1
Q
What disease processes commonly accompany vasculopaths?
A
DM, HTN, CRI and COPD
2
Q
What produces heparin in the body?
A
Basophils and mast cells
3
Q
What is the MOA of heparin?
A
Binds to AT III which then inactivates thrombin and factors XII, XI, IX and X
4
Q
Thrombin is responsible for activating what factors?
A
V and VII
5
Q
T/F: heparin inhibits platelet function
A
True
6
Q
List the common pharmacokinetics of heparin
A
Poorly lipid soluble
Poorly absorbed from GI tract
Does not cross placenta
Circulates bound to plasma proteins
7
Q
What is the dose-response relationship disproportionate effect of heparin?
A
Anticoagulation increases in intensity and duration with: increasing doses
But decreases effect in hypothermia, hepatic and renal dysfunction
8
Q
How does heparin affect hemodynamics?
A
Relaxation of vascular smooth muscle
Decreased MAP,PAP,SVR
9
Q
What findings indicate mild HIT?
A
Due to platelet aggregation
Platelet count <100,000
Begins hours-15 days after initiation of therapy
10
Q
What findings indicate severe HIT?
A
Platelet count <50,000 (actual diagnosis)
Occurs 5-10 days after initiation
Antibody (IgG) formation
11
Q
If HIT is confirmed, what drugs would you consider immediately starting to avoid thrombotic complications?
A
Bivalirudin (Angiomax)
Argatroban
12
Q
Where is IgG found?
A
In the blood and ECF
13
Q
What is the function of IgG?
A
Neutralize toxins, viruses, and bacteria
Opsonize them for phagocytosis
14
Q
What does IgG bind to on a platelet? What does this then subsequently cause?
A
The FC receptor
This activates the platelet which then releases pro-thrombotic substances and then activates further platelets
15
Q
What drug is a commonly used direct thrombin inhibitor for HIT?
A
Bivalirudin
16
Q
What cofactor(s) does Bivalirudin require to exert its effect?
A
None
Whereas heparin requires AT to work
17
Q
What is the dose of heparin for vascular cases?
A
1 mg/kg or 100 u/kg
18
Q
What is the goal ptt in vascular cases?
A
1.5 - 2.5x baseline (normal is 30 - 35 seconds)
19
Q
What is a normal ACT?
A
90 - 120 seconds
20
Q
How does protamine neutralize heparin?
A
It is a positively charged alkaline which then combines with the negatively charged acidic heparin molecule
21
Q
What clears heparin?
A
The RES (Reticuloendothelial system)
22
Q
What is the dose of protamine?
A
1 mg per every 1 mg or 100 units of heparin given
23
Q
What side effects to be aware of when giving protamine?
A
Hypotension
Histamine release
Injection central line vs peripheral IV
Allergic Reactions
Chronic protamine insulins, vasectomy, fish allergies
Require alternatives after vascular procedures (Platelet factor 4)
Pulmonary Hypertension
Rare
Secretion of thromboxane and serotonin
Pulmonary vasoconstriction…pulmonary edema and hypoxemia
Pretreated with cyclooxygenase inhibitors (indomethacin or ASA)
24
Q
If pulmonary HTN is of concern when giving protamine, what could you pre-treat the patient with to mitigate this?
A
Cyclooxygenase inhibitors (indomethacin or ASA)
25
At what GFR do s/sx of ESRD begin to manifest?
Less than 25 ml/min
26
At what GFR are you likely dialysis dependent?
Less than 10 ml/min
27
What metabolic abnormalities are common to ESRD?
Hyperkalemia
Hypermagnesemia
Hypocalcemia
Hypoalbuminemia
Water and sodium retention
Metabolic acidosis
28
What hematologic lab findings are common to ESRD?
Hgb generally around 6-8 g/dL
Impaired WBC and platelet function
29
T/F: CO is generally increased in ESRD
True
30
How does minute ventilation change in ESRD?
Increased to help offset the metabolic acidosis
31
What GI changes are common to ESRD?
Nausea, vomiting, ileus
Hypersecretion of gastric acid
Delayed gastric emptying
32
What are the pros/cons of an AV fistula?
Pros:
best long-term patency
lowest rate of infection
no foreign material used
Cons:
requires a longer “maturation” time (6 weeks or more)
may require more than one operation to create a functional dialysis fistula
33
What are the pros/cons to an AV graft?
Pros:
shorter time required for “maturation”
usually requires only one operation
Cons:
does not last as long
more prone to infections…complete removal
embolectomies/revisions
34
What fluids are generally used for ESRD patients in the OR?
Balanced crystalloids - Isolyte or NS
*LR should be avoided if potassium is elevated*
35
When should NS be the fluid of choice in ESRD patients?
If they are hypochloremic and alkalotic
36
Why does etomidate, barbiturates and BZDs have an increased effect in ESRD?
They are highly protein bound, in ESRD you have less circulating protein for them to bind to
37
What drugs have increased effect d/t elimination concerns in ESRD?
Opioid metabolites
Anticholinergics
Metoclopromide
H2 blockers
Pancuronium
Reversal agents...neostigmine
38
What is the theoretical concern with sugammadex use in ESRD?
The potential for re-emergence neuromuscular blockade d/t delayed elimination of the encapsulated paralytic/sugammadex complex
39
What are the indications for lower extremity revascularization?
1. Claudication
Metabolic requirements r/t oxygen delivery
2. Ischemic rest pain
3. Gangrene
May be considered emergent due to potential limb loss
Amputation occurs in approx. 25% of critical limb ischemia
40
What ABI indicates calcification/vessel hardening?
Greater than 1.4
41
What ABI indicates moderate arterial disease?
0.5 - 0.8
42
What ABI indicates severe arterial disease?
Less than 0.5
43
Why are iliac artery stents generally preferable to a fem-pop?
Higher initial success, and fem-pop has a lower initial success rate coupled with a higher incidence rate of thrombosis/restenosis
44
What are some examples of vascular synthetic grafts?
Aorta-bifemoral
Axilla-bifemoral
Femoral-femoral (fem-fem crossover)
45
What anesthesia considerations are common to a Aorta bi-fem/Axillo bi-fem/fem-fem crossover?
Type and cross
Large blood loss may occur
Large bore IV access
Central line/SVV monitoring
Heparin often redosed and usually reversed
46
T/F: you may not have to reverse heparin in a fem-pop/fem-tib bypass
True
47
What are the common post-op concerns with vascular cases?
Sudden loss of pulses
Sudden temperature change
Complaints of numbness/paresthesia
Loss of motion/sensation
48
What is the definition of an urgent surgery?
Threat to life/limb without surgical intervention, there may be time to clinically improve the patient, generally needs to get into the OR in 2 - 24 hours
49
What surgeries are intermediate risk on the cardiac risk assessment index?
Minor vascular, head/neck, ortho and urologic procedures
50
What are the common pulmonary complications from major vascular surgery?
Atelectasis, pneumonia, respiratory failure, exacerbation of chronic diseases
51
What are the obstructive pulmonary diseases common in major vascular surgery patients?
Bronchitis and emphysema
52
What are the restrictive pulmonary conditions common in major vascular surgery patients?
Pulmonary fibrosis and chest wall disease
53
What renal factors are independent risk factors for cardiac complications r/t surgery?
Creatinine > 2mg/dl
Creatinine clearance < 60 mL/min
Dye administration
Renal cross clamping
54
Why are the positive effects that statins have on improving outcomes in vascular surgery patients?
Anti-inflammatory, anti-oxidant effects
Preserves renal function and graft patency
55
What 2 vessels provide the most blood flow to the liver?
Hepatic artery (25 - 30%)
Portal vein (70 - 75%)
56
The metabolism of various substances in hepatocytes is dependent upon what?
The location or "zone" of the hepatocyte, different metabolism occurs in different zones of the hepatocyte
57
What zone of the hepatocyte is perivenous and primarily deals with glycolysis/glucuronidation?
Zone 3
58
What zone of the hepatocyte is periportal and is primarily responsible for aerobic metabolism?
Zone 1
59
What zone would you anticipate tylenol metabolism occurs in the hepatocyte?
Zone 3
60
Hepatic stellate cells make up what percentage of liver cells? What is their primary function?
8 - 10%
Specialized
Quiescent
Respond to cytokines during inflammatory periods
61
What are some common pathologies that create hepatic injury that could lead to cirrhosis?
Alcoholic liver disease
Hepatitis C
Hepatitis B
Non-alcoholic steatohepatitis
62
What is the difference between compensated and uncompensated cirrhosis?
Compensated: no portal HTN/varices/dysfunction, median survival rate is over 12 years
Uncomp: Ascites, + portal HTN, variceal hemorrhage and ~2 year survival rate
63
The release of what substances helps create esophageal varices?
NO and angiogenic factors
64
What blood flow is altered in response to the release of NO and angiogenic factors in portal HTN causing esophageal varices?
Increased azygos and hemiazygos venous flow (as portosystemic collaterals)
65
Where would you find the azygos and hemi-azygos veins?
Either side of the vertebral column
66
What is the primary function of the azygos and hemi-ayzgos veins?
Drain the thoracic and abdominal walls
67
What are esophageal varices?
Collaterals between high-pressure portal system
and low-pressure azygos system
68
What is the drug class of choice to help decrease pressure in portal HTN?
Non-selective BBs - Propranolol, Nadolol, Inderal
69
How does Octreotide help prevent variceal rebleeding?
Peptide hormone that inhibits the secretion of other hormones like insulin (is GHIH)
Vasoconstriction, decreases portal pressure, inhibits release of glucagon (splanchnic dilator)
70
What 2 vessels are connected with a catheter in a TIPS procedure?
The portal and hepatic veins to help decompress the portal circulation
71
What are the indications for a TIPs procedure?
Secondary prophylaxis of bleeding varices after failed medical therapy
Temporary relief of portal HTN while awaiting
transplantation
Treatment of refractory ascites
72
What are the common "concerns" r/t the TIPS procedure?
High rate of shunt stenosis, hepatic encephalopathy, high cost and lack of availability
73
Why are TIPS procedures generally an RSI?
Bleeding issues are common
Decreased LOC d/t encephalopathy?
Increased intra-gastric pressure…ascites?
74
How does portal HTN alter the heart?
Generally increases pressure on the right side of the heart
75
What factors does the liver produce?
Factors I, II, V, VII and IX - XIII
*note, factor V is made by both the liver and platelets*
76
How does cirrhosis alter pharmacokinetics/dynamics?
Increased volume of distribution
Decreased protein binding
Decreased drug metabolism
Decreased drug elimination
77
What are common anatomic locations for PEs to originate from?
Lower extremities, pelvic veins and the right heart
78
What pulmonary patho changes occur during a PE?
Increased dead space
Increased Mv Hypoxemia
Increased pulmonary vascular resistance
Loss of surfactant
Atelectasis within 24-48 hours
Potential pulmonary infarction
79
What should be part of your DD if a PE is suspected?
MI
Pericarditis
Pneumonia
Pneumothorax
Pleuritis
80
What are common pt s/sx of a PE?
Sudden dyspnea
Tachypnea
Pleuritic chest pain
Rales
Nonproductive cough
Tachycardia
Hemoptysis
Fever
*note how many of these would be difficult or unable to assess if a pt is under GA*
81
What 2 changes on an ABG could indicate a PE?
Hypoxemia and hypocapnia
82
What EKG changes could indicate a PE?
ST changes, A. Fib, tachycardia and RBBB
*Again, note how non-specific these are*
83
What TEE findings could indicate a PE?
Dilated RA/RV and LV wall motion abnormalities
84
A spiral CT and VQ study are looking for clots in what vessels?
Main, lobar, and segmental pulmonary arteries
85
What is the gold standard to diagnose a PE?
Pulmonary angiogram
86
What lab findings could indicate a PE?
+ D-dimer and elevated troponin
87
A SBP less than 90 or decrease greater than 40 mmHg greater than 15 minutes could indicate a PE if what other issues are ruled out?
Sepsis,
New-onset dysrhythmias
Hypovolemia
88
Why are IVC filters not left in place long term?
More complications the longer in place: fracture and migration
No significant survival benefit over anticoagulation alone
89
Why are IVC filters not routinely placed in pregnant patients?
Warfarin teratogenicity
LMWH appropriate…placenta previa?
IVC dilates in pregnancy
Displacement due to uterine growth
90
What are 2 common s/sx of carotid stenosis?
Asymptomatic bruit and TIA sx (transient blindness, paresthesia, speech problems clumsiness of extremities)
91
What scan is generally performed to diagnose carotid disease?
Duplex scan (Combines anatomic imaging with doppler flow velocity)
92
What are the 3 hallmark treatments of carotid disease?
ASA therapy
Platelet inhibitor therapy (P2Y12)
Clopidogrel, ticagrelor
Endarterectomy/Stenting
93
When is a CEA (carotid endarterectomy) indicated in carotid disease? When is a CAS (carotid artery stent) indicated?
CEA:
Surgery within 2 weeks of ischemic event
Stenosis 70% or greater
Poor anatomy (tortuosity)
DAPT contraindications
CAS:
Contralateral laryngeal palsy
Poor surgical candidate (CHF, USA, Advanced COPD)
94
What are the anesthesia goals during CEA?
Protect the heart
Protect the brain
Control heart rate/blood pressure
Ablate stress response
Awake patient at end of procedure
95
T/F: it is indicated to stop ASA prior to CEA surgery
False: dcing ASA increases rate of MI and TIA
96
What classes of medications should the patient continue prior to CEA?
Anti-anginal, anti-hypertensive, and anti-platelet meds
97
What kind of auto-regulation shift is common in carotid disease patients?
A right shift
98
What induction strategies are ideal for induction for a CEA?
Barbiturates: thiopental ↓ CMRO2 by 50%....focal protection
Etomidate: preserves cardiac stability and ↓ CMRO2
Small studies showing Barbs, Etomidate and Propofol prolong “tolerable” ischemia
Small doses of opioid
Short-intermediate acting NMBD
Sevo/Des d/t more rapid emergence
Esmolol/Phenylephrine/Sodium nitroprusside/Cardene
*essentially, make use of short acting downers/uppers*
99
Is placing a shunt required for a CEA?
No: you as long as you have intact collateral flow from the circle of Willis
100
What are potential issues with shunting during a CEA?
Kinking
Shunt occlusion against side wall
Air embolism
Injury to carotid artery
Impaired access due to shunt position
101
What monitoring modalities are as effective as shunting to reduce the chances of a perioperative stroke?
EEG, SP, SSEP and CBA
102
What would you expect to see if the baroreceptor reflex is activated during CEA?
Sudden bradycardia and hypotension
103
What steps/treatments should you start if the baroreceptor reflex is activated during CEA?
Cessation of manipulation
Infiltration with Lidocaine 1%
Glycopyrrolate IV
104
What regional block can be used for CEA surgery?
Superficial cervical plexus block
*Deep cervical plexus block is more likely to involve the phrenic nerve which may require conversion to GA*
105
What are the advantages of regional anesthesia for a CEA?
Easy to monitor adequacy of cerebral perfusion (Consciousness, speech, contralateral handgrip)
Greater stability of hemodynamics
Reduced operative site bleeding
Decreased cost
106
What are the advantages of GA for a CEA?
Ability to use pharmacologic cerebral protection
Avoid patient panic, loss of cooperation
Avoid phrenic nerve paresis
Avoid issues of poor neck anatomy or mobility
107
What is hyperperfusion syndrome?
Abrupt increase in flow and loss of autoregulation
Several days after CEA
HA, seizure, cerebral edema
Severe preoperative internal carotid stenosis or recent contralateral CEA
Beta adrenergic antagonists vs. calcium channel blockers, nitroprusside, ACE-I
108
T/F: nerve dysfunction s/p CEA is usually transient
True
109
What s/sx indicate unilateral laryngeal nerve injury? Bilateral?
Unilateral recurrent: hoarseness and impaired cough
Bilateral recurrent: life threatening respiratory obstruction
110
Carotid body denervation can cause what pulmonary/ventilatory changes?
Mild hypoxemia d/t impaired ventilatory responses
Bilateral dysfunction causes impaired response to acute hypoxia and elevated PaCO2
111
What multi-factorial conditions can increase the risk of an aneurysm occuring?
Adventitial elastin degradation
Chronic inflammation
Concomitant aortoiliac occlusive
disease (20-25%, think atherosclerosis)
112
When does an aneurysm become a dissection?
When the intimal layer ruptures
113
What is created when the intimal layer ruptures creating a dissection?
A false lumen
114
Why is blood pooling in a false lumen dangerous?
It can occlude the true lumen
115
What are common risk factors for a AAA?
Frequent in elderly men (8%)
Smoking
Family history of AAA
Atherosclerotic disease
116
What are risk factors for thoracic aneurysms?
Congenital syndromes
Trauma
Aortic cannulation
Bicuspid aortic valve
117
At what size of aneurysm is more serious intervention generally considered?
At 6 - 6.9 cm - the risk of rupture increases to 10 - 20%
118
What is the mortality rate for a AAA? What is the mortality rate if it ruptures?
2-4% surgical
50% if ruptured
90% if ruptured prior to hospital admission
119
What are the occurrence rates for unwanted outcomes for a thoracic abdominal aneurysm?
Paraplegia 4-40%
Renal failure 3-30%
Respiratory failure 8-14%
120
What is a saccular aneurysm? Fusiform?
Saccular - eccentric dilation with a variably sized neck, it looks like a balloon
Fusiform - uniform dilation of entire circumference and is more common
121
What s/sx can indicate a thoracic aneurysm is present?
Hoarseness
Stridor
Dysphagia
Upper body edema
Acute, sharp pain
BP pressure changes
Absence of peripheral pulses
122
What imaging modalities can help diagnose an aneurysm?
Widening of mediastinum
CT/MRI
Transesophageal echocardiogram (Easy and safe in acute dissection)
Angiography (Clearly identifies aortic branches -> Brachiocephalic, left common carotid, left subclavian)
123
What are the first 3 branches of the aorta?
Brachiocephalic trunk, left common carotid and left subclavian
124
What is the most common classification of an dissection?
Debakey I (Stanford A)
125
Describe the debakey classifications of each type of dissection
DB1 = goes from the root and extends distally, encompassing most of the aorta
DB2 = just the ascending aorta, does not affect the arch or the 3 vessels
DB3 = all descending
126
What is the occurrence rate of each type of dissection?
DB I - 60%
DB II - 10 - 15%
DB III - 25 - 30%
*Stanford A is both DB I and II*
127
Classify the aneurysm: the dissection is circumferential in nature distal to the aortic arch
DB III and/or stanford B
128
Classify the aneurysm: the dissection is partially circumferential in the ascending aortic arch
DB II and/or stanford A
129
Classify the aneurysm: the dissection is partially circumferential affecting the brachiocephalic trunk but not the left subclavian
DB II and/or stanford A
*If it is affecting any of the 3 takeoff vessels, the aneurysm is affecting the aortic arch*
130
What is the triad of abdominal aneurysm rupture?
Hypotension, back pain, pulsatile mass
Only 50% of ruptured aneurysms
*Suspected rupture/unstable…emergent OR without confirmation*
131
What location does an abdominal aneurysm rupture tend to accumulate?
The left retroperitoneum
132
What is the potential advantage of an abdominal aneurysm rupturing into the retroperitoneal space?
It can help tamponade the aneurysm
133
Why should you delay euvolemic resuscitation until proximal control of the aneurysm is achieved?
If you raise the BP too much you can actually increase bleeding from the aneurysm, keep the BP lower to allow the tamponade to control the bleeding
134
What preop assessments should be carried out in preop for an aneurysm?
Assessment of organ systems
Previous MI, presence of myocardia ischemia
Valvular dysfunction
CHF
Consider CABG/CEA
Hx of COPD/Smoking
PFT’s, ABG’s
Renal protection
Preop hydration, avoidance of low CO
Avoidance of nephrotoxic drugs
135
T/F: there is an ideal induction strategy for aneurysm repair
False
136
What are the goals for induction of an aneurysm repair?
Minimize hypertension/rupture
Double lumen for surgical exposure (for thoracic)
No renal clearance NMBD’s (Pancuronium, vecuronium and sux -> sux is metabolized in the plasma but it's metabolite is renally cleared, use with caution)
137
What are the 2 approaches for aneurysm repair?
Trans-peritoneal
Thoracic/abdominal midline incision
Aorta accessed through peritoneum
More fluid shifts, ileus, pulmonary complications, longer ICU stay
Retroperitoneal
Incision lateral border of left rectus muscle
Appropriate in obesity, COPD, previous abdominal surgeries
Less fluid shifts, less pulm/abd issues
More hernias, chronic wound pain
Poorer visualization
138
Why may surgeons prefer the trans-peritoneal approach despite the fact it has greater post-op complications?
It provides better visualization
139
What CV changes occur when the aorta is clamped?
Increased SVR
Initial decreased CO (no HR change)
Impedance to Ao flow, release of catecholamines
Renal vascular resistance increases by 70%
Renal hemodynamic changes last 30 minutes beyond unclamping
Post op mortality 4-5x higher if ARF develops
Active venoconstriction ↑ preload
140
What interventions should be carried out slightly before and/or during aortic clamping?
Small boluses of vasodilator prior to clamp
Afterload change/capacitance change
Preload alteration
Normalize/replace blood loss with packed cells as Hct drops
Use of epidural catheter
141
What CV changes occur when the aorta is unclamped?
Substantial ↓ in SVR
Hypotension
Blood pooling
Hypoxia-mediated vasodilation
Accumulation of metabolites
*sometimes, partially and slowly unclamping can help mitigate this*
142
What interventions can you use to help mitigate the negative effects of unclamping the aorta?
Prepare for sudden hemodynamic collapse
Fluid administration to CVP goal (common to go for 12 – 15)
Decrease volatiles
Small doses of vasoconstrictors
Frequent bedside labs to assess Hct, K+, ABG’s
Encourage surgeon to unclamp judiciously
Consider use of calcium, bicarbonate, and low dose pressors as needed
143
What are the MAP goals above/below the clamp?
Above = MAP of 100
Below = Map of 50
144
Where is the aorta clamp generally placed?
Distal to the subclavian or between the subclavian and common carotid
145
What column does SSEPs measure?
Dorsal column
MEPs measure the anterior column/motor tracks
146
T/F: drugs such as Mannitol, Dopamine and Fenoldopam are commonly used in aneurysm surgery to preserve renal function
False; their respective MOA's do have theoretical renal benefit, however they are not shown in studies to predict/modulate post-op renal function
147
T/F: opioids are preferred over LAs to control pain in a CEA
True: they have less hypotension issues relative to LAs
148
Paresis/paraplegia from aneurysm surgery could potentially be treated with what procedure?
Drainage of the CSF
149
How much does RBF decrease if the clamp is distal to the subclavian? If it is clamped infrarenally?
Sub - 90% decrease
Infra - 30% decrease
150
What kind of bypass can be performed to help perfuse the lower part of the body during aorta clamping?
Left heart bypass
Allows adjustment of flow
Oxygenator unnecessary
Relieves ↑ afterload
Full bypass dose of heparin -> not required
151
T/F: an oxygenator is not needed for left heart bypass
True
152
If the ascending arch is not clampable, what intervention is performed instead?
Circulatory arrest -> DHCA (deep hypothermic circulatory arrest)
153
What are the goals of DHCA (deep hypothermic circulatory arrest)?
18-20 degrees C
400-500cc/min flow (normal is 4 – 5 L/min)
30 minute “safe” zone
> 40min significant increase in brain injury
Anesthesia: neuroprotective measures
Mortality 10-15%...coagulopathies
154
What is the primary advantage of endovascular aneurysm repair?
Less significant hemodynamic forces
155
What occurs to the aneurysm sac after endovascular repair?
Sac thrombosis around stent and remodels aortic wall
156
What are potential complications of endovascular repair?
Endoleaks
Vascular injury during deployment
Inadequate sealing
Migration
Frame fracture
Thrombosis of stent
157
What is ALARA in OR radiation safety protocols?
As low as reasonably achieved (in terms of total radiation)
158
T/F: sodium bicarb and acetylcysteine do not have renal protective benefits in preventing contrast-induced nephropathy
True
159
What lab value indicates contrast induced nephropathy? When does it occur?
2 - 3 days postop and creatinine increases by 25%
160
What are the risk factors for contrast induced nephropathy?
Contrast load and pre-existing disease
*Try to limit contrast and adequately hydrate the patient*
161
What 2 vessels branch off the brachiocephalic artery?
The right subclavian and right common carotid
162
What 2 vessels branch off the proximal aorta to perfuse to coronary sinuses?
The R/L coronary arteries
163
What valve separates the RA and RV?
Tricuspid valve
164
What valve separates the LA/LV?
Mitral valve
165
Why do neonatal lungs only receive 5 - 10% of the CO?
High PVR and flow bypasses the lungs d/t foramen ovale (RA and LA) and the ductus arteriosus (connection between the aorta and pulmonary artery)
166
In neonatal circulation, what connects the RA and LA?
Foramen ovale
167
In neonatal circulation, what connects the pulmonary artery and aorta?
Ductus arteriosus
168
In neonatal circulation, what connects the umbilical vein to the IVC?
Ductus venosus
169
How does pulmonary circulation change at birth?
Marked decrease in PVR, PACO2 decreases, PAO2 increases
170
What closes the foramen ovale?
Increased pressure in the LA that becomes higher than the RA
171
What percentage of kids under 5 have a patent foramen ovale?
About 50%
172
Why does SVR drastically increase after birth?
The loss of a large low resistance vascular bed (placenta) increases SVR, IVC flow increases, RA pressure drops and aorta pressure increases over PAP
173
What closes the ductus arteriosus?
Increased oxygen levels and the decrease in PGE2 (prostaglandin E2)
174
What timeframe does the ductus arteriosus generally close?
Between 2 - 7 days after birth
175
What circulation changes may occur in neonatal hypoxia?
Pvr increases
Foramen ovale and ductus arteriosus may reopen
Significant proportion of blood bypasses lungs -> Rapid hypoxia, impaired tissue oxygenation…acidosis…further increase pvr…worsening hypoxia
*common conditions that can cause this include RDS and CDH*
176
What axis is the neonatal heart generally found?
~ 180 degree
177
How does the neonatal heart differ from an adult?
Less contractile tissue
Less compliant when relaxed
Limited sv
Cardiac output rate dependent
Immature myofibrils and sarcoplasmic reticulum
Calcium exchange more dependent on sarcolemma
Greater sensitivity to ccb drugs or citrated blood
Autonomic innervation immature
Further compromises co when stressed
178
What is an example of an extracardiac shunt?
Connections between a systemic and pulmonary artery
179
What determines the direction/magnitude of a shunt in ASD?
Ventricular compliance and AV valve function -> this means the shunt may or may not be clinically significant
180
In a VSD and/or PDA, what determines the magnitude?
The resistance of the pulmonary/systemic systems
181
In a VSD and/or PDA, what determines the direction of the shunt?
If PVR is high, it is a R -> L shunt
If SVR is high it is a L -> R shunt
182
What occurs in a L -> R shunt if the PVR is low?
Pulm blood flow increases
Volume overload for lungs
Increased workload of LV to maintain adequate CO which may lead to CHF
183
What are some examples of a L -> R shunt?
ASD, VSD, PDA, Coarctation of the aorta (narrowed aorta)
184
What is the other name of a L -> R shunt?
Acyanotic
185
What are the hemodynamic goals in a L -> R shunt?
Avoid vasodilators, 100% FiO2, decreased PCO2 and alkalosis
*Use a hypoxic gas mixture if needed*
186
What hemodynamic consequences can occur with a L -> R shunt?
Decreased systemic perfusion, low CO, hypotension, LV failure and LV overload
187
What occurs in a R -> L shunt?
PVR or pulmonary outflow tract > than svr
Decreased pulm blood flow
Admixture of deoxygenated blood to system
Systemic hypoxia
Rv failure
188
What are some examples of a R -> L shunt?
TOF, transposition, truncus arteriosus, hypoplastic left heart
189
What do you need to avoid in a R -> L shunt?
Sympathetic stimulation, decreased FiO2, increased PCO2 and acidosis
190
What are the hemodynamic consequences of a R -> L shunt?
Decreased pulmonary flow, hypoxemia, LV volume overload and LV dysfunction
191
What are the hemodynamic goals of a R -> L shunt?
Avoid decrease in SVR and decrease PVR (hyperoxia and/or hyperventilation)
192
How does a R -> L shunt affect an IV induction? Inhalation?
IV is faster, inhaled is prolonged
*paradoxical emboli are possible*
193
How does a L -> R shunt affect an inhalation induction?
No change
194
What is the largest group of cyanotic lesions?
Mixing lesions -> such as a truncus arteriosus
195
What pulmonary and systemic O2 saturation changes occur in a mixing lesion?
D/t extensive mixing, the sats should be nearly identical
196
What determines the extent of mixing in a cyanotic lesion?
The vascular resistance (PVR and/or SVR)
197
What direction is most common to a mixing lesion?
A R -> L shunt
198
What occurs to the LV in an obstructive lesion?
Pressure-overloaded ventricle proximal to obstruction
Profound lV failure
Impaired coronary artery perfusion
Systemic hypotension
Hypoxemia
199
What conditions are classified as an obstructive lesion?
Aortic stenosis, coarctation of the aorta
200
In a ductal lesion, what provides systemic flow?
The PDA
201
When does PVR reach adult levels after birth?
Around 6 months
202
What factors can we manipulate to increase PVR?
Increase PEEP, high airway pressures, atelectasis, low FiO2, acidosis, increased HCT, sympathetic stimulation, surgical manipulation and vasoconstrictors
203
What factors can we manipulate to decrease PVR?
No PEEP, low airway pressures, expand lungs to FRC, high FiO2, alkalosis, low HCT, blunt stress response, nitric oxide, vasodilators (milrinone, prostacyclin)
204
What is the usual dose of nitric oxide?
20 - 40 ppm
205
What is the primary concern with nitric oxide use?
Rebound HTN after DC
206
Why is a nasal RAE commonly used in pediatric CV surgery?
To prevent extubation from TEE
207
What side do you try to place your a-line and central line in pediatric CV surgery?
Right side
208
What is the heparin dose in neonates?
400u/kg
209
What is the heparin dose in children?
300u/kg
210
What is the goal ACT for going on pump in neonates?
480
211
IV induction is slow for peds CV cases, what shunt does it need to be especially slow/gentle?
R -> L shunt
212
What medication is commonly given in induction prior to giving fentanyl/sufentanil in a peds CV case?
Atropine
213
What paralytic may be a good choice if you want to avoid bradycardia on induction in a peds CV case?
Pancuronium (stimulates a sympathetic response)
214
What CVOR infusions are commonly used in a peds CV case?
Lactated ringers: low basal rate
Dopamine: 5mcg/kg/min
Epinephrine: 0.05 mcg/kg/min
Milrinone: 0.5 mcg/kg/min
Sufentanil: 0.5 mcg/kg/hr
215
What communicates in a patent PFO?
The LA and RA
216
What communicates in a primum ASD?
Inferior portion of the atrial septum near the AV valve
217
Where does a secundum ASD occur?
Close to the fossa ovalis causing a defect in the septum secundum
218
Where does a sinus venosus ASD occur?
High in the atrial septum close to the SVC
219
Where does a coronary sinus AD occur?
The coronary sinus, allowing blood to flow from the RA to the LA through the sinus
220
What occurs to the septum in a common atrium?
There is no atrial septum, may or may not also have abnormal valves
221
What are common anesthesia considerations for ASD surgeries?
Able to close many asd’s with percutaneous catheter device
Short acting drugs
Often extubated on table
Postop pulmonary hypertension rare
222
What is the most common congenital defect?
VSD
223
In a VSD, what type is generally physiologically insignificant?
Restrictive - the flow is small/low
224
In a VSD, what type is of more concern and may cause early onset CHF?
Unrestrictive - the low is much larger than restrictive
225
What are common anesthesia considerations for a VSD?
Able to close some with percutaneous, catheter device
Usually asymptomatic
Bidirectional shunts possible…care with air emboli
Maintain PVR to increase right to left shunt
Inotropic support may be required postop
Pulmonary hypertension if left to right shunt was significant
226
PDA is most common in preterm infants, what finding would raise suspicion for an PDA?
If mechanical ventilation is needed
227
What changes to PGE1 can cause a PDA?
*Make note, the slide says it is PGE1, I'm pretty sure this is meant to be PGE2*
Decreased degradation or increased production
228
What 2 approaches can be used to fix a PDA?
Thoracotomy or a sternotomy
229
Where do you place a pre and post-ductal pulse ox?
The right hand and the left foot
230
What findings would hint that the wrong structure was ligated during a PDA repair?
Major changes in BP, continued murmur or increased airway pressures
231
What are the 4 findings associated with TOF?
VSD
Overriding aorta
RVOTO - RV outflow tract obstruction
RVH
232
What are TET spells? What can cause them?
Acute worsening of TOF -> such as stress, crying, during feeding, metabolic acidosis or surgical stimulation. Causes hypercyanosis and worsens the RVOTO
233
Treatment of a TET spell?
Tx with o2, fluid, and esmolol or phenylephrine
234
Common anesthesia considerations for TOF?
Preop sedation
100% oxygen
Beta blockade to counter sympathetic stimulation
235
How is a complete repair for a TOF carried out?
By closing VSD and applying transannular patch at level of RVOTO
236
Where is a systemic/pulmonary shunt placed for a TOF surgery?
The subclavian artery to branch pulmonary artery
237
T/F: transposition of the great arteries is commonly associated with extra-cardiac anomalies
False
238
What cardiac changes occur in a transposition of the great arteries?
Ventriculoarterial discordance
Separate and in parallel
Aorta arises from RV
Pulmonary artery arises from LV
Some mixing occurs by PDA or VSD
239
Why is a repair needed early in transposition of the great arteries if no VSD is present?
Mixing is inadequate, the LV is only exposed to the low pressure lung
*conversely, if there is a large VSD you are at risk of pulmonary HTN d/t high flow*
240
What are common anesthesia considerations for a TGA (transposition of the great arteries)?
Arterial switch most common
Transection of arteries distal to valves
Disconnection of coronary arteries and re-anastamosis to aorta
A conduit inserted between rv and pulmonary artery if rvot is stenotic
Moderate hyperventilation with high fi02 reduces pvr…improves saturation
Pge continued
Nitroglycerin prior to cpb weaning…optimizes coronary artery flow
Blood loss…multiple suture lines…correct coagulopathy
241
What 3 heart changes are common in truncus arteriosis?
A common arterial outlet, a common valve, and a VSD
242
What is the basic blood vessel change in truncus arteriosis? Why is this of major concern?
There is a single arterial outlet (so one major vessel going to both the lungs and systemic circulation).
This creates high pulmonary flow causing pulmonary HTN
243
What syndrome is associated with truncus arteriosis?
Digeorge syndrome -> Aortic arch abnormalities, absent parathyroids (calcium issues), immune deficiency
244
Anesthesia considerations for truncus arteriosis?
Generally already intubated and on inotropes
Irradiated blood
Close watch of calcium levels
Circ arrest may be required
Nitric oxide postop
245
What heart changes are common to hypoplastic left heart syndrome?
Hypoplastic left ventricle
Mitral stenosis or atresia
Aortic stenosis or atresia
Hypoplastic aortic arch
Asd
246
How many stages is a hypoplastic left heart repaired in?
3 stages
247
What flow changes occur in hypoplastic left heart syndrome?
Pulmonary flow passive from svc/ivc…requires low pap
Children remain hypoxic (sats 80’s) -> eventually single ventricle fails and heart transplant is required
248
Why is low PAP a necessity in hypoplastic left heart syndrome?
Pulmonary flow is passive, in order to create a delta gradient high enough to get blood to the lungs the PAP must be low
249
Common anesthesia considerations for hypoplastic left heart syndrome?
Balance Pvr and svr
High pvr increases cyanosis
Pvr decreases…pulmonary overload; systemic hypoperfusion/acidosis
Caution with inotropes and changing svr
Keep PaCO2 high/normal
Keep FiO2 very low
Maintain pge infusion (to maintain patency of pda)
250
What structures make up the portal triad?
The portal vein, hepatic artery and bile duct
251
Of the direct factor Xa inhibitors, which has the shortest half life?
Edoxaban
252
Of the direct factor Xa inhibitors, which has the greatest amount of metabolism carried out by the liver?
Apixaban
253
Of the direct factor Xa inhibitors, which is not indicated for stroke prevention?
Betrixaban
254
Of the direct factor Xa inhibitors, which has little to no metabolism carried out by the liver?
Betrixaban
255
Of the direct factor Xa inhibitors, which are strong inhibitors of CYP3A4 and P-gp?
Apixaban and Rivaroxaban
256
Of the direct factor Xa inhibitors, which are indicated for post-op DVT prophylaxis and DVT/PE treatment?
Apixaban and Rivaroxaban
257
What organ primarily metabolizes Dabigatran?
Kidneys (80%) liver is the other 20%
258
What P2Y12 drugs are commonly used to manage carotid disease?
Clopidogrel and Ticagrelor
Semester 7 TxWes
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