Final Exam

gas
collection of molecules which move about freely
ideal gas model
model of matter in which the molecules are treated as non-interacting point particles which are engaged in a random motion that obeys conservation of energy.
standard temperature and pressure
22.4 liters of most gases at standard temperature and pressure will contain very nearly 6.022 ? 10^23 molecules (one mole).
gas laws
empirical laws that describe the relationship between thermodynamic temperature, absolute pressure and volume of gases.
Boyle’s law
inversely proportional relationship between the absolute pressure and volume of a gas, if the temperature is kept constant within a closed system.
Charle’s law
proportional relationship between temperature and the volume of a gas at constant pressure
Dalton’s law
the total pressure exerted by a gaseous mixture is equal to the sum of the partial pressures of each individual component in a gas mixture.
Henry’s Law
At a constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid.
Methemoglobin
Normal hemoglobin can have its Fe2+ oxidized to Fe3+ by a variety of drugs and chemicals including nitrites, sulfonamides, acetanilide
methemoglobin reductase
responsible for converting methemoglobin back to hemoglobin A
Normal percentage of methemoglobin
1-2%
O2 Capacity
The maximum amount of O2 which can be combined with hemoglobin
Oxygen saturation
measures the percentage of hemoglobin binding sites in the bloodstream occupied by oxygen
O2 Saturation of Hemoglobin equation
(O2 combined with Hb/O2 capacity) x 100
The oxygen dissociation curve
plots the proportion of hemoglobin in its saturated form on the vertical axis against the prevailing oxygen tension on the horizontal axis.
Bohr Effect
Changes associated with pCO2
Haldane effect
Deoxygenation of the blood increases its ability to carry carbon dioxide
Right shift
increase in temperature, 2,3-DPG, pCO2, and decrease in pCO, pH
Left Shift
increase in pCO, and pH decrease in temperature, 2,3-DPG, and pCO2
P50
The partial pressure of oxygen (pO2)at which the hemoglobin is 50% saturated, typically about 27 mmHg for a healthy person
increased P50
rightward shift of the standard curve
decreased p50
Left shift
What is responsible for elimination of CO2
alveolar ventilation
In acid-base balance, the kidney is responsible for 2 major activities
Reabsorption of filtered bicarbonate:
Excretion of the fixed acids
Henderson-Hasselbalch Equation
pH =pKa + log (A-/HA)
Acidosis
an abnormal process or condition which would lower arterial pH if there were no secondary change in response to the primary etiological factor
Alkalosis
an abnormal process or condition which would raise arterial pH if there were no secondary changes in response to the primary etiological factor
Simple (Acid-Base) disorders
are those in which there is a single primary etiological acid-base disorder
Mixed (Acid-Base) disorders
are those in which two or more primary etiological disorders are present simultaneously
Acidemia
arterial pH < 7.36
Alkalaemia
arterial pH > 7.44
Metabolic Acidosis etiology
uncontrolled diabetes (accumulation of ketoacids), lactic acid accumulation (exercise, poor perfusion, systemic infections), renal tubular acidosis (kidnets can’t execute H+/Na+ exchange), liver disease (impaired urea/ammonia formation), salicylate intoxication (hyperventiliation, loss of bicarbonate), poisonings (converted to acid), or ingestion of carbonic anhydrase inhibitors
Metabolic Acidosis Compensation methods
retention of HCO3, hyperventilation, or kidnye excretes organic acids and exchanges H+ for Na+, more acid urine
Metabolic Acidosis Laboratory findings
Decreased pH
Decreased HCO3
Initial pCO2 normal but will become decreased as compensating mechanisms are invoked
Negative base excess
In lactic acidosis there may be ^anion gap, ^K+, ^lactate,
Poisoning, i.e., drugs, methanol etc. there may be ^anion gap
Respiratory Acidosis
Based deficit disorder resulting from a decreased HCO3/H2CO3 ratio resulting from an increase in carbonic acid
Respiratory Acidosis etiology
disorders that interfere with the ability of the lungs to expel CO2: COPD, depression of the respiratory centers (drugs), respiratory distress syndrome (premies or adults in shock)
Respiratory Acidosis Compensation methods
hyperventilation to eliminate CO2, retain Na+ and HCO3 with increased acid excretion
Respiratory Acidosis Laboratory findings
Decreased pH
Increased pCO2
Initially a normal HCO3 which becomes increased as compensatory mechanisms are employed
Normal base excess
Coexisting metabolic lactic acidosis may exist due to tissue hypoxia
Metabolic Alkalosis
base excess, high pH, increase in bicarb with no change in carbonic acid
Metabolic Alkalosis Etiology
increased concentration of HCO3: Excessive intake of NaHCO3 (gastric disease, tums), loss of chloride (vomiting)
Respiratory Alkalosis
Disorder associated with a decrease in carbonic acid concentration usually resulting from over stimulation of the respiratory system.
Respiratory Alkalosis Etiology
hyperventilation, salicylate intoxification, impairment of CNS, aggressive mechanical ventilation
Respiratory Alkalosis Compensation methods
increased excretion of bicarbonate, slow respiration
Respiratory Alkalosis laboratory findings
Increased HCO3/H2CO3 ratio
Increased pH
Initially a decreased pCO2 but may increase as compensation is initiated
Initially normal with decreased concentrations as renal compensation is initiated
Decreased base excess
Alkaline urine with titratable HCO3
6 steps of systemic acid-base evaluation
(1) pH (2) pattern (3) clues (4) compensation (5) formulation (6) confirmation
pH in evaluation of acid-base disorder
arterial pH, acidaemia = acidosis, alkalaemia = alkalosis, normal = no disorder or compensation
pattern in evaluation of acid-base disorder
suggestive pattern in pCO2 and [HCO3, if both are low = metabolic acidosis or respiratory alkalosis, if both are high = metabolic alkalosis or respiratory acidosis, if they are opposite = mixed disorder
clues in evaluation of acid-base disorder
high anion gap = metabolic acidosis, hyperglycaemia = diabetic ketoacidosis, hypokalaemia/chloraemia = metabolic alkalosis
compensation in evaluation of acid-base disorder
if expectal and actual match = not mixed
if they don’t match = mixed
formulation in evaluation of acid-base disorder
consider everything together
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