Exam 4: Key Terms & Objectives Flashcards
predictors of coagulopathy in trauma patients
factors include age, injury severity score, systolic blood pressure, PRBC, pH, and temperature.
o ISS >25 = 70% coagulopathy
o SBP <34°C = 59% coagulopathy
carotid endarterectomy—-mortality rate for GA vs RA
about the same: GA = 4.8%, RA = 4.5%
hypothermia- physiological alterations
- depressed myocardial function/dysrhythmias
- increased hgb-oxygen affinity
- decreased hepatic metabolism of citrate (leads to citrate toxicity)
- increased wound infections/postop infections
- inhibition of platelet function/coagulation cascade ((hypothermia does NOT decrease clotting factor levels Fibrinolysis is stimulated when patient is hypothermic.))
aortic dissection- pathophysiology
splitting of the intima from the adventitia along the length of the vessel.
o Type A—proximal dissection involving the ascending aorta. 2/3 of dissections. High risk of extrusion into coronary and arch vessels
o Type B—distal dissection confined to thoracic and abdominal aorta. 1/3 of dissections.
causes of heat loss under anesthesia
- Altered responses to heat loss due to anesthesia (e.g. lack of shivering)
- environment exposure
- Cooling effect of anesthetic gases and intravenous fluids
- Reduced heat production due to reduced metabolic activity
aortic surgery, hypotension after cross clamp
Cross-clamping—increases afterload above the clamp (HTN), and causes hypotension below the clamp (buildup of anaerobic metaolites so when the clamp is released pt will get hypotensive everywhere—have volume load ready and uppers).
gastric contents, pH and pulmonary injury
lower the pH, greater chance of injury upon aspiration.
ALL trauma patients treated as FULL stomach
appropriate uses of sux in trauma pts
succinylcholine is the RSI relaxant of choice. It can still be used safely in open eye injuries, increased ICP pts (risk/benefit ratio), BURNS, spinal cord injury, massive trauma, crush injury→ do no use 24 hours after injury (not even 6-8 hours after injury) because of the risk of hyperkalemia.
hypertensive crisis
severe elevation in BP. Usually results from an acute hemodynamic event superimposed on a chronic hypertensive patient. Requires immediate treatment to decrease BP.
EFFECTS OF HYPERTENSIVE CRISIS—hypertensive crisis may cause:
o Hypertensive encephalopathy—headache, blurred vision, mental changes
o Papilledema—swelling of the optic disc due to increased ICP.
o Angina—due to increased afterload→ LVH→ increased oxygen demand.
stages of htn
- Prehypertension (120-139/80-89)→ lifestyle modifications (diet, exercise, decrease Na+ intake).
- Stage 1 HTN (140-159/90-99)→ usually 1 drug
- Stage 2 HTN (>160/>100)→ combination drug therapy
body temp and MAC value
HYPOthermia – decreases MAC
HYPERthermia – increases MAC
Think metabolism
glascow coma scale
neurological scale that is a way of recording the conscious state of a person for initial as well as subsequent assessment. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and 15.
< 8 = pt gets a tube
coagulopathy with massive transfusions
massive transfusion leads to clotting factor deficiencies, which lead to progressive systemic coagulopathy, which then lead to more blood loss.
• Trauma treatment of coagulopathy = correct hypoperfusion, shock and hypothermia; “shotgun” approach = give everything (CF, FFP, plts, cryo, ect).
pulmonary vascular resistance – definition and calculation
The resistance offered by the vasculature of the lungs.
Pulmonary Vascular Resistance = ( 80 * (PAP - LAP) / C.O )
drugs affecting LES tone
LES = lower esophageal sphincter
Decrease = benzos, gases Increase = Reglan*, Neostigmine, Succ
