Blood Gases Flashcards
List body buffer systems (and which one is the most important)
- Bicarb (most important)
- Proteins
- Phosphates
When is body acid-base at equilibrium?
pH = pKa
Equal conc of protonated and unprotonated spp. for given buffer system
CO2 transport
CO2 + H2O -> H2CO3 -> HCO3 + O2 + H cation -> HHb venous
Two main kidney functions
- Reabsorb bicarb from glomerular filtrate in proximal tubule
- Kidneys also excrete H+ for buffering capacity
How does increased plasma pH correlate with Na-H exchange and HCO3 reabsorption?
Both decreased Na-H exchange and HCO3 reabsorption
How does decreased plasma pH correlate with Na-H exchange and HCO3 absorption?
Both increased Na-H exchange and HCO3 reabsorption
Normal HCO3 to H2CO3 ratio and pH?
20:1 and pH = 7.0
Respiratory component of acid-base homeostasis
dissolved CO2 (dCO2) expelled by lungs
Metabolic component of acid-base homeostasis
How kidneys control bicarb conc by reabsorption or depletion
Reference range for pH
7.35-7.45
How does body compensate for metabolic acidosis?
Hyperventilation because the body compensates by altering the factor not associated with the primary process
Primary respiratory acidosis/alkalosis
Respiratory dysfunction caused by change in pCO2
Metabolic acidosis/alkalosis
Renal/metabolic dysfunction caused by change in bicarb level
Compensation
- Response to maintain acid-base homeostasis
- Accomplished by organ not associated with primary process
Fully compensated
pH returned to normal range and bicarb: carbonic acid is approaching 20:1
Partially compensated
pH approaching normal
Uncompensated
pH abnormal and body has not started compensating for acid-base imbalance
Causes of metabolic acidosis
- Overdose of acid-producers (aspirin, ethanol, methanol, ethylene glycol)
- Reduced excretion of H+ (renal tubular acidosis)
- Excessive loss of bicarb from diarrhea (hyperchloremic acidosis)
Causes of respiratory acidosis
- Hypoventilation -> reduced CO2 expelled from lungs -> increased pCO2 (hypercarbia/hypercapnia)
- Airway obstruction (COPD)
- Drug overdose that leads to hypoventilation and increases pCO2 in blood
- Decreased cardiac output (congestive heart failure) -> less blood presented to lungs and therefore higher pCO2
Causes of metabolic alkalosis
- Excessive loss of stomach acid through vomiting or nasogastric suctioning
- Prolonged use of diuretics -> increased H+ renal excretion
- Excess admin of sodium bicarb or excess ingestion of antacids
- Hypokalemia causes H+ to shift intracellularly -> increased bicarb reabsorption in the kidneys
Causes of respiratory alkalosis
- High altitudes decrease pCO2 -> hyperventilation
- Anxiety -> hyperventilation
- Aspirin overdose stimulates hyperpnea
- Pulmonary embolism or pulmonary fibrosis impair oxygen exchange
List primary and compensatory responses to metabolic acidosis
Primary
- Increased H+
- Decreased pH
- Decreased bicarb
Compensatory
Decreased PCO2 due to hyperventilation
List primary and compensatory responses to metabolic alkalosis
Primary
- Decreased H+
- Increased pH
- Increased bicarb
Compensatory
Increased PCO2 due to hypoventilation
Disturbances in which 7 conditions can result in hypoxia and poor tissue oxygenation?
- Binding of Hgb
- Available atmospheric oxygen
- Adequate ventilation
- Gas exchange btwn lungs and arterial blood
- Enough Hgb amt
- Adequate blood flow to tissues
- Ability of oxygen to release to tissues
How is a patient’s oxygen status evaluated?
Measure pO2, pH, and pCO2 in routine blood gas analysis
Percentages of oxygen, CO2, and N2 in air
- O2 = 21%
- CO2 = 0.3%
- N2 = 78%
How do the gas percentages and vapor pressures vary with altitude?
Percentages stay the same but vapor pressures vary
Tracheal/bronchial air pO2 and pCO2
pO2: 149 mm Hg
pCO2 0.2 mm Hg
Alveolar air pO2 and pCO2
pO2: 100 mm Hg
pCO2: 36 mm Hg
Venous circulation pO2 and pCO2 (pH 7.35)
pO2: 40 mm Hg
pCO2 46 mm Hg
Tissue surface pO2 and pCO2
pO2 20 mm Hg
pCO2: 60 mm Hg
Arterial circulation pO2 and pCO2 (pH 7.40)
pO2: 90 mm Hg
pCO2: 40 mm Hg
List factors that influence amount of oxygen that moves to the alveoli
- Destruction of the alveoli
- Pulmonary edema
- Airway blockage
List factors that influence the amount of O2 delivered to the tissue
- Inadequate blood supply
- Diffusion of CO2 and O2
-Intrapulmonary shunting - Anemia
Oxyhemoglobin (O2Hgb)
O2 hemoglobin containing ferrous (Fe2+) iron in the heme group that is reversibly bound to oxygen
Deoxyhemoglobin (HHb)
Reduced hemoglobin without oxygen
Carboxyhemoglobin COHb)
Hgb bound to carbon monoxide
Methemoglobin
Hemoglobin unable to bind oxygen because iron is in an oxidized (Fe3+) state instead of reduced
Hgb-O2 binding capacity
97-99% normal
Four parameters commonly used to assess pt’s oxygen status
- Oxygen saturation (SO2)
- Fractional % oxyhemoglobin (FO2Hb)
- Trends in oxygen sat assessed by transcutaneous and pulse oximetry (SpO2)
- Amount of oxygen dissolved in plasma (pO2)
Hgb affinity for O2 depends on which factors?
- pH
- pCO2
- pCO
- Body temp
- 2,3-DPG conc
Left shift
- Increased pH
- Decreased pCO2, 2,3-DPG, and temp
Right shift
- Decreased pH
- Increased pCO2, 2,3-DPG, and temp
T/F: Unique structure of Hgb allows it to act as both acid-base buffer and O2 buffer
True dat
Oxygen and gas exchange in tissue
Elevated CO2 and H+ results in enhanced O2 release (oxygen buffering) -> accelerates uptake of CO2 and H+ by hemoglobin (acid-base buffering)
Oxygen and gas exchange in lungs
Microenvironment promotes uptake of oxygen and release of CO2
Potentiometry
Measures electric potential between two electrodes -> change in voltage indicates concentration of each analyte (pCO2, pH)
List calculated parameters
- HCO3
- H2CO3
- Total CO2
- Base excess
