Exam 2 Review Flashcards
1
Q
Incidence of atherosclerosis and vascular diseases increases with
A
Advancing age.
2
Q
Predisposing risk factors for atherosclerosis include:
A
HTN Insulin resistance Dyslipidemia Abdominal obesity Cigarette smoking Increasing age Family History Pro-inflammatory states Pro-thrombotic state
3
Q
Development of atherosclerosis occurs in 2 stages:
A
Endothelial injury
Inflammatory response to injury
4
Q
Pathophysiology of Atherosclerosis: Primary injury and everything else
A
Primary injury occur as low density lipoprotein and apolipoprotein-B containing lipoproteins invade the vascular endothelium and become proinflammatory
As the inflammatory cascade starts, the subendothelial space is filled with atherogenic lipoproteins and macrophages, which form foam cells.
5
Q
What are foam cells?
A
They form the atheromatous core of a plaque, which becomes necrotic and further enhances the inflammatory process.
6
Q
How does plaque rupture?
A
Disruption of the fibrous cap over a lipid deposit can lead to plaque rupture and ulceration.
7
Q
Vascular disease is not a localized phenomenon, but rather a systemic one affecting
A
multiple organs including the heart with MI and the brain with CVA
8
Q
Leading cause of disability
A
Stroke
9
Q
Third leading cause of death in the US
A
Stroke
10
Q
PAD can cause
A
Claudication and Limb ischemia
11
Q
Coronary atherosclerosis that leads to MI is the
A
Leading cause of death and disability worldwide.
12
Q
Medical therapy for atherosclerosis
A
HTN, HLD, Diabetes,Obesity
13
Q
How do statins help treat Atherosclerosis
A
Reduces progression and may cause regression of atherosclerotic plaques
Improve endothelial function
Reduce CV events
14
Q
Management of atherosclerosis is basically
A
Management of contributing systemic diseases such as HTN, Hyperlipidemia, diabetes and obesity.
15
Q
3 things that significantly slow or reverse the progression of atherosclerosis
A
- Chronic therapy with aspirin
- ACE inhibitors
- Smoking Cessation.
16
Q
Therapies to be continued up to day of surgery and throughout the perioperative period?
A
Statins
ASA
B blockers
17
Q
Aspirin side effects
A
Platelet inhibition may lead to increased bleeding.
18
Q
Aspirin do you continue ?
A
Continue until day of surgery ESPECIALLY for carotid and PVD,
19
Q
Clopidogrel side effects are
A
Platelet inhibition
Rare thrombotic thrombocytopenic purpura
20
Q
Clopidogrel (Plavix) hold for
A
7 days before surgery EXCEPT CEA and Severe CAD or DES
21
Q
Clopidogral (Plavix) and neuraxial anesthesia
A
AVOID if not held for at least 7 days.
22
Q
Side effects of statins HMG CoA reductase inhibitors
A
Liver function test abnormalities
Rhabdomyolysis
23
Q
Beta Blockers side effects
A
Bronchospasm Hypotension Bradycardia, heart Block Induction hypotension Cough
24
Q
Beta Blockers and perioperative period
A
continue throughout the periop
25
ACE inhibitors side effects
Induction hypotension
| Cough
26
ACEI and perioperative period
Continue throughout the periop
| Consider one half dose on day of surgery
27
Diuretics and perioperative period
Continue through periop
28
CCB Side effects
Perioperative hypotension (especially with amlodipine)
29
Consider withholding this medication day of surgery and why?
Amlodipine, may cause perioperative hypotension
30
Oral Hypoglycemics may cause
hypoglycemia intra-operatively and perio-operatively.
31
When feasible for oral hypoglycemics switch to
insulin preoperatively , monitor glucose
32
If a coronary stent is placed, elective surgery should be delayed, for bare metal stents
minimum of 6 weeks
33
If a coronary stent is placed, elective surgery should be delayed, for Drug eluting stents
12 months or longer.
34
Recommended indefinitely to prevent in-stent thrombosis
Aspirin
35
Ischemia-reperfusion injury in the vascular surgery patient: fundamental concepts
Reduction or interruption of blood flow stop delivery of O2, --> glucose, and other essential nutrients that are needed for AEROBIC metabolism and therefore generation of ATP is slowed. When there is no ATP cellular processes fail and cellular integrity is lost. The duration of ischemia correlates directly with the degree of cellular injury. Toxic metabolites of anaerobic metabolism accumulate in the ischemic region. Upon reperfusion, toxic metabolites are released into the circulation.
36
Prevention of Post op acute renal failure.
Suprarenal aortic cross-clamping 15%
| Infrarenal aortic cross-clamping 5 %
37
During carotid endarterectomy What is the most common cause of stroke?
Emboli from the surgical site.
38
Aortic procedures can be associated with
Significant pulmonary complications due to LARGE FLUID SHIFTS and transfusion related acute lung injury.
39
After carotid endarterectomy , what happens
The carotid body on the operative side is denervated and this blunts the ventilatory response to hypoxemia.
40
The most urgent and potentially devastation complications of Carotid endarterectomy is
CLOT formation at the surgical site and the associated THROMBOEMBOLISM in the cerebral circulation.
41
***The most urgent and potentially devastation complications of Carotid endarterectomy is
CLOT formation at the surgical site and the associated THROMBOEMBOLISM in the cerebral circulation.
42
Major risk with Thoracic aortic procedures?
Compromise of the spinal cord vascular supply, especially the artery of ADAMKIEWICZ
43
Symptoms of Carotid artery stenosis
Sudden unilateral vision loss (AMAUROSIS FUGAX)
| Unilateral changes in motor function, dysarthria, and aphasia
44
When is a CEA urgent?
If preoperative medical management with anticoagulants, and antiplatelet drugs does not control the symptoms of carotid stenosis.
45
Should be avoided with CEA?
Sudden reduction in BP should be avoided.
46
The Artery of Adamkiewicz usually arises at the
T11 - T12 level and provides the blood supply to the lower spinal cord.
47
Why do some patient are kept away during CEA?
Providing regional is good because awake patient can report neurological changes most reliably.
48
Other CEA cases done under GA relies on what monitors
EEG
SSEPs
Transcranial Doppler
Cerebral Oximetry.
49
Anesthesia for CEA
Both General and regional safe
50
For both types of anesthesia patient should be
awake and cooperative at the end of the procedure for ongoing neurological assessment.
51
CEA pts have a high incidence of
CAD and hypertensive heart disease
52
Use in combination to offset the ETT stimulation
Etomidate
| Esmolol
53
The majority of CVAs are caused by
Emboli from the surgical site.
54
Regional anesthesia for CEA
Deep and superficial Cervical Plexus blocks
Cervical anesthesia
Local infiltration
55
Recommended CEA monitors
ASA monitors
| Intra-arterial BP Because BP control is vital during CEA
56
Carotid Angioplasty with stenting, vs CEA
Carotid stenting is associated with a higher risk of periprocedural stroke and death.
57
What should prompt immediate Ultrasound after CEA?
New onset neurologic change after surgery should prompt immediate US and possible reoperation.
58
Other possible adverse effects after CEA
Hypotension
hypertension
MI
Recurrent nerve injuries
59
Associated with increased mortality and increase cardiac and neurologic complications?
Uncontrolled severe hypertension with CEA.
60
CEREBRAL HYPERPERFUSION SYNDROME symptoms
Headaches
Seizures
Focal neurological signs.
61
Can obstruct the airways?
Expanding wound hematoma.May need emergent evacuation of the hematoma before an adequate airway can be re-established.
62
One of the greater anesthetic management challenge
Rupture of an Aortic aneurysm
63
True surgical emergency
Rupture of an Aortic aneurysm
64
Risk factors for AAA (MASHHLL)
```
Male sex
Advanced age
Smoking
Hypertension
High Fibrinogen
Low serum high density lipoprotein (low HDL)
Low platelet
```
65
Aneurysm that should be consider for surgical endovascular repair
>5 cm
66
Task force screening for Aortic Aneurysm
Screening for AAA is recommended for men> 65 years with a SMOKING HISTORY
67
Medical management of aortic aneurysm includes
Smoking cessation
| Control of HTN, dyslipidemia, DM and diet
68
Smaller AAA such as size_________require what?
4 - 5.4 requires frequent ultrasound monitoring for progression.
69
Dominant treatment modality for AAA is
Endovascular aneurysm repair (EVAR)
70
First line/Dominant treatment modality for AAA is
Endovascular aneurysm repair (EVAR)
71
In EVAR what artery is used to introduce the stent grafts inside the aneurysm?
Femoral artery
72
Stent grafts inserted to prevent
further enlargement and rupture.
73
Complications of EVAR
Graft leak
intraoperative conversion to open repair
Vascular injury
Inability to seal the graft against the wall of the aorta.
74
When compared EVAR to open surgical repair
EVAR is associated with shorter recovery times
| lower 30-day mortality rates
75
For the open surgical repair two approaches?
Anterior Transperitoneal laparotomy
| Anterolateral retroperitoneal approach
76
Retroperitoneal appraoach for open aortic aneurysm repair- Advantages
Less fluid shifts
Faster return of bowel function
Lower pulmonary complications
Shorter ICU stays
77
The higher the level of clamping
The greater the stress will be on the LV and the HIGHER the incidence of ischemic injury to the gut, kidney, and spinal cord.
78
Must be used during open repair of aortic aneurysm
Systemic anticoagulation
79
Can be employed to enhance spinal perfusion pressure
Spinal fluid drainage during thoracic aneurysm
80
One of the greatest anesthetic management challenges
Thoracoabdominal aortic aneurysm surgery because it involves the descending thoracic and abdominal aorta requiring expansive incision extending into these cavities, one lung ventilation, and the use of CPB.
81
During thoracic procedures, spinal cord ischemia may be detected through the use of
SSEPs
| MEPs
82
Done to improve spinal cord perfusion?
Lumbar subarachnoid drain used to remove CSF
83
Most common reason for emergency Aortic surgery?
Rupture or leaking of an aortic aneurysm
84
Aortic aneurysm rupture has a mortality rate of
85%
85
Aortic aneurysm rupture has a mortality rate of 85% unless surgery is done immediately, rate is then
50%
86
If patient survives aortic aneurysm surgeries they are at risk for
MI, pulmonary injury
| SCI
87
Rupture most common occur into the
Retroperitoneum
88
Needed for emergency aneurysm surgeries
Massive blood loss
Preparations for blood replacement
Rapid infusion devices.
89
Lower Extremity revascularization surgery : 3 indications
Claudication
Ischemic rest pain or ulceration
Gangrene
90
High risk LE revascularization procedures
ileofemoral bypass
Femoral-femoral bypass
Aortafemoral bypass
91
LE revascularization procedures done to
Reestablish blood flow to an ischemic extremity and relieve debilitating symptoms of claudication.
92
LE revascularization what is painful and can lead to tachycardia?
Tunneling the graft
| Deployment of the stent.
93
What is given prior to the deployment of a graft?
Heparin
94
Use to keep graft patency after the procedure
Heparin.
95
Atherosclerosis occurs in 2 stages, the first is _______
Endothelial injury
96
Atherosclerosis occurs in 2 stages, the first is endothelial injury, the second is
An inflammatory response
97
What % of men over the age of 65 have carotid stenosis?
Over 40%
98
How long should elective surgery be delayed after the placement of a DES?
12 months
99
The risk of cardiac related death or nonfatal MI after CEA is
less than 5%
100
S/S of cerebral hyperperfusion syndrome after CEA include
Headaches, seizures and focal neurological deficits
101
At what diameter should an aortic aneurysm be considered fro surgical repair?
Greater than 5.0cm
102
AAA Incidence and age
3-10% Over 50 years old (Nagelhout)
103
AAA more common in
Men
104
AAA #1 Risk factors
Smoking
105
Surgery intervention is recommended for AAA
AAA > 5.5 cm or GREATER
106
AAA other Risk factors
```
Male
Older Age (>50)
CAD
HTN
Low HDL
High Fibrinogen
High Cholesterol
Family History
```
107
Ruptured AAA Incidence
35-94%
108
ABove the clamp you get _____below to the clamp you get ______
HTN ; HoTN
109
The higher the level of the cross clamping the
greater the stress to the LV
110
Most common site is of clamping and why?
MOST COMMON site is INFRARENAL because most aneurysm are below the levels of the renal artery.
111
Preclamp you can give this medication
Mannitol 0.25 - 0.5 g/kg IV to maintain UO and preserve renal function
112
Five minutes before cross clamp give
heparin
113
Obtain baseline _______ ,_____Mns after administration, and then every _______ while the clamp is in place
5 minutes, 3 minutes, every 30 minutes.
114
Cross clamping derangements
| IADPI
```
Sudden increase afterload
decrease preload
Increased filling pressure
Decreased renal perfusion
Decrease perfusion of viscera below clamp
```
115
The placement of the clamp determines the
Degress of derangement.
116
Infrarenal clamp avoids
Ischemia to most major organ
117
LEAST Hemodynamics effects : CLAMP
InFRARENAL
118
MOST Hemodynamics effects : CLAMP
SUPRACELIAC
119
Most dramatic changes occur during
Cross clamping
120
AORTIC CLAMPING leads to an
Increase in SNS stimulation catecholamines, aldosterone, cortisol
increase in Afterload
121
2 concerns during aortic clamping
CHF and LV dysfunction is a concern.
122
Metabolites from ANAEROBIC metabolism →
LACTATE
123
Effects of release :
Vasodilation, decrease SVR, decrease venous return which is called DECLAMPING SHOCK SYNDROME (DSS)
124
Declamping shock syndrome is characterized
Vasodilation, decrease SVR, decrease venous return
125
Declamping associated with: BP
HYPOTENSION
126
2 main mechanism with hypotension after declamping
Relative Hypovolemia
| Myocardial depression
127
Partally responsible for declamping hemodynamic instability:
Venous endothelin “ET1” is partially responsible
128
ET1 effect on Heart
ET1, Positive inotrope on heart, Vasoconstricting effect on blood vessels
129
Ischemic REPERFUSION INJURY →
occurs during cross clamping and unclamping (cross clamping -ischemia; unclamping - reperfusion)
130
Declamping Release substances include
reactive oxygen species, increased intracellular calcium which inhibits mitochondrial activity and ATP.
131
NO REFLOW PHENOMENON occurs when the
microvasculature is occluded by platelets, neutrophils and thrombi causing inadequate perfusion and further increase in cellular necrosis.
132
Other manifestations with ischemic reperfusion include
tissue injury, ARDS, compartment syndrome, MODS.
133
LIST the physiologic changes associated with aortic cross-clamping
```
Increase arterial BP above the clamp
Decrease BP below the clamp
Increase wall motion abnormalities
Decreased EF and CO
Decrease Renal blood flow
Increase pulmonary occlusion pressure (PAOP)
Increase in CVP
```
134
Increase arterial BP above the clamp → leads to what metabolic changes?
decrease total body O2 consumption
135
Intra-operative interventions of increase arterial BP above the clamp
TX: DECREASE AFTERLOAD with sodium nitroprusside, volatile anesthetics, milrinone and shunts
136
Decrease BP below the clamp what metabolic changes?
Decrease in the CO2 production
137
Decrease BP below the clamp : intraoperative interventions?
REDUCE PRELOAD with nitroglycerine, atria-femoral bypass
138
Increase wall motion abnormalities leads to what metabolic changes?
Increase mixed venous O2 saturation
139
Increase wall motion abnormalities intraoperative interventions:
RENAL PROTECTION with fluid and diuretics : mannitol, furosemide, dopamine, N-Acetylcysteine
140
Decreased EF and CO leads to what metabolic changes?
Decrease Total body oxygen extraction
141
Decreased EF and CO Intraoperative interventions
Miscellaneous : hypothermia, decrease minute ventilation, and sodium bicarbonate
142
Decrease Renal blood flow leads to what metabolic change
INCREASED CATECHOLAMINE RELEASE
143
Increase pulmonary occlusion pressure (PAOP) metabolic changes
respiratory alkalosis
144
Increase in CVP leads to what metabolic changes
leads to METABOLIC ACIDOSIS
145
ACUTE KIDNEY INJURY (AKI)
| Tissue distal to the aortic clamp are
underperfused
146
RBF can be decreased by as much as
80%
147
Suprarenal Cross clamp Time longer than_____increase risk of what?
30 minutes increases risk of renal failure.
148
Most IMPORTANT INTERVENTION to protect from AKI are :
Minimize aortic clamp time, aggressive hemodynamics stabilization
149
4 Medications that can help prevent AKI are:
Dopamine, bicarbonate, furosemide, mannitol
150
SPINAL CORD ISCHEMIA can Causes
PARAPLEGIA
151
Incidence of spinal cord ischemia
1-13% of the time
152
Spinal arteries supplying the spinal cord are
2 posterior arteries (20%) , 1 anterior artery (80%), supplies the cord
153
ARTERY OF ADAMKIEWICZ provides
transverse levels
154
Level of ARTERY of ADAMKIEWICZ is
T8 - T12
155
Interruption of blood flow to the artery of adamkiewicz in absence of collateral blood flow can cause
PARAPLEGIA
156
Interruption of blood flow to which artery can cause PARAPLEGIA →
ARTERY OF ADAMKIEWICZ
157
SPINAL CORD PROTECTION Strategy :
Mild hypothermia, CSF drainage, Distal aortic perfusion with SBP > 120mmHg
158
Ischemic colon injury from
INFERIOR MESENTERIC ARTERY
159
2nd most common vascular surgery in US
CEA
160
The risk of cardiac - related death or nonfatal MI after CEA is
less than 5%
161
1st most common VASCULAR surgery is
CORONARY REVASCULARIZATION
162
Framingham Study: Stroke Risk _____after a TIA and ___% ____years after a TIA
30% 2 years after a TIA, and 55% 12 years after TIA
163
Leading cause of death after vascular surgery?.
STROKE
164
Stroke often related to a
decrease Cerebral blood flow
165
What is AMAUROSIS FUGAX →
Unilateral (monocular) blindness, 25% of people with high grade carotid artery stenosis
166
AMAUROSIS FUGAX -> caused by
microthrombi in the internal carotid artery leading to a decreased blood flow to the OPTIC NERVE
167
Nerve affected by amaurosis Fugax
OPTIC NERVE
168
The most URGENT and devastation complication of CEA is
CLOT FORMATION at THE SURGICAL SITE and the associated thromboembolism to the cerebral circulation
169
BEST Measure of adequate CBF is
an AWAKE PATIENT
170
What is the Gold standard for identifying neurological deficits related to coronary artery cross clamping
EEG monitoring
171
EEG assesses for
CORTICAL electrical function and a
| LOSS OF BETA WAVE ACTIVITY, LOWER AMPLITUDE, and emergence of SLOW WAVE ACTIVITY
172
STUMP PRESSURE assess what
To assess COLLATERAL FLOW
173
Stump pressure is a Gross measurement of the pressure within
the circle of WIllis
174
A stump pressure of less than______Means what?
40-50 mmHg means NEUROLOGIC HYPOPERFUSION and is an INDICATION FOR A SHUNT
175
SOMATOSENSORY EVOKED POTENTIALS reflect what
Reflect sensory integrity of the spinal cord in the brain
176
List 5 ways of neuromonitoring during CEA
```
EEG
Stump pressure
SSEPs
TCD
NIRS
```
177
TRANSCRANIAL DOPPLER : Assess
velocity of blood flow in the MIDDLE CEREBRAL ARTERY
178
Transcranial Doppler assesses which artery
Middle cerebral artery
179
NEAR INFRARED SPECTROSCOPY : Assess
CEREBRAL REGIONAL OXYGEN SATURATION.
180
NIRS indication of cerebral ischemia?
>20%reduction is indicative of CEREBRAL ISCHEMIA
181
Which technique best assess regional cerebral oxygen saturation ->
Near infrared spectroscopy.
182
3 ways to protect the brain and prevent ischemia (IDA)
1. INCREASE collateral flow with a SHUNT
2. DECREASE CMRO2 with volatile anesthetics
3. AVOID hyperglycemia
183
CO2 during neurosurgery
Maintain normocarbia
184
Anesthetics to avoid
AVOID ETOMIDATE, and NITROUS
185
Which gas provide the BEST PROTECTION AGAINST CEREBRAL ISCHEMIA?
ISOFLURANE
186
Signs and symptoms of cerebral hyperperfusion syndrome after CEA include
headaches, seizures and FOCAL NEUROLOGICAL DEFICITS
187
Most common complication of CEA is
STROKE by microemboli
188
Other Complications of CEA
MI, Bradycardia , HoTN
Stent thrombosis, HORNER’s SYNDROME
Hemorrhage
Carotid Artery rupture
189
Leads to anterior spinal cord syndrome?
Damage to artery of adamkiewitcz
190
Regional for surgery of Lower extremities
EPIDURAL BEST option with MANY ADVANTAGES
191
If they have combined general and epidural is associated with
30% reduction in death
192
Lower incidence of (3) with epidural anesthesia
MI, stroke and respiratory failure
193
A positive consideration for administering INHALATIONAL and IV Anesthetics is that they
DECREASE the rate of OXYGEN DEMAND
194
RISK that neuraxial can lead to
EPIDURAL Hematoma formation
195
STUMP PRESSURE To assess
COLLATERAL FLOW
196
Provide the blood flow to the CIRCLE of willis during the CEA
NON-OPERATIVE carotid artery and the BASILAR artery
197
Stump pressure Gross measurement of the
pressure within the circle of WIllis
198
EVAR is good because it associated with
LOWER MORTALITY , Shorter recovery time, decrease procedure time.
199
More common with EVAR
Re-interventions or having 2 surgeries
200
EVAR is associated with no
cross clamping , no prolonged period of extreme hypotension
201
During EVAR what is done?
FEMORAL ARTERY used to introduce stent graft to aneurysm
202
Endovascular Aortic repair (EVAR) →
because of the ENDO leak or GRAFT LEAK
203
Most significant advantages EVAR
NO CROSS CLAMPING, NO LARGE INCISION (chest to pelvis.
204
Open approaches: 2 approaches
anterior transperitoneal OR anterolateral retroperitoneal approaches
205
Questions: All are indications for FFPs except
Question 2:
Question 3;
Hypovolemia with a normal Hgb (FFP is not used for volume status, only for blood)
206
For surgeries with significant blood loss, the best alternative to RBC transfusion is
Blood Salvage with cell Saver.
207
For craniotomy indication for platelet is when platelet is
100,000,
208
(No spontaneous bleed until platelets
less than 10,000,
209
Recommended indications for platelet infusion include all EXCEPT
Platelet count 25,000 in asymptomatic patients.
210
Major surgeries indications for platelets
50000
211
It is the component of choice to improve oxygen carrying capacity.
1 unit increases Hgb by 1 g/dl and Hematocrit by 3 %
PRBCS
212
One unit of PRBCs is good for
40 days,
213
One unit of PRBC contains _____ml of RBCs
250 ml of RBCs,
214
PRBCs hematocrit is
65%.
215
PRBCs give
Given 1 ml for each 2 ml of blood loss
216
1 unit of PRBCs increases Hgb by ____and Hct by ___
1 g/dl; 3%
217
FFPs Contains all the
coagulation factors
218
FFP : It is stored for
1 year at -10 C
219
FFP Thawed, kept in the fridge
for 5 days
220
FFP Volume
Volume 200-250 ml
221
Indications for FFP administration:
Reversal of effect of warfarin
Vitamin K deficiency
Correction of coagulopathy
222
FFP and PT/PTT
Used to treat elevated PT/PTT that is greater than 1.5 x normal
223
FFP Dose for reversal of warfarin
is 5-8 ml/kg
224
FFP Dose for ALL Other purpose of administration except for reversal of heparin
Dose is 10-20 ml/kg
225
FFP discouraged if
INR < 2
226
FFP and coagulation levels
increase coagulation levels by 20-30 %
227
1 unit of whole blood is about
6 units of platelet concentrate
228
Platelets shelf life and implications
SHORT Shelf life - 5 days because PRONE TO BACTERIAL GROWTH
229
Dose of platelet
1 platelet concentrate per 10 kg of body weight
230
1 unit raise platelet count by
30,000 - 60,000
231
Indication for platelet Less than
50,000
232
CRYOPRECIPITATE and factor VII
Contains 100 units of factor VIII
233
Cryoprecipiate Contains
fibrinogen, fibronectin, and von willebrand Factor
234
- Recommended for von willebrand disease, and for deficit of fibrinogen < 100
Cryoprecipitate
235
How is Cryo administered
Must be administered RAPIDLY through a FILTER
236
Cryo and fibrinogen
10 units of cryoprecipitate contains 2 g of fibrinogen
237
Colloids administration should be AVOIDED with
SUSPECTED or known TBI
238
Colloids expands what volume?
plasma volume rather than interstitial fluid volume
239
Colloids have less
fluid requirement, LESS PERIPHERAL AND PULMONARY EDEMA
240
No mortality difference of colloids administration in
septic patients
241
Worst OUTCOMES AND HIGHER MORTALITY.(not in US)
Hydroxethyl starch (HES)
242
Crystalloids are
inexpensive, non allergenic, and do not inhibit coagulation
243
Colloids are (disadvantages)
expensive, allergenic, and linked to RENAL FAILURE AND COAGULATION
244
Colloids advantages: infusion volume , edema and length of time in plasma volume?
Smaller infused volume
Less peripheral edema
Prolonged increase in plasma volume
245
Colloids Disadvantages:
```
Greater cost
Coagulopathy
Pulmonary EDEMA
Decreased GFR
Osmotic diuresis
Greater duration of excessive volume expansion
```
246
Crystalloids advantages
Lower cost
Greater urinary flow
Interstitial fluid replacement
247
Crystalloids disadvantages
Transient increase in Intravascular volume
| Transient hemodynamic improvement
248
Crystalloids edema diagnosis
```
Peripheral edema (protein dilution)
Pulmonary edema (protein dilution + high PAOP)
```
249
All of the following IV solution are ISOTONIC , Except:
25% Albumin
250
ISOTONIC SOLUTIONS are :
LR, plasmalyte, NS
251
NS composition
| Na, CL, ph, OsmoLality
154 Na+
154 Cl-
pH 5.6
OsmoLAlity 310
252
LR composition
Sodium, Chloride, Potassium, Calcium, Lactate
253
LR ph and osmolality
pH 6.2
| OsmoLAlity 275
254
LR composition numbers
```
Na+ 130
Cl- 110
K+ 4.0
Ca 3.0
Lactate 28
pH 6.2
OsmoLAlity 275
```
255
Plasmalyte composition
Sodium, Potassium, chloride, Magnesium, Glucose
256
Plasmalyte composition
| Na, K, Cl, Mag, glucose ph and osmoloLality
```
Na 140
K+ 5
Cl- 98
Mag 3.0
Glucose 23
pH 7.4
OsmoLALITY is 295
```
257
Plasma Composition
Sodium, Potassium, Chloride, Magnesium, Calcium,
258
Plasma composition numbers :
| Na+, K+, Cl-, Mag Ca2+, ph, osmolality.
```
Na 142
K+ 4
Cl 103
Mag 2.0
Ca2+ 5
pH 7.4
OsmoLAlity is 291
```
259
Preferable for resuscitation of dehydration conditions such as fasting , active GI losses, polyuria, and
Crystalloids
260
Administration of isotonic affects the entire ECV
Crystalloids
261
MOST COMMONLY ADMINISTERED IV FLUIDS, however is the LEAST PHYSIOLOGICAL
NSS crystalloid
262
Large volume of NS lead to
increase SALT and WATER retention
263
3% Saline is given to
trauma and head injury patients, and for VOLUME EXPANSION
264
Can lead to HYPERCHLOREMIC METABOLIC ACIDOSIS
NSS crystalloids
265
Hyperchloremia does what?
impairs renal handling of bicarbonate and DECREASES GFR
266
HYPERMETABOLIC conditions fluid
NSS crystalloids
267
Beneficial for restoration of circulating intravascular volume, decrease in hormone mediated vasoconstriction
NSS crystalloids
268
Preservation of microcirculatory flow
| LAck of allergic potential
NSS crystalloids
269
NSS and crystalloids metabolism
Easily metabolized and renally cleared
| Ability to expand plasma volume transient
270
Can lead to mild METABOLIC ALKALOSIS
LR
271
LR and Blood Products
Contraindicated with BLOOD PRODUCTS because of risk of coagulation
272
Compatible with blood products
PLASMA LYTE and NSS
273
T/F Crystalloids are more ALLOGENIC than colloids?
FALSE
274
Used to estimate fasting deficit and surgical and insensible losses
4-2-1
275
Used to replace fluid deficit
4-2-1
276
Prophylactic volume administration is outdated,
and can lead to fluid overload
277
Fluid management techniques that account for
3rd spacing, results in poor clinical outcomes
278
Urine output as an indicator of volume status is
NOT ACCURATE
279
Positive fluid balance in a trial resulted in an
increase rate of Acute Renal Failure in those with sepsis
280
ERAS and clear fluid
Allows clear fluid 2 HOURS prior to surgery so the patient is in a euvolemic state
281
Bowel Prep And ERAS
It avoids the routine use of a BOWEL PREP
282
Carbohydrate drinks and ERAS
2 hours before (carb loading, NO fasting)
283
ERAS and glucose
Maintain adequate insulin and glucose level
284
ERAS and dehydration
Decrease state of dehydration prior to surgery
285
ERAS and NG tube
NO NG tube, early PO, early foley removal
Early MOBILIZATION
NO drains
286
Less likely to develop hypotension from hypovolemia
Early discontinuation of IV fluids
| Start PO intake soon
287
Hyponatremia Symptoms
```
Cerebral edema
Impaired thermoregulatory control
Lethargy, coma, seizures
Nausa
Reflex impairments
```
288
Hypernatremia Symptoms
Weakness
Lethargy, coma, seizures
DEMYELINATING LESIONS
Intracerebral or Subarachonid hemorrhage
289
Hypokalemia
```
Muscle weakness
Respiratory failure
Rhabdomyolosis
Ileus
Cardiac arrhythmias
```
290
ECG changes
(blunted T waves and the presence of U waves)
291
Hypokalemia Symptoms
```
Muscle weakness
Respiratory failure
Rhabdomyolosis
Ileus
Cardiac arrhythmias
Nephrogenic DI
```
292
ECG changes
blunted T waves and the presence of U waves
293
HYPERKALEMIA Symptoms
```
Severe muscle weakness
Ascending paralysis
Cardiac conduction abnormalities
ECG changes
Cardiac arrhythmias
```
294
Mild Hyperkalemia 5.5 - 6.5 →
Peaked T waves,Prolonged PR segment
295
Moderate Hyperkalemia 6.5 -8 →
Loss of P wave, Prolonged QRS, ST segment elevation, Ectopic beats and escape rhythms
296
Severe Hyperkalemia > 8 ->
Sinus wave, Progressive widening of QRS complex, Vfib, asystole, axis deviations, BB blocks, Fascicular blocks.
297
Hypertonic fluids :
Mannitol and Hypertonic Saline
298
Hypertonic Saline is MOST commonly used for
sympatomatic hyponatremia
299
Mannitol is used to
reduce ICP
300
Hypertonic fluids draw
interstitial fluid into the intravascular space
301
Mannitol and Mechanism
inhibitsREABSORPTION of free WATER and Sodium in the kidney resulting in a Large diuresis.
302
Mannitol,For the Treatment of
elevated ICP, HYPERTONIC SALINE is SUPERIOR
303
Clinical indicators of tissue hypoxia
```
Base deficit > 2 mEq/L
Lactate > 2.5 mmol/L
Cap refill > 2 sec
Cold mottled skin
Mixed venous oxygen saturation < 65%
Central Venous oxygen saturation < 70%
```
304
Most common cause of Transfusion related death
TRALI
305
National heart and lung diagnostic criteria:
Acute, NONCARDIOGENIC pulmonary edema with Bilateral infiltrates and a P/F < 300
306
Pathology of TRALI
Breakdown of capillary alveolar membrane
Interstitial pulmonary edema
Microscopic alveolar hemorrhage
307
Occurs as a result of Alloantibodies
TRALI
308
TRALI definition
Defined as ACUTE LUNG INJURY within 6 hours of Blood transfusion
309
Presenting symptoms of TRALI:
| Cause
Increase O2 requirements to ARDS
310
TRALI treatment
Treatment is supportive
| DOES NOT RESPOND to diuretics.
311
Theories for the cause of TRALI
Theory 1. Antibodies in the donor plasma activate neutrophils leading to pulmonary capillary leakage. Theory 2. Stressor like sepsis, leads to neutrophils in the lungs.
312
Most IMPORTANT complication of heparin therapy
Heparin Induced Thrombocytopenia
313
HIT is Characterized by
microvascular thrombosis secondary to platelet activating IgG antibodies to the heparin and platelet factor IV complex
314
HIT and lovenox
Less likely to occur with lovenox
315
When is HIT suspected?
Should be suspected in anyone with decrease >50% decrease in platelet count from baseline OR total platelet count of < 100 while on heparin with normal baseline levels.
316
1 out 5 % of patients TYPICALLY after
5-10 DAYS
317
Classical PRESENTATION of HIT:
Thrombocytopenia, RESISTANCE TO HEPARIN, THROMBOSIS, Positive assay
318
Worst type of HIT
Type II HIT i
319
HIT: Type I onset
1-4 days
320
HIT: Type II onset
5 days - 15 days
321
Recombinant activated factor seven (VII) used for
| WIll reverse prolonged INR
For hemophilia A and B
| Inhibitor disorders of factor, VII, VIII, IX
322
UNIVERSAL HEMOSTATIC AGENT
Recombinant activated factor seven (VII)
323
Mechanism of action of Recombinant activated factor seven (VII)
ACCELERATED thrombin formation at the site of endothelial injury.
324
Dose of factor VII
Dose 20-100 mcg/kg
325
Dose of factor VII for Hemophillia
90-120 mcg/kg
326
Factor VII is good for
GOOD for patients suffering from critical bleeding
327
Reverse prolonged INR
Activated factor Seven
328
Factor VII does not work with
Does NOT WORK IN ACIDOSIS or HYPOTHERMIA
329
Prothrombin complex concentrates (PCC)
| Usually
Factor II, IX, X and sometimes VII
330
Indicated for Hemophillia patients
PCC
| Factor VII
331
Most commonly used for REVERSAL AGENT FOR WARFARIN and oral anticoagulants
PCC
332
Risk. with PCC
RISK: Arterial and thromboembolism
333
CONTRAINDICATIONS of PCC:
DIC
334
Anesthetic medications that promote cerebral protection
Propofol
Dexdemetomidine
Inhalation anesthetics
335
Propofol and cerebral protection
It decreases CMRO2 by 40%
336
Dexdemetomidine and cerebral protection→
decrease CMRO2
337
Inhlation anesthetics and cerebral protection→
decrease CMRO2 in a dose dependent
338
How soon must fresh frozen plasma be transfused
| once thawed?
Within 24 hours
339
Six hours after a patient received a transfusion with 2 units of fresh frozen plasma and 1 unit of platelets, she presents with hypoxia, ever, and noncardiogenic pulmonary edema. What complication do you suspect?
Transfusion-related acute lung injury
340
A 44-year-old 50-kg male received 750 mL of fresh frozen plasma. What percent of normal would you expect his clotting actor concentration to achieve post transfusion?
(D) 30%
341
Which is NOT an indication of cryoprecipitate administration?
Antithrombin deficiency
342
Indication of cryoprecipitate administration?
Fibrinogen levels < 80-100 mg/dL
Factor XIII deficiency
Preoperative prophylaxis or patient with von
Willebrand disease
343
What is the approximate half-life of serum albumin?
21 days
344
A patient receives large volumes of 0.9% normal saline during a case. What is the risk associated with this?
Hyperchloremic Metabolic acidosis
345
An adult patient’s platelet count is 25,000/μL. After transfusing the patient with 2 units of apheresis platelets, what would you expect the platelet count to be?
85,000-145,000/μL
346
Which statement about fresh frozen plasma (FFP) administration is correct?
(A) Each unit of FFP will increase the level of each
| clotting factor by 2-3% in adults.
347
Each unit of FFP will increase the level of each
| clotting factor by
2-3% in adults.
348
The initial therapeutic dose of FFP is
10-15 mL/kg.
349
What is the treatment of choice or hyponatremic patients with decreased total body sodium content?
0.9% NS
350
Heparin Induced Thrombocytopenia is a
TYPE-II CYTOTOXIC Hypersensitivity REACTION
351
At what value do serious complications of hyponatremia
| manifest?
120 mEq/L
352
Which sodium disturbance increases Minimum Alveolar Concentration (MAC)?
HYPERNATREMIA
353
A patient’s serum potassium level is 7.2 mEq/L. In
which sequential order will cardiac manifestations of
hyperkalemia progress?
Peaked T waves
Widened QRS complex
loss of P wave
Sine wave
354
The goal of FFP administration is to achieve
30% of the normal coagulation factor concentration.
355
A unit of FFP will increase the level of each clotting actor by
2-3% in adults
356
A patient is undergoing an elective abdominal aortic aneurysm (AAA) repair. What drug are you most likely to administer after aortic clamping?
NITROGLYCERIN
357
A patient undergoing repair of a descending thoracic
aortic aneurysm is found postoperatively to exhibit
loss of lower extremity motor function bilaterally.
What is the most likely cause?
Blood flow to the anterior spinal cord was
| damaged during the surgery.
358
Which type of surgical procedure will result in the
greatest increase in afterload accompanied by acute
hypertension during aortic cross-clamping?
Stanford type A dissection of the Ascending Aorta
359
The more proximal the clamp is applied
the more marked the effects.
360
Since the ascending aorta is most proximal, it
| will experience the
greatest increase in afterload if it is cross-clamped with the heart beating.
361
The most serious acute complication associated with carotid artery stenting (CAS) is
stroke
362
The most serious acute complication associated with carotid artery stenting (CAS) is stroke, which can occur due to
thromboembolism, hypoperfusion, hyperperfusion syndrome, or hemorrhage.
363
Regional anesthesia for carotid endarterectomy
Superficial/deep cervical plexus blocks
364
What type of plasma donor has the highest risk of causing TRALI in recipient?
Multiparous female donors.
365
Recipient antibodies to HLA on donor leukocytes ->
influx of neutrophils
366
Which complications are most concerning following
| carotid endarterectomy?
HTN and hypoxemia
367
One unit of whole blood or packed red cells will raise the
| hematocrit by_____and the hemoglobin by_____
3% ; 1 g/dL.
368
In adults, a pool of six platelet concentrates, or a single
| apheresis unit should increase the platelet count by
20 000- 60 000/μL.
369
Commonly, the platelet count is raised to at least
50 000/μL,
370
A pool of _____platelet concentrates make one unit
six platelets.
371
Recombinant activated factors VII (rFVII)—This product
is known to enhance thrombin generation and has
been approved specifically for patients with
Factor VII deficiency (hemophilia).
372
Prothrombin Complex Concentrate (PCC) (trade name Octaplex or Ocplex[1]) is a combination of blood clotting
factors II, VII, IX and X, as well as protein C and S.[1] It
373
This product Reverses the effect of warfarin (a coumarin anti-coagulant) and is used in cases of significant bleeding in patients with a coagulopathy (INR > 8.0, prolonged prothrombin time, raised d-dimer).
Prothrombin Complex Concentrate (PCC)
374
What is the PRINCIPAL RISK FACTOR for TRALI?
The presence of HLA antibodies in DONOR PLASMA
375
In TRALI, 1st theory:
HLA-Antibodies activates the complement cascade, resulting in neutrophils recruitment to the pulmonary vasculature, and subsequent activation. Neutrophil activation leads to endothelial damage and capillary leak, the basis for pulmonary edema.
376
In TRALI ,2nd theory : Two-hit model
The first hit involves neutrophil sequestration in the lungs due to a trigger (surgery, massive transfusion, infection). Upon receiving a transfusion with donor antibodies against HLA or HNA subtypes, the antibodies activate the sequestered neutrophils causing neutrophil-mediated lung injury.
377
A TRALI reaction meets the following criteria:
* An acute onset of hypoxemia within 6 hours of transfusion.
* Bilateral pulmonary infiltrates on chest X-ray.
* No cardiogenic cause of the pulmonary edema (pulmonary capillary wedge pressures <18 mm Hg).
* No preexisting lung injury.
378
Can have a detrimental effect on TRALI -->
Diuretics
379
TRALI-> It is most closely associated with
fresh frozen plasma (FFP) transfusion, but also occurs with packed red blood cells (PRBCs).
380
The Biggest concern with heparin therapy is
Heparin Induced Thrombocytopenia
381
Unfractionated heparin interacts with
PLATELET FACTOR 4 (PF4) → trigger igG mediated antibody specific to the heparin-platelet 4 complex
382
2 types of HIT
| Type 1 mild →
causes mild Thrombocytopenia and recovers within a few days even in the presence of heparin.
383
PCC coagulation factors - how much FFP is one dose of PCC equivalent to
II, VII, IX, X 8-16 units of FFP
384
Which factor is FFP deficient in
VIII
385
Prevention of AKI after AAA aortic cross clamping
A. mannitol - inc. RBF, vasodilator, inc. renal prostaglandin, dec. renal renin furosemide
B. vasodilator maintain adequate vascular volume
386
Factors effecting hemodynamic changes after aortic cross clamping
1. level of cross clamp (most important) volume status pre-existing cardiac disease (coronary disease, aortic regurg, CHF
387
Treatment of hypertension after cross clamp placement
preload reduction - nitroglycerin
| afterload reduction - nitroprusside
388
Risk of PPC open and EVAR
endovascular 3% vs open 16% AAA repair risk of PPC -
389
PPC : Spinal vs general
spinal/epidural anesthetics less PPC than general anesthesia
390
Which blood product has the highest incidence of transfusion related sepsis?
platelets because stored at room temperature
391
Incidence of HIT is
2.5%
392
What fluid should be used as carrier for blood?
plasmalyte normal saline ^do not contain any calcium*
393
TRALI antibodies
antibodies in donor plasma activating recipient leukocytes -> recipient neutrophil activation
394
Fresh frozen plasma contains what clotting
| factors?
contains all coagulation factors except platelets.
395
Which factors are most abundant in FFP?
Factors V and VIll are most labile and are the most abundant factors in FFP
396
Factor with the shortest half life?
Factor VII has the shortest half-life, which is 4-6 hours.
397
Transfusions of fresh frozen plasma (FFP) are indicated for:
( l) isolated coagulation factor deficiencies;
(2) reversal of warfarin therapy;
(3) correctionof coagulopathies associated with liver disease
(4) after massive transfusions with continued bleeding even after platelet transfusions.
398
What is the dosing for fresh frozen plasma (FFP)?
General dosing of fresh frozen plasma (FFP) is 10-15 ml/kg, which is expected to bring clotting factor levels to at least 30% of normal.
399
What is the dosing of FFP for reversal of warfarin?
Dosing of FFP for reversal of warfarin therapy is 5-8 ml/kg.
400
What coagulation factors are found in cryoprecipitate?
Cryoprecipitate contains factor VIII:C, VIII:vWF, XIII and fibrinogen (factor I).
401
Cryoprecipitate is a concentrated source ofl. Remember:
fibrinogen (I), Factor VIII, Factor XIII, and vWF.
402
One unit of cryoprecipitate has enough
fibrinogento increase fibrinogen levels 5-7 mg/dL
403
How do you obtain cryoprecipitate?
is recovered from fresh frozen plasma thawed at 4 degrees C.
404
What may be given to treat the patient with a fibrinogen {factor I) deficiency?
Cryoprecipitate
405
Transfusion-related acute lung injury (TRALI) is characterized by
dyspnea and arterial hypoxemia secondary to noncardiogenic pulmonary edema.
406
The diagnosis ofTRALI is confirmed when pulmonary edema occurs in the
absence of left atrial hypertension and the pulmonary edema fluid has high protein content.
407
The edema in TRALI has a
High protein content
408
Why should hypotension be avoided in the patient undergoing carotid endarterectomy surgery?
There is a loss of autoregulation in ischemic areas of the brain. Because perfusion in these areas is pressure dependent, hypotension should be avoided.
409
Postoperative hypertension may be due to
surgical denervation of the ipsilateral carotid baroreceptor, chemical denervation of the baroreceptor OR carotid sinus dysfunction from surgical trauma.
410
When the clamp is removed after repair of an abdominal aortic aneurysm, would you increase or decrease minute
ventilation? Does this change in minute ventilation promote "steal" or "inverse steal" (Robin Hood effect)?
```
A temporary increase in minute ventilation may be useful for the control of acidosis. The hypocarbia associated with increased ventilation would tend to constrict vessels and decrease perfusion to tissues located proximal to
the clamp, thereby diverting blood to ischemic tissues (those tissues distal to the clamp). This is inverse steal,
Hood effect (robbing from the rich and giving to the poor).
```
411
Symptomatic hyperkalemia is often not present until serum levels are >6.5 mEq/L, and its treatment should initially include
administration of parenteral calcium as a cardiac membrane stabilizer.
412
Abnormalities of serum sodium are most often due to some form of
abnormal renal water regulation.
413
Hypernatremia should not be corrected more quickly than
∼0.7 mEq/hr, t
414
Hypokalemia Early electrocardiogram (ECG) findings include
blunted T waves and the presence of U waves.
415
After carotid endarterectomy, the carotid body on the operative side is
denervated and this blunts the ventilatory response to hypoxemia and virtually eliminates this response after bilateral carotid endarterectomy.
416
When compared with open surgical repair, EVAR is associated with
shorter recover times and lower 30-day mortality rates (1.4% vs. 4.2%) but no difference in mortality rates at intermediate and long-term follow-up.
417
The annual risk of aneurysmal rupture is directly related to its diameter:
1% for aneurysms measuring <4.0 cm, 2% for aneurysms 4.0 to 4.9 cm, and 20% for aneurysms >5.0 cm. All aneurysms >5.0 cm should be considered for surgical or endovascular repair.
418
Aortic aneurysm rupture has a mortality rate of
85% unless surgery is performed immediately, and even then the mortality rate is 50%.
419
Nevertheless, EVAR is not without complications, including
graft leak and intraoperative conversion to open repair because of aneurysm rupture, vascular injury, or inability to seal the graft against the wall of the aorta
420
Risk of cardiac related death or nonfatal MI after carotid endarterectomy is
5%
421
What coagulation factor is responsible for conversion of fibrinogen to fibrin?
Thrombin
