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S5 - Principles III - Test 3 > Vascular Anesthesia > Flashcards

Vascular Anesthesia Flashcards

1
Q

What is the primary process leading to CAD, stroke, extremity ischemia, and aneurysms?

A

Atherosclerosis

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2
Q

What is the presumed progression of atherosclerosis?

A

Fatty streaks –> Fibrous plaques –> Complicated lesions

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3
Q

What locations does atherosclerosis commonly form?

A
  • Coronary arteries
  • Carotid bifurcation
  • Infrarenal abdominal aorta
  • Iliac arteries
  • Superficial femoral artery
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4
Q

Risk factors for atherosclerosis (11)

A
  • Hyperlipidemia
  • Smoking
  • Diabetes
  • Hypertension
  • Family history
  • Male
  • Advanced age
  • Insulin resistance
  • Physical inactivity
  • Elevated C-reactive protein
  • Elevated lipoprotein
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5
Q

T/F Atherosclerosis is a slow gradual process

A

True

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6
Q

3 causes of ultimate injury in atherosclerosis

A
  1. Plaque enlargement reducing blood flow
  2. Embolism of plaque-associated platelet thrombi or debris
  3. Complete occlusion of arteries by advanced plaque
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7
Q

What three major vessels does arteriosclerosis occur in?

A

Infrarenal abdominal aorta

Thoracoabdominal aorta

Descending thoracic aorta

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8
Q

What is cystic medial necrosis and where does it occur?

A

Degeneration of the aortic media

Occurs in ascending aorta

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9
Q

When is elective repair of aortic aneurysm recomended?

(Hint: at what diameter?)

A

> 5 cm

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10
Q

Mortality rate of elective AAA repair vs ruptured aneurysms

What about if it ruptures outside of the hospital?

A

Elective 1-11%

Ruptured 35-94% or ~75%

Pre-hospital mortaility combined 80-90%

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11
Q

Mortality if aneurysm left untreated for 5 years?

10 years?

A

5 years: 81%

10 years: 100%

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12
Q

How much do aneurysms grow per year?

A

approximately 4 mm/year

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13
Q

complications of atherosclerosis (4)

A
  • MI
  • Cerebral infarct
  • Gangrene of extremities
  • Abdominal aortic aneurysm
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14
Q

At what age do you begin to see fatty streaks in vessels?

A

20’s

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15
Q

At what age do you begin to see atheroma in vessels?

A

30s

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16
Q

At what age do you typically begin to see atheromas with complications?

What are the complications?

A

40’s

  • Thrombosis
  • Plaque rupture
  • Hemorrhage
  • Wall weakening
  • Calcification
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17
Q

Law of Laplace formula

A

T = P x r

T = wall tension

P = transmural pressure

r= vessel radius

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18
Q

What happens as the radius of the vessel increases?

A

Wall tension increases

AKA the bigger the aneurysm the higher risk of rupture

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19
Q

Which type of aneurysm is described?

Originates in proximal aorta and usually involves ascending aorta, arch and can go into abdominal aorta

A

Debakey Type 1

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20
Q

Which type of aneurysm is described?

Confined to descending thoracic aorta

A

Debakey Type IIIA

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21
Q

Which type of aneurysm is described?

Confined to ascending aorta

A

Debakey Type II

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22
Q

Which type of aneurysm is described?

May extend into abdominal aorta and iliac arteries

A

Debakey Type IIIB

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23
Q

Which type of aneurysm is described?

Descending thoracic aorta involved with or without proximal or distal extension

A

Stanford Type B

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24
Q

Which type of aneurysm is described?

Ascending aorta is involved with or without the arch or descending aorta

A

Stanford Type A

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25
Q

Which type of aneurysm?

A

Debakey Type 1

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26
Q

Which type of aneurysm?

A

Debakey Type II

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27
Q

Which type of aneurysm?

A

Debakey Type IIIa

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28
Q

Which type of aneurysm?

A

Debakey Type IIIb

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29
Q

Which type of aneurysm?

A

Stanford Type A

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30
Q

Which type of aneurysm?

A

Stanford Type B

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31
Q

Where are the two places aneurysms most commonly occur?

A

Ascending thoracic aorta close to aortic valve

Descending thoracic aorta just distal to left subclavian artery

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32
Q

Why do aneurysms commonly occur in ascending thoracic aorta close to aortic valve?

A

Pressure is highest just outside the aortic valve

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33
Q

Why do aneurysms commonly occur in descending thoracic aorta just distal to left subclavian artery?

A

Right after the bifurctation, just past subclavian artery the stress of that pressure can cause a break in the intima that allows blood flow in between the layers of the artery

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34
Q

When doing an aneurysm repair, do we think that one operative vessels is the only diseased one in the whole body?

A

NO

prob have vascular/atherosclerotic disease other places

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35
Q

Major causes of M&M for aortic aneurysm repair patients

A
  • MI
  • Respiratory failure
  • Renal failure
  • Stroke
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36
Q

What percent of patients having AAA reconstruction have CAD?

What percent of deaths after repair attributed to MI?

A

50% have CAD

40-70% of deaths attributed to MI

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37
Q

What part of AAA repair puts patients at risk of MI and heart failure?

A

The cross clamping causes significant stress on heart potentially causing ischemia and heart failure

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38
Q

If a patient has hypertension, what do we also assume they have until proven otherwise?

A

CAD

Proven otherwise = clear heart cath

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39
Q

What 3 things determine hemodynamic effects of aortic cross clamping?

A
  1. Site of clamp
  2. Patient’s pre-op cardiac reserve
  3. Patient’s intravascular volume
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40
Q

What is required due to stagnant blood flow when the aortic cross clamp is applied?

A

Heparinization

(not to the degree of CPB)

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41
Q

3 considerations in heparinizing patient for aortic cross clamping

A
  1. ensure good blood return in IV
  2. hypotension may occur after heparin bolus
  3. know exact minute and second you admin heparin to be able to tell surgeon when he can cross clamp (usually 2-3 minutes after heparin admin)
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42
Q

When the aorta is cross clamped, what happens to BP above and below level of the clamp?

A

Hypertension above clamp

Hypotension below clamp

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43
Q

Hemodynamic effects of aortic cross clamping:

What happens to afterload?

MAP and SVR?

HR?

CO?

LVEDP?

A
  • Afterload increased
  • MAP and SVR increase
  • HR unchanged
  • CO may decrease or remain unchanged
  • LVEDP may increase or show no change
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44
Q

Why does HR remain unchanged in aortic cross clamping when you would think it woud decreased related to increased SVR and HTN?

A

Release of catcholamines offsets compensatory decrease

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45
Q

If a patient has poor cardiac reserve, what will you expect with cross clamping?

A

May have decreased ventricular function and myocardial ischemia

Will see an increase in LVEDP

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46
Q

How to assess patients cardiac reserve?

“How many flights of stairs can you climb”?

A

NO

Ask them what they do on a daily basis

If sedentary, expect poor cariac reserve

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47
Q

What causes increased preload in aortic cross clamping?

A

Active venoconstriction proximal and distal to clamp

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48
Q

Which will have more hemodynamic effects.. placing cross clamp more proximal or more distal?

A

Distal (infrarenal) has little effect of hemodynamics

Proximal (supraceliac) has major hemodynamic effects

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49
Q

Besides location of cross clamp, what other factor has major impact on hemodynamics?

A

Length of duration of cross clamping

Longer duration = greater increase in SVR and decrease in CO

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50
Q

What kind of pulmonary damage can occur related to cross clamping?

What contributes to this process?

A

Pulmonary edema

Related to:

  • increased pulmonary vascular resistance (>at unclamping)
  • increased capillary membrane permeability
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51
Q

What worsens pulmonary edema r/t aortic cross clamping?

A
  • Hypervolemia
  • Junk AKA Prostaglandins, oxygen free radicals, activation of RAAS, and complement cascade
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52
Q

Effect of infrarenal aortic cross clamping on renal blood flow and renal vascular resistance

A

Decrased renal blood flow 40%

Increased renal vascular resistance 75%

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53
Q

Effect of suprarenal and juxta-renal aortic cross clamping on renal blood flow

A

Decreases renal blood flow as much as 80%

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54
Q

Renal failure is common post aortic surgery

What is the cause?

A

Acute tubular necrosis related to ischemic reperfusion injury

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55
Q

Why is spinal cord damage associated with aortic cross clamping?

A

Artery of Adamkiewics is occluded with no collateral flow to the anterior portion of cord

Anterior = motor

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56
Q

Greater risk of paraplegia when aortic clamp is more proximal or distal?

A

More proximal

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57
Q

Why is SSEP not good monitoring for spinal cord ischemia in aortic cross clamping?

A

SSEP looks at posterior

Does not provide good information about anterior which is what we are worried about

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58
Q

Incidence of anterior spinal syndrome with elective infrarenal vs rupture of descending aorta

A

Elective infrarenal 0.2%

Rupture of descending aorta 40%

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59
Q

Main blood supply to anterior spinal cord

Where does it originate?

Why is this problematic?

A
  • Artery of Adamkiewicz
  • Origin varies but somewhere between T5 and L2
  • Almost always emerges from left side
  • Variations among individuals make it hard to identify
60
Q

Spinal cord perfusion formula

What two ways can we help with perfusion?

A

MAP - CSF pressure

Drainage of CSF has allowed best avoidance of ischemia

Limiting cross clamp time to 30 minutes

61
Q

Preventative measures for anterior spinal syndrome

(Long list so sry)

A
  • Shunt from left atruim to common femoral artery
  • Maintenance of HTN during cross clamp
  • Methylprednisone
  • Moderate hypothermia (30-32 degrees C) below clamp
  • Avoiding hyperglycemia
  • Mannitol to lower CSF pressure by decreasing production
  • Drainage of CSF
62
Q

How may nipride increase risk of spinal cord ischemia?

A

Decreases pressure proximal to the clamp but also distal to clamp

63
Q

S/s of anterior spinal syndrome

What is preserved?

A

S/S: Loss of motor function and pinpric sensation

Sense of vibration and proprioception are preserved because they are posterior

64
Q

Major metabolic abnormality seen in cross clamping

Why may this not show up on ABG?

A

Metabolic acidosis because tissues distal to the clamp are hypoxic causing accumulation of metabolites including lactate

May not be seen on ABG because they are building up below level of clamp and ABG is drawn above level of clamp

May be seen on ABG after unclamping

65
Q

What effect does aortic cross clamping have on oxygen consumption?

Total body extraction?

MvO2?

CO2 production?

Catecholamines?

A
  • O2 consumption decreased due to portion of tissues not being perfused
  • Total body oxygen extraction decreased
  • Increased MvO2
  • Decreased CO2 production = respiratory alkalosis
  • Increased catecholamines
66
Q

Major goals during aortic cross clamping

A
  • Reduce afterload
  • Reduce proload
  • Renal protection
  • Hypothermia below clamp
  • Decrease minute ventilation
  • Correct acidosis with bicarb
67
Q

How to reduce afterload in aortic cross clamping?

A
  • Nipride
  • Inhalation agents
  • Milrinone
  • Shunt or aorta to fem bypass
68
Q

How to reduce preload in aortic cross clamping?

A
  • Nitroglycerine
  • Atrial to fem bypass
69
Q

How to provide renal protection in aortic cross clamping?

A
  • Fluid
  • Renal cold perfusion
  • Pharmacologic (mannitol, renal dose dopamine?)
70
Q

Effect of release of cross clamp and built up metabolites

A

Metabolites such as lactate are ciruclated causing vasodilation, increased EtCO2, and hypotension

71
Q

how does aortic cross-clamp release affect:

  • afterload/SVR?
  • MAP?
  • Preload?
  • CO?
  • PCWP?
  • ETCO2 and PH?
  • Temperature?
A
  • Afterload and SVR decrease
  • MAP decreases
  • Preload decreases
  • CO increases, or no change or increases
  • PCWP decreases
  • ETCO2 increases and pH decreases
  • Temperature decreases
72
Q

When releasing aortic cross clamp significant acidosis may occur requiring what drug?

A

Bicarb

73
Q

When releasing aortic cross clamp, what potential lethal arrhythmia can result from profound hypothermia?

A

V fib

74
Q

Why may CO increase when aortic cross clamp is released?

A

May increase if ventricle has nothing to pump against

(Major decrease in afterload)

75
Q

What contributes to unclamping hypotension?

A

Blood shifting to periphery

Hypoxia related vasodilation below level of clamp

Release of vasoactive and myocardial depressant metabolites

76
Q

How to minimize hypotensive effects of cross clamp release?

A
  • Maintain or restore intravascular volume
    • Replace blood loss
    • Raise PCWP 3-4 mmHg above pre-clamp values just prior to release
  • Lower site of clamping = less drastic change
  • Release clamp gradually
77
Q

What drug should you have ready before releasing cross clamp?

A

Phenylephrine

78
Q

Interventions you can use during unclamping to decrease effects

A
  • Decrease anesthetic depth (MACamnesia) to reduce vasodilation
  • Decrease vasodilators
  • Increase fluids
  • Increase vasoconstrictors
  • Consider mannitol to pull volume back intravascularly
  • Nabicarb to correct acidosis
79
Q

What can you ask the surgeon to do if you have tried everything to correct hypotension after unclamping?

A

Reapply cross clamp

80
Q

What monitoring and equipment do you need for aortic aneurysm repair?

A
  • 2 large gauge IVs, blood warmer, blood filter
  • Radial art line
  • PA catheter (to monitor left sided filling pressures and fluid)
  • ECG- leads II and V5
  • Esophageal stethoscope
  • Foley
  • TEE
81
Q

Advantages of GA with inhalation agent for aortic aneurysm repair

A
  • Rapid adjustment of level
  • Rapid emergence
  • Potentially early extubation
82
Q

Advantages and disadvantages of GA with narcotics for aneurysm repair

A
  • Advantages:
    • Cardiac stability
    • Excellent post-op analgesia
  • Disadvantages:
    • No amnesia
    • Unreliable supression of autonomic stimulation
    • Respiratory depression
83
Q

Advantages of regional for aneurysm repair

A
  • Decreased preload and afterload
  • Preserved myocardial oxygenation
  • Increased graft flow to lower extremities
84
Q

Risks and considerations of regional for aortic aneurysm repair

A
  • Requires 1600-2000 ml more IV fluids
  • Potential for epidural hematoma

Study showed 20 patients out of 3164 epidurals had neurologic complications

Epidural placed before surgery due to use of heparin intra-op and then usually dosed at the end of the case

Want to check an INR before removing the catheter

85
Q

Why is combined GA and regional good for aneurysm repair?

A

Benefits of regional plus amnesai and controlled ventilation

Epidural good for post-op pain relief

86
Q

What places aneurysm repair patients at high risk for bleeding?

A
  • Anticoagulation
  • Back-bleeding after clamped and aneurysm is opened
87
Q

What guides fluid volume replacement for aneurysm repairs?

A

Want to maintain pts normal cardiac filling pressures and normal CO

UOP goal of 1 ml/kg/hr

88
Q

What reduces need for banked blood in aneurysm repair?

A

Cell saver

(75% less banked blood used)

80% of AAA done with only cell-saver and no banked blood

89
Q

Drugs to improve CO if LV is struggling after cross clamp removed

A

Dopamine and dobutamine

90
Q

What is the best prevention of renal failure in aortic aneurysm repair pts?

A

Prevention of hypovolemia

91
Q

What drug may be administerd 20-30 minutes prior to cross clamping?

A

Mannitol (0.5 gm/kg)

(Surgeon may just assume you know he wants this so ask preceptor)

92
Q

What is the renal dose of dopamine that is not necessarily proven effective?

A

3-5 mcg/kg/min

93
Q

What 4 factors increase risk of renal failure after aortic aneurysm repair?

A
  1. Emergency procedures
  2. Long aortic cross clamp time
  3. Prolonged hypotension
  4. Pre-existing renal disease
94
Q

3 cardiac goals for post-op care of aortic aneurysm repair

A
  1. Avoid hypertension
  2. Maintain intravascular volume
  3. Maintain myocardial oxygenation
95
Q

After aortic aneurysm repair we must evaluate need for post-op ventilation

Which particular types of these surgeries may need this?

A

Surgery involving:

  • Ascending aorta
  • Aortic arch
  • Thoracic aorta
96
Q

Renal goals after aneurysm repair

A
  • Maintain UOP at 1 ml/kg/hr
  • Maintain volume
  • Maintain normotension
  • Use dopamine if necessary
97
Q

Symptoms of ruptured AAA

A
  • Abdominal pain with pulsatile mass
  • Back pain,
  • Hypotension
98
Q

Induciton for ruptured AAA is similar to induction for what type of patient

A

Trauma patient

Use scopolamine not midazolam

Goal is hemodynamic stability

“Saving their life is the goal, amnesia is just icing on the cake”

99
Q

Considerations for fluid replacement in ruptured AAA

A

Give whatever you have on hand

You prob will only have crystalloids at first so give that dont want until you have colloid or blood, but you can give those once you have them

100
Q

Hemodynamic and respiratory considerations of ruptured AAA

A

HD effects of cross-clamping will be more pronounced in these patients

Most will need post-op ventilation due to potential for lung injury related to blood products

101
Q

mortality if AAA is ruptured or even just leaking prior to surgery

A

50%

102
Q

Risk factors associated with increased risk of mortality in patients with AAA rupture

(Box 28.7)

A
  • Increased age
  • Female
  • Non-white race
  • Insurance status (higher for self-pay or Medicaid in US)
  • Comorbid conditions
  • CHF
  • Renal failure
  • Valvular heart disease
103
Q

Post op considerations for patients having AAA repair (8)

(Box 28.5)

A
  • Continue invasive HD monitoring
  • Treat acute BP extremes and arrhythmias (a. fib)
  • Assess for postop MI
  • Provide ventilatory mgmt with weaning and extubation
  • Assess for abdominal compartment syndrome
  • Evaluate Hgb, Hct, coag status, and adequacy of volume replacement
  • Assess BUN/creatinine and UOP
  • Institute DVT prophylaxis per protocol
104
Q

What is unique/more scary about surgical repair of ascending aorta?

A

Requires CPB

Anesthesia is similar to cardiac anesthesia and requires median sternotomy

105
Q

What potentially futher complicates repair of ascending aorta?

A
  • Aortic regurgition
  • Large blood loss
  • AV replacement
  • Coronary reimplantation
106
Q

Where should art line be placed in ascending aortic aneurysm repair?

Why?

A

Left radial

Because inominate artery may be clampled

107
Q

What would you want to avoid in patient undergoing ascending aorta repair who also has aortic regurg?

A

Bradycardia

(F,F,F bby)

108
Q

What is unique about aortic arch repair?

A

May need circ arrest after CPB

  • hypothermia 15-18 degress C allows arrest of 30-40 mins
  • Ice to head, cooling on bypass, thiopental
  • Long rewarming may increase blood loss

Need median sternotomy

109
Q

What is unique about repairs of descending thoracic aorta?

A
  • Require left thoracotomy so one-lung ventilation
  • Does not require CPB
  • Use of shunts with cross clamp
110
Q

Risk of descending thoracic aneurysms compared to AAA

A
  • Greater HD effects with cross clamping and clamp release
  • Greater risk of spinal cord ischemia
  • Greater risk of renal insufficience

All related to the clamp being placed higher in this procedure

111
Q

What determines level of monitoring in peripheral vascular surgeries?

A

Co-existing disease in

  • coronary arteries
  • cerebral arteries
  • renal arteries
112
Q

Common anesthetic for peripheral vascular surgeries

Why?

A

Regional + sedation (dexmedetomidine or sedation dose propofol)

SNS blockade with regional increases peripheral blood flow, helps with postop pain

Good because these patients are sick sick so may not want to put them to sleep

113
Q

Considerations with existing AV graft

A

Assess pre and post op

Protect graft (put BP cuff on other side, dont stick there)

114
Q

Why are CEAs so important?

A

Becasue strokes are the 5th leading cause of death in the US

with 80% of them being ischemic and 20% being hemorrhagic

115
Q

What is the most significant predictor of post op stroke incidence?

A

Pre-op neuro funciton

Document pre-op deficits

116
Q

Incidence of perioperative strokes related neuro history

A
  • Asymptomatic pts: 3%
  • Symptomatic pts: 5%
  • Existing strokes: 10%
117
Q

Two common co-existing diseases in patients undergoing CEA

Significance?

A
  • Hypertenison
  • Diabetes

Hypertensive pateints autoregulation shifted higher so need to maintain higher CPP

118
Q

Operative mortality of CEA?

Most common cause?

A

0.5-2.5%

Mostly due to MI

119
Q

What factors increase risks in CEA? (6)

A
  • Age greater than 75
  • Symptomatic lesions
  • Uncontrolled HTN
  • Angina
  • Carotid thrombus
  • Occlusions near carotid siphon (really high up in 🧠 )
120
Q

Major anesthetic goal in CEA

A

Balance cerebral and myocardial protection

Increasing pressure for cerebral perfusion causes increased myocardial oxygen consumption

121
Q

Why do we want rapid awakening in CEA?

A

for neuro assessment

prefer to do this in the OR in case there are deficits that could be fixed

122
Q

How to provide cerebral protection in CEA?

A
  • Increasing collateral flow by maintaining good vertebral flow
  • Decreasing CMRO2
    • Barbiturates (pentothal decreases more but has hangover, propofol satisfactory)
    • Passive hypothermia
123
Q

When is autoregulation maintained?

Hypertension effect on curve

A

50-150 mm Hg

HTN shifts curve to right causing CBF decrease with hypotension

124
Q

CPP formula

A

CPP = MAP - ICP

ICP shouldnt be elevated so CPP should = MAP

125
Q

Monitoring for CEA

A
  • Art line
  • EtCO2 monitoring
  • SSEP or EEG (but EEG is gold standard) – but the goldest standard is an awake pt
126
Q

Indications of neurologic dysfunction on EEG

A
  • Loss of beta-wave activity
  • Loss of amplitude
  • Emergence of slow-wave activity
127
Q

How to determine if shunt placement is necessary in CEA?

A

Measure the carotid stump pressure distal to the clamp

Surgeon will hand us sterile pressure tubing to hook up to transducer

Need shunt if pressure <50 mm Hg

128
Q

Value of cerebral oximetry in CEA

A

Monitoring for a significant change

One single value doesnt really mean anything

??? someone indicate if this is right because we never used these

129
Q

Regional technique for CEA

A

Infiltration of local or deep cervical plexus block (C2-C4)

Surgeon performed

130
Q

Advantages and disadvantages of regional for CEA

A
  • Advantages
    • Shorter, less cardiopulmonary complications
    • Directly assess neuro function (LOC, speech, grip on opposite side)
  • Disadvantages
    • Requires patient cooperation and acceptance
131
Q

Advantages and disadvantages of GA for CEA

A
  • Advantages
    • Inhalation agents provide better HD stability and may benefit cerebral circulation
    • muscle relaxants beneficial for low agent
  • Disadvantages
    • Narcotics can prolong wake-up
    • Volatiles interfere with EEG and SSEP monitoring if >1 MAC
132
Q

Which is better for CEA: regional or GA?

A

No difference in M&M with either type

133
Q

What HD changes should you be ready for with CEA?

A

Both hypertension and hypotension

Patients are hypertensive pre-op but can easily become hypotensive

134
Q

How common is hypotension during CEA?

What is the cause?

How to treat?

A
  • 10-20% of patients become hypotensive
  • Carotid sinus baroreceptor stimulation
  • Treatment:
    • Ephedrine or phenylephrine infusion
    • Atropine if bradycardic
    • Surgeon can prevent with LA infiltration
135
Q

How common is hypertension in CEA pts?

What is the cause?

Treatment?

A
  • 10-66% will have HTN
  • Caused by carotid sinus denervation
  • Treatment/prevention:
    • Have patient take antihypertensive pre-op
    • Beta-blockers, hydralazine
    • Nitroglycerine, nipride
136
Q

What effect may carotid sinus denervation have on ventilation?

A

Decreases ventilation response to hypoxemia

137
Q

BP goal after carotid is cleaned out

A

“normotension”

138
Q

Why is it super easy to overshoot BP one way or the other in pts undergoing CEA?

A
  • These patients have history of hypertension so they are baseline vasoconstricted and volume depleted
  • Makes them have enhanced response to vasodilators and vasocontrictors
139
Q

Postop complications of CEA (10)

A
  • HD instability
  • myocardial ischemia/infarction
  • cerebral hypoperfusion syndrome
  • Stroke
  • respiratory insufficiency
  • RLN/SLN damage
  • Hematoma
  • Carotid body dysfunction
  • Tension pneumo
  • Acute carotid occlusion
140
Q

Implications of bleeding and hematoma after CEA

A

May cause airway obstruction

Requires emergency surgery

This is why surgeons do not cover the neck with a big dressing anymore these days

141
Q

Effect of HTN (SBP >180) after CEA

A

Associated with higher incidence of stroke or MI

Incidence of neuro deficits increased 3x in patients who become hypertensive postop

142
Q

3 major things you want to evaluate and document when dropping you CEA off in the PACU

A
  1. Do they MAE to command? is this the same as they could do pre-op?
  2. Respiratory status- are they breathing on their own?
  3. Responsiveness- should be awake and alert
143
Q

When do CEAs usually go home?

A

The next day after surgery

144
Q

What is mesenteric traction syndrome associated with?

A

Traction on the mesentery that is used to expose the aorta

145
Q

S/S of mesenteric traction syndrome

A

Decrease in blood pressure and SVR

Tachycardia

Increased CO

Facial flushing

146
Q

When does hemodynamic stability return after mesenteric traction syndrome?

A

As reperfusion occurs

147
Q

what should you do with PCWP prior to cross clamp release? why?

A

raise 3-4 mmHg above pre-clamp value to prevent hypotension and decreased CO assoc. with clamp release

S5 - Principles III - Test 3 (3 decks)

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