Pre-bypass Flashcards

1
Q

What are components of goal directed therapy

A
  • optimize myocardial oxygen supply/demand balance
  • optimize ventricular pressure-volume relationship
  • maintain contractility and CO
  • control heart rate and rhythm
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2
Q

what is it important to protect against pre-bypass

A

ischemia

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3
Q

Periods of high stimulation

A
  • incision
  • sternotomy
  • pericardiotomy
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4
Q

periods of low stimulation

A
  • pre-incision
  • IMA harvest
  • cannulation of aorta
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5
Q

Why do you bring systolic own to 90 during cannulation of aorta

A

to prevent embolic incidents

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6
Q

Risks of redo sternotomy

A
  • be prepared to crash on bypass

- adhesions of vessels to posterior side of sternum, auricular appendage

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7
Q

Two common risks with sternotomy

A

IMA dissection and brachial plexus injury

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8
Q

Other risks with sternotomy

A
  • retractor compression of left subclavian artery
  • radial nerve injury from post supporting the pittman retractor
  • risk of sternal fracture
  • papaverine - hypotension and anaphylaxis
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9
Q

Sources for graft

A
  • IMA
  • Radial artery
  • saphenous vein
  • gastroepiploic artery
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10
Q

common issues pre-bypass

A
  • ischemia
  • hypotension
  • hypertension
  • rate probelms
  • hyperglycemia
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11
Q

What reduces the incidence of perioperative MI before bypass

A

prevention and rapid treamtent of ischemia

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12
Q

major risk factor for ischemia?

A

tachycardia

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13
Q

considerations for why the patient is ischemic

A

tachycardia
hypertension
hypotension
hypoxia

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14
Q

How can you alter your anesthetic plan to remedy ischemia

A
  • lighten/deepen your anesthetic
  • vasodilator
  • BBlocker
  • pressor/inotrope (with caution)
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15
Q

Nitroglycerine mechanism of action on preload and afterload

A

Decrease preload through venodilation resulting in decreased LV filling pressures and decreased diastolic chamber size

Decreased afterload with decreases systolic pressures, decreases SVR and improves coronary circulation

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16
Q

Nitrates role in coronary circulation

A
  • epicardial cornoary artery dilation
  • reactive areas only
  • athermatous vessels do not react/dilate
  • increase collateral coronary artery flow and vessel diameter
  • improves subendocardial flow
  • reversal and prevention of coronary vasospasm and vasoconstriction
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17
Q

Beta blockers role in ischemia

A
  • reduce myocardial 02 consumption
  • decrease HR and contractility
  • improve coronary artery blood flow
  • prolong diastolic time
  • improves both collateral flow and ischemic flow
  • overall improves myocardial supply/demand ratio
  • reduce mortality post-MI
18
Q

Calcium channel blockers and their role in preventing ischemia

A
  • slow the ventricular response rate in afib/aflutter
  • cornary vasodialtors
  • depress contractility and vascular tone, decrease SV
19
Q

Verapamil

A

-ca channel blocker best for tachyarrhythmias

20
Q

nifedipine and diltiazem

A

ca channel blocker best for vasodilation

21
Q

benefit of diltiazem

A

ca channel blocker vasodilates with the least myocardial depression

22
Q

Potential causes of hypotension

A
mechanical (surgical)
technical
deep anesthesia
occult blod loss into chest
typically hpovolemia
23
Q

Treatment of hyotension

A

fluid bolus (colloid, crystalloid)
vasopressors
inotropes (w/ caution)

24
Q

causes of hypertension

A

most commonly light anesthesia
hypoxia (consider ET position)
hypercarbia
hypervolemia

25
Q

Treatment of hypertension

A

increase depth of anesthesia
resolve ventilation problems
beta blockers

26
Q

HR problems: SB

A

common causes: narcotic effect, ischemia, myocardial supply/demand

27
Q

HR problems: ST

A
much more ominous than SB
most common cause of ischemia
light anesthesia?
ventilation problems?
treat with narcotics or beta blockers
28
Q

efffects of hyperglycemia

A
  • impaired leukocytes and immune function
  • impaired endothelial vasodilation
  • inhibits development of collateral coronary blood flow
  • higher mortality rate from MI
  • impaired wound healing
  • increased infection rate
29
Q

CBP causes a temporary state of insulin ______

A

resistance

30
Q

Heparin dosing

A

300 u/kg (3 mg/kg)

31
Q

heparin administration

A

give via central line

aspirate before and after

32
Q

heparin and act

A

draw act 3 min after dose

ACT must be >400

33
Q

AT-III deficiency

A

heparin resistance - inability to get adequate anticoagulation despite conventional heparin doses more common in those who have been on heparin preoperatively

34
Q

How to tx AT-III deficiency

A

usually responds to increased dosing

may give 1,000 units of AT-III or 2-4 units of FFP to restore AT-III activity

35
Q

HIT type 1

A

usually of little clinical significance

36
Q

HIT type II patho

A

IGE antibodies develop to heparin-platelet factor 4 complexes on the surfaces of the platelets and endothelial cells. Complex activation and platelet aggregation

37
Q

symptoms of HIT II

A

throbocytopenia, heparin tachyphlaxis, bleeding, thrombosis

38
Q

treatment of HIT II

A

discontinue heparin, aspirin thereapy
Alt: LMWH, Heparinoids (dermatan sulfate and danapariod)
direct thrombin inhibitors
plasmapheresis (wait until antibodies disappear)

39
Q

direct thrombin inhibitors

A

hirudin, bivalirudin and agatroban, ancrod

40
Q

Are you ready to go on pump?

A
LAMPS
labs
anesthetic (midaz, narc, relaxant)
monitors
patient/pump
support