Unit 3 - CV Patho Flashcards
1
Q
what is the risk of perioperative MI if the patient had an MI < 3 months ago?
A
30%
2
Q
what is the risk of perioperative MI in the general population?
A
0.3%
3
Q
when should a patient be referred to a cardiologist before surgery?
A
a pt with an NYHA classification of 3 or 4 who is scheduled for a high- or intermediate-risk surgery
4
Q
risk of perioperative MI if MI > 6 months
A
6%
5
Q
risk of perioperative MI if previous MI within 3-6 months
A
15%
6
Q
highest risk of reinfarction
A
within 30 days of acute MI
7
Q
ACC/AHA minimum recommended time before considering elective surgery in a patient with recent MI
A
4-6 weeks
8
Q
6 risk factors for perioperative cardiac morbidity & mortality for non-cardiac surgery
A
- high risk surgery
- history of IHD (greatest risk with unstable angina)
- history CHF
- history cerebrovascular disease
- DM
- serum Cr > 2 mg/dL
9
Q
what factor confers the greatest risk of perioperative MI
A
unstable angina
10
Q
3 important biomarkers released by infarcted myocardium
what’s more sensitive of MI diagnosis?
A
- creatine kinase-MB
- troponin I
- troponin T
troponins are more sensitive
11
Q
when do biomarkers released by infarcted myocardium initially elevate
A
3-12 hours
12
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
13
Q
when does CK-MB return to baseline after MI?
A
2-3 days
14
Q
when do troponin I levels return to normal after infarction?
A
5-10 days
15
Q
when do troponin T levels return to normal after infarction
A
5-14 days
16
Q
EKG lead that aids in identification of inferior wall ischemia & monitors for dysrhythmias
A
lead II
17
Q
best leads for detecting intraoperative LV ischemia
A
V3, V4, V5
18
Q
which lead may be best for detecting ischemia & why
A
V4
closest to isoelectric level on baseline EKG
19
Q
combination of what 3 leads has an ischemic detection rate of up to 96%
A
leads II, V4, V5
20
Q
intraop EKG monitoring in CAD pt
A
RA, RL, LA, LL, and a V lead to monitor for LV ischemia
21
Q
goal of myocardial ischemia interventions
A
make the heart smaller, slower, and better perfused
22
Q
how to treat intraop increased myocardial O2 demand caused by increased PAOP
A
nitroglycerin
23
Q
what is diastolic compliance
A
describes filling pressure that results from a given EDV
24
Q
what happens to the diastolic pressure-volume curve with decreased compliance
A
curve shifts up and left
higher EDP for given EDV
25
what happens to diastolic pressure-volume curve with increased compliance
shifts down and right
lower EDP for given EDV
26
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. HOCM
5. pericardial pressure (increased external pressure)
27
what happens to filling pressures in a poorly compliant ventricle
higher filling pressures required to prime poorly compliant ventricle
28
CVP and PAOP with reduced ventricular compliance
may overestimate LVEDV
29
why is there a risk of pulmonary edema in a poorly compliant ventricles
higher filling pressures required
30
2 conditions that dilate the heart and increase compliance
1. chronic aortic regurg
2. dilated cardiomyopathy
31
what type of heart failure is associated with a pumping problem
HF with reduced ejection fraction
aka systolic failure
32
what type of heart failure is assoc. with a filling problem
HF with preserved EF
aka diastolic failure
33
3 etiologies of systolic heart failure (HFrEF)
1. myocardial ischemia
2. valve insufficiency
3. dilated cardiomyopathy
34
7 etiologies of diastolic failure (HFpEF)
1. myocardial ischemia
2. valve stenosis
3. HTN
4. hypertrophic cardiomyopathy
5. cor pulmonale
6. obesity
7. aging
35
what is HF with reduced EF?
heart can't pump enough blood to satisfy body's metabolic requirements
volume overload
36
what is HF with preserved EF
heart can't relax and accept incoming volume d/t decreased ventricular compliance
37
contractility with HFpEF
generally preserved unti late in disease
38
compensation for HFrEF
- increased SNS
- increased RAAS
- increased preload
39
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
40
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
41
defining characteristic of HFpEF (diastolic failure)
symptomatic heart failure with normal EF
42
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
43
how can myocardial remodeling with heart failure be reversed
ACE inhibitors & aldosterone antagonists
44
3 physiologic functions of BNP
1. natriuresis
2. diuresis
3. vasodilation
45
why does the failing heart release natriuretic peptides into systemic circulation
improve Na+ and fluid balance
46
useful biomarker for assessing risk in pt with heart failure
BNP
47
MOA of neprilysin inhibitors
neprilysin degrades natriuretic peptides
inhibition can be used to treat heart failure by increasing concentration of natriuretic peptides in blood
48
goals of HFrEF (systolic failure)
(preload, afterload, contractility, HR)
- diuretics if preload too high
- decrease afterload to reduce myocardial work, maintain CPP (SNP)
- augment contractility with inotropes PRN (dobutamine)
- HR usually high; may need to stay high to preserve CO with low EF
49
HD goals of HFpEF (diastolic failure)
(afterload, contractility, HR)
- keep afterload elevated to perfuse thick myocardium (neo)
- contractility usually normal
- slow/normal HR to increase diastolic time and CPP
50
most common cause of right heart failure
left heart failure
51
6 conditions that increase PVR and right heart work
- hypoxia
- hypercarbia
- acidosis
- hypothermia
- high PEEP
- N2O
52
4 surgical procedures with high cardiac risk (risk \> 5%)
1. emergency surgery (especially in elderly)
2. open aortic surgery
3. peripheral vascular surgery
4. long surgical procedures with significant volume shifts/blood loss
53
5 surgical procedures assoc. with intermediate cardiac risk (risk = 1-5%)
1. CEA
2. head/neck surgery
3. intrathoracic or intraperitoneal surgery
4. orthopedic surgery
5. prostate surgery
54
5 surgical procedures assoc. with low cardiac risk (risk \< %)
1. endoscopic procedures
2. cataract surgery
3. superficial procedures
4. breast surgery
5. ambulatory procedures
55
what is the modified NY association functional classification of heart failure
```
class 1: asymptomatic
class 2: symptomatic with moderate activity
class 3: symptomatic with mild activity
class 4: symptomatic at rest
```
56
how is coronary perfusion pressure calculated
aortic diastolic pressure - LVEDP
57
what's the difference in primary and secondary HTN
primary: no identifiable cause (95%)
secondary: identifiable cause (5%)
58
treatment of RV failure
- inotropes (milrinone, dobutamine)
- pulmonary vasodilators (iNO, sildenafil)
- reverse causes of increased PVR
59
how does HTN cause organ damage
increased BP increases myocardial work
higher arterial driving pressure damages nearly every organ in the body
60
6 complications of HTN
- concentric LVH
- IHD
- CHF
- arterial aneurysm (aorta, cerebral)
- stroke
- ESRD
61
how does LVH contribute to infarction
- leads to CHF
- increased MvO2 results in coronary insufficiency
62
diagnosis of HTN
BP measured on 2 separate occasions at least 1-2 weeks apart to confirm
63
normal, elevated, and HTN stages 1-3
- normal: SBP \< 120 & DBP \< 80
- elevated: SBP 120-139 & 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
64
cause of primary HTN
increased CO, SVR, or both (SVR almost always the cause)
65
what plays an integral role in increasing SVR
vascular smooth muscle tone (increased intracellular Ca2+ concentration)
66
what leads to increased SVR in primary HTN
SNS overactivity, chronic vasoconstriction
67
how does chronic vasoconstriction assoc. with primary HTN lead to water and Na+ retention
- results in increased renin release
- increases AT1, AT2 and aldosterone
- increases Na+/water retention
68
why do pts with primary HTN have a vasodilator deficiency
decreased NO and prostaglandins
69
how do patients with primary HTN develop increased vascular stiffness
collagen and metalloproteinase depositition in arterial intima
70
cerebral perfusion pressure remains constant with BP of:
50-150 mmHg
71
BP beyond the limits of autoregulation is dependent on:
pressure
72
cerebral autoregulation curve in pts with chronic HTN
shifted to right, narrower
difficult to predict on individual basis
73
how does HTN contribute to CHF?
- increased myocardial wall tension
- LVH
- increased MvO2
- coronary insufficiency
74
what is the cerebral autoregulation curve
describes the range of BPs where cerebral perfusion pressure remains constant
75
why does the cerebral autoregulation curve shift to the right in pts with chronic HTN
helps the patient's brain tolerate a higher range of BPs
comes at the expense of not tolerating a lower BP
76
6 causes of secondary HTN
1. coarctation of aorta
2. renovascular disease
3. hyperadrenocorticism (Cushing's syndrome)
4. hyperaldosteronism (Conn's disease)
5. pheochromocytoma
6. pregnancy-induced HTN
77
anticipated HD response to anesthesia in pts with HTN
- exaggerated hypotensive response to induction
- exaggerated hypertensive response to intubation & extubation
78
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
79
how to promote HD stability in patients with HTN
adequate hydration before induction
80
perioperative beta blocker use in hypertensive pts
- continue throughout periop period if already on
- starting DOS increases risk of hypotension, bradycardia, stroke, death
81
should ACE inhibitors and ARBs be taken DOS?
decision made on case-by-case basis
82
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
83
surgery should be delayed for optimization when BP is what?
SBP \> 180
DBP \> 110
84
most common cause of intraoperative HTN
surgical stimulation
85
what is a hypertensive crisis
BP \> 180/120
86
when is a hypertensive emergency declared
evidence of end-organ injury
- CNS: encephalopathy, stroke, papilledema
- cardiac: CHF
- renal: HTN-induced acute renal dysfunction
87
treatment of hypertensive crisis
depends on cause
beta blockers, CCBs, vasodilators (Nipride)
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 Conn's disease
- HTN
- hypokalemia
- alkalosis
- weakness/fatigue
- paresthesia
- nocturnal polyuria & polydipsia
91
clinical findings of pheo
- headache
- palpitations
- diaphoresis
92
clinical findings of pregnancy-induced HTN
- peripheral and pulmonary edema
- headache
- sz
- RUQ pain
93
2 major classes of CCBs
- dihydropyridines: nifedipine, nicardipine, amlodipine, clevidipine
- non-dihydropyridines
94
example of CCB in phenylalkylamine class
verapamil
95
example of CCB in benzothiazepine class
diltiazem
96
how do alpha 1 antagonists reduce BP
- decreased vascular calcium causes vasodilation
- decreased SVR
97
how do beta 1 antagonists decrease BP
decreased: inotropy, chronotropy, dromotropy, renin release
vasoconstriction in muscle
98
beta 1 selective beta blockers
- acebutolol
- atenolol
- bisoprolol
- esmolol
- metoprolol
99
alpha:beta anagonistic properties in labetolol
```
IV = 1:7
PO = 1:3
```
100
how do alpha 2 agonists decrease BP
decreased SNS outflow
101
how do CCBs decrease BP
- decreased vascular calcium (vasodilation)
- decreased SVR
- decreased inotropy, chronotropy, dromotropy
102
class of CCBs that target vasculature
dihydropyridines
103
class of CCBs that target myocardium \> vessels
non-dihydropyridines
104
how do arteriodilators and venous dilators decrease BP
increased NO
venodilators decrease venous return
105
how do ACE inhibitors decrease BP
- inhibits vasoconstriction d/t AT2
- inhibits aldosterone release
106
how do AT2 receptor blockers decrease BP
- inhibits vasoconstriction r/t AT2
- inhibits aldosterone release
107
how do loop diuretics decrease BP
inhibits Na-K-Cl transporter in thick portion of ascending loop of Henle
diuresis = decreased VR
108
how do thiazide diuretics decrease BP
inhibits Na-Cl transported in distal convoluted tubule
decreased VR
109
how do K+ sparing diuretics decrease BP
inhibit K+ excretion and Na+ reabsorption by principal cells of collecting ducts
110
MOA of CCBs
bind to alpha-1 subunit of L-type calcium channel & prevent calcium from entering cardiac and vascular smooth muscle cells
111
which cardiac marker is the least sensitive for MI?
CK-MB
112
what are the 3 best EKG leads to monitor intraoperative ST changes?
V3
V4
V5
113
how does a decrease in ventricular compliance affect PAOP
PAOP may overestimate LVEDV
114
how do patients with CHF maintain BP?
rely on elevated levels of circulating catecholamines (increased SNS tone)
115
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)
116
primary mechanism of CHF that activates RAAS
CHF reduces renal blood flow
117
why do CHF patients release natriuretic peptides
atrial dilation increases release of ANP & BNP
118
how does CHF affect beta receptors
causes down-regulation
119
most common cause of secondary HTN
renal artery stenosis
120
how does renal artery stenosis cause secondary HTN
- narrowed renal artery reduces renal blood flow
- kidneys activate RAAS in attempt to increase GFR
121
why are ACE inhibitors contraindicated in a pt with bilateral renal artery stenosis
can significantly reduce GFR and precipitate renal failure
122
examples of arteriodilators
- hydralazine
- Nipride
123
examples of venodilators
- NTG
- Nipride
124
examples of loop diuretics
- furosemide
- bumetanide
- ethacrynic acid
125
examples of thiazide diuretics
- HCTZ
- metolazone
- indapamide
- chlorthalidone
126
potassium sparing diuretics
triamterene
amiloride
127
CCB that is a useful coronary antispasmodic
nicardipine
128
only CCB proven to decrease M&M from cerebral vasospasm
nimodipine
129
CCBs that reduce HR in pts with tachycardia, A-fib, or A-flutter
verapamil
diltiazem
130
CCB contractility impairment from greatest to least
verapamil \> nifedipine \> diltiazem \> nicardipine
131
best CCBs for HTN r/t increased SVR
nifedipine, amlodipine, nicardipine (vasodilators)
132
MOA of clevidipine
arterial vasodilation decreases SVR without affecting preload
133
contraindications of clevidipine
- egg allergy
- soybean allergy
- impaired lipid metabolism (pathologic HLD, lipid nephrosis, acute pancreatitis with HLD)
- severe aortic stenosis
134
CCB prepared as a lipid emulsion
clevidipine
135
clevidipine dosing
1-2 mg/hr, max 16 mg/hr
136
PK of clevidipine
- onset 2-4 min
- half life 1 min (full recovery 5-15 min after gtt off)
- tissue and plasma esterase metabolism
137
function of pericardium
surrounds heart and provides minimal friction environment
138
where do the visceral and parietal layers of the pericardium attach
visceral - attached to myocardium
parietal - anchored to mediastinum
139
3 conditions that affect the pericardium
1. acute pericarditis
2. constrictive pericarditis
3. cardiac tamponade
140
what causes constrictive pericarditis
fibrosis or any condition that causes pericardium to be thicker
141
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)
142
cause of acute pericarditis
usually inflammation
(most commonly viral)
143
does acute pericarditis affect diastolic filling
not usually unless inflammation leads to constrictive pericarditis or tamponade
144
anesthetic management of constrictive pericarditis
- avoid bradycardia (CO dependent on HR)
- preserve contractility
- maintain afterload
145
causes of constrictive pericarditis
- cancer (radiation)
- cardiac surgery
- RA
- TB
- uremia
146
causes of acute pericarditis
- viral infection
- Dressler's syndrome
- lupus
- scleroderma
- trauma
- cancer (radiation)
147
what is Dressler's syndrome
pericardial inflammation from necrotic myocardium s/o MI
148
s/s constrictive pericarditis
- Kussmaul's sign (JVD during inspiration)
- pulsus paradoxus
- pericardial knock
149
what is pulsus paradoxus
- SBP decreased \> 10 mmHg during inspiration
- indicates impaired diastolic filling
may be seen with constrictive pericarditis
150
treatment of constrictive vs. acute pericarditis
pericardiotomy
151
risks & mortality assoc. with pericardiotomy
risk hemorrhage and dysrhythmias
mortality 6-19%
152
s/s acute pericarditis
acute chest pain with pleural discomfort
- increased pain with inspiration, postural changes
- pain relieved when leaning forward or supine
pericardial friction rub
ST elevation with normal enzymes
fever
153
which type of pericarditis usually resolves spontaneously
acute
154
drugs to relieve acute pericarditis pain
- salicylates
- oral analgesics
- corticosteroids
155
drugs to use in anesthetic management of constrictive pericarditis
- ketamine
- pancuronium
- volatiles with caution
- opioids, benzos, etomidate OK
156
what is Kussmaul's sign
paradoxical rise in CVP and JVD during inspiration
result of RV filling defect (impaired RV compliance)
157
what separates pericardial tamponade from effusion
excess fluid excerts external pressure on the heart, limiting ability to fill and act as a pump
158
CVP in pericardial tamponade
rises in tandem with pericardial pressure
159
CVP and PAOP in pericardial tamponade
as ventricular compliance deteriorates, left and right diastolic pressure (CVP and PAOP) begin to equalize
160
best method of pericardial tamponade diagnosis
TEE
161
best treatment of pericardial tamponade
- pericardiocentesis
- pericardiostomy
162
effects of increased pericardial pressure
- increased LV pressure
- decreased coronary perfusion
- decreased ventricular filling
- decreased LV volume
- decreased SV
- decreased CO
- increased contractility
- increased HR
- increased renal fluid retention
163
2 conditions commonly associated with Kussmaul's sign
1. constrictive pericarditis
2. pericardial tamponade
(can occur with any condition limiting RV filling)
164
2 conditions assoc. with pulsus paradoxus
1. constrictive pericarditis
2. pericardial tamponade
165
treatment for pericardial effusion
seldom requires treatment
166
pressure volume loop in pericardial tamponade
- loop shifts to left (decreased LVEDV)
- narrower (decreased SV)
- higher slope during ventricular filling (decreased ventricular compliance)
167
beck's triad
- hypotension
- JVD
- muffled heart sounds
168
causes of the symptoms in becks triad
- hypotension: decreased SV
- JVD: impaired VR to right heart
- muffled heart tones: fluid accumulation in pericardial space attenuates sound waves
169
preferred anesthetic technique for acute pericardial tamponade undergoing pericardiocentesis
local anesthesia
170
primary goal if GA is required for pericardiocentesis
preserve myocardial function
171
drugs to avoid with pericardiocentesis
- volatiles
- propofol
- thiopental
- high dose opioids
- neuraxial anesthesia
172
safer drugs to use in pericardiocentesis
- ketamine (best choice d/t SNS activation)
- N2O
- benzos
- opioids
173
why should spontaneous ventilation be maintained until pericardial tamponade relieved
PPV can impair venous return and CO (CV collapse)
174
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
175
why do patients with pericardial tamponade have decreased EKG voltage
excess fluid around the heart attenuates the electrical signal recorded by electrodes
176
why do pts with pericardial tamponade have increased contractility and afterload
increased SNS tone
177
complications of pericardial tamponade treatment
- PTX
- re-accumulation of fluid
- puncture of coronary vessels or myocardium
178
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)
179
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)
180
ACC/AHA guidelines for infective endocarditis antibiotic prophylaxis
only if pt is at high risk of developing and more likely to suffer adverse outcomes
181
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
182
is antibiotic prophylaxis required for unrepaired cardiac valve disease, CABG, or coronary stent placement?
nope
183
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
184
2 definitive procedures for treatment of cardiac tamponade
1. pericardiocentesis
2. pericardiostomy
185
most common autosomal dominant CV disease
hypertrophic obstructive cardiomyopathy (HCOM)
186
most common cause of sudden cardiac death in young athletes
obstructive hypertrophic cardiomyopathy
187
what causes LVOT obstruction in HCOM
1. congenital hypertrophy of interventricular septum
2. systolic anterior motion of anterior leaflet of mitral valve
188
3 key determinants of flow through LVOT
1. systolic LV volume
2. force of LV contraction
3. transmural pressure gradient
189
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
190
conditions that distend LVOT and decrease obstruction
- increased systolic volume (inc. preload or dec. HR)
- decreased contractility
- increased aortic pressure
191
what is systolic anterior motion (SAM)?
systolic anterior motion of anterior leaflet of mitral valve
produces mechanical obstruction to flow through LVOT
192
venturi effect in SAM
blood rapidly flows across LVOT
velocity increases through stricture
193
how is hypertrophic obstructive cardiomyopathy diagnosed
TEE
194
SAM can be a postop complication after which surgery
mitral valve **repair** (not replacement)
195
what happens if some of LV stroke volume can't pass into aorta
- takes retrograde path actoss mitral valve
- leads to mitral regurg
196
sign of turbulent flow through LVOT obstruction or mitral regurg
systolic murmur
197
what leads to diastolic dysfunction in HCOM
LVH
198
why is it v important to promptly treat A-fib or junctional rhythms in pt with hypertrophic obstructive cardiomyopathy
preserving LA contraction is very important
199
why is nitroglycerin not a good choice for a pt with hypertrophic obstructive cardiomyopathy
reduces preload - reduces systolic LV volume - narrows LVOT - worsens obstruction
200
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
201
is phenylephrine a good or bad choice for HCOM pt
good - increases aortic pressure, which increases transmural pressure and opens LVOT
202
3 surgical options to correct LVOTO
1. septal myomectomy
2. alcohol injection into septal perforator arteries
3. mitral valve replacement
203
how long should elective surgery be delayed after PCI angioplasty without stent
2-4 weeks
204
how long should elective surgery be delayed in pt after PCI with bare metal stent?
30 days (3 months preferred)
205
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
206
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
207
how long should elective surgery be delayed in pt after a CABG?
6 weeks (3 months preferred)
208
what meds are involved in dual antiplatelet therapy (DAPT)
- aspirin
- thienopyridine (ADP receptor antagonist, usually clopidogrel or ticlopidine)
209
when should a pt on DAPT stop taking aspirin before surgery
continue unless absolutely contraindicated
if contraindicated stop 3 days preop
210
when should a pt on DAPT stop taking clopidogrel before surgery
7 days preop
211
when should a pt on ticlodopine for DAPT stop taking preop?
14 days before surgery
212
what can be given to reverse platelet inhibition in emergency surgery on a pt taking DAPT
platelets
213
should UFH/Lovenox be used to "bridge" patients off antiplatelet therapy?
no - paradoxically increases platelet aggregation in the stent
214
whats the best treatment for stent thrombosis
PCI
best outcome if blood flow restored \< 90 min
215
purpose of roller pump in CPB
compresses blood tubing, creates occlusion point as it mechanically propels blood forward
216
CPB pump flow with afterload changes
remains constant d/t roller pump
217
how can roller clamp cause tubing rupture
if arterial inflow line is clamped, pump continues pushing forward and can rupture inflow tubing
218
complication with roller pump on CPB if venous reservoir runs dry
air embolism
219
what type of CPB is less traumatic to blood cells
centrifugal pump
220
which CPB tends to not entrain air
centrifugal pump - can't produce excessive negative pressure, tends to not entrain air
221
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
222
component of CPB where gas exchange occurs
oxygenator
223
which CPB oxygenator is safer
membrane oxygenator (uses blood-membrane-gas interface)
224
which CPB oxygenator carries risk of cerebral air embolism
bubble oxygenator (uses a blood-gas interface)
225
what is the CPB circuit primed with
- mannitol
- albumin
- heparin
- bicarb
226
when is awareness most common with CPB
during sternotomy
227
ACT goal for CPB
\> 400 seconds
228
what should be used for anticoagulation for CPB if pt has heparin allergy
- bivalirudin
- hirudin
- another factor 10 inhibitor
229
SBP goal before aortic cannulation
\< 100 mmHg (HTN can cause dissection)
230
best way to reduce myocardial O2 consumption during CBP
cardioplegia (K+ containing solution that arrests heart in diastole)
231
where is antegrade cardioplegia introduced
into aortic root
solution enters coronaries
232
required for antegrade cardioplegia to work
competent aortic valve & clamped aorta
233
where is retrograde cardioplegia introduced
through a cannula into coronary sinus
234
alpha-stat ABG
- doesn't correct for pt's temp
- aims to keep constant pH across all temps
235
which blood gas measurement in CPB is assoc. with better outcomes in adults
alpha-stat
236
which blood gas measurement in CPB is assoc. with better outcomes in peds
pH-stat
237
pH-stat ABG
- corrects for pt's temp
- aims to keep constant pH across all temperatures
238
dose of protamine after off bypass
~1 mg for each 100 units heparin given
239
radial artery pressure immediately after CPB
may be artificially low
240
common post-bypass AEs
- myocardial depression
- heart block
(may need vasoactives and pacing)
241
why is MAP not a good surrogate for organ perfusion during CPB
blood flow is non-pulsatile
242
what is the difference in full bypass and partial bypass
- full: all venous return drained in venous reservoir
- partial: heart receives and pumps a fraction of venous return
243
why is an LV vent used during CABG surgery?
- removes blood from LV
- this blood usually comes from Thesbian veins and bronchial circulation (anatomic shunt)
244
how does protamine reverse heparin
neutralization reaction (forms acid/base complex)
245
how should post-bypass protamine dose be calculated
account for amount of heparin predicted to remain in circulation after bypass
if based on initial heparin dose, may contribute to protamine overdose
246
administration of protamine
over 10-15 min to reduce systemic vasodulation and pulmonary vasoconstriction
247
indications for IABP
- cardiogenic shock
- MI
- intractible angina
- difficult CPB separation
248
contraindications for IABP
- aortic insufficiency
- descending aortic disease (aneurysm)
- severe PVD
- sepsis
249
where is IABP inserted
through femoral artery and advanced along descending aorta
250
what is an IABP?
a counterpulsation device that improves myocardial o2 supply while reducing O2 demand
251
how does IABP function in diastole?
pump inflation augments coronary perfusion
252
how does IABP function in systole?
pump deflation reduces afterload and improves CO
253
what do IABP inflation and deflation correlate with on monitoring waveforms?
- inflation correlates with dicrotic notch and T wave
- deflation correlates with R wave
254
where should the IABP distal tip be and why
- 2cm distal to left subclavian
- more proximal can occlude left common carotid and brachiocephalic arteries
255
how is proper IABP position confirmed
- CXR
- TEE
- fluoro
256
effects of priming the CPB circuit with anything other than blood
hemodilution:
- decreased Hct
- decreased plasma concentration of drugs and plasma proteins
- decreased O2 carrying capacity
- decreased blood viscosity
- increased microvascular flow
257
what can happen if air enters the venous line of CPB circuit
air lock
258
MOA of potassium based cardioplegia
- arrests heart in diastole
- K+ increases RMP, which locks voltage-gated Na+ channels in closed-inactive state
259
contraindication to antegrade cardioplegia
incompetent aortic valve
260
when does the IABP inflate and deflate
- inflates during diastole (increases coronary perfusion pressure/O2 supply)
- deflates during systole (reduces afterload, decreases O2 demand)
261
when is aortic pressure higher with IABP
higher in diastole than during unassisted systole
262
most common IABP complications
- vascular injury
- infection at insertion site
- thrombocytopenia
263
purpose of an LVAD
mechanical device that unloads failing heart by pumping blood from LV to aorta
264
where is the inflow cannula of LVAD inserted
in apex of LV
265
conditions that require surgical correction before LVAD can be used
- PFO
- AI
- tricuspid regurg
266
purpose of LVAD
- bridge to recovery
- bridge to transplant
- destination therapy
267
why might SpO2 and NIBP be ineffective with LVAD
flow may be non-pulsatile depending on native function
consider AL and cerebral ox
268
most common cause of death with LVAD
sepsis
269
common long-term complication with LVAD
GI bleeding (requires anticoagulation)
270
what 3 things are CO dependent on in a pt with LVAD
1. LV preload
2. pump speed
3. pressure gradient across pump (afterload)
271
what is LV suck down with LVAD & how is it treated
- low preload + relatively high pump speed produces suction
- part of LV sucked into LV cavity, occludes inflow cannula
- treated with IVF to increase preload, decrease pump speed
272
consequences of suction with LVAD
- hypotension
- ventricular dysrhythmias
- L shift of interventricular septum
- decreased RV contractility
- decreased compliance
273
consequences of mechanical shear stress with LVAD
- coagulopathy
- platelet dysfunction
274
Crawford aneurysm classification: type 1
involves all or most of descending thoracic aorta and upper abdominal aorta
275
Crawford aneurysm classification: type 2
involves all or most of descending thoracic aorta, most of abdominal aorta
276
Crawford aneurysm classification: type 3
involves lower descending thoracic aorta and most of abdominal aorta
277
Crawford aneurysm classification: type 4
involves most of abdominal aorta only
278
DeBakey aneurysm classification: type 1
tear in ascending aorta + dissection along entire aorta
279
DeBakey aneurysm classification: type 2
tear + dissection only in ascending aorta
280
DeBakey aneurysm classification: type 3a
tear in proximal descending aorta with dissection limited to thoracic aorta
281
DeBakey aneurysm classification: type 3b
tear in proximal descending aorta with dissection along thoracic & abdominal aorta
282
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
283
Stanford Aneurysm classification
- type A: involves ascending aorta
- type B: doesn't involve ascending aorta
284
in which types of dissection should you be worried about aortic insufficiency
DeBakey 1/2 or Stanford A (involve ascending aorta)
285
which type of aortic aneurysms are most difficult to repair
crawford types 2 & 3
286
which type of aortic aneurysm has the most significant perioperative risks & why
crawford type 2
- paraplegia
- renal failure
mandatory period for stopping blood flow to renal arteries and some radicular arteries that perfuse anterior spinal cord
287
aortic aneurysms that are surgical emergencies
acute dissection of ascending aorta
| (Debakey 1/2, Stanford A)
288
type of aortic aneurysm that is often managed medically
dissection of descending aorta (meds for HR, BP, pain)
289
incidence of AAA in pts \> 50
3-10%
290
independent risk factors for AAA
- cigarette smoking
- male
- advanced age
291
how is AAA most commonly detected
- pulsatile abdominal mass
- generally asymptomatic
292
primary mechanism of AAA
destruction of elastin and collagen that form matrix of vessel wall
293
pathologic changes that cause abdominal aorta to weaken/dilate
- atherosclerosis
- inflammation
- endothelial dysfunction
- platelet activation
294
what AAA measurements correlates with risk of rupture
diameter (increased radius = increased transmural pressure = increased wall stress)
295
when is surgical correction of AAA recommended
when \> 5.5cm or if it grows \> 0.6-0.8 cm/year
296
risk of AAA rupture when \> 8 cm diameter
30-50%
297
classic triad of symptoms in AAA rupture
- hypotension
- back pain
- pulsatile abdominal mass
\*\*only in ~50% of patients\*\*
298
where do most AAA rupture
left retroperitoneum
299
most common cause of AAA postop death
MI
300
how does aortic cross clamp contribute to risk of anterior spinal artery syndrome?
- clamp above artery of Adamkiewicz may cause ischemia to lower anterior spinal cord
- can result in anterior spinal artery syndrome (Beck's syndrome)
301
how does anterior spinal artery syndrome present
- flaccid paralysis of lower extremities
- bowel and bladder dysfunction
- loss of temp and pain sensation
- preserved touch and proprioception
302
why dont most AAA rupture pts immediately exsanguinate
most aneurysms rupture in left retroperitoneum, allowing for tamponade and clot formation
303
effects of aortic cross clamp:
- 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 (inc venous return)
304
physiologic effects of removing aortic cross clamp
- LV wall stress
- MVO2
- coronary blood Q
- renal blood Q
- total body VO2
- SvO2
- LV wall stress increased (inc preload/afterload)
- MVO2 increased
- coronary blood Q increased
- renal blood Q decreased
- total body VO2 decreased (aerobic metabolism distal to clamp)
- SvO2 increased (decreased total body VO2)
305
infrarenal clamp time associated with increased risk ARF
\> 30 min
306
effects of aortic cross clamp removal:
- venous return
- CO
- MAP
- SVR
- PAOP
- VR decreased (central hypovolemia, capillary leak)
- CO decreased (dec. preload & contractility)
- MAP decreased (dec. preload & SVR)
- SVR decreased (anaerobic metabolites, vasodilation)
- PAOP increased (increased PVR)
307
effects of aortic cross clamp release:
- LV wall stress
- MVo2
- coronary blood Q
- renal blood Q
- total body VO2
- SvO2
- LV wall stress decreased
- MVo2 decreased (increased if PAOP increased)
- coronary blood Q decreased
- renal blood Q decreased/unchanged (depends on MAP)
- total body VO2 increased (cells distal to clamp receive O2)
- SvO2 decreased (increased total body VO2)
308
advantages of EVAR over open repair
- decreased operative time
- decreased transfusion rate
- shorter LOS
- decreased morbidity
- no need for aortic cross clamp
- avoid resp risks assoc. with midline abdominal incision
309
complications of EVAR
- baroreceptor reflex activation
- massive hemorrhage
- aortic rupture
- cerebral embolism
- endoleak
310
what is an endoleak
EVAR complication - original graft fails to prevent blood from entering aortic sac
311
endoleak treatment
sometimes resolve spontaneously (especially early), may require placement of 2nd graft or open repair
312
amaurosis fugax
blindness in one eye
sign of impending stroke. emobli travel from internal carotid to opthalmic artery & impairs perfusion of optic nerve
causes retinal dysfunction
313
what perfuses the posterior 1/3 spinal cord
posterior spinal arteries
314
perfuses anterior 2/3 spinal cord
anterior spinal artery (1)
315
where does artery of Adamkiewicz originate
on left side between T11-T12
- 75% of population: originates between T8-T12
- another 10%: originates L1-L2
316
what are watershed areas
some regions of spinal cord only have a single blood supply
317
why does a patient with Beck syndrome present with flaccid paralysis of lower extremities
the corticospinal tract is perfused by anterior blood supply
318
why does pt with Beck's syndrome have bowel & bladder dysfunction
ANS fibers perfused by anterior blood supply
319
why does pt with beck syndrome lose pain and temp sensation
spinothalamic tract perfused by anterior blood supply
320
why does a pt with beck syndrome have preserved touch & proprioception
dorsal column perfused by posterior blood supply
321
thoracic cross clamp time that significantly increases risk of cord ischemia
\> 30 min
322
method to reduce spinal cord O2 consumption
moderate hypothermia (30-32 deg C)
323
what does spinal cord perfusion pressure depend on
pressure gradient between anterior spinal artery and CSF
CSF will drain with decreased pressure and increased gradient
324
BP goals during cross clamp to prevent beck's syndrome
maintain proximal HTN (MAP ~ 100)
325
monitoring that monitors posterior cord
SSEP
326
spinal cord protecting drugs
- corticoteroids
- CCBs
- mannitol
327
incidence of amaurosis fugax
in 25% of pts with high grade stenosis
328
regional techniques for CEA
- local infiltration
- superficial plexus block (C2-C4)
- deep cervical plexus block (C2-C4)
329
risk of regional anesthesia in CEA pt
risk of ipsilateral phrenic nerve block - caution with severe COPD
330
cerebral perfusion pressure =
MAP - ICP
331
what does cerebral perfusion depend on during carotid artery clamp (CEA)
collateral flow from circle of willis (contralateral carotid and vertebral vessels)
332
EEG findings that indicate risk of cerebral hypoperfusion
- loss of amplitude
- decreased beta wave activity
- slow wave activity
333
things that increase frequency in EEG
- mild hypercarbia
- early hypoxemia
- seizure
- ketamine
- N2O
- light anesthesia
334
things that decrease EEG frequency
- extreme hypercarbia
- hypoxia
- cerebral ischemia
- hypothermia
- anesthetic OD
- opioids
335
what is cerebral oximetry
what indicates cerebral perfusion is at risk
uses NIRS to monitor cerebral O2 sat (rSO2) in frontal lobe
perfusion at risk when reduced 25%+ from baseline
336
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
337
anesthesia considerations for SSEP
- requires light plane of anesthesia
- monitors sensory pathways only
- volatiles decrease amplitude and increase latency (mirror ischemia)
338
where is carotid stump pressure measured
distal to clamp
339
carotid stump pressure that indicates risk of ipsilateral cerebral hypoperfusion
stump pressure \< 50m mmHg
340
risk assoc. with carotid shunt placement
increased risk embolic stroke
341
BP goal during carotid clamping (CEA)
keep BP normal/slightly elevated - brain perfusion is pressure dependent d/t loss of autoregulation
342
what reflex can be activated during CEA or following carotid balloon inflation
baroreceptor reflex
343
ETCO2 goal in CEA
maintain normocapia or mild hypocapnia
cerbral vessels distal to stenosis may be maximally dilated - hypercarbia dilates cerebral vessels and shunts blood from hypoperfused tissue
344
lab value that increases risk stroke or death in CEA
blood sugar \> 200 mg/dL DOS
345
5 complications assoc. with CEA
- hematoma
- RLB injury
- hemodynamic instability (altered baroreceptor sensitivity)
- stroke (usually embolic)
- carotid denervation
346
when is carotid denervation a problem
hx bilateral CEA
reduced ventilatory response to hypoxia
347
what is carotid artery angioplasty stenting (CAS)
uses percutaneous transvacuolar access to pass stent to carotid
348
ACT goal for CAS
\> 250 sec
349
most common complication of CAS & how is it treated
thromboembolic stroke
treat w recombinant tPA
350
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
351
BP in subclavian steal
much lower in ipsilateral arm
352
treatment of choice for subclavian steal syndrome
subclavian endarterectomy
353
s/s subclavian steal
- syncope
- vertigo
- ataxia
- hemiplegia
- arm ischemia
- weak pulse in ipsilateral arm
354
why does the RV subendocardium remain well perfused throughout cardiac cycle
vs. LV subendocardium - thinner wall
doesn't generate enough pressure to occlude its own circulation
355
when is LV subendocardium primarily perfused
during diastole
356
which region of myocardium receives the least amount of perfusion during systole & why
LV subendocardium
tissue compresses its own blood supply as aortic pressure increases
357
why is LV subendocardium predisposed to ischemia
high compressive pressures in LV + decreased coronary flow during systole increases coronary vascular resistance
358
2 factors assoc. with highest O2 consumption
pressure work
HR
359
MOA of aldosterone antagonists & example
- inhibit K excretion & Na reabsorption by principal cells of collecting ducts
- block aldosterone at mineralocorticoid receptors
spironalactone
