CPB (Renal/Thermo)

Question 1

Does AKI affect outcomes after cardiac surgery?

Answer 1

Yes (occurs 5-42% after cardiac surgery); a creatinine increase of 0.3 mg/dL can increase mortality by 6%

Question 2

What part of the kidney more prone to ischemic injury?

Answer 2

The renal medulla because of its low baseline PO2 (10-20 mmHg) compared to the renal cortex (50 mmHg)

Question 3

How does CPB cause hypoperfusion to the kidney?

Answer 3

Increases renal vascular resistance via RAAS to maintain renal blood flow + non-pulsatile flow inhibits autoregulation + hemodilution decreases O2 delivery (greatest factor in AKI) + during rewarming, O2 demand increases (but supply doesn’t) + embolic occlusion + free Hbg from CPB scavenges nitric oxide causing more vasoconstriction

Question 4

Besides hypoperfusion, how else does CPB cause renal injury?

Answer 4

Oxidative stress and inflammation from contact inflammatory response (cytokines attract neutrophils and macrophages to renal parenchyma) + Toxicity via ACE inhibitors, ARBs, and aminoglycosides whih can cause renal damage (as well as contrast use before CPB and free iron producing reactive O2 species)

Question 5

What are preoperative risk factors for cardiac surgery-associated AKI?

Answer 5

Age > 70yo + Female + creatinine > 2.5 mg/dL + anemia (<9 g/dL) + EF < 35% + Use of high dose contrast agent

Question 6

What are intraoperative risk factors for cardiac surgery-associated AKI?

Answer 6

Hypotension (MAP < 65 mmHg for 5+ min) + DO2 < 272 mL/min/mm2 + prolonged CPB

Question 7

What are postoperative risk factors for cardiac surgery-associated AKI?

Answer 7

Hypotension + nephrotoxins + atheroembolism + sepsis + cardiogenic shock

Question 8

What is the Cleveland Clinic Score?

Answer 8

Risk assessment tool for AKI; looks at 10 factors (gender, CHF, LV function, IABP, COPD, IDDM, previous cardiac surgery, emergency surgery, surgery type, and preop creatinine); ranges from 0-17 points

Question 9

What is the Mehta score (STS)?

Answer 9

Risk assessment tool for AKI: looks at 10 factors (last creatinine, age, surgery type, DM, recent MI, race, chronic lung disease, previous cardiac surgery, NYHA class, cardiogenic shock); ranges from 0-83

Question 10

What is the prophylactic or therapeutic treatment for AKI after cardiac surgery?

Answer 10

There are no effective prophylactic or therapeutic treatments for AKI after cardiac surgery as of now

Question 11

What should you do preoperatively to reduce the risk of AKI after cardiac surgery?

Answer 11

Discontinue ACEi and ARBs + limit contract use + corticosteroids (no evidence though) + remote ischemic conditioning (no real evidence yet) + N-acetylcysteine (scavenges reaction O2 species, no real effect though) + statins (attenuates inflammation and oxidative stress but no benefit as of yet)

Question 12

What should you do intraoperatively to reduce the risk of AKI after cardiac surgery?

Answer 12

Leukocyte filtration + higher MAP (low-grade evidence) + vasopressors (when vasoplegic, dopamine not shown to decrease risk) + goal-directed O2 delivery (DO2 > 280 mL/min/mm2) + dexmedetomidine (not shown to work) + transfusion (no difference if restrictive or liberal)

Question 13

What should you do postoperatively to reduce the risk of AKI after cardiac surgery?

Answer 13

KDIGO bundle (optimize hemodynamics and volume status + avoid nephrotoxic agents + prevent hyperglycemia –> shown to reduce AKI in high-risk patients) + Renal replacement therapy (early use in high-risk patients)

Question 14

What are the most beneficial measures for preventing AKI after cardiac surgery?

Answer 14

KDIGO bundle and maintaining renal DO2 > 280 mL/min/mm2 during CPB

Question 15

How much does CMRO2 drop with each degree C drop?

Answer 15

6-7% decrease per 1C

Question 16

How does hypothermia provide CNS protection?

Answer 16

Preserves high-energy phosphate stores + reduces excitatory neurotransmitter release + hastens recovery of protein synthesis + diminished membrane-bound protein kinase C activity + delayed onset of depolarization + reduced formation of O2 reactive species + suppresses nitric oxide synthetase activity

Question 17

What is a Q10 concept?

Answer 17

Increase or decrease in rates or metabolic processes in relation to a temperature change of 10C; usually 2-3 (double/half or triple/third per 10C)

Question 18

What happens to the cardiac system with hypothermia?

Answer 18

HR decreases but contractility remains the same (or even increases) + dysrhythmias (PVCs, AV block, etc)

Question 19

What happens to the pulmonary system with hypothermia?

Answer 19

Progressive decrease in ventilation + dead space increases via dilation of the bronchi + gas exchange is largely unaffected

Question 20

What happens to the renal system with hypothermia?

Answer 20

Kidneys show the largest proportional decrease in blood flow of all organs; increased renal vascular resistance + impaired ability to concentrate urine + increased urine flow (from decreased tubular reabsorption) but it can be masked by increased stress-induced ADH release + glycosuria

Question 21

What happens to the hepatic system with hypothermia?

Answer 21

Decrease in metabolic and excretory function + hepatic blood flow decreases with decreased CO

Question 22

What happens to the circulatory system with hypothermia?

Answer 22

Tissue water content is increased (cellular edema) primarily due to hemodilution + decreased K + increased osmolarity + SVR and PVR increases (below 26C) due to increased blood viscosity from plasma volume loss from cellular edema + Hct increases (loss of plasma volume) + thrombocytopenia + complement activation + increased bradykinin

Question 23

What happens to the endocrine system in terms of glucose control and corticosteroids with hypothermia?

Answer 23

Hyperglycemia (decreased insulin production + increased glycogenolysis and gluconeogenesis from increased catacholamines) + corticosteroid release is supressed with long-term hypothermia below 28 but normal if short periods

Question 24

What happens to the acid-base system with hypothermia?

Answer 24

Blood pH is slightly alkaline + solubility of gas increases (at a constant CO2 content, PaCO2 decreases as temperature falls)

Question 25

What are two strategies to manage blood gases and pH during CPB?

Answer 25

Alpha stat and pH-stat

Question 26

What is alpha-stat?

Answer 26

ABG is uncorrected for actual blood temperature; therefore, as body temperatures fall, pH rises and PaCO2 decreases (CO2 becomes more soluble) -> relative respiratory alkalosis at the patients actual body temperature

Question 27

What is pH-stat?

Answer 27

Patient’s pH is maintained at a constant level by managing the pH at the patient’s temperature; it will aim for a PaCO2 of 40 and pH of 7.40 at the patient’s actual temp so if the patient is hypothermic, CO2 dissolves and PaCO2 is lower than at normal temps so sweep gas flow is reduced or CO2 is even added

Question 28

What are the benefits of alpha-stat?

Answer 28

Preserves cerebral autoregulation + prevents intracranial HTN and cerebral edema (not increases CO2) + decreases micro-embolism

Question 29

What are the disadvantages of alpha-stat?

Answer 29

Cerebral O2 consumption is decreased + Cerebral steal (if there is additional aorto-pulmonary collateral blood flow)

Question 30

What are the advantages of pH-stat?

Answer 30

Increased cerebral blood flow (added CO2) + faster cooling of the brain + counteracts the left-shift of the oxyhemoglobin dissociation curve caused by hypothermia and alkalemia

Question 31

What are the disadvantages of pH-stat?

Answer 31

Loss of cerebral auto-regulation + Increases intracranial pressures (due to cerebral vasodilation) + increased risk of cerebral microembolism + mismatch of cerebral blood flow and CMRO2

Question 32

Where can you measure core temperatures?

Answer 32

PA catheter tip + esophageal + tympanic membrane + nasopharyngeal + bladder + rectal

Question 33

How fast should you rewarm from CPB?

Answer 33

If core temperature is >/= 30C: </= 0.5C/min or a difference of </= 4C between the arterial outlet temperature and the venous inflow temperature; if core temperature is </= 30C: Can have a difference of </= 10C between arterial and venous