505 Exam 1

embolus

a blood clot, air bubble, piece of fatty deposit, or other object which has been carried in the bloodstream to lodge in a vessel

3-500 microns

emboli with greatest tendency to obstruct microcirculation

pulmonary embolism, myocardial infarction, stroke

most common pathologies caused by emboli

stroke

most common pathology caused by emboli on CPB

30%

about what percent of patients on CPB suffer a stroke

1-5%

what percent of CPB strokes are clinically obvious

foreign material, gaseous, bloodborne biologic

three sources of emboli

bloodborne biologic

most common source of emboli

manufacturing or circuit assembly, operative field, spallation

where do foreign material emboli come from

gross gaseous, gaseous microemboli

two types of gaseous emboli

potential sources of gross gaseous emboli

Inattentive perfusionist may drain venous reservoir and introduce air to patient, Air introduced to aortic root from cardioplegia system, Reversal of flow through vents into the left ventricular or aortic vent, Atrial septal defects (ASD) or ventricular septal defects (VSD), Cavitation, Closed circuits which lack a venous or cardiotomy reservoir have less air handling capability, Inadequate de-airing of the heart prior to cross clamp removal, Cardiotomy suction (consists of mostly nitrogen-->CO2 field flush)

potential sources of gaseous microemboli

extracorporeal circuit and oxygenator, poor de-airing techniques, low reservoir volumes

persistent GME

GME that adheres to quiescent areas of the oxygenator/reservoir/filters, Can be sent to patient upon initiation or sudden movement to circuit

inattentive perfusionist

the most common cause of a gaseous embolus

bubble oxygenators

Common source for gaseous microemboli

physical damage, elevated transmembrane pressure ratios

Common reasons for air formation in a membrane oxygenator

elevated transmembrane pressure ratios

occurs when pressure on gas side is higher than pressure on blood side

sweep too high, failure to maintain positive pressure on blood side

reasons for elevated transmembrane pressure ratios

indirect

relationship between temperature and solubility of gas in blood

10-17 C

gradient between heat exchanger and venous blood that should not be exceeded

Microthrombi from fibrin formation, Lipid emboli, Platelet aggregates, RBC aggregates

Autologous aggregates of cell products forming bloodborne biologic emboli

fibrin formation

Inadequately anticoagulated blood contacts a foreign surface

heparin

Blocks coagulation cascade by binding to antithrombin III (ATIII) and inhibiting formation of thrombin

cardiotomy suction

most common source of lipid emboli

cerebral embolism

lipid emboli usually results in

fat embolism syndrome

where fat emboli are released from the disruption of fat cells, enter through capillaries of site of trauma and travel to capillaries of organ tissues where they obstruct blood flow

duration of CPB

embolic load is proportional to

30-50%

percent of platelet count drop due to platelet activation early on in CPB

thrombocytopenia

consumption of activated platelets on CPB leads to

platelet aggregates

why do we need to filter packed red blood cells (PRBC’s) and stored platelet concentrates

cold agglutinin disease

Antibodies the normally attack bacteria, usually Immunoglobulin M (IgM) class, attach themselves to RBC’s when blood reaches temperature threshold

arterial line, cardiotomy, venous return, pre-bypass

circuit filters

filters, adequate heparinization, CPB circuit coatings, acid/base management, chemical defoaming agents, CO2 field or circuit flush

embolic event mitigation

alpha stat

thought to reduce embolic load to cerebral tissues by managing PaCO2

polyurethane foam

most common chemical defoaming agent

20x more soluble

CO2 solubility versus O2

2x more soluble

O2 solubility versus N2

direct visualization, doppler ultrasound

intra-operative emboli detection

CT/MRI, histologic exams

post-operative emboli detection

counts and accumulation

Morbidity and mortality commonly linked to GME is related to

greater than 35-40 microns

GME size associated with increased morbidity

10-70 microns

Small capillary and arteriolar dilations (SCADS) range

GME <35 microns

present in arterial return lines, despite arterial line filtration

19-38%

what percent of patients experience “mild, moderate, or severe deterioration” in post CPB neurologic testing

50-70%

what percent of ECC patients exhibit cognitive deficits 1 week after CPB

30%

what percent of patients exhibit long term neuropsychologic dysfunction after CPB

stealth perfusion

minimal extracorporeal circuitry

less than or equal to 6 C

best practice rewarming gradient to reduce GME

less than or equal to 10 C

best practice cooling gradient to reduce GME

MAP 60-90 mmHg

best practice for maintaining cerebral blood flow on CPB

pressure, temperature, volume

gas characteristics are governed by

Boyle’s Law

pressure of a gas is inversely proportional to the volume it occupies

P1V1 = P2V2

Boyle’s Law

V1/T1 = V2/T2

Charles’ Law

P1/T1 = P2/T2

Gay Lussac’s Law

P = P1 + P2 + P3 + P4

Dalton’s Law

Henry’s Law

amount of dissolved gas in a liquid is proportional to the partial pressure above the liquid

4

how many O2 binding sites per Hb molecule

methemoglobin

changes heme iron configuration, O2 does not bind

fetal hemoglobin

two gamma not two beta chains, increases O2 affinity

SaO2 x Hb x 1.37

bound oxygen content equation

PaO2 x 0.003

dissolved oxygen content

(SaO2 x Hb x 1.37) + (PaO2 x 0.003)

CaO2 =

Q x CaO2

DO2 =

Q x (CaO2 - CvO2)

VO2 =

CO = VO2/(CaO2 - CvO2)

Fick equation

tissue mass, patient age, temperature, muscle activity, distribution of blood flow, dead tissue

variables affecting VO2

indirect

relationship of volume of gas and pressure exerted on it (at constant temperature)

direct

relationship between temperature and volume

surfactants

substances with molecules with hydrophobic and hydrophilic parts

7.35-7.45

normal blood pH

bases

proton acceptors

bicarbonate, biphosphate

physiological bases

acids

proton donors

carbonic acid, phosphoric acid, pyruvic acid, lactic acid

physiologic acids

chemical buffers, respiratory regulation, renal regulation

pH range maintained by

pCO2

how is pH range controlled through respiratory regulation

excretion and reabsorption

how is pH range controlled by renal regulation

CO2

byproduct of aerobic respiration

C6H12O6 + 6O2 -> 6CO2 + 6H2O + energy (38 ATP molecules and heat)

aerobic respiration equation

glycolysis, fermentation

anaerobic respiration stages

2 ATP, lactic acid

products of anaerobic glycolysis

cytoplasm

location of anaerobic glycolysis

cytoplasm and mitochondria

location of aerobic glycolysis

glycolysis, fermentation

stages of anaerobic glycolysis

glycolysis, link reaction, krebs cycle, electron transport chain

stages of aerobic glycolysis

acidosis

relative increase in H+, relative decrease in HCO3-

alkalosis

relative decrease in H+, relative increase in HCO3-

35-45 mmHg

arterial blood gas pCO2

75-100 mmHg

arterial blood gas pO2

22-26 mEq/L

arterial blood gas HCO3-

-2 to 2 mEq/L

arterial blood gas base excess/base deficit

greater than 95%

arterial blood gas O2 sat

lowers

high pCO2 impact on pH

raises

low pCO2 impact on pH

raises

high bicarb impact on pH

lowers

low bicarb impact on pH

respiratory acidosis

high pCO2, low pH, normal bicarb

respiratory alkalosis

low pCO2, high pH, normal bicarb

metabolic acidosis

low bicarb, low pH, normal pCO2