Goljan High Yield Cell Injury EC Flashcards
PO2
driving force for diffusion of O2 into tissue
SaO2
percent heme groups occupied by O2
Cyanosis
decreased O2 saturation (SaO2)
O2 content
1.34HbSaO2 + PaO2
Oxygen
electron acceptor in oxidative pathway
Hypoxia
inadequate O2 leads to ATP depletion
Ischemia
Decreased blood flow
Respiratory acidosis
retention of CO2 always decreases PaO2
Ventilation defect
impaired delivery of O2 to alveoli
Intrapulmonary shunting of blood (ie RDS)
Perfusion defect
absent blood flow to alveoli
Increased alveolar dead space (ie PE)
Methemoglobin
Decreased SaO2
Heme Fe +3
Oxidizing agents (sulfur/nitro drugs) cause
Treat with IV methylene blue
Clinical methemoglobinemia
Cyanosis not corrected by O2
Chocolate colored blood
Carbon monoxide
Decreased SaO2
Left-Shifted OBC
inhibits cytochrome oxidase
Causes carbon monoxide poisoning
Car exhaust
Space heaters
Smoke inhalation
S/S carbon monoxide poisoning
Headache (#1 sign)
Cherry red color of skin (masks cyanosis)
Cyanide
inhibits cytochrome oxidase
Systemic asphyxiant
Carbon monoxide + cyanide poisoning
House fire
Left shifted O2 curve
decreased 23-BPG, CO, alkalosis, HbF, methemoglobinemia, hypothermia
Right shifted O2 curve
increased 23-BPG, high altitude, acidosis, fever
High altitude
respiratory alkalosis enhances glycolysis
Increased synthesis of 23-BPG
Mitochondrial poisons
damages membrane and drains off protons
Alcohol and salicylates
Uncoupling agents in mitochondria
drain off protons
Dinitrophenol, thermogenin (brown fat)
Complication of mitochondrial poisons/uncoupling agents
Hyperthermia
Decreased ATP
Impaired Na/K ATPase pump (cellular swelling)
Reversible