Chapter 10 Gravelee - Myocardial Protection , CH 15 324-35 WBCs Flashcards
Anesthetic Agents - do what?
provide some degree of cardioprotection.
Ameliorate deleterious effects of reactive oxygen species on myocardium during ischemia reperfusion
EX Isoflurane
Anesthetic Agents do what for preconditioning ?
↑ preconditioning
Acute normovolemic hemodilution how does it enhance myocardial protection?
- avoids blood transfusion to patient
- **-↓A fib and conduction block ***
- Less myocardial injury, CK-MB release and decreased inotrope requirement.
CK-MB
shows levels of of CK released from damaged myocardial muscle
Acute normovolemic hemodilution cons?
Some patients are too anemic from this
Efficacy not always proven
Neutrophil depletion, how does it enhance myocardial protection?
↓ V fib – post bypass
Lower inotrope use and lower postop cardiac enzyme release
How does Neutrophil deletion work?
Neutrophils are released during CPB, and then cause tissue injury by the release of enzymes, reactive oxygen species and other toxic substances
Use Neutrophil filtration
Erythropoietin how does it enhance myocardial protection?
↓ myocardial injury
How does Erythropoietin work?
- its a noncardioplegia medication
- it is the primary growth factor that controls the precursor to RBC production. Commonly used in pts with depressed bone marrow or depressed erythropoietin production
- ALSO has antiapoptic effects
- it protects myocytes from hypoxia and oxidative stress
Myocytes
are long, tubular cells that develop from myoblasts to form muscles in a process known as myogenesis. There are various specialized forms of myocytes: cardiac, skeletal, and smooth muscle cells, with various properties.
N-acetylcysteine how does it enhance myocardial protection?
**↓ oxidative stress **
How does N-acetylcysteine work?
- Noncardioplegia medication
- A reactive oxygen species scavenger
Reactive Oxygen Species
chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.[1] However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[1] This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress
Deferoxamine how does it enhance myocardial protection?
↓lipid peroxidation *******
Increase LVEF
Decreased postop wall motion abnormalities
Statins how does it enhance myocardial protection?
**↑NO release **
Anti-inflammatory properties
Antioxidative properties
Decreased monocytes adhesion
How does Deferoxamine work?
- Noncardioplegia medication
- it is an iron chelator that reduces myocardial injury by reducing the amount of hydroxyl radical formation by iron catalyzed Fenton reactions (aka reduces amount of iron)
What are statins?
Statins are a class of drugs used to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver, which produces about 70 percent of total cholesterol in the body. Also increase NO release
Ischemic preconditioning
an initial sublethal ischemic injury conveys protection against subsequent ischemic insults
Having to do with adenosine receptor , multiple kinase and alterations in the Katp channels
(bc ATP repletion following brief episodes of ischemia occurs slowly)
Fibrillatory Arrest
relies in principle of ischemic preconditioning bc the protective events of short intervals of ischemia have been related to adenosine receptor, multi kinase and alterations in Katp channel.
Fib Arrest Cons
Repeated aortic clamping
Anastomotic time limited
Perfusion-assisted direct coronary artery bypass (PADCAB)
This is used during OFF PUMP cases.
directly perfuses myocardium supplied by a bypassed coronary artery by providing a controlled flow down the conduit.
Inflow to the circuit and pump is provided by a catheter placed in the ascending aorta or femoral artery. Use of MPS - a computer controlled blood delivery system, allows for exact control of coronary perfusion pressure.
This pressure is independent of systemic pressure bc body is taking care of that
Selectin Family
transmembrane molecules expressed on the surface of leukocytes and activated endothelial cells.
The initial attachment of leukocytes from the blood stream during inflammation is afforded by the selectin family and causes slowing of downstream move until a complete stop of leukocytes along endothelium.
Members in Selectin Family -
P, E and L-selectin
P-selectin does what?
released by exocytosis within minutes of activation of agents such as histamine/thrombin ect.
Largely responsible for the rolling phase of leukocyte adhesion cascade.
Neutrophil activation during CPB how?
through interaction with activated vascular endothelium, shown through loss of L-selectin
