastomoses. What options are there?
End-to-side to patent arterial grafts.
Use RIMA in situ if possible.
Can also place grafts on innominate artery.
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?
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.
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?
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.
What are the important diagnostic studies for post-infarct VSD?
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.
Post-infarct VSD mortality?
Poor - 25% within 24 hrs, increasing with time up to 97% in 1 year.
This is an indication for urgent surgery.
Manage a post-infarct VSD preop.
What are your hemodynamic goals and what meds or methods do you use to achieve them?
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.
How do you do an anterior septal rupture repair (pt w/ post-infarct VSD)?
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.
How do you do apical VSD repair (postinfarct VSD)?
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).
How do you do posteroinferior VSD repair (postinfarct VSD)?
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).
When is delayed repair for post-infarct VSD acceptable?
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.
What is the greatest predictor of post-operative mortality in pts w/ postinfarct VSD?
Time in cardiogenic shock
Is asymptomatic severe aortic stenosis an indication for AVR replacement (TAVI or SAVR)?
Discuss this.
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
How can you “unmask” asymptomatic severe (>4 Vm) aortic stenosis to objectively confirm a patient is without impairment?
exercise stress test (treadmill) - positive if…
- Symptoms.
- SBP dec by >10 mm Hg.
- Dysrhythmias.
- ST changes.
What is the peak gradient equation (in the context of aortic stenosis)?
How is it directly obtained/measured (as opposed to calculated as above)?
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.
In what scenario may a patient with severe aortic stenosis have a low gradient?
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.
How can a low flow/low gradient AS be confirmed in a patient w/ normal EF (>50)?
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%.
How can a low flow/low gradient AS be confirmed if the patient has a low EF (<50%)?
Dobutamine stress echo - if gradient increases while AVA remains the same, AS is confirmed.
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?
pseudo-AS
In the workup of AS, a significant subvalvular gradient and asymmetric septal hypertrophy is found, what treatment may be required?
Septal myectomy and possible mitral valve surgery
If the diagnosis of AS is uncertain by echo, including dobutamine stress testing, what else can be done to evaluate the gradient?
Cardiac cath to cross the valve and obtain a hemodynamic AV study.
Can directly measure gradients.
In a potential TAVR candidate for AS, what imaging needs to be obtained?
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.
What are the diagnostic criteria for severe AS?
What else should you rule out?
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.
How do you decide on SAVR vs TAVR for severe symptomatic AS?
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.
What STS risk score is prohibitive for SAVR for symptomatic severe AS?
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.
What are the likely complications for TAVR vs SAVR?
TAVR - perivalvular leak, heart block requiring permanent pacemaker, access injuries.
SAVR - bleeding, re-hospitalization, atrial fibrillation.
What are the benefits of a mechanical aortic valve compared to bioprosthetic?
Lower reintervention rate in <60 yrs old.
Superior survival at 15 yrs if b/w 50-70 yrs.
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.
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.
An AS patient undergoes TAVR CT showing bicuspid aortic valve. The valve is functional, and the patient is low risk. Discuss TAVR use.
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.
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?
4.5 cm
What is the EOA and why is it useful for aortic valve placement?
Effective orifice area (obtained by sizing valve and finding the corresponding EOA published by the manufacturer)/BSA.
Used to predict patient-prosthesis mismatch.
An aortic valve’s EOAI is < 0.85. What does this mean?
Predictive of PPM. 0.65-0.85 is predictive of moderate PPM. <0.65 is severe.
Is EOAI <0.85 a contraindication for aortic valve surgery?
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.
During workup for CABG, moderate AS is found. How do you manage?
Class IIb indication for replacement at time of surgery.
You are doing surgery for AS, but the heart is not arresting well. How do you manage?
What do you have to rule out?
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.
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?
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.
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?
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.
What can make an asymptomatic severe AS more of a SAVR candidate (higher grade of recommendation) as opposed to TAVR?
Low gradient w/ <50% EF.
Critical AS (>5m/s velocity).
Severe LVH.
Concomitant cardiac operation.
Severe calcification.
A patient with aortic regurgitation gets an echo. What are you looking for?
Confirm diagnosis and severity, assess for etiology, valve morphology, LV assessments, aortic root size.
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?
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.
Which AR patients need a heart cath?
Need: significant risk factors for CAD or those older than 40 in whom AVR is considered.
It may be good to assess RV/pulm HTN as well.
In workup of AR, what test can be done to confirm diagnosis if echo is inconclusive or discordant w/ physical findings?
LHC w/ root angiography and measurement of LV pressures
Severe AR is defined by what echo/angio parameters?
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+
Diagnosis of chronic severe AR requires evidence of what?
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.
Guideline indications for surgery for chronic AR?
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)
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?
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.
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.
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.
During AR case, what if you injure the coronary sinus and/or retrograde cardioplegia becomes unreliable?
Initiate CPB, clamp, give ostial cardioplegia.
During AR case, TEE and direct visualization shows a prolapse of the R cusp. What are the surgical options?
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
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?
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.
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?
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.
You complete an AVR, but there is periprosthetic regurgitation.
What do you do?
What does a leak around the non-coronary sinus imply?
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.
Symptomatic acute aortic regurgitation should be taken care of expeditiously. Why?
The ventricle has not had time to develop any adaptation to overcome the increased volume which can lead to rapid deterioration.
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?
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.
Describe the benefits of aortic valve repair in AR surgery?
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.”
How do stented pericardial aortic valves tend to fail?
By aortic stenosis of the biologic prosthesis, but tend to last longer than porcine valve.
What type of aortic valve is generally favored in younger (<55) patients?
Mechanical valves, though they do limit lifestyle d/t need for anticoagulation, and they limit future TAVR options.
Ideally, <50 gets a Ross.
What tests should you obtain before a redo AVR?
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
Compared to TAVR, redo AVR is associated with what risk profile?
Ie compare risks of specific complications.
Redo AVR has…
Lower vascular complications and perivalvular leak.
Higher short-term stroke rate, atrial fib rate, AKI, bleeding.
How do you decide b/w valve in valve TAVR vs redo SAVR?
Pros of ViV TAVR? Contraindications?
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.
In considering valve-in-valve TAVR, what would be considered a small in place prosthetic valve?
<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.
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?
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.
A previous AVR fails d/t AI (as opposed to AS). What are the considerations for procedural management (TAVR vs SAVR)?
There needs to be a compelling reason to NOT do redo SAVR.
Most current TAVRs are designed for AS, not AI.
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?
Prior CABG w/ LIMA (esp if near sternum).
HFrEF, >75-80 yrs, poor condition, renal failure.
Calcified ascending aorta.
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?
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).
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?
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.
Discuss cannulation strategy for redo AVR.
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.
Discuss myocardial protection in a redo AVR w/ AI.
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.
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?
Higher risk of heart block. Make sure you have reliable wires, and consider a-wires.
Near the underside of the R/non commissure.
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?
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)
Discuss operative plan for redo AVR w/ previous CABG.
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.
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?
Transect aorta.
During redo AVR, you tear the aorta/outflow tract when removing the old valve. How do you fix this?
Patch.
May need homograft recon if extensive - Bentall.
During redo AVR, you injure R coronary ostia while removing the valve. How do you manage?
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.
Coming off bypass from redo AVR, and there is RV dysfunction. Assessment and plan?
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.
How can you be sure coronary ostia are open after redo AVR?
Before closing aortotomy, visualize the ostia. Can place R angle into them.
Give retrograde plegia and look for blood return from the os.
After redo AVR, you cannot close the aortotomy d/t tension on the aorta.
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.
77yr pt w/ mechanical AVR has failed w/ AS to the point of requiring intervention, and there is MR. CKD. Assessment and plan?
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.
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)?
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
In terms of valve sizing, what info can be obtained before AVR to ensure no PPM?
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.
Primary mitral regurgitation is generally caused by what?
primary leaflet abnormalities - usually result of degenerative disease
Secondary MR is generally caused by what?
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
LV dysfunction and secondary MR prognosis compared to either abnormality in isolation?
Is revascularization or addressing MR of value?
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
Carpentier’s Type 1 MR?
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
Carpentier’s Type II MR?
leaflet prolapse - can be degenerative, acute papillary rupture after MI
1) normal
2) too much
3) not enough
Carpentier’s Type IIIa MR?
leaflet restriction, systole and diastole - rheumatic
Carpentier’s Type IIIb MR?
restriction during systole alone - chronic ischemic disease
Dilated cardiomyopathy is likely to cause what type of MR?
type 1 - normal leaflet motion
pts may have severely depressed LV fct
Ischemic MR tends to cause what type of MR?
What is mechanism?
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
What is the study of choice to clarify the mechanism and anatomy of MR?
What is a problem with this study?
TEE - however, MR severity may be lower intraoperatively d/t anes and ventricular unloading
At the time of CABG for severe ischemic MR, what is the preferred surgery for the mitral valve?
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
What is an Alfieri stitch and when is it appropriate?
Any technical considerations depending on disease process? What about valve orifice size concern?
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.
In CABG MVR, why do you do distal anastomoses first before valve?
avoids excess manipulation of heart that predisposes to AV groove dissociation
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?
LVAD. Consider Alfieri suture after apical coring.
A patient who requires CABG is found to have moderate ischemic MR. What do you do for the MR?
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).
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.
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).
What is often the mechanism for acute mitral regurgitation 2-7 days after MI?
How do you manage?
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.
Papillary muscle/blood supply/mitral commissure mnemonic:
The PDA is posterior and medial.
The LAD is anterior, and the LCX is lateral.
How does the jet in primary mitral regurgitation predict leaflet affected?
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
Vena contracta for severe mitral regurgitation?
0.7 cm
Regurgitant volume for severe MR?
60 ml
Regurgitant fraction for severe MR?
50%
Central jet (percentage of LA or characteristics) for severe MR?
40% LA or holosystolic eccentric jet
In primary mitral regurgitation, which patients should get an operation? Do they have to have severe findings?
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) or 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.
If doing a mitral valve repair, what is a necessary adjunct to reinforce most repair techniques?
Ring or band annuloplasty
During mitral repair, what is at risk if you place deep stitches at the anterior leaflet while moving from the right to left trigone?
Aortic valve (L/non commissure) - look for aortic insufficiency that wasn’t there preop.
While doing a mitral repair, what is at risk if placing deep retraction stitches outside the annulus of the P3 scallop?
Coronary sinus
In MVR w/ Barlow’s valve, what is often the best repair?
There is excess tissue in almost all scallops.
Perform quadrangular resection w/ sliding plasty.
(B) in picture***
For MV approach, when might L atriotomy be best approach?
How is it done?
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.
For MV approach, when might vertical transseptal be best approach?
How is this done?
Any advantages?
Any disadvantages?
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.
For MV approach, when might extended superior transseptal (Guiraudon) be best approach?
How is this done?
Disadvantages?
Any advantages?
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.
For MV approach, when might horizontal transseptal (Dubost) be best approach?
Any advantages/disadvantages?
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.
For MV approach, when might transaortic be best approach?
How is this done?
Any advantages?
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.
Describe the pathophysiology of SAM after mitral surgery?
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.
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
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.
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?
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.
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?
Complete heart block 2/2 AV node damage 2/2 deep/wide posteromedial mitral commissure stitch during MVR or ring annuloplasty.
How can you cause conduction block during mitral surgery?
Sutures too deep near the posterior leaflet near the PM commissure - bundle of His.
What complication will occur in mitral surgery if there is aggressive debridement or retraction/lifting of the heart?
How do you prevent this?
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.
What are the three principal goals of surgical intervention for AF?
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)
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?
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 - linear lesion connecting the box to the mitral annulus.
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?
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.
You perform a CMIV w/ LAA clip placement. TEE shows a small pouch with clot in the appendage. What happened?
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.
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?
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).
During CMIV, after completion of the RA appendage line, you come off CP bypass and notice the pt in complete heart block. What happened?
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.
Where is Bachmann’s bundle (CMIV surgery)?
Medial and superior to the roof lesion - transecting this will delay the arrival of a sinus impulse from the RA to the LA.
What is the “flutter line” and “isthmus lesion”?
Why should it be avoided during CMIV surgery?
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).
During TV surgery, where will the AV node be?
Triangle of Koch
Describe a tricuspid ring annuloplasty.
Interrupted mattress sutures with a gap a Koch’s triangle (1cm from anterospetal commissure to midpoint on septal leaflet).
During tricuspid annuloplasty, what can be injured when placing sutures near the anteropostero commisure?
RCA.
In carcinoid valvular disease, what is the gross appearance and management of an affected TV?
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.
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.
You are finishing an AVR/MVR when TEE shows lateral WMA.
What happened?
What do you do?
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.
What important structure is behind p2-p3 of the mitral valve?
Circumflex artery
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?
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
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?
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.
A pt undergoes AVR/MVR. You come off bypass, and TEE shows the following, with increased gradient across the LVOT. What happened?
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.
When should early valve surgery be performed for L side IE?
- 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
You are doing surgery for IE on mitral valve. The entire posterior annulus is involved with abscess.
What should you do?
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.
How do you manage acute AI in the setting of iatrogenic ascending aortic dissection?
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.
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.
What are the indications for repairing a TAA?
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).
In pt w/ aortic root aneurysm requiring surgery, how do you manage the valve operatively?
If valve is normal, a valve sparing procedure can be performed - David.
If <40 yrs old, consider Ross.
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).
You are doing a redo aortic root replacement, but cannot safely dissect the tissue around the aortic root posteriorly. What are your options?
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.
Diameter indication for surgical repair of sporadic ascending/root aortic aneurysm?
5.5 cm.
5 for Marfan, Ehler-Danlos, or with experienced surgeons.
Diameter indication for surgical repair of sporadic aortic arch aneurysm?
5.5 cm.
There isn’t a 5.0 or 4.5 caveat here, unlike ascending aneurysms.
What are the size cutoffs for intervention in patients with an arch aneurysm compared to ascending aneurysm?
The same for the cutoff for sporadic disease. Ascending aorta has caveats for centers of excellence for 5.0 cm cutoff.
For descending TAA, what are the asymptomatic indications for repair?
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.
When would you do an exercise echo for HOCM? What are you looking for?
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.
For HOCM treatment, what are the pertinent decision-making points?
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.
A patient has a LA myxoma. What could cause pulm HTN and obstructive heart failure?
Tumor causes diastolic mitral orifice inflow obstruction.
