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55 Cards in this Set
- Front
- Back
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What are the benefits of LMWH compared to unfractionated heparin?
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1. dose independent clearance,
2. longer half-life, 3. better bioavailability, 4. HIT occurs less |
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What are guidelines on the use of LMWHs with neuraxial anesthesia?
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1. the smallest effective dose of LMWH should be given periop,
2. Therapy should be delayed as long as possible - min of 12 and 24hrs 3. remove indwelling catheters 10-12 hours following last dose of LMWH, as opposed to 6-8 hrs after last dose of heparin |
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What is the most frequent cause of death of patients undergoing major vascular surgery?
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MI (eval for CHF, unstable angina)
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What preop testing should be done on all AAA patients?
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EKG, BUN, Creatinine, electrolytes, could also argue for a CXR, if has COPD do abgs
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How do high abdominal incisions affect pulmonary function?
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1. increase work of breathing,
2. decrease FRC, 3. cause hypoxia |
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Why should you consider not to extubate a patient after an open AAA repair?
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1. high abdominal incision,
2. use of moderate to large doses of narcotics, 3. large fluid shifts |
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What increases the risk of renal failure during open AAA repair?
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1. contrast before surgery,
2. intraop hemorrhage or hypotension, 3. cross clamping whether above or below the renal arteries |
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What are the main causes of renal dysfunction in patients with a AAA?
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atherosclerotic vascular disease and HTN
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How does infrarenal aortic cross clamping affect renal blood flow?
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decreases renal blood flow
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What is the general risk of operative mortality in patients undergoing open AAA?
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4-8%
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What symptoms do you need to avoid with premedication in patients with a AAA?
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tachycardia and hypertension, small dose of benzo often adequate
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What invasive monitors should you consider during an open AAA repair?
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A-line, PAC (detect LV failure during cross clamping)
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What are maintainance agents of choice for GA during open AAA repair?
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N2O, isoflurane, narcotics
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What is a good induction technique during open AAA repair?
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high dose narcotics (fentanyl 7-10mcg/kg), low dose thiopental with vec/roc
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What is a good predictor of LV failure during cross clamping for an open AAA surgery?
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increased PCWP
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What is a good medication to prevent large increases in SVR following cross clamping? What does it do?
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nitroglycerin (0.2mcg/kg/min); decreases preload, it also increases coronary blood flow
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Why would you use SNP versus nitroglycerin in decreases blood pressure during AAA repair when the cross clamp is already in place?r
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faster onset of action
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What should you base extubation on at the conclusion of open AAA repair?
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1. length of surgery,
2. preop pulmonary fxn, 3. age, 4. amount of blood transfused, 5. temperature at end of surgery |
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Why would you use dextran or promit during open AAA repair?
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dextran: decreases thromboembolic events by:
1. decreasing blood viscosity, 2. diluting clotting factors, 3. inhibiting platelet aggregation; promit: same as dextran but lower incidence of anaphylactic rxns - binds to antibodies but does not lead to immune complex formation and anaphylaxis |
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What reactions can occur with use of dextrans?
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allergic reactions: hypotension, shock, cardiac arrest
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What are indications for CEA?
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1. acute carotid occlusion,
2. fluctuating neurological deficits, 3. TIA's: deficit>24hr and assoc stenosis(>70%) or ulcerated plaque |
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What stimulates the carotid or aortic bodies?
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decreased PaO2, increased PaCO2
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What has a larger response when stimulated, the aortic or carotid bodies?
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carotid
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Where are the chemoreceptors located that mediate the hyperventilation produced by increases in PaCO2
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medullary chemoreceptors in the medulla oblongata
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How can you monitor for cerebral ischemia in patients undergoing CEA?
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1. keep them awake with superficial and deep cervical plexus block,
2. EEG - only monitors the cortex not the deeper structures |
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If cerebral ischemia develops during a CEA what should you do?
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1. release carotid clamp,
2. shunt placed, 3. BP and oxygenation maximized |
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What is the mortality from CEA and what are the causes?
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4%: stroke, myocardial ischemia/infarction, CHF
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How can a defecit be reversed that is from an embolization from plaque, air, or thrombus after CEA surgery?
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surgical reexploration within 12 hours
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Why are patient's prone to HTN after CEA?
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Denervation of carotid sinus nerves and baroreceptor reflexes may result in HTN
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What can happen if the carotid body is injured during CEA?
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reduced respiratory response to hypoxia
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How is the ventilatory response to hypoxia and CO2 altered after CEA?
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ventilatory response to hypoxia is lost; response to CO2 is attenuated(chronic elevation of CO2)
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How do you do a deep cervical plexus block?
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deposit 3-4mL 0.5% marcaine at the transverse process of C2-4 or deposit 20mL at one of these locations
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how is the superficial cervical plexus block done?
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subcutaneous injection in the area of incision and dissection
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After a cervical plexus block what should you do if horner's syndrome develops?
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injection is superficial to the deep cervical plexus; redo the injection
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what are complications of cervical plexus block?
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phrenic nerve palsy, vertebral artery injection
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Risk of AAA rupture based on size.
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5 cm = 10% per year
>= 7 cm = 40% per year |
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Where are carotid and aortic bodies located? What do they respond to?
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Carotid bodies - near the carotid bifurcation
Aortic bodies - near the aortic arch They respond to decreased PaO2 or increased PaCO2. |
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What happens in humans in whom both carotid bodies have been removed.
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1. Little change in ventilation at rest
2. Ventilatory response to hypoxia is lost 3. 30% reduction in Ventilatory response to carbon dioxide |
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2 hypotheses proposed about mechanism of hypotension post cross clamp release.
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1. Myocardial depression caused by washout of acid, acid metabolites, and vasoactive substances from ischemic extremity.
2. Relative volume depletion |
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If hypotension occurs for greater than 4 min post cross clamp despite adequate fluid replacement, what should you do?
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Seek other causes such as:
1. Hidden bleeding 2. Misjudged replacement of blood deficits 3. Allergic reaction to graft material 4. myocardial depression sec to ischemia or citrate toxicity |
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Most important temporizing tx if severe hypotension post cross clamp release
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Reclamp the aorta
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Overall mortality rate of dissecting aortic aneurysm. What is the most important determinant?
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15-90%, time of onset of symptoms to control of bleeding the key to outcome
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Prep for pt with a ruptured aortic aneurysm. What are BP goals?
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1. Placement of at least 1 large bore IV
2. Blood sample to determine hct, blood type, amd cross matching of 10-12 units of blood 3. Request 5 units of type specific or type O neg be sent immediately to the OR 4. Infusion of sufficient crystalloid to achieve a BP of 80-100 (BP higher than this can overcome retro peritoneal tamponade of the rupture site 5. Place Aline if circumstances permit |
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How is pt prepped and draped with a ruptured aortic aneurysm?
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Abdomen is prepped and draped while pt is still awake Bc induction of anesthesia and muscle paralysis results in loss of abdominal tone and may promote hemorrhage by releasing tamponade. Anesthesia is induced with surgeon standing by and ready to proceed.
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induction of ruptured AAA
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Induction with fentanyl or sufentanil
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Fluid management during CEA
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Admin of more than about 10 cc/kg of crystalloid or other fluids in the typically 2 hr procedure is not recommended Bc it may contribute to postop htn and myocardial ischemia
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What do the carotid bodies do as PO2 drops below 60? What do they activate?
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They activate the medullary respiratory center via CN IX causing minute ventilation to increase
- magnitude of this increase remains small until PO2 drops to <40 with a consequent inc in MV of 50-60% - this is considerable smaller than the up to 10 fold inc in MV caused by changes in PCO2. |
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Explain Ventilatory drive in COPD pts.
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The carotid body response is clinically significant in COPDers bc they can lose their hypercapnic Ventilatory drive over time. Consequently when these pts receive supplemental O2, the absence of hypoxia eliminates their only remaining drive to breathe and apnea can result.
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What can happen suddenly during CEA? Why does this happen?
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Bradycardia can occur when the surgeon stretches the baroreceptor nerve directly
- nerve endings are super sensitive since they usually have not been stretched by BP changes for many years due to atherosclerosis |
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How can bradycardia during CEA be prevented?
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By injection of 1% lidocaine in the area of the bifurcation 10-15 min before the carotid artery is occluded
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What can happen during carotid artery occlusion?
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Decreased pressure within the isolated portion can initiate sympathetic NS via the carotid sinus resulting in tachycardia and hypertension
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What EEG finding correlates with postop neurological defects?
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Intraop ischemic EEG changes for >10 min
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Evidence suggests that most strokes from CEAs are...
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Embolic and not related to cross clamping
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Chief function of carotid bodies.
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As a peripheral chemoreceptor for changes in blood O2 and CO2 tension
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What else do carotid bodies serve as peripheral receptors for?
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Indirectly for BP
- as MAP drops below 80, the ordinarily high perfusion and flow to the carotid bodies drops, resulting in the development of an A-V O2 content gradient - carotid bodies perceive this as a drop in Po2 amd signal medullary respiratory and vasomotor centers to increase MV and BP. |
