APEX... FML > Unit 3 - CV Patho > Flashcards

Unit 3 - CV Patho Flashcards

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1
Q

Which surgical procedures have the highest risk of cardiovascular morbidity and mortality for the pt with CAD?

A
  • Open abdominal aortic aneurysm repair
  • emergency surgery (especially in elderly)
  • peripheral vascular surgery
  • long procedures with significant volume shifts and/or blood loss

POLE

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2
Q

General risk factors for MI, CHF and death

A
  • High risk sx
  • hx of ischemic heart disease (unstable angina is the greatest risk)
  • hx of CHF
  • hx of CV disease
  • DM
  • creatinine >2 mg/dL
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3
Q

Unstable angina definition

A
  • angina at rest
  • new-onset angina <2 months
  • increasing symptoms (intensity, frequency or duration)
  • duration >30min
  • s/s becoming less responsive to medical therapy

pts with unstable angina should be optimized before elective non-cardiac sx

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4
Q

what is the risk of perioperative MI if the patient had an MI < 3 months ago?

A

30%

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5
Q

what is the risk of perioperative MI in the general population?

A

~0.3%

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6
Q

Timeline for highest risk of reinfaction of the pervious MI?

A

highest risk of reinfarcation is within 30 days after an acute MI

  • for this reason, the AHA guidelines recommend 4-6 weeks before considering elective sx for a pt with a recent MI
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7
Q

risk of perioperative MI if previous MI is >6 months

A

6%

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8
Q

risk of perioperative MI if previous MI within 3-6 months

A

15%

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9
Q

What procedures does AHA define as a pt with high risk for a perioperative MI? (>5%)

A
  • Emergency sx
  • open aortic sx
  • peripheral vascular sx
  • long procedures with significant volume shifts

POLE

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10
Q

What procedures does the AHA define as a pt with intermediate risk for a perioperative MI?
(1-5%)

A
  • carotid endarterectomy
  • head and neck sx
  • intrathoracic or intraperitoneal sx
  • orthopedic sx
  • prostate sx

CHIPO

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11
Q

What procedures does the AHA define as a pt with low risk for a perioperative MI? (<1%)

A
  • endoscopic procedures
  • cataract sx
  • superficial procedures
  • breast sx
  • ambulatory procedures
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12
Q

NYHA classifications of heart failure

A

1: no symptoms with physical activity
2: symptoms appear during normal activity but no symptoms at rest
3: symptoms appear with less than normal activity, but no symptoms at rest
4: symptoms appear with mimimal activity or even at rest

prudent to get a cardiologist referral for a class 3 or 4 if your procedure requires GA and is a procedure with high or intermediate risk

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13
Q

3 important biomarkers released by infarcted myocardium

what’s more sensitive of MI diagnosis?

A
  1. creatine kinase-MB
  2. troponin I
  3. troponin T

troponins are more sensitive

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14
Q

when do biomarkers released by infarcted myocardium initially elevate

A

3-12 hours

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15
Q

peak elevation with infarcted myocardium:

CK-MB
Troponin I
Troponin T

A
  • CK-MB: 24 hours
  • Troponin I: 24 hours
  • Troponin T: 12-48 hours
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16
Q

Which cardiac marker is least sensitive for MI?

A

CK-MB

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17
Q

when does CK-MB return to baseline after MI?

A

2-3 days

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18
Q

when do troponin I levels return to normal after infarction?

A

5-10 days

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19
Q

when do troponin T levels return to baseline after infarction

A

5-14 days

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20
Q

Why is lead II suggested to use in the OR?

A

aids in identification of inferior wall ischemia & monitors for dysrhythmias

  • specific for narrowed QRS and where P wave analysis is critical for diagnosis
  • examples: junctional, a-flutter, and a-fib

newer data says V1 is also useful for detecting dysrhythmias

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21
Q

best leads for detecting intraoperative LV ischemia (AKA: best leads to monitor intraop ST changes)

A

V3, V4, V5

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22
Q

which lead may be best for detecting ischemia & why

A

V4

closest to isoelectric level on baseline EKG

V5 is the classic teaching, but all V3, V4 and V5 is great, if you have to choose between the 3 choose V4 (according to apex)

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23
Q

combination of what 3 leads has an ischemic detection rate of up to 96%

A

leads II, V4, V5

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24
Q

intraop EKG monitoring in CAD pt

A

RA, RL, LA, LL, and a V lead to monitor for LV ischemia

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25
goal of myocardial ischemia interventions
make the heart smaller, slower, and better perfused
26
how to treat intraop increased myocardial O2 demand caused by an MI
- if HR is too high, use Beta blocker for HR <80 - if BP is too high, increase anesthesia depth or use vasodialator - if PAOP is too high, use nitroglycerin
27
How to treat intraop decreased O2 supply caused by an MI
- if HR is too low, use anticholinergic and pacing - if BP is too low, use vasoconstrictor or reduce depth of anesthesia - if PAOP is too high, use nitroglycerine or inotrope
28
LV compliance curve, describe the curves and examples of each
LV compliance curve shows how the LV pressure changes at a given volume. A more complianct ventricle has a smaller pressure rise than a less compliant ventricle - Curve A: greater rise is pressure at a given volume (non compliant ventricle) *examples: MI and advanced age* - Curve B: normal - Curve C: increased compliance *examples: aortic insufficiency (dialated LV) or dialated cardiomyopathy*
29
what is diastolic compliance
describes filling pressure that results from a given EDV
30
what happens to the diastolic pressure-volume curve with decreased compliance
curve shifts up and left higher EDP for given EDV
31
what happens to diastolic pressure-volume curve with increased compliance
shifts down and right lower EDP for given EDV
32
Compliance of ventricle equation
33
5 conditions that make the heart "stiffer" and decrease compliance (things that affect the diastolic pressure-volume relationship)
1. age \> 60 2. ischemia 3. pressure overload hypertrophy (aortic stenosis or HTN) 4. Hypertrophic obstructive cardiomyopathy 5. pericardial pressure (increased external pressure) | Age, 2 pressures inside, no O2 and 1 pressure outside
34
what happens to filling pressures in a poorly compliant ventricle
higher filling pressures required to prime poorly compliant ventricle ## Footnote preservation of NSR and atrial kick are critically important to maintain the priming function
35
CVP and PAOP with reduced ventricular compliance
may overestimate LVEDV ## Footnote PAOP and CVP are indirect measurements of volume
36
why is there a risk of pulmonary edema in a poorly compliant ventricles
higher filling pressures required
37
2 conditions that dilate the heart and increase compliance
1. chronic aortic regurg 2. dilated cardiomyopathy
38
what type of heart failure is associated with a pumping problem
HF with reduced ejection fraction aka systolic failure
39
what type of heart failure is assoc. with a filling problem
HF with preserved EF aka diastolic failure
40
3 etiologies of systolic heart failure (HFrEF)
1. myocardial ischemia 2. valve insufficiency 3. dilated cardiomyopathy DIV into systolic HF
41
6 etiologies of diastolic failure (HFpEF)
1. myocardial ischemia 2. valve stenosis 3. HTN 4. hypertrophic cardiomyopathy 5. cor pulmonale 6. obesity OH - CHIV
42
what is HF with reduced EF?
heart can't pump enough blood to satisfy body's metabolic requirements volume overload
43
what is HF with preserved EF
heart can't relax and accept incoming volume d/t decreased ventricular compliance
44
With HFrEF, what compensatory mechanisms are active?
- less oxygen is delivered to the periphery d/t less EF - Therefore the arterial-venous oxygen content difference is increased - Compensatory mechanisms include - increased SNS, RAAS and preload *volume overload commonly causes systolic dysfunction*
45
Defining characteristic of HFpEF
symptomatic HF with normal EF
46
contractility with HFpEF
generally preserved unti late in disease
47
EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFrEF (systolic failure)
- increased EDV - increased EDP - increased ESV - decreased/normal SV - increased LV mass - eccentric hypertrophy
48
EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFpEF (diastolic failure)
- normal EDV - increased EDP - normal ESV - normal or decreased SV - increased LV mass - concentric hypertrophy
49
5 ways the body adapts to heart failure & consequences of each
1. SNS activation - increased myocardial work 2. excessive vasoconstriction - decreased CO 3. chronic SNS activation - downregulation of beta receptors 4. fluid retention - ventricular dilation, increased wall stress 5. myocardial remodeling - decreased myocardial performance Saul Expresses Chronic Flyboy Mentality
50
how can myocardial remodeling with heart failure be reversed
ACE inhibitors & aldosterone antagonists ## Footnote -pril drugs and spironolactone
51
3 physiologic functions of BNP
1. natriuresis 2. diuresis 3. vasodilation ## Footnote BNP is a useful biomarker for assessing risk in the pt with HF
52
why does the failing heart release natriuretic peptides into systemic circulation
improve Na+ and fluid balance
53
MOA of neprilysin inhibitors
Neprilysin inhibitors work by inhibiting the enzyme neprilysin, which breaks down vasoactive peptides like atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). Inhibiting this breakdown increases natriuretic peptide levels, causing increased vasodilation, enhanced natriuresis, diuresis, and reduced cardiac fibrosis and remodeling
54
goals of HFrEF (systolic failure) (preload, afterload, contractility, HR)
- diuretics if preload too high - decrease afterload to reduce myocardial work, maintain CPP - augment contractility with inotropes PRN (dobutamine) - HR usually high; may need to stay high to preserve CO with low EF
55
goals of HFpEF (diastolic failure) (preload, afterload, contractility, HR)
- Volume is requires to stretch noncompliant ventricle. *LVEDP does not correlate with LVEDV so TEE is best* - keep afterload elevated to perfuse thick myocardium (neo) - contractility usually normal - slow/normal HR to increase diastolic time and CPP
56
most common cause of right heart failure
left heart failure
57
6 conditions that increase PVR and right heart work
- hypoxia - hypercarbia - acidosis - hypothermia - high PEEP - N2O
58
Treatment of RV failure
- Inotropes - milrinone, dobutamine - pulmonary vasodialators - iNO or sildenafil - reversing causes of increased PVR
59
how is coronary perfusion pressure calculated
aortic diastolic pressure - LVEDP
60
how does HTN cause organ damage
increased BP increases myocardial work higher arterial driving pressure damages nearly every organ in the body
61
6 complications of HTN
- concentric LVH - Ischemic Heart disease - CHF - arterial aneurysm (aorta, cerebral) - stroke - ESRD
62
how does LVH contribute to infarction
- leads to CHF - increased MvO2 results in coronary insufficiency
63
diagnosis of HTN
BP measured on 2 separate occasions at least 1-2 weeks apart to confirm
64
normal, elevated, and HTN stages 1-3
- normal: SBP < 120 **&** DBP < 80 - elevated: SBP 120-129 **&** DBP < 80 - stage 1 HTN: SBP 130-139 **or** DBP 80-89 - stage 2 HTN: SBP > 140 **or** DBP > 90 - stage 3 HTN (crisis): SBP > 180 **and/or** DBP > 120
65
cause of primary HTN
increased CO, SVR, or both (SVR almost always the cause)
66
what plays an integral role in increasing SVR
vascular smooth muscle tone (increased intracellular Ca2+ concentration)
67
what leads to increased SVR in primary HTN
SNS overactivity, chronic vasoconstriction
68
how does chronic vasoconstriction assoc. with primary HTN lead to water and Na+ retention
- results in increased renin release b/c the kidneys don't get enough blood supply - RAAS activated - increases AT1, AT2 and aldosterone - increases Na+/water retention
69
why do pts with primary HTN have a vasodilator deficiency
decreased NO and prostaglandins
70
how do patients with primary HTN develop increased vascular stiffness
collagen and metalloproteinase depositition in arterial intima ## Footnote Metalloproteinases are a family of zinc-dependent enzymes that break down extracellular matrix (ECM) proteins like collagen, elastin, and gelatin
71
with autoregulation of the heart, **cerebral** perfusion pressure remains constant with BP of:
50-150 mmHg ## Footnote this adaptation helps the pts brain tolerate a higher range of BPs - but at the expense of not being able to tolerate lower pressures
72
BP beyond the limits of autoregulation is dependent on:
pressure
73
cerebral autoregulation curve in pts with chronic HTN
shifted to right, narrower curve and therefore difficult to predict on individual basis ## Footnote many texts lead you to believe that the width of the curve remains the same in the HTN pt, but there is good evidence that the range of autoregulation becomes narrower and very difficult to predict for each pt
74
Hypertensive crisis BP value
>180/120
75
Hypertensive emergency is called when there's evidence of end-organ injury (otherwise its urgency). Issues with the following systems - CNS - CV - Renal
- CNS: encephalopathy, stroke, papilledema - CV: CHF - Renal: HTN-induced acute renal dysfunction
76
Treatment of hypertensive crisis
Depends on underlying cause - B-blockers - CCBs - sodium nitroprusside
77
how does HTN contribute to CHF?
- increased myocardial wall tension - LVH - increased MvO2 - coronary insufficiency
78
anticipated HD response to anesthesia in pts with HTN
- exaggerated hypotensive response to induction - exaggerated hypertensive response to intubation & extubation
79
risk of using myocardial depressants and vasodilators with anesthesia in pts with HTN
hypertensive pts are volume contracted agents that cause myocardial depression & vasodilation unmask volume contracted state
80
how to promote HD stability in patients with HTN
adequate hydration before induction
81
perioperative beta blocker use in hypertensive pts
- continue throughout periop period if already on - starting day of surgery increases risk of hypotension, bradycardia, stroke, death
82
should ACE inhibitors and ARBs be taken DOS?
decision made on case-by-case basis
83
effects of ACE inhibitors and ARBs with GA
can produce vasoplegia and cause a state of hypotension unresponsive to vasopressors and fluids may need to treat with vasopressin, terlipressin, methylene blue
84
surgery should be delayed for optimization when BP is what?
SBP \> 180 DBP \> 110
85
most common cause of intraoperative HTN
surgical stimulation
86
6 causes of secondary HTN
1. coarctation of aorta 2. renovascular disease **(renal artery stenosis is the most common cause)** 3. hyperadrenocorticism (Cushing's syndrome) 4. hyperaldosteronism (Conn's disease) 5. pheochromocytoma 6. pregnancy-induced HTN
87
Definitive treatment for Renal artery stenosis inducing secondary HTN and what should you never give them?
- Definative treatment = renal artery endarterectomy or nephrectomy - **never give an ACEi** = can significantly reduce GFR = renal failure
88
clinical findings with coarctation of aorta
- upper limb BP \> lower limb BP - weak femoral pulse - systolic bruit
89
clinical findings with renovascular disease
- bruit (epigastric or abdominal) - severe HTN in young pt
90
Clinical findings with hyperadrenocorticism (cushings)
- truncal obesity - hyperglycemia - muscle and bone weakness - weakened immunity - hirsutism - moon face
91
clinical findings with hyperaldosteronism (Conn's disease)
- HTN - hypokalemia - alkalosis - weakness/fatigue - paresthesia - nocturnal polyuria & polydipsia
92
clinical findings of pheo
- headache - palpitations - diaphoresis
93
clinical findings of pregnancy-induced HTN
- peripheral and pulmonary edema - headache - sz - RUQ pain
94
2 major classes of CCBs
- dihydropyridines: nifedipine, nicardipine, amlodipine, clevidipine - non-dihydropyridines
95
example of CCB in phenylalkylamine class
verapamil
96
example of CCB in benzothiazepine class
diltiazem
97
how do alpha 1 antagonists reduce BP
- decreased vascular calcium causes vasodilation - decreased SVR
98
how do beta 1 antagonists decrease BP
decreased: inotropy, chronotropy, dromotropy, renin release vasoconstriction in muscle
99
beta 1 selective beta blockers
- acebutolol - atenolol - bisoprolol - esmolol - metoprolol
100
alpha:beta anagonistic ratio in labetolol
``` IV = 1:7 PO = 1:3 ```
101
how do alpha 2 agonists decrease BP
decreased SNS outflow
102
how do CCBs decrease BP
- decreased vascular calcium (vasodilation) - decreased SVR - decreased inotropy, chronotropy, dromotropy (non-dihydropyridines duh)
103
class of CCBs that target vasculature
dihydropyridines
104
class of CCBs that target myocardium \> vessels
non-dihydropyridines
105
how do arteriodilators and venous dilators decrease BP
increased NO venodilators decrease venous return
106
how do ACE inhibitors decrease BP
- inhibits vasoconstriction d/t AT2 - inhibits aldosterone release
107
how do Angiotensin receptor blockers decrease BP
- inhibits vasoconstriction r/t AT2 - inhibits aldosterone release
108
how do loop diuretics decrease BP
inhibits Na-K-Cl transporter in thick portion of ascending loop of Henle diuresis = decreased Venous return
109
how do thiazide diuretics decrease BP
inhibits Na-Cl transported in distal convoluted tubule decreased VR ## Footnote HCTZ, metolaxone, indapmide, chlorthlidone
110
how do K+ sparing diuretics decrease BP
inhibit K+ excretion and Na+ reabsorption by principal cells of collecting ducts Acts independently of aldosterone ## Footnote Triamterene, amiloride
111
How do aldosterone sparing diuretics decrase BP?
Inhibits K+ excretion and Na+ reabsorption by the principla cells in the collecting ducts Blocks aldosterone at mineralocorticoid receptors ## Footnote spironolactone
112
why can a standard 2 mg/kg propofol induction cause CV collapse in pts with CHF
CHF patients rely on increased SNS tone to maintain BP 2 mg/kg propofol reduces SNS tone while simultaneously reducing contractility (instead, slow titration of lower dose)
113
why do CHF patients release natriuretic peptides
atrial dilation increases release of ANP & BNP
114
why are ACE inhibitors contraindicated in a pt with bilateral renal artery stenosis
can significantly reduce GFR and precipitate renal failure
115
examples of arteriodilators
- hydralazine - Nipride
116
examples of venodilators
- NTG - Nipride
117
examples of loop diuretics
- furosemide - bumetanide - ethacrynic acid
118
examples of thiazide diuretics
- HCTZ - metolazone - indapamide - chlorthalidone
119
potassium sparing diuretics
triamterene amiloride
120
MOA of CCBs
all clinically used CCBs bind to alpha-1 subunit of L-type calcium channel & prevent calcium from entering cardiac and vascular smooth muscle cells
121
CCB of choice for arrythmias
Verapamil and diltiazem (great treatment for tachycardia, a-fib or a-flutter)
122
CCBs impair contractility in this highest to lowest order
1. verapamil 2. nifedipine 3. diltiazem 4. nicardipine *in the pt with decrased contractility or decreased EF, dilt is a better choice than verapamil*
123
Nicardipine is best used for what reason
coronary antispasmodic
124
Nimodipine is best used for what reason
only CCB proven to decrease M&M from cerebral vasospasm
125
best CCBs for HTN r/t increased SVR
nifedipine, amlodipine, nicardipine (vasodilators)
126
MOA of clevidipine
arterial vasodilation decreases SVR without affecting preload
127
Ingredients to know about inside clevidipine
- prepared as a lipid emulsion (*contains EDTA preservative)* - eggs - soy/soy beans
128
contraindications of clevidipine
- egg allergy - soybean allergy - impaired lipid metabolism (pathologic HLD, lipid nephrosis, acute pancreatitis with HLD) - severe aortic stenosis
129
clevidipine dosing
1-2 mg/hr, max 16 mg/hr
130
Pharmacokinetics of clevidipine (onset, halflife, metabolism)
- onset 2-4 min - half life 1 min (full recovery 5-15 min after gtt off) - tissue and plasma esterase metabolism ## Footnote no need for dosing change if renal/liver failure
131
Some anesthetic considerations for constrictive pericarditis
- Kussmaul's sign is ususally present - Bradycardia should be avoided
132
What is Kussmaul's sign?
Paradoxical rise in CVP and Jugular venous distension during inspiration. its the result in RV filling defect (impaired RV compliance)
133
function of pericardium and how much fluid is in the pericardial sac?
surrounds heart and provides minimal friction environment 10-50mL of clear fluid
134
where do the visceral and parietal layers of the pericardium attach
visceral - attached to myocardium parietal - anchored to mediastinum
135
3 conditions that affect the pericardium
1. acute pericarditis 2. constrictive pericarditis 3. cardiac tamponade
136
what causes constrictive pericarditis
fibrosis or any condition that causes pericardium to be thicker
137
effects of constrictive pericarditis
1. ventricles can't fully relax during diastole (decreased compliance and diastolic filling) 2. increased ventricular pressure creates back pressure on peripheral circulation 3. ventricles increase myocardial mass (impairs systolic function over time)
138
cause of acute pericarditis
usually inflammation (most commonly viral)
139
does acute pericarditis affect diastolic filling
not usually unless inflammation leads to constrictive pericarditis or tamponade
140
anesthetic management of constrictive pericarditis
- avoid bradycardia (CO dependent on HR) - preserve contractility - maintain afterload
141
causes of constrictive pericarditis
- cancer (radiation) - cardiac surgery - RA - TB - uremia **C**onstrictive = CC RUT
142
causes of acute pericarditis
- viral infection (n=most common) - Dressler's syndrome (inflammation from necrotic myocardium s/p MI) - lupus - scleroderma - trauma - cancer (radiation) Louis Vitton Dresses Sauve Teaching Chemistry
143
s/s constrictive pericarditis
- Kussmaul's sign (JVD during inspiration) - pulsus paradoxus - Increased venous pressure - atrial dysthythmias d/t atrial distension - pericardial knock KAPPI ## Footnote A pericardial knock is a high-pitched, early diastolic heart sound caused by the sudden cessation of ventricular filling due to a stiff, scarred, or calcified pericardium in patients with constrictive pericarditis. It is heard shortly after the second heart sound, and signals that the heart cannot expand further, typically indicating severe diastolic dysfunction
144
what is pulsus paradoxus
- SBP decreased \> 10 mmHg during inspiration - indicates impaired diastolic filling may be seen with constrictive pericarditis
145
s/s of acute pericarditis
acut chest pain with pleural component: - pain with inspiration and postural changes - releaved by leaning forward or supine - pericardial friction rub - ST elevation with normal enxymes - Fever
146
treatment of constrictive pericarditis
pericardiotomy
147
risks & mortality assoc. with pericardiotomy
risk hemorrhage and dysrhythmias are common mortality 6-19%
148
which type of pericarditis usually resolves spontaneously
acute
149
drugs to relieve acute pericarditis pain
- salicylates - oral analgesics - corticosteroids
150
drugs to use in anesthetic management of constrictive pericarditis
- ketamine - pancuronium - volatiles with caution - opioids, benzos, etomidate OK *want to preserve HR and contractility*
151
What is Beck's triad and what is it indicative of?
- muffled heart tones - JVD - HoTN *indicative of Pericardial tamponade*
152
what separates pericardial tamponade from effusion
excess fluid excerts external pressure on the heart, limiting ability for diastolic filling and act as a pump
153
CVP in pericardial tamponade
rises in tandem with pericardial pressure
154
CVP and PAOP in pericardial tamponade
as ventricular compliance deteriorates, left and right diastolic pressure (CVP and PAOP) begin to equalize
155
best method of pericardial tamponade diagnosis
TEE
156
Pressure volume loop of pericardial tamponade
- decrease LVEDV (left shift) - decreased SV (narrow loop) - decreased ventricular compliance (higher slope during filling)
157
Presentation of pericardial tamponade
- Beck triad - Pulsus paradoxus - Kussmauls sign - reduced EKG voltage - compression of heart, lungs, trachea and esophagus
158
best treatment of pericardial tamponade
- pericardiocentesis - pericardiostomy
159
What is the preferred anesthesia technique for pericardiocentesis?
Local anesthesia - if GA is required, preserve myocardial function is the primary goal - the heart is relying on the SNS tone - so choose ketamine for induction *any drug that depresses the myocardium or reduces afterload can cause CV collapse*
160
Vent considerations for pericardial tamponade
PPV can impair venous return and CO - best to maintain spont. vent until tamponade is relieved
161
effects of increased pericardial pressure - ____ LV pressure - ____ coronary perfusion - ____ ventricular filling - ____ LV volume - ____ SV - ____ CO - ____ contractility - ____ HR - ____ renal fluid retention
- increased LV pressure - decreased coronary perfusion - decreased ventricular filling - decreased LV volume - decreased SV - decreased CO - increased contractility - increased HR - increased renal fluid retention
162
2 conditions commonly associated with Kussmaul's sign
1. constrictive pericarditis 2. pericardial tamponade (can occur with any condition limiting RV filling)
163
2 conditions assoc. with pulsus paradoxus
1. constrictive pericarditis 2. pericardial tamponade
164
drugs to avoid with pericardiocentesis
- volatiles - propofol - thiopental - high dose opioids - neuraxial anesthesia VP - TON
165
safer drugs to use in pericardiocentesis
- ketamine (best choice d/t SNS activation) - N2O - benzos - opioids
166
what happens to SNS tone, HR, inotropy, LVEDP, LVEDV, coronary perfusion pressure, CO, and SV with pericardial tamponade
- SNS increased - HR increased - inotropy increased - LVEDP increased - LVEDV decreased - CPP decreased - CO decreased - SV decreased
167
why do pts with pericardial tamponade have increased contractility and afterload
increased SNS tone
168
complications of treating pericardial tamponade
- PTX - re-accumulation of fluid - puncture of coronary vessels or myocardium
169
goals for HR and rhythm in pts with pericardial tamponade
- maintain HR (CO is HR dependent since SV is reduced) - maintain NSR (properly timed atrial kick required to prime less compliant ventricles)
170
preload, inotropy, and afterload goals in pts with pericardial tamponade
- maintain or increase preload; avoid decrease (PPV, hypovolemia, venous pooling) - maintain or increase inotropy - maintain afterload (essential to compensate for decreased SV and CO)
171
ACC/AHA guidelines for infective endocarditis antibiotic prophylaxis
only if pt is at high risk of developing and more likely to suffer adverse outcomes ## Footnote Hisotrcally, the guidelines for prophylaxis against infective endocarditis were broad. Overtime, the number of indications has been decreased d/t concerns about abx resistance as well as **very few cases of IE can be prevented with prophylactic abx**
172
6 patients at highest risk of infective endocarditis (need preop antibiotic prophylaxis)
1. previous infective endocarditis 2. prosthetic heart valve 3. unrepaired cyanotic CHD 4. repaired CHD < 6 months 5. repaired CHD with residual defects that have impaired endothelialization at graft site 6. heart transplant with valvuloplasty 2 valves, 3 CHD, 1 big kahuna
173
is antibiotic prophylaxis required for unrepaired cardiac valve disease, CABG, or coronary stent placement?
nope
174
3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis
1. dental procedures involving gingival manipulation and/or damage to mucosal lining 2. respiratory procedures that perforate mucosal lining (incision/biopsy) 3. biopsy of infective lesions on skin or muscle ## Footnote pt at high risk of developing bacteremia after ertain "dirty" procedures should receive abx prophylaxis
175
Antibiotic prophylaxis options for IE (PO and then if PCN allergy)
PO: amoxicillin 2g PCN allergy: clinda (600mg), azithro (500mg), or clarithromycin (500mg)
176
Antibiotic prophylaxis options for IE (IV or IM and if PCN allergy)
IV/IM: ampicillin (2g), cefazolin (1g), or ceftriaxone (1g) PCN allergy: clindamycin (600mg)
177
What 3 things deterine blood flow through the LVOT?
- systolic LV volume - force of LV contraction - transmural pressure ## Footnote As a general rule, in obstructive hypertrophic cardiomyopathy things that distend LVOT are good and things that narrow are bad. Connection: treat (SAM) systolic anterior mitral leaflet obstruction the same way (from CV valve deck)
178
most common autosomal dominant CV disease
hypertrophic obstructive cardiomyopathy (HCOM)
179
most common cause of sudden cardiac death in young athletes
obstructive hypertrophic cardiomyopathy
180
All the names for cardiomyopathy
- obstructive hhypertrophic cardiomyopathy - hypertrophic obstructive cardiomyopathy - asymmetric septal hypertrophy - idiopathic hypertrophic subaortic stenosis
181
what causes LVOT obstruction in HCOM
1. congenital hypertrophy of interventricular septum 2. systolic anterior motion (SAM) of anterior leaflet of mitral valve
182
what factors reduce CO in pts with HCOM?
things that narrow the LVOT: - decreased systolic volume (preload or inc. HR) - increased contractility - decreased aortic pressure
183
conditions that distend LVOT and decrease obstruction
- increased systolic volume (inc. preload or dec. HR) - decreased contractility - increased aortic pressure
184
venturi effect in SAM
blood rapidly flows across LVOT velocity increases through stricture ## Footnote The effect is based on **Bernoulli’s Principle**. When a fluid travels through a narrowed space, its velocity must increase to maintain flow, while its pressure simultaneously drops. Narrowed Path: In patients with HCM, the heart muscle is thickened, making the LVOT much narrower than usual. High Velocity: As the heart pumps, blood has to "zip" through this narrow gap at very high speeds. Pressure Drop: According to the Venturi effect, this high-velocity flow creates a zone of low lateral pressure. The "Suck" Factor: Because the pressure in the LVOT is now lower than the pressure behind the mitral valve leaflets, the leaflets are drawn into the outflow tract, obstructing the blood's exit to the aorta. **think like a curtain getting pulled into a fan**
185
how is hypertrophic obstructive cardiomyopathy diagnosed
TEE
186
SAM can be a postop complication after which surgery
mitral valve **repair** (not replacement)
187
what happens if some of LV stroke volume can't pass into aorta
- takes retrograde path actoss mitral valve - leads to mitral regurg
188
sign of turbulent flow through LVOT obstruction or mitral regurg
systolic murmur
189
what leads to diastolic dysfunction in HCOM
LVH
190
why is it important to promptly treat A-fib or junctional rhythms in pt with hypertrophic obstructive cardiomyopathy
preserving LA contraction is very important
191
why is nitroglycerin not a good choice for a pt with hypertrophic obstructive cardiomyopathy
reduces preload - reduces systolic LV volume - narrows LVOT - worsens obstruction
192
is esmolol good or bad for HCOM pt?
good - slower HR extends LV filling time, so esmolol increases systolic LV volume also decreases contractility, which improves LVOT obstruction
193
is phenylephrine a good or bad choice for HCOM pt
good - increases aortic pressure, which increases transmural pressure and opens LVOT
194
3 surgical options to correct LVOTO
1. septal myomectomy 2. alcohol injection into septal perforator arteries 3. mitral valve replacement (can reduce SAM)
195
Dual antiplatelet therapy (DAPT) consists of
- aspirin: irreversible cyclooxygenase inhibitor - Thienopyridine: ADP receptor antagonist (usually clopidogrel or ticlopidine)
196
how long should elective surgery be delayed after PCI angioplasty without stent
2-4 weeks
197
how long should elective surgery be delayed in pt after PCI with bare metal stent?
30 days (3 months preferred)
198
how long should elective surgery be delayed in pt after PCI with drug eluding metal stent in stable ischemic heart disease?
first generation DES = 12 months minimum current generation DES = 6 months minimum
199
how long should elective surgery be delayed in pt after PCI with drug-eluding metal stent in pt with acute coronary syndrome?
12 months minimum
200
how long should elective surgery be delayed in pt after a CABG?
6 weeks (3 months preferred)
201
when should a pt on DAPT stop taking aspirin before surgery
continue unless absolutely contraindicated if contraindicated stop 3 days preop
202
when should a pt on DAPT stop taking clopidogrel before surgery
7 days preop
203
when should a pt on ticlodopine for DAPT stop taking preop?
14 days before surgery
204
what can be given to reverse platelet inhibition in emergency surgery on a pt taking DAPT
platelets
205
should UFH/Lovenox be used to "bridge" patients off antiplatelet therapy?
no - paradoxically increases platelet aggregation in the stent
206
whats the best treatment for stent thrombosis
PCI best outcome if blood flow restored < 90 min
207
How is venous blood drained into the venous reservoir in the bypass machine?
venous blood (usually from SVC/IVC) is drained into the venous reservoir by **gravity** *an airlock can occur if air enters the venous line*
208
purpose of roller pump in CPB
- compresses blood tubing, creates occlusion point as it mechanically propels blood forward - this is traumatic to blood cells
209
CPB pump flow with afterload changes
Pump flow remains constant regardless of the pts afterload if the arterial inflow line is clamped, the pump continues pushing blood forward. *This can rupture the arterial inflow tubing*
210
complication with roller pump on CPB if venous reservoir runs dry
air embolism (more likely to entrain air when the reservoir runs dry)
211
what type of CPB is less traumatic to blood cells
centrifugal pump - nonocclusive. It uses gravity and spins the blood through a cone
212
which CPB tends to not entrain air
centrifugal pump - can't produce excessive negative pressure, tends to not entrain air
213
Is the centrifugal pump affected by afterload?
yes- this pump cannot produce high positive pressure, so the pump flow decreases then confronted by excessive afterload reduced risk of line rupture if the arterial inflow line is clamped
214
disadvantage of centrifugal CPB pump
lack of an occlusion point if afterload is excessively high, blood backs up towards venous circulation and decreases circulating blood volume
215
component of CPB where gas exchange occurs
oxygenator
216
which CPB oxygenator is safer
membrane oxygenator (uses blood-membrane-gas interface)
217
which CPB oxygenator carries risk of cerebral air embolism
bubble oxygenator (uses a blood-gas interface)
218
what is the CPB circuit primed with
- blood - mannitol - albumin - heparin - bicarb
219
5 effects of priming the CPB with something other than blood - ____ Hct - ____ O2 carrying capacity - ____ blood viscosity - ____ plasma concentration of drugs and plasma proteins - ____ microvascular flow
Hemodilution 5 effects: - decreased Hct - decreased O2 carrying capacity - decreased blood viscosity - decreased plasma concentration of drugs and plasma proteins - increased microvascular flow
220
when is awareness most common with CPB
during sternotomy ## Footnote d/t intense surgical stimulaiton next most common time is rewarming
221
ACT goal for CPB
\> 400 seconds
222
what should be used for anticoagulation for CPB if pt has heparin allergy
- bivalirudin - hirudin - another factor 10 inhibitor
223
SBP goal before aortic cannulation
< 100 mmHg (HTN can cause dissection) ## Footnote Idea range SBP 90-100 with MAP <70
224
Blood transfusion has risk, what are the 2 ways to conserve blood?
- antifibrinolytics (aminocaproic acid or TXA) - cell saver
225
best way to reduce myocardial O2 consumption during CBP
cardioplegia (K+ containing solution that arrests heart in diastole)
226
where is antegrade cardioplegia introduced
into aortic root solution enters coronaries
227
required for antegrade cardioplegia to work
competent aortic valve & clamped aorta
228
where is retrograde cardioplegia introduced
through a cannula into coronary sinus
229
alpha-stat ABG
- doesn't correct for pt's temp - aims to keep intracellular charge nutrality across all temps ## Footnote associated with better outcomes in adults
230
which blood gas measurement in CPB is assoc. with better outcomes in peds
pH-stat
231
pH-stat ABG
- corrects for pt's temp - aims to keep constant pH across all temperatures
232
Full vs partial bypass
Full bypass = when all of the venous return is drained in the venous reservoir Partial bypass = heart receives (and pumps) a fraction of the venous return
233
What removes blood from the LV on CPB?
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation
234
Damage that CPB produces
systemic inflammation that can result in critical organ injury and/or failure
235
dose of protamine after off bypass
~1 mg for each 100 units heparin given ## Footnote of 30,000 unit of heparin remain the pts circulation, calculated dose of protamine is 300 mg
236
radial artery pressure immediately after CPB
may be artificially low
237
common post-bypass Adverse events
- myocardial depression - heart block is a side effect of the cardioplegia solution (may need vasoactives and pacing)
238
how does protamine reverse heparin
neutralization reaction (forms acid/base complex)
239
administration of protamine
over 10-15 min to reduce systemic vasodulation and pulmonary vasoconstriction
240
indications for IABP
- cardiogenic shock - MI - intractible angina - difficult CPB separation
241
contraindications for IABP
- severe aortic insufficiency - descending aortic disease (aneurysm) - severe PVD - sepsis
242
where is IABP inserted
through femoral artery and advanced along descending aorta
243
Proper position of an IABP
The tip of the balloon should be positoned 2cm distal to the left subclavian a. (proximal position can lead to occlusion fo the L common carotid and brachiocephalic) *proper position is confirmed with CXR, fluoro or TEE*
244
what is an IABP?
a counterpulsation device that improves myocardial o2 supply while reducing O2 demand
245
how does IABP function in diastole?
- balloon inflates during diastole (when the aortic valve closes) - inflation correlated with the dicrotic notch on the aortic pressure waveform - the balloon will created backpressure on the coronary arteries - this augments coronary perfusion and increases myocardial O2 supply
246
how does IABP function in systole? what wave on EKG does it correlate with?
- the balloow deflates just before systole - **coorlates with R wave on EKG** - balloon deflation causes a vacuum-like effect that reduces afterload and LV work - reduced myocardial O2 demand - aortic pressure dips lower than after an unassisted systole (also reduces aortic EDP)
247
what do IABP inflation and deflation correlate with on monitoring waveforms?
- inflation correlates with dicrotic notch and T wave - deflation correlates with R wave
248
when is aortic pressure higher with IABP
higher in diastole than during unassisted systole
249
most common IABP complications
- vascular injury - infection at insertion site - thrombocytopenia
250
CO with an LVAD is dependent on what 3 things
- LV preload - Pump speed - pressure gradient across the pump (afterload)
251
purpose of an LVAD
mechanical device that unloads failing heart by pumping blood from LV to aorta
252
where is the inflow cannula of LVAD inserted
in apex of LV *then blood flows through the LVAD and is returned to the aortia through the outflow cannula*
253
conditions that require surgical correction before LVAD can be used
- PFO - Aortic insufficiency - tricuspid regurg
254
purpose of LVAD
- bridge to recovery - bridge to transplant - destination therapy
255
why might SpO2 and NIBP be ineffective with LVAD
If flow through the LVAD is non-pulsatile, then measuring SpO2 and NIBP will be ineffective consider ALine, ABGs and cerebral ox
256
most common cause of death with LVAD
sepsis
257
mechanical sheer stress can cause what with an LVAD?
coagulopathy and platelet dysfunction
258
common complication with LVAD
GI bleeding
259
what is LV suck down with LVAD & how is it treated
- low preload + relatively high pump speed produces suction (**LV suck down**) - part of LV sucked into LV cavity, occludes inflow cannula - treated with IVF to increase preload, decrease pump speed
260
consequences of suction with LVAD
- hypotension - ventricular dysrhythmias - L shift of interventricular septum - decreased RV contractility - decreased compliance
261
Crawford aneurysm classification: type 1
involves all or most of descending thoracic aorta and upper abdominal aorta
262
Crawford aneurysm classification: type 2
involves all or most of descending thoracic aorta, most of abdominal aorta
263
Crawford aneurysm classification: type 3
involves lower descending thoracic aorta and most of abdominal aorta
264
Crawford aneurysm classification: type 4
involves most of abdominal aorta only
265
DeBakey aneurysm classification: type 1
tear in ascending aorta + dissection along entire aorta
266
DeBakey aneurysm classification: type 2
tear + dissection only in ascending aorta
267
DeBakey aneurysm classification: type 3a
tear in proximal descending aorta with dissection limited to thoracic aorta
268
DeBakey aneurysm classification: type 3b
tear in proximal descending aorta with dissection along thoracic & abdominal aorta
269
Crawford vs. Debakey aneurysm classification
- Crawford: classifies aortic aneurysms into 4 types based on involvement in thoracic/abdominal aorta - DeBakey: classified according to location of dissection
270
Stanford Aneurysm classification
- type A: involves ascending aorta - type B: doesn't involve ascending aorta
271
Most difficult aneurysms to repair
Crawford 2 and 3 because they involve the thoracic and abdominal aorta
272
Aneurysm that has to most significant perioperative risk
Crawford 2: paraplegia and/or renal failure - b/c there is a mandatory period of stopping blood flow to the renal arteries and some radicular arteries that perfuse the anterior spinal cord (possibly artery of Adamkiewicz)
273
Acute dissection of which classifications is a surgical emergency?
DeBakey 1 or 2 or Stanford A
274
type of aortic aneurysm that is often managed medically
dissection of descending aorta (meds for HR, BP, pain)
275
Which law describes aneurysmal diameter?
Law of LaPlace (not Poiseuille) states that increased diameter increases wall tension. - the greater the wall tension, the greater the risk of rupture - Sx is indicated when AAA diameter >5.5cm
276
incidence of AAA in pts \> 50
3-10%
277
independent risk factors for AAA
- cigarette smoking - male - advanced age
278
how is AAA most commonly detected
- pulsatile abdominal mass during routine exam - generally asymptomatic
279
primary mechanism of AAA
destruction of elastin and collagen that form matrix of vessel wall
280
pathologic changes that cause abdominal aorta to weaken/dilate
- atherosclerosis - inflammation - endothelial dysfunction - platelet activation A PIE! ## Footnote Thrombus formation may reduce the diameter of the aortic lumen
281
when is surgical correction of AAA recommended
when > 5.5cm or if it grows more than 0.6-0.8 cm/year
282
risk of AAA rupture when \> 8 cm diameter
30-50%
283
classic triad of symptoms in AAA rupture
- hypotension - back pain - pulsatile abdominal mass \*\*only in ~50% of patients\*\*
284
Which space do most AAA rupture into?
left retroperitoneum
285
how is rapid exsanguination usually prevented in a ruptured AAA?
clot formation and the tamponade effect of the retroperitoneum
286
most common cause of AAA postop death
MI
287
Which factors increase following the cross-clamp removal during a AAA repair? - PVR - Venous return - MVO2 (body o2 consumption) - Coronary blood flow
PVR and MVO2 - When the clamp is released, ischemic tissues release acid and vasoactive substances (increased PVR) - removal of the clamp increases the size of the vascular tank, so venous return falls - HoTN reduces coronary flow
288
The Pts physiologic response to the aortic cross-clamp (AoX) is releated to what 3 factors
- location of AoX (infrarenal most common) - intravascular volume status - cardiac reserve
289
3 things that cause central hypervolemia after application of the aortic cross-clamp
- reduces venous capacity - shifting more blood proximal to the clamp - increasing venous return
290
4 things that cause central hypovolemia by removing the aortic cross-clamp
- restoring venous capacity - shifting a greater proportion of blood to the lower body - decreasing venous return - creating capillary leak (contributes to loss of intravascular volume
291
application of cross-clamp starves distal tissues of O2 causing anerobic metabolism, leading to.... - ____ lactic acid production (metabolic acidosis) - ____ prostaglandins - ____ activated complement - ____ myocardial depressant factors - ____ temp
- increased lactic acid production (metabolic acidosis) - increased prostaglandins - increased activated complement (immune cascade) - increased myocardial depressant factors - decreased temp
292
The ____ the proximal clamp is placed on the aorta, the ____ the physiological insult. Even an ____ clamp reduces renal blood flow, and puts the pt at risk for ____
The **higher** the proximal clamp is placed on the aorta, the **greater** the physiological insult. Even an **infra-renal** clamp reduces renal blood flow, and puts the pt at risk for **acute kidney injury**
293
effects of aortic cross clamp application: - venous return - CO - MAP - SVR - PAOP
- VR increased (blood shift proximal to clamp) - CO decreases or doesn't change (depends on reserve) - MAP increased (inc. preload & SVR) - SVR increases (mechanical effect, catecholamine release, RAAS activation) - PAOP increased/unchanged (depends on cardiac reserve)
294
effects of aortic cross clamp removal: - venous return - CO - MAP - SVR - PAOP
- venous return: decreased - central hypovolemia and capillary leak - CO: decreased - reduced preload and contractility - MAP: decreased - lower preload and SVR - SVR: decreased - washout of anerobic metabolites = vasodilation - PAOP: increased - lactic acidosis
295
Physiological effects of aortic cross clamp application for: - LV wall stress - MVO2 - coronary blood Q - renal blood Q - total body VO2 - SvO2
- LV wall stress: increased - increased preload/afterload - MVO2: increased - preload, wall stress and afterload - coronary blood Q: increased - increased AoDBP - renal blood Q: decreased (even with infrarenal clamp) - total body VO2: decreased - less O2 delivery distal to clamp = anerobic metabolism - SvO2: inc/dec - less O2 but also less consumed
296
physiologic effects of removing aortic cross clamp - LV wall stress - MVO2 - coronary blood Q - renal blood Q - total body VO2 - SvO2
- LV wall stress: decreased - less preload/afterload - MVO2: decrased - less preload/afterload - coronary blood Q: decreased - less AoDBP - renal blood Q: decreased (depends on MAP) - total body VO2: increased - cells distal to clamp finally receive O2 - SvO2: inc/dec - more O2 but more consumed
297
infrarenal clamp time associated with increased risk ARF
\> 30 min
298
advantages of EVAR (endovascular aneurysm repair) over open repair
- decreased operative time - decreased transfusion rate - shorter Length of stay - decreased morbidity and mortaility - no need for aortic cross clamp - avoid resp risks assoc. with midline abdominal incision
299
complications of EVAR
- baroreceptor reflex activation - massive hemorrhage - aortic rupture - cerebral embolism - endoleak
300
what is an endoleak
EVAR complication - original graft fails to prevent blood from entering aortic sac
301
endoleak treatment
sometimes resolve spontaneously (especially early), may require placement of 2nd graft or open repair
302
Where do the 2 posterior spinal arteries arise from?
- Aorta - segmental a. - posterior radicular a. - posterior spinal a. - Aorta - subclavian a. - vertrbral a - posterior spinal a.
303
what perfuses the posterior 1/3 spinal cord
posterior spinal arteries
304
perfuses anterior 2/3 spinal cord
anterior spinal artery (1)
305
Where does the anterior spinal artery arise from?
- Aorta - segmental a. - anterior radicular a. - anterior spinal a. - Aorta - subclavian a. - vertrbral a. - anterior spinal a.
306
How many radicular arteries supply the spinal cord?
6-8 paired radicular arteries
307
where does artery of Adamkiewicz originate
on left side between T11-T12 - 75% of population: originates between T8-T12 - another 10%: originates L1-L2
308
what are watershed areas
some regions of spinal cord only have a single blood supply *These areas are particularly vulnerable to ischemia* ## Footnote The spinal cord is perfused at each segment - but not necessarily along its entire length
309
An aortic cross-clamp placed above the artery of Adamkiewicz can cause what?
Ischemia to the lower portion of the anterior spinal cord - this can cause anterior spinal artery synrome (AKA Beck's syndrome)
310
Classis s/s of Beck's syndrome
- flaccid paralysis of the lower extremities - Bowel and bladder dysfunction - loss of temperature and pain sensation *Touch and proprioception are preserved*
311
why does a patient with Beck syndrome present with flaccid paralysis of lower extremities
the corticospinal tract is perfused by anterior blood supply
312
why does pt with Beck's syndrome have bowel & bladder dysfunction
ANS fibers perfused by anterior blood supply
313
why does pt with beck syndrome lose pain and temp sensation
spinothalamic tract perfused by anterior blood supply
314
why does a pt with beck syndrome have preserved touch & proprioception
dorsal column perfused by posterior blood supply
315
thoracic cross clamp time that significantly increases risk of cord ischemia
\> 30 min
316
method to reduce spinal cord O2 consumption
moderate hypothermia (30-32 deg C)
317
what does spinal cord perfusion pressure depend on
pressure gradient between anterior spinal artery and CSF pressure CSF drain will decreased CSF pressure and increased gradient
318
BP goals during cross clamp to prevent beck's syndrome
maintain proximal HTN (MAP ~ 100)
319
monitoring that monitors posterior cord
SSEP
320
spinal cord protecting drugs
- corticoteroids - CCBs - mannitol
321
What is Amaurosis fugax? and what is it a sign of?
Blindness in one eye - sign of impending stroke
322
How is amaurosis fugax caused?
Embolie travel from the internal carotid artery to the ophthalmic artery - this impairs perfusion of the optic nerve and causes retinal dysfunction
323
incidence of amaurosis fugax
in 25% of pts with high grade carotid stenosis
324
regional techniques for CEA
- local infiltration - superficial plexus block (C2-C4) - deep cervical plexus block (C2-C4) *Awake pt is the best monitor of neuro status*
325
risk of regional anesthesia in CEA pt
risk of ipsilateral phrenic nerve block - caution with severe COPD
326
**cerebral** perfusion pressure =
MAP - ICP *or MAP - CVP (whichever is higher)*
327
what does cerebral perfusion depend on during carotid artery clamp (CEA)
collateral flow from circle of willis (contralateral carotid and vertebral vessels)
328
EEG findings that indicate risk of cerebral hypoperfusion
- loss of amplitude - decreased beta wave activity - slow wave activity
329
things that increase frequency in EEG
- mild hypercarbia - early hypoxemia - seizure - ketamine - N2O - light anesthesia ## Footnote However there is a high incidence of false-negatives with EEG
330
things that decrease EEG frequency
- extreme hypercarbia - hypoxia - cerebral ischemia - hypothermia - anesthetic OD - opioids
331
what is cerebral oximetry what indicates cerebral perfusion is at risk
uses Near-infrared spectroscopy (NIRS) to monitor cerebral O2 sat (rSO2) in frontal lobe perfusion at risk when reduced 25%+ from baseline
332
use of transcranial doppler in CEA
assess continuous blood flow velocity in middle cerebral artery (where most emboli lodge) may indicate when shunt should be placed
333
anesthesia considerations for SSEP
- requires light plane of anesthesia - monitors sensory pathways only - volatiles decrease amplitude and increase latency (mirror ischemia)
334
where is carotid stump pressure measured
distal to clamp
335
carotid stump pressure that indicates risk of ipsilateral cerebral hypoperfusion
stump pressure \< 50m mmHg *a low stump pressure is an indication to place a carotid shunt*
336
risk assoc. with carotid shunt placement
increased risk embolic stroke This increased risk of stoke will make many surgeons not place a carotid shunt unless there is good reason to do so (i.e. low stump pressure or concerning data from other monitors)
337
BP goal during carotid clamping (CEA)
keep BP normal/slightly elevated - brain perfusion in ischemic regions are maxiamally vasodialated and therefore is pressure dependent d/t loss of autoregulation
338
what reflex can be activated during CEA or following carotid balloon inflation
baroreceptor reflex ## Footnote Bradycardia and HoTN
339
ETCO2 goal in CEA
maintain normocapia or mild hypocapnia cerbral vessels distal to stenosis may be maximally dilated - hypercarbia dilates cerebral vessels (it can crease a *steal* phenomenon by shunting blood from hypoperfused tissue
340
lab value that increases risk stroke or death in CEA
blood sugar \> 200 mg/dL DOS
341
5 complications assoc. with CEA
- hematoma - RLN injury - hemodynamic instability (altered baroreceptor sensitivity) - stroke (usually embolic - not HoTN or hyperperfusion) - carotid denervation - reduces ventilatory response to hypoxia (more likely a problem with bilat CEA)
342
what is carotid artery angioplasty stenting (CAS)
uses percutaneous transvascular access to pass stent to carotid
343
ACT goal for CEA
\> 250 sec
344
most common complication of CEA & how is it treated
thromboembolic stroke - A distal protection filter placed beyond the angioplasty balloon will catch most of the debris - Embolic stroke is treated with recombinant tPA
345
what is subclavian steal syndrome
occlusion of subclavian or innominate artery proximal to origin of ipsilateral vertebral artery (usually on left side) - causes vertebral blood flow to reverse flow toward ipsilateral subclavian artery - AKA: the arterial blood is "stolen" from the posterior cerebral circulation and diverted to the ipsilateral arm
346
BP in subclavian steal syndrome
much lower in ipsilateral arm - pulse may be deminished
347
treatment of choice for subclavian steal syndrome
subclavian endarterectomy
348
s/s subclavian steal
- syncope - vertigo - ataxia - hemiplegia - arm ischemia - weak pulse in ipsilateral arm
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