Perf Tech 3 Test 5 Flashcards
Hemostasis
activation- clot formation- clot lysis
- platetes form plug, CF reinforce platelets, fibrin acts as glue
- clot strength; platelets 80-90%, fibrin 10-20%
Component Measurement Tests
- PT/INR= extrinsic clotting factor (II, VII, X)
- PTT= intrinsic clotting factors (II, IX, XI, XII)
- fibrin concentration (doesn’t consider thrombin)
- platelet count
Component Interaction Tests
TEG, ROTEM, Sonoclot
TEG
Thromboelastography (TEG)- whole blood hemostasis analyzer, point of care
-cup moves, pin stays still
TEG Parameters
- R (enzymatic, CF, thrombin formation)- reaction time
- alpha (fibrinogen)- speed of fibrin accumulation (speed as it gets stronger)
- K (fibrinogen)- time until reaches fixed strength
- MA (platelets)- ultimate strength of fibrin + platelets clot
- LY30 (fibrinolysis) - rate of amplitude reduction 30 min after MA, indication of stability
TEG tracing abnormalities
- elongated R= thrombin formation issue, too much hep or low CF= give protamine or FFP
- low alpha angle= fibrinogen issue, low fibrinogen, thrombin, or platelet= give FFP or cryoprecipitate
- low MA= platelet issue, low platelet count or fibrinogen= give platelets
- high MA= hyperactive platelets= give anti platelet
TEG Assays
1) Standard= kaolin
2) Rapid TEG= tissue factor and kaolin= activates extrinsic/intrinsic pathways
3) Heparinase= runs one with heparin (normal) and one with heparinase which removes heparin
4) Platelet Mapping= tells you which pathway it inhibits
- -AA, arachidonic acid, aspirin
- -ADP, clopidogrel
- -GPIIb/IIIa inhibitor, abcixamab, tirofiban, eptifibatide
ROTEM
Rotational Elasometry (ROTEM)- cup stays still, pin turns -additional tests available
Sonoclot
- viscoelastic detection system
- provides info on enter hemostatic process (with graft and numbers)
Kidneys arutoregulation pressures
80-160 mmHg MAP
- so we loss this during bypass= less urine output
- but low GFR doesn’t mean AKI
- kidneys respond to decrease BF/volume
- decrease urine due to pain, anxiety, nausea = increase ADH independent of BV
Ways to measure Kidney function
1) blood creatinine
2) creatinine clearance
3) blod urea nitrogen: creatinine ratio
Estimated GFR (eGFR) Formulas
- better predictor of renal outcome
1) Cockroft-Gault Formula= uses serum creatinine with creatinine clearance or GFR
2) Modification of Diet in Renal Disease (MDRD)= 4 variables= serum creatinine, age, ethnicity, gender
3) Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)= use cystatin C= which is only eliminated by glomerular filtration
Operative Renal Risk Factors on
so things on bypass that have risk for renal dysfunciton
- low flow, CO, need IABP
- bypass time >180 min, SIRS
- hemodilution with HCT <21%
- embolic events
- –aoric atherosclerosis (9-17% will have dysfunction)
Pharmacological Intervention
Goal= prevent AKF that requires dialysis
1) dopamine low dose= renal dilation, lower Na reab
2) loop diuretics (furosemide)= block Cl,Na transport (lower O2 demand)
3) Osmotic Diuretics (mannitol)= flush out debris, ROS, increase renal flow. GIVE before ischemic insult
4) calcium channel antagonists
5) anti-inflmamatoy/antioxidant drugs
Operative Assessment of Renal Function
-low urine output = renal hypo perfusion (but doesn’t mean post op dysfunction)
-Oliguria- urine output less than .25-.33 ml/kg/hr
…..want to maintain proper perfusion
Neurologic Injury
decrease psychomotor speed, attention, concentration, learning, memory
-dysfunction present in 25-80% of patients
Classification
1) Transient Ischemic Attack (TIA)- localized, rapid onset/recovery, no permanent damage
- causes= atherosclerosis, A-fib, thrombi, emboli, plaque
2) Reversible Ischemic neurologic Defect (RIND)- similar to TIA but 24-72 hours with full recovery
3) Lacunar Brain Infarct= specific cerebral artery occlusion, deep in brain, doesn’t resolve, aka stroke
4) Global Ischemia= long periods of hypo perfusion or massive emboli, poor recovery >50% die
Pre-Op Risk Factors
- AGE <60 yo 1% >70 yo 4-8%
- ATHEROSCLEROSIS
- HTN 55%, DM 25%= both change auto regulation, collateral BF and decrease ischemic tolerance
- previous incident (13% of heart patients have TIA history)
- carotid stenosis=
- genetic APOE4, arrhythmias
Surgical Stress that causes Brain Ischemia
1) Hypo perfusion= vascular disease, low MAP
2) emboli= on pump #1 cause brain injury during cardiac surgery, plaques, clots, GME, filling the heart
3) inflammation= due to impact vascular lining= thrombosis, tone, fluid transport, inflammation
- activates WBC/platelets
- 26-50% post op delirium
Cerebral Metabolic Requirement for O2 (CMRO2)
- 3 ml/100 mg of brain tissue/min
- brain regulates BF by O2 demand
Cerebral Blood Flow
55-60 ml/100g/min
-influenced by CMRO2, PaCO2, HCT, MAP
Utilization of total resting O2
20%
- also 20% of CO
- brain weighs 1400g
CBP and Cerebral Perfusion
1) Temperature- 10 degrees lower= 50% metabolic rate decrease
- below 23 degrees, flow/metabolism disconnect
2) MAP= autoregulation of CBF at 50-150 mmHg
3) CO2= changes in PaCO2 change CBF independent of O2 demand = auto regulation with alpha stat
4) HCT= hemodilution decreases viscosity/resistance and increase CBF
Interventions to Decrease Neurological Morbidity
- watch aorta, do carotid study, less aortic manipulation
- flood chest with CO2, watch decannulation, use TEE
- pharm to lower O2 demand (thiopental/propofol)
- CO2 flush, filters, ACT
- slow rewarm
- alpha stat= preserves CBF auto regulation and decrease cerebral emboli
