EXAM II Flashcards
(416 cards)
1
Q
What are the components of the basic cardiac exam?
A
Inspection
Palpation
Auscultation
2
Q
Inspection for cardiac
A
Assess RIJ distention and determine if JVD is present
3
Q
Slide 3 pic of pt in CV
A
Shows: EJ Path of IJ Clavicular head of SCM (sternocleidomastoid) Clavicle Sternal head of SCM
4
Q
What are we palpating when doing cardiac exam?
A
Precordium to determine location of PMI (Point of maximum impulse)
5
Q
Cardiac auscultation sites APTM plus ERB’s point
A
Aortic 2nd intercostal space (2-3) right sternal border
Pulm 2nd intercostal space (2-3) Left sternal border
Erb’s 3rd ICS left sternal border
Tricus 4th left ICS left sternal border
Mitral 5th ICS left mid-clavicular line
6
Q
Where is S2 heard best?
A
Erb’s point
7
Q
SLIDE 8 CV KNOW THE PRESSURE/VOLUME loop!
CO formula and #s
SV formula and #s
CI formula and #s
Atrial kick amount
A
CO = SV x HR 5-6 L/min
SV = EDV - ESV 50-110 mL/beat
CI = CO/BSA 2.8-4.2 L/min/m^2
Atrial kick 5-10%
8
Q
What does Tito equate to afterload?
A
SVR
9
Q
Ejection fraction define
2 formulas
Normal Values
A
Percentage of end-diastolic volume ejected during systole
EF = (EDV-ESV)/EDV
EF = SV/EDV
Normal 60%-70%
10
Q
Which of the two drugs would you give a pt with low EF?
Prop or Etomidate
A
Etomidate cause it won’t mess with their CO
11
Q
What are the factors that increase the Coronary Supply?
A
Coronary artery Diastolic pressure Diastolic time (good HR) O2 extraction -Hb -SaO2 HR
12
Q
What are the factors that influence demand on the Coronary/heart?
A
HR
Preload
Afterload
Contractility
13
Q
During anesthesia what do we want to do to coronary supply and demand?
A
Increase supply
Decrease demand
14
Q
Value of coronary blood flow and % of the CO?
A
225-250 mL or 4-7% of CO
15
Q
What things can cause tachycardia in the OR?
A
Blood loss
Light anesthesia (such as in emergence)
Pain
16
Q
If pt tachycardic and we want to try and fix it how do we go about it?
A
Make one adjustment at a time so we know what is working and what isn’t. Do not try several things at once
17
Q
What do the right and left coronary arteries supply?
A
The myocardium with oxygenated blood
18
Q
When does most perioperative MI occur?
A
24-48 hrs post op which accounts for 20% mortality
19
Q
What values of MAP do the coronary arteries autoregulate?
A
MAP of 60-140 mm HG
20
Q
Factors that effect myocardial O2 consumption (MVO2)
A
50% increase in any of these will result in:
HR 50% increase in MVO2
Pressure work 50% increase in MVO2
Contractility 45% increase in MVO2
Wall stress 25% increase in MVO2
Volume work 4% increase in MVO2
21
Q
In the pressure volume loop what does the net external work output represent?
A
Myocardial workload
22
Q
In the pressure volume loop if the area of the loop widens what can we predict?
A
The heart’s workload has increased
23
Q
In the pressure volume loop if the area of the PV increases in height what can we predict?
A
The heart’s workload has increased
24
Q
List factors that decrease O2 delivery to coronaries as related to decreased coronary flow
A
Tachycardia
decreased aortic pressure
Decreased vessel diameter (Spasm or hypocapnia)
Increased end diastolic pressure
25
List factors that decrease O2 delivery to coronaries as related to decreased arterial oxygen content (CaO2)
Hypoxemia
| Anemia
26
List factors that decrease O2 delivery to coronaries as related to decreased Oxygen fraction
Left shift oxyhemoglobin dissociation curve
| Decreased capillary density
27
List factors that increase O2 demand of coronaries
```
Tachycardia
HTN
SNS stimulation
Increase wall tension
Increased end diastolic volume
Increased afterload
Increased contractility
```
28
SLIDE 14 pic of conducting system CV
Middle internodal tract
| Posterior internodal tract
29
According to the WHO what is the FIO2 required to be maintained during colorectal surgery
80% FIO2
30
SLIDE 15, 16, 17 CV
P/V loop and Ventricular function curve
31
List all 8 CV reflexes
```
Baroreceptor
Valsalva
Cushing
Chemoreceptor
Brainbridge reflex
Oculocardiac
Celiac
Bezolh-Jarish
```
32
SLIDE 19 CV
Baroreceptor reflex
33
What is the valsalva maneuver?
Forced expiration against a closed glottis stimulates bareceptor
Inhibits the SNS and stimulates PNS
- decreases HR
- decreases contractility
- vasodilation
Increases intrathoracic pressure
34
When might we need to use valsalva maneuver in OR?
Surgeon might ask us to test this for suture integrity or test urination
35
How can we induce Valsalva maneuver in the OR?
Open APL to 70 and switch pt off vent and squeeze the reservoir bag a little.
36
Slide 20 CV
Shows medulla, CN 9 and 10, carotid body, aortic bodies
37
What is the cushing reflex and what are signs?
Physiologic response to INITIAL CNS ischemia caused by increase ICP causes tachycardia, HTN, and increased contractility.
LATE SIGN!!!!! of high sustained ICP prior to cerebral herniation
- Wide pulse pressure (systolic shoots up)
- Bradycardia
- irregular respirations (last sign)
38
Bainbridge reflex
slide22 has a pic CV
increase in right-sided filling pressure causes stretch receptors in right atrial wall send vagal afferent signals to CV centers in medulla
- inhibits PNS activity to increase HR
- acceleration of the HR also from direct effect on the SA node by stretching the atrium
39
Oculocardiac reflex/Five & dime mechanism
- Traction on extraocular muscles (especially the medial
rectus)
- traction on conjunctiva
- traction on orbital structures
all of these cause hypotension & reflex slowing of HR as well as arrhythmias
40
Oculocardiac reflex/Five & dime mechanism nerve paths
Afferent path - trigeminal nerve
| Efferent branch - vagus
41
Oculocardiac reflex/Five & dime mechanism how to blunt reflexes prophylactically and when it happens?
Prophylactically:
- retrobulbar block
- glycopyrulate
Reactive:
- release of the offending stimulus (tell surgeon to stop and still give more glyco)
- vagal response inhibited by anticholinergics
42
Celiac reflex
Traction on mesentery or gallbladder or stimulation of vagus nerve in the other areas of body like thorax and abdominal cavity. Can occur indirectly as a result of pneumoperitoneum
causes bradycardia
apnea
hypotension
stop it by stopping stimulus
43
Chemoreceptor reflex
pic slide 25 CV
chemosensitive cells are located in carotid bodies and aortic body
response to pH changes (usually acidotic) in blood O2 tension
44
Oculocardiac reflex/ Fiv & dime which nerves stimulated and what types of procedures can we see this reflex happen with?
CN v1 of trigeminal nerve and vagus nerve
Big time in face-lifts
Brain surgery
ENTs
45
What types of procedures cause Celiac reflex?
15 mm Hg insuplation (fill thorax with CO2) for laparoscopic surgery like gallstone.
Can be initiated clinically with pneumoperitoneum
46
What drugs to give to blunt Celiac reflex?
For the bradycardia atropine
| For the hypotension ephedrine
47
Alternative to medical intervention for Celiac reflex?
Stop the initiating stimulus
48
Where are chemosensitive cells located and what changes do they respond to?
Carotid bodies and aortic body respnd to changes in pH and blood O2 tension
49
Values of PaO2 or pH that cause chemoreceptors to respond and how do they signal the CNS?
PaO2 less than 50 mm Hg
Signal through nerve of Hering (branch of CN IX) and vagus nerve to chemosensitive are of medulla
50
What does activation of chemoreceptors in medulla cause?
stimulation of the respiratory centers to increase resp drive
activate PNS
- increase HR and myocardial contractility
- which increase BP
51
What is the Bezold- Jarisch reflex?
A DEFENSE MECHANISM which is caused by noxious stimuli such as irritants that stimulate LV and cause
- hypotension
- bradycardia
- coronary dilation (most protective to heart)
52
What are some irritants that cause Bezold?
Dobutamine and????????
53
What is the Bezold reflex pathway?
Irritant in LV
Afferent impulse ---> CN X-----> brain
Efferent impulse to heart ----> heart
54
How does the BP cuff work?
Senses oscillations in cuff pressure which correlate with arterial pulsation
Inflated beyond the point at which oscillation ceases then slowly deflated
Oscillation begins at systolic pressure, peaks at MAP and disappears once again at diastolic
55
Allen's test
Occlude both arteries
squeeze hand 10 times
release ulnar and look for <6 sec cap refill
56
What does a positive allens test indicate?
??????
57
What does right lateral position mean?
Pt is right side down
58
If pt is in right lateral position what will their right arm cuff BP difference be?
increase in 15 mm Hg in right arm for both systolic and diastolic
59
If pt is in right lateral position what will their left arm cuff BP difference be?
decrease in 15 mm Hg in right arm for both systolic and diastolic
60
If pt is in right lateral position what will their left and right arm a-line BP difference be?
No difference, still 120/80
61
With a 20 cm gradient how much does this change our cuff BP?
+/- 15 mm Hg depending on the arm that is up or down
62
What are the 5 differences between the distal A-line waveform and the aortic arch?
Distal:
- wider PP
- delayed upstroke
- slurred dicrotic notch
- more prominet diastolic wave
- incrased SBP due to distance from aorta and increased resistance
63
A-line waveform abnormalities
Aortic stenosis
A stenosis - pulsus parvus (narrow PP)
| - pulsus tardus (delayed upstroke)
64
A-line waveform abnormalities
Aortic regurg
```
Bisferiens pulse (double peak)
wide pulse PP
```
65
A-line waveform abnormalities
Hypertrophic cardiomyopathy
Spike-and-dome pattern (midsystolic obstruciton)
66
A-line waveform abnormalities
Systolic LV failure
Pulsus alterans (alternating PP amplitude)
67
A-line waveform abnormalities
Cardiac tamponade
Pulsus paradoxus (exaggerated decrease in systolic BP during inspiration - greater than 10 mm Hg drop)
68
CVP use, when to place, and where?
Monitor fluid status
before/after induction
Multiport
Can place on either IJ
69
CVP how to confirm cath tip position?
X-ray (tip @ T4-T5 interspaces
| Aspirate (BRB?)
70
CVP how to confirm cath tip position?
X-ray (tip @ T4-T5 interspaces)
| Aspirate (BRB?)
71
CVP complication
when we place on left IJ could nick thoracic duct and cause chylothorax
72
CVP waveform/art line/ekg slide 36 CV
Shows each waveform component
73
CVP waves and phases of cardica cycle
```
a - end diastoly
c - early systole
x - mid systole
v - late systole
y- early diastole
h- only in bradycardia but mid to late distole
```
74
a wave
atrial contract
75
c wave
isovolumetric contraction
76
v wave
systolic filling of atrium
77
h wave
diastolic plateu
78
x decent
atrial relax (systolic collapse)
79
y decent
early vent filling (diastolic collapse)
80
CVP waveform abnormalities
A-fib
loss of a wave
| prominent c wave
81
CVP waveform abnormalities
Cardiac tamponade
Dominant x descent
attenuated y descent
82
PA catheter uses and complications
Open hearts and sooooooometimes neuro
Complications
- arrhytmias
- Pulm artery rupture (hemoptisis)
83
PA wave slide 39 CV
Tip of catheter must go in zone 3
84
Cardiac drugs
```
Milrinone (PDE)
Nipride (vasodilator decrease afterload)
Lasix
Dig (cardiac glycoside)
NTG (mostly venous dilator to decrease preload but)
NEO (increase SVR)
```
85
Cardiac drugs
```
Milrinone (PDE)
Nipride (vasodilator decrease afterload)
Lasix
Dig (cardiac glycoside)
NTG (mostly venous dilator to decrease preload but)
NEO (increase SVR)
```
86
Before surgery we must assess MI and heart failure risks based on whos guidelines?
American college of cardiology (ACC)
American heart association (AHA)
87
What are the guidelines of ACC and AHA for heart risk for surgery?
1. condsider urgency of surgery
2. consider an active cardiac condition
3. consider risosk of the procedure
4. Assess pt functionality
5. consider pt with poor or indeterminate functional capacity scheduled for vascular, intermediate, or high risk
procedures
88
Step 1. Urgency Surgery
Emergency cases
Focus perioperative surveillance and risks reduction
Surveillance-serial ecgs, cardiac enzyme, monitoring
Risk reduction- beta blockers, statins, pain management
89
Step 2. Active cardiac condition
1. unstable coronary syndrome
2. decompensated HF
3. Significant arrhythmias
4. Severe valvular dz
90
Step 2. Active cardiac condition
1. unstable coronary syndrome
2. decompensated HF
3. Significant arrhythmias
4. Severe valvular dz
91
Step 2. Active cardiac condition
Unstable coronary syndrome characteristics
Unstable or severe angina @ rest increasing sx> 30 min and sx become less responsive to MONA
Acute MI past 7 days, elective surgery postpone
Recent MI 7-30 days with myocardium risk (+stress test and persistent sx), elective surgery postpone
92
Class 1 HF
No limitaion on exercise toleration
no sx during usual activity
93
Class 1 HF
No limitaion on exercise toleration
no sx during usual activity
94
Class 2 HF
Mild exercise limitation
comfy with rest or mild exertion
95
Class 3 HF
Moderate exercise limitation
comfy only @ rest
96
Class 4 HF
Sever exercise limitaiton
any physical activity brings discomfort and sx at rest
DECOMP HF
97
Step 2. Active cardiac condition
Significant Arrhythmias
```
Mobitz II
3rd degree hrt blck
SVT or A-fib with RVR or new onset
Symptomatic vent arrhythmia or bradycardia
New vent tachycardia
```
98
Step 2. Active cardiac condition
Severe valvular dz
Severe aortic or mitral stenosis
99
Step 3. Surgical procedure
Low risk vs high risk cases
100
Step 3. Surgical procedure
high risk procedures defined
Vascular > 5% chance of CV death or nonfatal MI
Intermediate 1-5% chance of CV death or nonfatal MI
101
Step 3. Surgical procedure
Vascular procedures
Aortic and other major vascular surgery
peripheral vascular surgery
102
Step 3. Surgical procedure
intermediate procedures
Intraperitoneal & intrathoracic surgery
Carotid endarterectomy
Head and neck surgery
Ortho
Prostate
103
Step 3. Surgical procedure
low risk procedures defined
<1% chance of cardiac death or nonfatal MI
104
Step 3. Surgical procedure
low risk procedures procedures
Endospcopic procedures
superficial procedure
cataract surgery
breast surgery
Ambulatory surgery
105
Do the low risk procedures require further preoperative cardiac testing
No, unless the pt has an unstable cardiac condition
106
Step 4 Pt functionality
Functional capacity or exercise capacity expressed as MET (metabolic equivalent units) units
O2 consumption at rest 3.5 mL/kG/min or 1 MET
=> 4 METs go to surgery
asymptomatic pt with average capacity can walk 1-2 flights or 4 blocks on level surface can go to surgery
107
Step 5. Clinical predictors
```
Ischemic heart dz
compensated or prior HF
CVA or TIA
DM
Renal insufficiency
```
108
Step 5. Clinical predictors
```
Ischemic heart dz
compensated or prior HF
CVA or TIA
DM
Renal insufficiency
```
109
The LEE revised cardiac risk index (RCRI) w/ 6 risks
```
High risk surgery
Ischemic Hrt dz
Hx of CHF
Hx of CVA or TIA
DM w/insulin
Creatine > 2.0 mg/dL
```
110
After adding all the RCRI components what are the % risks for cardiac death, nonfatal MI, or nonfatal cardiac arrest?
0 = 0.4%
1 = 1.0%
2 = 2.4%
=> 3 5.4%
111
Lee revised cardiac index (modified Goldman Index)
What is considered hx of ischemic hrt dz?
- Hx of MI
- Hx of positive exercise test
- Current chest pain considered 2/2 MI
- Nitrite therapy use
- ECG with pathological Q waves
112
Lee revised cardiac index (modified Goldman Index)
What is considered hx of CHF?
```
Hx of CHF
Pulm edema
Paroxysmal nocturnal dyspnea
bilateral rales or S3 gallop
Chest radiograph showing pulmonary vascular redistribution
```
113
What are the noninvasive tests for step 5?
Exercise ECG considered good when pt can exercise to @ least 85% of their target HR (220- age)
Pharmacologic stress tests for pt who can't exercise, pacemakers, or significant bradycardia, or high dose Beta blockers
- dobutamine echocardiography
- dipyridamole myocardial perfusion scintigraphy
114
What can be done for a pt who wants to have elective non cardiac surgery but their risk stratification doesn't allow them?
1. revascularization by surgery
2. revascularization by PCI w/ or w/out stents
3. optimal medical management
115
To confirm HTN dx
2 seperate results at least 1-2 wks apart
116
What causes HTN
increased CO, SVR, or both
SVR usually the cause tho
117
What causes a SVR elevation usually?
Vascular smooth muscle tone (intracellular Ca++ concentration)
118
Primary HTN
no identifiable cause
| 95% of cases
119
Secondary HTN
identifiable causes
| 5% of cases
120
How is BP regulated?
Slide 70 and 71 CV
Feedback mechanism using
SNS (baroreceptors)
RAAS
Vasopressin
121
How does chronic vasoconstriction cause primary HTN
increase renin ---->>
increase angiotensin 1, angiotensin II, and aldosterone -->
increase Na and H2O retention
122
How does SNS overactivity cause primary HTN
Chronic vasoconstriction-----> increase SVR
123
How does vasodilator deficiency cause primary HTN
these people have a decrease in NO2 and prostaglandins which increases SVR
124
How does collagen and metalloproteinase deposition in the arterial intima cause primary HTN
increase vascular stiffness----> increase SVR
125
How does diet cause primary HTN
increase in Na intake, hold H2O
126
How is secondary HTN acquired and how to tx
Usually 2/2 a particular cause and if we tx cause BP normalizes
127
What are the 4 pharmacologics for HTN
Adrenergic receptor drugs
Target myocardium and VSM
Renal meds
CCB
128
What are the 6 renal medicaiton catagories?
```
ACEi (prils)
AT-2 receptor blockers (sartans)
Loop diuretics
Thiazide diuretics
K+ sparing diuretics
Aldosterone antagonists
```
129
How do ACEi work?
inhibit ATII mediated vasoconstriction
| inhibit aldosterone release
130
How do AT-2 receptor blockers work?
Inhibit ATII mediated vasoconstricion
| inhibit aldosterone release
131
How do loop diuretics work?
Inhibit Na-K-2Cl transporter in the thick portion of the ascending loop of henle
132
How do thiazide diuretics work?
Inhibit Na-Cl transporter in the distal convoluted tubule
133
How do K+ sparing diuretics work?
Inhibit K excretion and Na reabsorption by the principal cells in the collecting ducts
acts independently of aldosterone
134
How do aldosterone antagonists work?
Inhibit K excretion and Na reabsorption by the principal cells in the collecting ducts
Blocks aldosterone at mineralocorticoid receptors
135
Name loop diuretics
Furosemide
bumetanide
ethacrynic acid
136
Name thiazide diuretics
HCTZ
metolazone
indapamide
chlorthalidone
137
Name K+ sparing diuretics
Triamterene
| amiloride
138
Name aldosterone antagonist
Sprinolactone
139
Name the 4 drugs that target myocardium and VSM for HTN
CCB dihydropyridines (dipine)
CCB non-dihydropyridines
Arteriodilators
Venodilators
140
CCB dihydropyridines how they work
Target vasculature mostly
| decrease vascular Ca++ ---> vasodilation ---> decrease SVR (afterload)
141
CCB nondihydropyridines how they work
```
Target myocardium
decrease inotropy
decrease chrono
decrease dromo (conduction velocity)
decrease SVR (afterload)
```
142
Arteriodilators how they work
```
Increase NO2 ---> vasodilation
Decrease SVR (afterload)
```
143
Venodilators how they work
increase NO2 ---> vasodilation
| Decrease venous return (preload)
144
CCB dihydropyridines list
Suffix "dipine"
145
CCB non-dihydro list
Verapamil (class = phenylalkylamine)
| Diltiazem (class = benzothiazepine)
146
Adrenergic receptor 4 drug classes for HTN
a1 antagonists
B1 antagonists
mixed a1/B1, B2 antagonists
a2 agonists
147
A1 antagonists names and how they do what they do when they do what they do dawg
"Zosin"s and phenoxybenzamine and phentalomine (a1/a2)
decrease vascular Ca++
decrease SVR
148
B1 selective antagonists names and how they do it
acebutolol, atenolol, bisoprolol, esmolol, metoprolol
(AABEM like hawkbeem)
decrease inotropy
decrease chrono
decrease dromo (conduction velocity)
decrease renin release by JGA
149
B1 & B2 non-selective antagonists names and how they do their thang
nadolol, pindolol, propranolol, sotalol, timolol
(NPPST like N ppsssst!)
in addition to B1 effects they cause vasoconstriction
150
mixed a1/B1, B2 antagonists names and how work
bucindolol, carvedilol, labetalol
mixed a1/B1, B2 effects
Labetalol a : B antagonistic potency
IV = 1:7
PO = 1:3
151
a2 agonists names n how they do it
Clonidine, precedex
decrease SNS outflow
152
CHF definition
Systolic, ventricle cant empty good
| Diastolic, ventricle cant fill good
153
Discuss cardiac remodeling
Occurs when HF happens
Changes shape, size, and function to preserve CO
Eventually this defense mechanism fails and causes myocardial dysfunction
154
How to reverse remodeling
ACEi
| Aldosterone inhibitors
155
Systolic HF etiology
MI
Valve insufficiency
Dilated Cardiomyopathy
156
Diastolic HF etiology
```
MI
Valve stenosis
HTN
Hypertrophic cardiomyopathy
Cor pulmonale
Obesity
```
157
Hallmark of S HF
decreased EF with an increase in LVED
- hrt cant squeeze well blood remains in the ventricle
- less O2 rich blood to peripheral circulation
158
Hallmark of D HF
symptomatic HF with normal EF
- because of decreased ventricular compliance hrt is unable to relax and receive incoming volume
- contractility is generally preserved until the late stage
159
How to deal with preload, afterload, contract, and HR in S HF
preload- already high (use diuretics if too high)
afterload- decrease to reduce hrt work and maintain CPP
Contract- inotropes as needed like dobutamine
HR- usually high d/t increased SNS tone
- if EF low, then higher HR needed for CO
160
How to deal with preload, afterload, contract, and HR in D HF
Preload- need volume to stretch noncompliant ventricle
afterload- keep elevated to perfuse thick myocardium (neo), maintain CPP
Contract- usually normal
HR- slow/noral to increase diastolic time and CPP
161
Coronary perfusion pressure (CorPP) formula and normal range
CorPP = DBP- LVED
normal range 60 -80 mm Hg
162
ASK ABOUT and READ slide 85 CV
contradicts notecards 163 and 164
163
Which hrt is thinner, more compliant and weaker?
Right
164
What kinds of conditions cause increase in PVR?
Hypoxia
Hypercarbia
Acidosis
All will impair RV impairment
165
How to treat R-sided HF
Inotropes
Decreasing PVR
NO2
166
In OR best ways to monitor for MI and what do you look for?
Most cost effective is to do EKG
leads II, V4, V5
II good for analysis of cardiac rhythm disturbances
167
Inferior MI lead changes, heart side, and artery
II, III, aVF
right heart
RCA
168
Septal MI lead changes, heart side, and artery
V1, V2
Left heart
LAD
169
Anterior Inferior MI lead changes, heart side, and artery
V3, V4
Left heart
LAD
170
Lateral Inferior MI lead changes, heart side, and artery
I, aVL, V5, V6
Left
Circumflex
171
Lab assessment for MI
O2 deprived myocardium releases:
- Creatine kinase-MB (more sensitive for dx)
- Trop I
- Trop T
Cross reference lab with EKG readings
172
CK-MB
Trop I
Trop T
initial Peak return to baseline
3-12 hrs 24 hrs 2-3 days
3- 12 hrs 24 hrs 5-10 days
3- 12 hrs 12-48 hrs 5-14 days
173
Causes of increased O2 demand and the interventions
Increased HR
Increased BP
Increased PAOP
use Beta block to HR <80
increase depth of anesthesia
vasodilator
nitroglycerin
174
Causes of decreased O2 supply and the interventions
Decreased HR
Decreased BP
Increased PAOP
```
Use anticholinergic
pace
vasoconstrict
reduce depth of anesthesia
nitroglycerin
inotrope
```
175
T/F most perioperative MI are caught in the OR?
False, usually undiagnosed and undertreated and events occur 24-48 hrs post-op
176
T/F most perioperative MI are caught in the OR?
False, usually undiagnosed and undertreated and events occur 24-48 hrs post-op
177
What usually happens with hemodynamics with valvular dz?
tolerated at first but eventually cause the heart muscle dysfunction CHF or sudden death
178
Pressure and volume overload correlation with which valvular diseases?
Pressure overload
- mitral stenosis
- aortic stenosis
Volume overload
- mitral regurgitation
- aortic regurgitation
179
T/F CHF is a frequent sign of valvular disease?
True
180
S1 hrt sound
GOOD PRESSURE VOLUME LOOP PIC ON 96 slide
Close A-V
systole begin
End of LV filling and beginning of isovolumic contraction
volume proportionate to force of contraction
- sound louder with vigorously contracting ventricle
- sound softer with poorly contracting ventricle
181
S2 hrt sound
Close aortic and pulmonic
diastole begin
end LV ejection and begin isovolumic relaxation
Volume proportionate to LV pressure decrease at end of systole
- sound is louder with htn
- sound is softer with hypotension
182
S3 hrt sound
Flaccid and inelastic heart - HF
Heard during middle 1/3 diastole after S2
Gallop rhythm- rumbling sound
183
S4 hrt sound
Atrial systole
| Heard before S1
184
Normal aortic valve cross sectional area
2.5-3.5 cm^2
185
What is the resultant pressure gradient in aortic valve
2-4 mm Hg is normal but stenosis increases
186
What is the most common valve lesion in the US?
Aortic stenosis
Causes
- Congenital defective bicuspid AV
- Calcification of the cusps
187
Severity and grades of Aortic valve stenosis
Velocity jet Mean P gradient Valve area
mild <3 m/s <25 mm Hg => 1.5 cm^2
moder 3 - 4 25 - 40 1 - 1.5
severe 4 - 4.5 40 - 50 0.7 - 1
Critical >4.5 >50 <0.7
188
Severity and grades of Aortic valve stenosis
Velocity jet Mean P gradient Valve area
mild <3 m/s <25 mm Hg => 1.5 cm^2
moder 3 - 4 25 - 40 1 - 1.5
severe 4 - 4.5 40 - 50 0.7 - 1
Critical >4.5 >50 <0.7
Critically severe = >50 AND <0.7
189
Survival rates in years if pt experiencing valvular sx
```
Angina = 5 years
Syncope = 3 years
HF = 2 years
```
190
Classic signs of Aortic stenosis
Angina pectoris
-caused by increased O2 demand from hypertrophied LV
syncope
-caused by uncompensated decrease in vascular tone upon exertion
dyspnea on exertion
-CHF
191
What is the clinical presentation of aortic stenosis?
Systolic murmur
timing- midsystole
Crescendo - decrescendo radiates to carotids
Concentric hypertrophy
192
PV loop for aortic stenosis
Slight increase in EDV and ESV
| Super htn
193
Death spiral from aortic stenosis
Hypotension for whatever reason pt is dealing with will:
myocardial ischemia--> ichemic contractile dysfunction-->
decrease CO--> worsen hypotension --> increase ischemia
194
Why won't chest compression be very effective on pt going in to death spiral?
tough to generate enough mechanical force to create adequate SV across the stenotic valve
195
How to perioperatively manage HR and Rhythm of pt with aortic stenosis?
70-80 BPM and NSR
196
What does tachycardia do to folks with aortic stenosis?
Decreases vent filling
decreases LVEDV
Decreases SV and CO
Increases Myocardial O2 demand and supply
197
What does bradycardia do to folks with aortic stenosis?
2/2 fixed lesion at the aortic valve limiting the amount of blood ejected during each cardiac cycle a drop in HR can super decrease CO leading to hypotension and peripheral perfusion problems
198
Why do we need decent HR and rhythm for aortic stenosis folks?
2/2 decrease in vent compliance (hypertrophy), we really need atrial kick which can be exaggerated to 40% from 30% of the CO
Loss of sinus rhythm can lead to rapid clinical deterioration
199
What should we do about afterload for aortic stenosis?
Maintain or increase SVR cause if they get hypotensive for any reason, could death spiral
200
What should we do about preload for aortic stenosis?
Increase, give fluids
201
How to tx hypotension for aortic stenosis
a1 agonist to increase SVR and coronary perfusion pressure without tachycardia
202
Do we need to worry about contractility with our aortic stenotic pt?
sure we can maintain it but it usually isn't a big deal till late in the dz state.
203
Aortic regurg, first how she look?
LV eccentric hypertrophy
CO decreased because part of the SV is back in the LV
Acute or chronic
204
What worsens aortic regurg?
Bradycardia (increases filling time)
Elevated SVR (increases Aortic-LV pressure gradient)
Bigger or larger valve orifice (large opening for blood to re-enter)
205
Aortic regurg clinical presentaiton
Diastolic murmur 3rd and 4th L ICS PSL
- holodiastolic (the entire diastole)
- decrescendo, high pitched
- eccentric hypertrophy
- LV cavity increases in size out of proportion to the LV wall thickness
- Large V wave in PA catheter suggestive of LV dilation
206
Pressure volume loop for aortic regurg slide 116 CV
High EDV, ESV, and SBP
207
HR and Rhythm management for Aortic regurg
HR Increase but NSR to slight tachy (80-100) helps CO and decreases diastolic time so decreases regurgitant flow and increases CO.
Bradycardia leads to LV overload and we need forward flow to cause end-organ perfusion
208
What to do about preload for Aortic regurg
Maintain or increase but be careful because LV may not be able to take it, plus could cause pulm edema
avoid hypovolemia since we lose so much during diastole
209
What to do about afterload with aortic regurg
Decrease otherwise the increased SVR decreases forward flow and will just come back to LV
210
What to do about contractility with aortic regurg
Maintain
| LV failure give inotrope or vasodilator
211
Mitral valve normally should look like
opening
classification
# of leaflets
SLIDE 122 CV has the leaflets labeled
opening 4 - 6 cm^2
Bicuspid
Carpentier classification
- posterior leaflet P1 (lateral), P2, P3 (medial)
- anterior leaflet
212
Mild, moderate, severe mitral stenosis
Mild 1.5 - 2.5 cm^2 5 mm Hg
Moderate 1.1 - 1.4 cm^2 6-10 mm Hg
Severe 0.6 - 1.0 cm^2 >10 mm Hg
213
What usually causes mitral stenosis?
Rheumatic hrt dz (under-developed countries)
calcification due to atherosclerosis and endocarditis in the US
214
Pulmonic clinical presentation of mitral stenosis
Pulm venous pressure increased with the increased LAP
fluid build in pulmonary interstitial space decrease pulm compliance, increase WOB, leading to progressive dyspnea on exertion
a-fib from dilated L atrium leading to failure and chronically causing thrombosis
a-fib pt need anticoag otherwise atrial thrombus
pulm hypertension and R HF may occur with significant stenosis
215
CV clinical presentation of mitral stenosis
a-fib from dilated L atrium leading to failure and chronically causing thrombosis
a-fib pt need anticoag otherwise atrial thrombus
pulm hypertension and R HF may occur with significant stenosis
216
Hrt sound of mitral stenosis
Diastolic murmur- heard best at apex mid diastole and low pitched radiating to axilla
217
P-V loop for mitral stenosis
decrease EDV, ESV, SBP
218
HR and Rhythm management for mitral stenosis
low end of NSR cause tachy decreases CO by decreasing diastolic filling time and we already have an issue with that and it causes increased LA pressure
219
What to do about tachyarrhytmias and tachycardia and why for mitral stenosis. Also drugs to avoid
tachyarrhythmias treated with amiodarone, beta-blockers, CCB, digoxin or cardioversion
Avoid drugs that increase HR (atropine, ketamine, atracurium)
Tachycardia increases LA pressure (pulm edema)
220
What to do about preload in mitral stenosis
Maintain normal
LV not filling well already so we can't decrease
Hypervolemia will back up into lungs
221
How can we estimate LAP and what about the waveform?
| Drugs to decrease LAP
With PA catheter PAOP will overestimate LVEDV but still use. Says if we read 10 its probably 8
In the PAOP waveform there will be a prominent a wave (LA hypertrophy) and decreased y descent
Use diuretics but to normal preload
222
Whats up with afterload pertaining to Mitral stenosis
Maintain
low SV and CO systemic vasoconstriction increases the SVR and preserves BP
223
Lets talk anesthesia and mitral stenosis
Decrease SVR may causes baroreceptors to increase HR
NOT GOOD
Hypotension should be treated with phenylephrine or vasopressin
224
What about contractility and mitral stenosis?
Maintain
| usually not a problem
225
Mitral regurg, type of hypertrophy, SV, and overall what happens
LA eccentric hypertrophy
Volume overload hypertrophy
SV goes in 2 directions
226
Where to auscultate mitral regurg
5th ICS
Systolic murmur - apex
holosystolic
high pitched radiating to axilla
227
P-V loop mitral regurg
Potato sac for chronic
-high EDV low ESV low SBP
Acute
- high EDV (same as chronic) super high ESV super low SBP
228
Anesthesia HR and Rhythm management of mitral regurg
High 90-100 NSR
- regurg during isovolumic contraction
- higher HR reduces regurgitant volume
- too fast increases O2 demand and decreases O2 supply
Profound brady not well tolerated
-leads to acute left ventricular fluid overload and lots of it going back to LA
229
What to do about preload in mitral regurg in OR
maintain or increase
higher preload helps out since we are losing some to LA
low preload = low CO
230
PAOP waveform for mitral regurg
enlarged v wave (all that pressure coming back to LA)
PAOP overstimates LVEDP so not reliable for LV filling pressure
231
Afterload management for mitral regurg
decrease
decrease SVR allows forward flow of blood
increased SVR prevents forward flow of blood
232
Contractility with mitral regurg
Maintain
| not often an issue
233
How quickly does clot dissolution occur?
depending on the size a couple minutes to days later
234
T/F coagulation proteins are in the activated form
False: inactivated
until we add an a at the end
example: Factor 3a
235
Do clotting factors attach to endothelial layer when uninjured?
No, this layer is smooth
236
Tissue factor and collagen is expressed in what type of endothelium
damaged
237
What does damaged or injured endothelium activate?
platelet
| coagulation cascades
238
Describe the intima (endothelial layer)
primarily endothelial cells
separates flowing blood from vessel
239
What do endothelial cells secrete and why?
Procoagulants
anticoagulants
Fibrinolytics
240
What do endothelial cells release?
Vasoconstrictors
| Vasodilators
241
vWF is which factor and what does it do?
Factor VIII
| helps with adherence of platelets to the subendothelial layer
242
Factor III does what?
Tissue factor
| activates the extrinsic clotting cascade
243
Name some mediators that help with vasoconstriction
```
thromboxane A2
Adenosine diphosphate (ADP)
```
244
Which mediators help with vasodilation and how they do it
nitric oxide promotes SM relaxation
prostacyclin inhibit platelet formation and aggregation & promotes SM relaxation
245
How many factors total
12
246
Name the 5 types of procoagulant mediators and their functions
Coagulation factors = Coagulation
Collagen = Tensile Strength
vWF = Adhesion
Fibronectin = Mediates cell adhesion
Thrombomodulin = Regulates anticoag pathway
247
2 anticoag mediators and their function
Antithrobin III Degrades factors XII, XI, X, IX, II
(HEPARIN??)
Tissue pathway factor inhibitor inhibits tissue factor
248
3 Fibrinolytic mediators and their function
plasminogen converts to plasmin
tPA activates plasmin
Urokinase activates plasmin
249
3 Vasoconstrictor mediators and their function
Thromboxane A2
ADP
Serotonin
250
Which amino acid belongs to nitric oxide
L-arganine
251
What is the second (subendothelial) layer of vessels and what does it do
Media
- extremely thrombogenic and active
- contains collagen
- contains fibronectin
252
What is collagen and what does it do?
A potent procoag that stimulates platelet attachment to the injured vessel wall
253
What is fibronectin and what does it do?
A potent procoag that facilitates the anchoring of fibrin during the formation of a hemostatic plug
254
Name all mediators in endothelial layer
```
vWF
Tissue factor
Prostacyclin
nitric oxide
fibrinolytics
vasoconstrictors
vasodilators
anticoags
procoags
```
255
What is the adventitia and what does it do?
Outer vessel layer
| controls blood flow through degree of contraction by endothelial vasoconstrictors or vasodilators or SNS
256
What does a dilated vessel do to coagulation?
increases blood flow which limits the activity of procoagulant mediators by washing them away
257
Where does NO synthesis occur and describe the process?
metabolic reaction occurs within the endothelial lining
nitric oxide synthetase (NOS) converts l-arginine to NO
258
How does NO do its thing?
diffuses out of the endothelial lining to the muscles cells of adventitia and activates soluble guanylate cyclase subsequently producing a second messenger cyclic GMP which causes SM relaxation
259
What are eicosanoids?
they are signaling molecules from arachidonic acid conversion
Prostaglandins and related compounds
Prostacyclin
Leukotrienes
Thromboxane
260
Name that lipid molecule made from prostaglandin which is a powerful vasodilator and interferes with platelet formation and aggregation
Prostacyclin
261
What is the order in slide 14 HEME that creates the 3 cycloendoperoxides
Membrane phospholipid broken down by phospholipase A2
This creates A.A
A.A> converted to COX 1 and 2
COX 2 becomes cycloendoperoxides
Thromboxanes, Prostacyclin, Prostoglandins (PGE2 PGF2)
262
Where are Thromboxanes seen
Platelets
263
Where are Prostacyclin seen
Endothelium
264
Where are Prostaglandins seen
smooth muscle
265
Where are leukotreines seen
Leukocytes
266
Pathway for Leukotreines
Membrane phospholipid broken down by phospholipase A2
This creates A.A
A.A> converted to 5-lipoxygenase
lipoxygenase to 5-HPETE
becomes leukotreines
267
What are the four phases of hemostasis and coagulation
```
Vascular phase (vascular spasm)
Primary hemostasis (Formation of platelet plug)
Secondary hemostasis (Coagulation & formation of fibrin)
Fibrinolysis (Lysis of clot)
```
268
Describe the vascular phase
Damage blood vessel causes vascular spasm of smooth muscle in vessel wall to slow down or stop bleeding with small localized cuts
269
What are the primary hormones involved in vascular phase and what do they do
Endothelins stimulate smooth muscle contractiton and division of endothelial cells, smooth muscle cells, and fibroblasts to help repair damaged site
270
Describe primary hemostasis
If vascular phase doesn't tamponade then primary hemostasis, injured blood vessel attracts platelet (plug produced).
271
What does primary hemostasis initiate?
phases of platelet formation
- adherence
- activation
- aggregation
272
Why are platelets typically flowing near the blood vessel wall?
They are smaller than the other blood constitutes so they get pushed there which is good cause thats where they need to work anyway.
273
Where are platelets formed
Megakaryocytes in bone marrow
274
Normal platelet count and lifespan
150,000 - 300,000
| 1-2 wks lifespan
275
Who clears platelets
Macrophages in the reticuloendothelial system
| Spleen
276
How much does spleen sequester?
1/3 of circulating for later use so gotta be careful during trauma
277
What receptors does the exterior platelet structure have that help with antiplatelet therapy
```
ADP
Thrombin
TxA2
GPIb
GPIIb-IIIa
```
278
What do the glycoproteins do on external platelet membrane do
Adhere to injured endothelium, collagen, and fibrinogen
GpIb sticks/attaches PLT to vWF
GpIIb-IIa complex links activated PLT together to form plug
279
What do the phospholipids do on external platelet membrane do
Substrates to prostaglandin synthesis
Produce TXA2 which activates PLT
280
What are the interior structures of platelets
```
Actin & Myosin
- contraction to form PLT plug
Thrombosthenin
- PLT contracion
ADP
- PLT activation and aggregation
Calcium
- clotting cascade
Fibrin-stabilizing factor
- Cross links fibrin
Serotonin
- Activates nearby PLT
Growth factor
- Repairs damaged vessel walls
```
281
Lets talk adherence
Platelet antenaes its GPIb and attaches to vWF that leaves endothelium.
vWF is poking out of platelet now and makes it sticky to site of injury
282
Lets talk activation
Tissue factor causes platelet to have confirmational change during activation which means it swells oval and irregular
NOW (bill cosby) GpIIb and IIIa antenae out to attach to other platelets' antenae and now they create plug (mesh)
and then they seal and heal site of injury
283
Talk to me about aggregation as it relates to mediator release
```
PLT during metamorphosis release
alpha
dense granules
contractile granules
thrombin
to promote procoag activity
```
284
What do mediators released during aggregation cause?
primary unstable clot formation and if injury is small and not threatening we end process here otherwise activate clotting cascade for repair and create a 2ndary clot
285
Secondary hemostasis discuss fibrin
Fibrin is the strongest most stable and single most important protein involved in clotting
286
For fibrin formation what is necessary
Fibrin production requires all the clotting factors
287
What is secondary hemostasis
A series of enzymatic reactions (clotting cascade) that ultimately activate prothrombin to thrombin, the enzyme that converts soluble fibrinogen to fibrin
288
What are the pathways for secondary hemostasis
intrinsic, extrinsic, common (thrombin activation)
289
Factors that are vitamin K dependent and their sources
II (Prothrombin) Liver
III (tissue factor/thrombo-plastin) vascular wall & extracellular membrane from injured cells
VII (Proconvertin) Liver
IX (Xmas Factor) liver and other tissues
X (Stuart-Prower factor) Liver
290
Factors that are vitamin K independent and their sources
```
I (Fibrinogen) Liver
IV (Calcium) Diet
V (Proaccelerin) Liver
VIII:C (Antihemo-philiac factor) Liver
VIII: vWF vascular endothelial cells
XI (plasma thromboplastin antecedent) Liver
XII (Hageman Factor) Liver
XIII (Fibrin Stabilizing factor) Liver
```
291
Extrinsic pathway...discuss
III released from sub-endothelium during trauma
activates factor 7
7 activates 10 in presence of calcium (IV)
292
How quickly does clot form in extrinsic pathway?
12-15 sec
293
With extrinsic pathway what happens after factor 10 activated?
Prothrombin activator and platelet phospholipids activate factor 2 (thrombin)
Factor 5 accelerates the positive feedback mechanism (increase production of prothrombin activator)
294
Intrinsic pathway...explain
1. Blood trauma exposure to collagen @ endothelium
activates XII
2. Factor XI activated by factor XIIa
- requires HMW kininogen
- This step is accelerated by prekalikrein
3. Factor XI a activates IX
4. Factor IXa and VIII in presence of Ca++ activate X
5. Prothrombin activator and tissue phospholipids avtiate thrombin (factor IIa)
This last step 5 is the same as in extrinsic
295
Which factor is missing with hemophelia A in intrinsic pathway and at what step in the process?
hemophelia A missing factor VIII
296
How long does it take to form a clot in the intrinsic pathway?
6 min but a larger clot than intrinsic
297
Common pathway...talk to me, dawg
Prothrombin activator changes prothrombin (II) to thrombin (IIa)
prothrombin changes fibrinogen to fibrin in the presences of Ca++
Fibrin is added to the aggregated platelet plug
Activated fibrin-stabilizing factor (XIIIa) cross-links fibrin-fibers to complete the clot (mesh)
Clot formed, stays in place until vascular tissue is repaired
298
Which pathway does ACT and PTT test and which drug
Intrinsic pathway, Heparin
299
Which pathway does PT and INR test
Coumadin
300
Is thin blood good or bad for surgery?
Good
301
When is fibrinolysis activated
When clotting cascade is activated to control size of clot and prevent excessive deposition of fibrin
302
What is the main mechanism in fibrinolyiss
release of tissue plasminogen activator by damaged endothelial cells
303
What are misc fibrinolysis mediators
urokinase from kidneys released to protect kidney from small clots getting lodged in the kidney tissue
Kallikrein and neutrophil elastase are fibrogenic factors
304
What do the previous circulating activators do?
Convert plasminogen to plasmin which breaks down fibrin degradation split products
305
Labs
Bleeding time (BT) 3 -10 min
Prothrombin time (PT) 12- 14 sec Extrinsic and common pathway
International normalized ratio (INR) <1.1 goes with PT
activated partial thromboplastin time (aPTT) 25 - 35 sec Intrinsic and common pathway
Thrombin time (TT) 30 sec Common pathway
Activated clotting time (ACT) 80-150 sec heparin measure
Fibrinogen => 150 mg/dL
306
Break down whole blood into its 2 large compartments
Plasma 55%
| Formed elements 45%
307
Break down Plasma by its consitutes
Proteins 7%
Water 92%
Other solutes 1%
308
Break down formed elements into its constitutes
Platelets 140,000 -340,000 per m^3
Leukocytes 5,000-10,000 per m^3
Erythrocytes 4.2-6.2 million perm^3
309
Break down Leukocytes
Neutrophils 40%-60%
Lymphocytes 20%-40%
Monocytes 2%-8%
Eosinophils 2%-4%
Basophils 0.5%-1%
310
What is normal hemeglobin molecule structure
2 alpha and 2 bata chains
311
Universal donor and receipent
Donor O -
| Receipient AB +
312
All the different blood products that can be given
```
RBC
FFP
Cryo
PLT
Specific clotting factors
```
313
What is added to banked blood for storage
Citrate phosphate dextrose adenine (CPDA-1)
314
What is in Citrate phosphate dextrose adenine
Citrate for chelation of Ca++ to prevent clotting b/c calcium helps with clotting cascade
Phosphate as buffer
Dextrose as fuel source
Adenine as a substrate for the synthesis of ATP to extend storage time from 21-35 days
315
Which of the calcium products worsk fastest?
Ca++ chloride > Ca++ gluconate
316
How are PRBCs acquired
PRBCs derived from whole blood which has had plasma removed
317
What do some PRBCs have done to them to help with infection risks?
They have Leukocytes removed to reduce transmission of cytomegalovirus (herpes -type) or reduce TRALI
318
What happens as stored blood ages?
Decreases levels of 2,3-DPG which shifts the Oxyhemoglobin dissociation curve to the left.
319
How long do we have to be able to use blood once its out of the cooler?
30 min for bacterial growth
320
How much does 1 unit of PRBCs increase Hgb and HCT
Hgb 1 g/dL increase
Hct 3% increase
321
What is TRALI typically caused by?
A, B, O mismatch
322
T/F FFP has all clotting factors in it
False, has em all except platelets
323
How do they acquire FFP
Plasma separated from RBC & PLT
324
FFP is a source of? how big is a bag? how long to expire? Dosing
Source of antithrombin III
200-250 mL
Expires 12 months after donation
Dose 10-15 mL/kG
325
Indication for FFP
Correction of inheretid factor deficiencies when there is no specific factor concentrate (eg. factor V) and when PT or aPTT is >1.5 times the mean control
Correction of acquired multi-factor deficiencies with clinical evidence of bleeding or in anticipation of major surgery or an invasive procedure with PT or aPTT >1.5 times the control
- Liver dx w/ signs of bleeding
- DIC w/ signs of bleeding
- Reversal of Vitamin K antagonists
- Heparin resistance secondary to antithrombin deficiency
when AT concentrate not available
Tx thrombotic microangiopathies like HELLP or thrombotic thrombocytopenic purpura or hemolytic uremic syndrome
Tx hereditary angioedema when C1 esterase inhibitor is not available
Microvascular bleed with massive transfusion and estimated blood loss> one blood volume
326
What other blood products would you give your patient if you need to give them blood but don't have a TEG to tell you about their coagulation?
FFP
327
What is cryo?
protein fraction taken off the top of the FFP when being thawed then frozen up to 1 yr.
328
What factors does cryo have in it?
1, vWF, VIII, XIII
329
Indications for cryo
Microvascular bleed with hypofrbrinogenemia
- DIC with fibrinogen <80-100 mg/DL
- Hemorrhae or massive transfusion w/ fibrinogen< 100- 150
Prophylaxis in pt with hemoph A and vWD dz (if specific
factor concentrates unavailable or ineffective due to inibitors)
Prophylaxis for patients with congenital dysfibrinogenemiasa
330
Platelets (thrombocytes) how we get them, how much in a bag, what number it increases the PLT by
From whole blood or platepheresis donation
contains PLT only
one bag = random value
one bag pheresis = 250 - 300 mL
one unit increases PLT by 5,000- 10,000
331
Indications for PLT transfusion
Stable pt without evidence of bleeding or coagulopathy
<10,000 uL
Prohylaxis for invasive procedures <50,000 uL
- lumbar puncture
- neuraxial anesthesia
- CVC
- endoscopy w/ biopsy
- major surgery
Stable pt with clinical evidence of bleed or coagulopathy
<50,000 uL
Pt w/ DIC and signs of ongoing bleed <50,000 uL
Pt undergoing massive transfusion <75,000 uL
Pt surgery at critical sites such as eye or central nervous system <100,000 uL
Microvascular bleeding attributed to platelet dysfunction such as uremia, liver dz, post-cardiopulmonary bypass use clinical judgment
332
WHen would we give PRBC to pt who have CAD
Heme of 10% or less
333
What is the Sickle cell hemeglobin beta chain disorder?
Substitution of glutamate by valine at the 6th position of the S heme molecule in the beta chain
334
What does the Hb A HbS chain look like?
7 chains, possibly more in pairs
Valine, histidine, leucine, threonine, proline, glutamate, glutamate
335
Glutamate and valine are they polar or nonpolar
glutamate has polar R group
| valine has nonpolar R group
336
Which hemeglobin molecule causes the biggest issue for sickle cell when it is exposed to low O2 concentrations
Heme S around 40-45 mm Hg
337
What happens in Sickle cell to heme S molecule during low O2 sats?
The molecule becomes unstable and polymerizes with other heme S molecules to form a crystaline gel thaat deforms the RBC into the characteristic sickel shape
338
What happens to the damaged sickled molecule?
It is more prone to hemolysis and removed by the spleen
339
What is the RBC lifespan for SCD?
12-17 vs normal of 120 days
340
What are some clinical manifestations of SCD?
Obstruction of small blood vessels
tissue ischemia
chronic anemia
Acute chest syndrome (ACS)
Aplastic crisis
sequestration crisis
Asthma
Pulm htn
341
What are some things that can cause sickling of RBC
Hypovolemia
Hypothermia
Low O2
Stress
342
What is VOC, how to treat normal, and severe, and incidence rate in perioperative period
Caso-occlusive crisis (usually peripheral)
-the first and most frequent manifestation of SCD which
is secondary to tissue ischemia and infarction
tx mild w/ oral analgesics and hydration
tx severe w/ hospilitiazation, parenteral narcotis, IV hydration, O2
incidence of VOC in perioperative period is 10%
343
Who is VOC most common in?
Children
344
What is the single greatest threat to SCD pt?
ACS which has a 20% mortality rate
345
How to dx ACS
new lung infiltrates (usually 1 lung) that follows:
- CP
- cough
- dyspnea
- wheeze
- or hypoxemia
346
Why does ACS possibly occur in SCD pt
thrombosis
embolism (clot and fat)
infection (ACS higher in children and related to this)
347
How to tx ACS and how to decrease incidence of postoperative ACS
supportive tx
perioperatively give transfusion and postop IS
348
What is a sequestration crisis in SCD?
Splenic removal of RBCs exceeds rate of RBC production
349
What does sequestration crisis in SCD cause?
Causes severe anemia and hemodynamic instability
350
What might a SCD pt have done if they have hx of sequestration crisis?
Early splenectomy
351
What is Aplastic crisis in SCD?
Production of RBCs is suppressed by a viral infection (parovirus B19)
352
T/F pt with mild bone marrow suppression can cause rapid onset of anemia with SCD pt?
True because SCD pt typically must maintain a high and continuous rate of production of PRBCs since so many are deffective
353
What are the incidences of asthma and pulm htn in SCD?
Asthma 50%
Pulm htn 10%
Mortality of SCD increased when these 2 are present
354
What are some anesthesia considerations for SCD pt
preop heme level obtain and transfuse if needed
preop echo for pt with
- lmited physical activity
- hypoxemia
- respiratory distress
- or symptoms consistent with cor pulmonale
355
Common echocardiographic findings in SCD pt
Left vent hypertrophy
Right vent dilation
Atrial enlargement
356
What is the typical heme level of SCD pt, what do we want to raise it to?
5-8 g/dL, raise it to 10 preop and intraop if pt experiencing significant blood loss
357
Can cell saver blood salvage be used for pt with SCD?
yes and it helps reduce complications
358
What are some things we need to do to decrease complications of SCD intraoperatively?
IV hydration
normothermia
analgesia to prevent pain and narcotic induced hypoventilation to reduce ACS postoperatively so might wanna do regional anesthesia
359
Can we use tourniquets for pt with SCD during surgery and if so for how long and what is incidence of complication?
Yes if they are critical to the performance of surgery and can be released every 60 min for SCD, and 120 min for normal pt
Incidence of complication with tourniquet in SCD is 12%
360
What is HELLP syndrome
red cell hemolysis (H)
elevated liver enzyme levels (EL)
low PLT count (LP)
361
What is the tx for HELLP?
HTN control
deliver baby
stabilize mom by htn control and sz prevention
362
How does MgSO4 tx HELLP?
decreases CNS irritability (raise sz threshold)
decrease activity at the neuromuscular junction (weakness)
relax uterine and VSM (increase uterine blood flow)
Usually given as 4g load over 5 min followed by 1-2 g/hr
MgSO4 crosses placenta
363
What is the antidote for mag toxicity?
Calcium chloride (is faster than gluconate)
364
What does mag toxicity look like
```
Hypotension
Bradycardia
Decrease deep tendon reflexes
skeletal weakness
Cardiac arrest
```
365
What is the therapeutic range for Mg?
4-6mEq/L
366
What are some anesthetic issues of Mg for HELLP
Mg inhibits ACh release and many preeclamptics have decreased plasma cholinesterase levels NMBDs must be used very carefully
decrease sedative and opiate use
exaggerated hypotension response to regional anesth
367
What is an additional tx for HELLP
High-dose steroids >24 mg of beta or dexamethasone in 24 hrs to tx fetal lung maturity may prevent worsening in platelet count or even increase platelet count
368
vWF discuss
most common hereditary bleeding disorder w/ varying clinical features that depending on type and classification
vWF plays critical role in platelet adherence/adhesion
easy bruising
RECURRENT EPISTAXIS
Menorrhagia
Pt usually unaware till questionnaire/surgery
369
vWF type 1 patho and comments
partial quantitative deficiency of vWF
mildest; most common; resonds to DDAVP
370
vWF type 2A patho and comments
dysfunction in platelet adhesion
may respond to DDAVP
371
vWF type 2M patho and comments
Dysfunction in platelet adhesion
may respond to DDAVP
372
vWF type 2B patho and comments
increased platelet-binding affinity
Thrombocytopeinia with DDAVP
373
vWF type 2N patho and comments
Decreased F VIII-binding affinityy
Often confused with hemophilia A
374
vWF type 3 patho and comments
severe quantitative deficiency of vWF
rarest; most severe; usually requires factor concentrates
375
How to dx vWF
PT & aPTT normal in these pt
BT is prolonged
Hematologist to analyze labs
376
Tx of vWF
Correct the deficiency of vWF
desmopressin
transfuse specific factor if no cryo
Cryo if desmo not working
377
What is DDAVP?
1-deamino-8-D-arginine vasopressin is a synthetic analogue of vasopressin and stimulates release of vWF by endothelial cells
378
DDAVP dosing, peak, duration, when to give
IV 0.3 ug/kg in 50 mL NS over 15-20 min
30 min peak
6-8 hr duration
give 60 min before surgery and confirmation of normalized BT and improved F VIII
379
DDAVP SE
Push too fast = hypotension
HA
rubor (skin flush)
tachycardia
hyponatremia
water intoxication
380
How to decrease H2O intoxication w/ DDAVP?
restrict 4-6 hrs after drug given which will decrease hyponatremia and consequential sz
381
Hyponatremia levels, CNS changes, and ECG changes
120 confusion,restless ; widened QRS
115 somnolence, nausea ; elevated ST seg, wide QRS
110 sz, coma ; Vtach or Vfib
382
Cryo for vWF unwanted issues, when to use, how much raises fibrinogen levels
If DDAVP unresponsive use it but it can increase risk of infection because cryo not submitted to viral attenuation
1 unit raises fibrinogen by 50 mg/dL
383
Know Chem 7 lab skeleton
Chem 7 top of graph: Na Cl Bun Glucose
| Chem 7 bottom graph: K CO2 Crt
384
CBC lab skeleton
Left: WBC
Top: Heme
Right: PLT
Bottom: HCT
385
Factor VIII (vWF)
prepared from pool of plasma from large number donors
undergoes viral attenuation
has F VIII and vWF
give preop and intraop
386
If we are having nasal surgery with a pt who has vWF what would we consider
Tuck pt arms in so surgeons and assistance can work
South facing oral ray tube
A-line
type/screen
387
What type of anesthesia should we consider with vWF?
GA because neuraxial block increases risk of developing hematoma and compression of neurological structures
avoid traumas during anesthesia
arterial puncture not recommended
Laryngeal trauma may cause hematoma = post ob obstruction
Avoid IM
388
What are 4 types of drugs that may cause acquired bleeding disorder?
Heparin
Warfarin
Fibrinolytics
Antiplatelets
389
Heparin discuss
negative charge CHO containing glucuronic acid residues
Inhibits thrombin by activating antithrombin III
390
What to monitor with heparin
PTT and ACT
391
What are LMWH used for?
More effective at VTE prophylaxis
more predictable pharmaco
fewer effects on PLT
reduce risk of HIT
Don't monitor them routinely
UFH can cause osteoperosis
392
Warfarin how works, reversals
Interferes with hepatic synthesis of vitamin K-dependent coags
-Factors II, VII, IX, and X
Vitamin K reversal takes 6-8 hrs
Prothrombin complex concentrates, recombinant factor VIIa, and FFP work faster than vitamin K
393
How do fibrinolytics work and which ones are out there?
convert plasminogen to plasmin --->
cleaves fibrin ---->
causes clot dissolution
Tissue plasminogen activator (tPA)
Streptokinase (SK)
Urokinase (UK)
394
Anti-fibrinolytis which are they and how do they do it
tranexamic acid
E-aminocaproic acid
aprotinin
all inhibit the conversion of plasminogen to plasmin
395
When would we not use tranexamic acid as an anti-fibrinolytic?
When pt has had previous thrombotic stroke hx cause it will cause a clot
396
What to do if pt bleeding from antiplatelet drugs?
D/C drug
PLT transfuse
397
What is DIC?
Disseminated intravascular coagulopathy
Systemic activation of the coag system simultaneously leading thrombus formation and exhaustion of platelets and coag factors
398
What can cause DIC?
```
trauma
amniotic fluid embolus
malignancy
sepsis
incompatible blood transfusions
```
399
Why is regional anesthesia good for oncotic patients?
Regional anesthesia decreases the rate of recurrence vs GA
400
DIC pathway slide 90 Heme
Increase release or expression of tissue factor--->
Systemic activation of coagulation (Thrombin production overwhelms physiologic inhibitors) ..... [split into the next 2]
1. Intravascular fibrin deposition---> Thrombosis of small and midsized vessels with organ fx
2. Depletion of platelets + coagulation factors---> Bleeding
401
What are the labs we monitor for DIC?
Decrease in PLT
prolong PT, PTT, TT
elevated concentrations of soluble fibrin degradation products
402
How to manage DIC
manage underlying condition precipitating this
403
How to tx DIC
blood component transfusions to replete coag factors and PLT that are consumed
antifibrinolytic therapy contraindicated in DIC because potential for catastrophic thrombotic complications
404
What are 2 prothrombotic disorders
Factor V Leiden (mutation)
HIT
405
What is factor V normal job in clotting casade?
It is a protein that when enough fibrin has been made, activated protein C inactivates factor V which helps stop the clot from growing larger than necessary (beginning of fibrinolysis)
406
What is the pathology of factor V leiden?
Mutation of the factor V resists action of activated protein C which it then continues to make more fibrin
407
If we have factor V leiden what do we need to worry about and do?
increased risk of DVT (w or without PE)
Because of this high risk pt put on anticoags
408
When does factor V mutation usually show itself?
Pregnancy, otherwise silent and we might see
- 1st presentation of DVT
- repeated missed abortions
- recurrent late fetal losses
409
What would we do with pregnant patients that may show signs of factor V?
Prophylactic anticoagulation with warfarin, UFWH, and LMWH
410
What is HIT, incidence, what happens to blood, lab findings
heparin-induced thrombocytopenia
autoimmune-mediated drug reaction
5% of pt after expsure to unfractionated heparin or rarely LMWH
See thrombocytopenia occurring 5-14 days after initial therapy
Hallmark is PLT<100,000
Results in platelet activation and potential for venous and arterial thromboses
411
HIT pathophys
mediated by immune complexes composed of IgG antibody, platelet factor IV, and heparin
412
What is the risk of thrombosis with HIT?
30%-75%
413
HIT cascade graph slide 99 Heme
Activated platelets...[split 1 and 2]
1. Cause clotting ---> VTE, MI, CVA, Emboli
- Hypercoagulable state
2. Deplete platelets ---> low platelet count (bleeding rare)
- Thrombocytopenia
414
When to suspect HIT and what to do about it if discovered
Think HIT when pt has thrombosis or thrombocytopenia when given Heparin
Fix by D/C heparin STAT
Give alternative anticoagulation
- Most of time give direct thrombin inhibitor
- bivalirudin
- lepirudin
- argatroban
- fondaparinaux to tx VTE
415
What is fondaparinaux?
A synthetic factor Xa inhibitor and its off label use
416
How long does it take for PFIV heparin immune complexes clear from the body?
3 months but still want to avoid future exposure to unfractionated Heparin
