Case 34 - open AAA repair Flashcards

1
Q

What is LaPlace Law, how does it relate to aortic aneurysm?

A

Laplace Law

  • Wall Stress = Pressure x Radius / 2 x Wall thickness
    • increase radius will increase aortic wall stress and make more prone to rupture
  • elective sx - aneurysm > 6cm or symptomatic or increase rate of growth
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2
Q

How do you evaluate myocardial reserves for patients undergoing aortic repair?

A

Assess 1) RF, 2) cardiac reserve via testing

Risk factors for myocardial ischemia

  • previous MI
  • angina
  • CHF
  • Male
  • Smoking
  • DM
  • limited excercise tolerence

Assessment

  • Low Risk –> proceed with sx without further eval
  • negative stress w/i 2 yrs or CABG and asymptom –> proceed with sx without further eval
  • Moderate Risk –> Stress test
  • High Risk for MI –> consider cath

negative stress test wi

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3
Q

What is stress tresting?

A

There are two components to stress testing: 1) stressing the myocardium, 2) detecting ischemia or infarction

Stressing

  • mechanical (exercise treadmill)
  • pharmacologic
    • dobutamine - increase myocardial O2 demand
    • dipyridamole - purposely cause myocardial steal
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4
Q

With stress testing, how do you detect myocardial ischemia?

A

Detection

  • EKG, Nuclear Studies, Echo
  • EKG
    • changes in ST segment (elevation, depression)
  • Nuclear Studies
    • a) reversible defect
      • rest - nuclear tracer uptake, stress - nuclear tracer absent
    • b) old infarction
      • absent nuclear uptake with rest and stress
  • Echo
    • a) reversible defect
      • wall motion abnormalites with stress
    • b) old infarction
      • akinetic segment with rest and stress
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5
Q

Why is stress testing important?

A
  • 1) allows us to determine if myocardium is a risk (ischemia with stress) as opposed to myocardum that is infarcted (old vs new)
  • 2) if myocardium at risk, should patient be further optimized (pharmacologic vs intervential)
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6
Q

If patient undergoes myocardial revascularization, how long should they be on antiplatelet therapy for prior to surgical procedures?

A

Myocardial Revascularization –> PCI or CABG –> pts placed on dual anti-plt therapy (ASA + clopidogrel)

PCI

  • balloon angioplasty
    • anti-PLT for 2-4 weeks
  • BMS
    • anti-PLT for 6 weeks
  • DES
    • anti-PLT for at least 12 months

CABG

  • unknown duration of anti-PLT therapy
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7
Q

Why do patients after myocardial revasc need to be on anti-PLT?

A
  • all PCI procedures are assoc with re-stenosis
  • During surgery, inflammation and hypercoagulable response, as well as premature d/c of anti-PLT therapy can lead in-stent thrombosis.

**If pts require aortic surgery and have significant CAD requiring PCI, type of interventiion and type of stent placed (if any) must be weighted against urgency of surgery.

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8
Q

What meds should administered preop to aortic sx pts?

A
  • should take all anti-HTN and anti-angial meds prior to sx
  • anxiolysis is recommended to decrease preop HTN and tachy –> increase o2 demand and stress on aortic wall –> myocardial ischemia and risk of rupture
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9
Q

What are main goals during aortic sx? What are the main goals during ruptured AAA sx?

A
  • HD stability
  • Anesthesia –> amnesia, analgesia, immobility
  • Strict control of BP to limit risk of rupture or extent of dissection
    • beta blockers, vasodilators

Ruptured (hypovolemic shock secondary to hemorrhage)

  • maintain volume status
  • secure airway
  • immediate surgical control
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10
Q

Should patients continue beta blockers or start beta blockers when presenting for aortic surgery?

A

Beta blockers

  • decrease contractility, decrease HR via B1 receptor antagonism in heart–> decrease O2 demand

To start to not start Beta blockade

  • patients on beta blockers should continue beta blockers during sx
    • acute d/c of long-term BB leads to increase myocardial events
  • patients at high risk for ischemia should be started on Beta blockers
    • titrate to HR and BP
    • POISE Trial (periop ischemic evaluation) –> BB had lower incidence of myocardial events, but greater incidence of hypotension and assoc risk of stroke and mortality.
    • Therefore TITRATE BB TO EFFECT
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11
Q

What are the goals for induction of anesthesia in aortic sx patients?

A

emergent sx

  • RSI –> full stomach

Overall

  • Goal - avoid hemodynamic aberrations during induction and tracheal intubation
    • HTN = risk of rupture, Hypotension = decrease organ perfusion
  • doesn’t matter what you use as long as you follow this induction goal
  • vasoactive meds (nitroprusside, NTG, Esmolol) - fast on and off
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12
Q

How are patients undergoing aortic anuerysm surgery monitored?

A
  • Standard ASA monitors
  • EKG - Leads II and V5
    • detects most MI and arrhythmias
  • Foley Catheter
    • monitor UOP, provide early indication of renal malprefusion
  • Core temp (bladder, esophageal, PA)
    • normothermia to prevent MI, coagulopathy, wound infection
  • Arterial line
    • beat to beat monitor of arterial pressure, frequent blood sampling
  • CVP
    • central route for drug admin, rapid infusion of fluids, measure filling pressures of heart
    • right IJ or left SC preferable. Left IJ assoc with increas incidence of innominate vein perf
  • PA vs TEE
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13
Q

What are causes of decreased blood pressure during aortic sx?

A

Major Causes:

  • shifts in intravascular volume
  • effects of anesthetic agents
  • surgical manipulation

Intravasc Volume

  • hemorrhage from intercostal artery back-bleeding
  • aortic disruptions
  • anastomotic suture leaks
  • evaporative/ third space losses

Maintain Intravasc volume

  • large bore IV
  • CVC
    • for rapid transfusion system

Blood salvaging techniques (cell saver)

  • Pros
    • scavanges and washes erythrocytes
    • may decrease overall allogenic blood prod
  • Cons
    • takes time to wash blood cell (need to fill reservoir before process)
    • lose plasma volume, protein, coag factor, PLT
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14
Q

Are CVP measurement accurate in measuring left heart pressure?

A
  • CVP is indirect measure of left heart filling pressure by measuring right sided pressure
  • correlates with left side if pt has good LV function
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15
Q

What are the benefits of pulmonary artery catherization?

A

Indications

  • decrease LV function
  • pulm HTN
  • severe valv disease
  • advanced systemic organ dysfucntion

Benefits

  • determine afterload
  • CO by thermodilution
  • o2 delivery via MVO2 sample
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16
Q

What are the benefits of using a TEE during aortic sx?

A

Indications

  • ventricular function
  • intravascular volume

Beneits

  • dx RWMA / ventricular dysfunction
  • measure stroke volume and EF
  • valvular pathology
  • aortic and pericardial pathology
17
Q

What happens during aortic cross-clamping?

A
  • overall, aortic cross clamp assoc with abrupt increase in afterload –> increase in prox aortic pressure
    • afterload is the sum of resistance of all systemic arterioles (SVR)
    • SVR = ( (MAP-CVP) / CO) x 80

Supraceliac aortic occlusion

  • clamp above celiac artery (perfuses gut)
  • Inc Preload
    • volume redistribution from veins distal to clamp. Shorter circuit the blood circulates through.
    • less blood in splanchnic circlation (reservoir for blood)
  • Inc Afterload
    • occlusion of aorta, increase prox aortic pressure due to increase back pressure
  • initial Inc in contractility and CO
    • preload/contractility matches afterload initially, until afterload increase surpasses ability of heart to push blood further
18
Q

What can you do to maintain normal blood pressure during aortic cross clamping?

A
  • aortic cross clamp assoc with increase in afterload and initial inc in preload
    • afterload - due to mechanical obstruction of aorta, causing Inc back pressure of blood.

methods

  • Preload - maintain low before occlusion
    • during clamp - maintain preload as it may decrease due to surgical blood loss
  • venodilators (NTG/nitroprusside)
    • start prior to clamp
    • will help reduce afterload effect from clamp
19
Q

Intraop hypotension during aortic sx can be a result of the following?

A

Main causes

  • hypovolemia (evap, third space, blood loss)
  • myocardial depression (increaes O2 demand with clamping, myocardial stunning from lactate, ischemia)
  • decrease in afterload with unclamping
  • lactate washout

Unclamping hypotension

  • redistribution of blood flow now to reperfused tissue –> blood pooling / larger cirucit for blood to circulate thru
  • lactate accumulation
    • myocardial depressant
  • vasodilator mediator accumulation
    • decrease in SVR –> hypotension
  • electrolyte derangements (hyper K+, hypo Ca2+)

Tx:

  • correct acidosis, hypovolemia, hypocalcemia
  • use pressors/inotropes
  • always consider re-clamping to catch up with metabolic derangements
20
Q

What can you do to prevent renal insuff in aortic sx patients?

A
  • Mannitol
    • 30 min prior to clamping
  • Fuorsemide
    • may protect ishchemic injury to renal medulla (o2 tension typically low in this area)
    • may increase prostaglandin produciton –> increase renal blood flow
    • little evidence
  • ask sx to redirect blood flow into renal arteries (temporary grafts)
  • sx may give kidney cocktail (nutrients to organ, hypothermic solution)
  • dopamine???
    • renal protective dose (1-3 mcg/kg/min)
    • dilate renal afferent arteriole
    • no advantage when compared to keeping pt euvolemic
21
Q

What are options for post-op analgesia?

A
  • IV opioids
    • PCA vs intermittent boluses
    • larger doses may be required –> increase in SE
  • Epidural
    • LA SE
      • sympathetic blockade (hypotension and tachy unless cardioaccel fibers knocked out)
      • motor blockade
      • LAST
    • opioids SE
      • N/V, pruritis, urinary retention, resp depress