Wilson 2

Question 1

Arterial blood samples

Answer 1

• Arterial pCO2
  
  • measured with CO2 electrode
    
    • 40 torr is normal
• Arterial pH
  
  • measured with a pH electrode
    
    • pH 7.35-7.45 is normal
• Arterial bicarbonate
  
  • typically CALCULATED from the conc of CO2 an the pH
    
    • normal is 24 mmol/L
  • Can be measured directly –> gives total CO2

Question 2

urinary ammonium ion

Answer 2

• measured chemically, enzymatically, or by ion-specific electrode
  
  • 20-40mEq/day considered normal
  • up to 250 mEq/day during an acidosis

Question 3

Anion gap

Answer 3

• Calculated as
  
  • [plasma Na+] - ([plasma HCO3-] + [plasma Cl-])
• 8-12 mEq/L typically accepted as normal
• LARGE ANION GAP often observed in metaboic acidosis
  
  • production of ingestion of fixed acid
  • conjugate base of acid is an UNMEASURED ANION

Question 4

effects of respiratory acidosis imbalances

Answer 4

• pH of blood DECREASED due to INCREASE pCO2
  
  • results in INCREASE H2CO3, dissociation yields INCREASE H+
• Recovery requires restoration of nromal ventilation but kidney can compensate
• ACUTE RESPIRATORY ACIDOSIS
  
  • UNCOMPENSATED –> severe asthma, pneumonia, aspiration of foreign body, drugs that depress respiratory drive etc.
• CHRONIC RESPIRATORY ACIDOSIS
  
  • COMPENSATED –> emphysema, chronic bronchitis

Question 5

Acute Respiratory acidosis

Answer 5

• HCO3- conc SLIGHTLY increased and remains on normal buffer slope
• UNCOMPENSATED resperiatory acidosis

Question 6

Chronic respiratory acidosis

Answer 6

• Increased H+ conc STIMULATES H+ excretion by renal tubule cells
• all filtered HCO3- reabsorbed
• excretion of H2PO4- and NH4+ INCREASES
  
  • new HCO3- added to plasma
• Increase in pCO2 partially offset by INCREASE in [HCO3-]

Question 7

Respiraotory alkalosis imablances

Answer 7

• decreased pCO2
  
  • pH of blood INCREASED
• Slow renal compensation allows distinction between acute and chornic cnoditions

Question 8

ACUTE RESPIRATORY ALKALOSIS

Answer 8

• causes include fear, anxiety, trauma, salicylate intoxication
• HCO3- conc DECREASES SLIGHTLY due to buffering

Question 9

Chronic respiratory alkalosis

Answer 9

• Causes include mechanical hyperventialtion, many cardiopulmonary disorders
• Increase in pH DECREASES secretion of H+ by renal tubular cells
  
  • lack of H+ secretion prevents complete reabsorption of HCO3- (lost in urine)
• B-type intercalated cells of collecting tubule (actively secrete HCO3- into filtrate)

Question 10

Causes of metabolic acidosis –> base deficit

Answer 10

• Decrease in plasma conc of HCO3-
  
  • use of HCO3- in buffering rxns
    
    • inability to excrete normal daily acid load
    • increase in acid load (diabetic ketoacidosis)
  • Loss of HCO3- from body
    
    • diarrhea

Question 11

High anion gap metabolic acidosis

Answer 11

• Increase acid load
  
  • HCO3- consumed by buffering reactions
  • anions (acetoacetate, lactate) accumulate in ECF
• Rapid respiratory resposne
  
  • hyperventialtion decreases pCO2, and increases pH

Question 12

describe the renal response to metabolic acidosis

Answer 12

• reabsorption of all filtered HCO3-
• increased titratable acid and ammonia excretion

Question 13

HYPERCHLOREMIC (non-gap) METABOLIC ACIDOSIS

Answer 13

• with gastrointestinal or renal loss of HCO3-
  
  • kidney retains NaCl to maintain extracellular volume
    
    • net excahgne of HCO3- for Cl-
• yeilds reciprocal changes in HCO3- and Cl- conc
  
  • sum of conc of HCO3- and Cl- remains constant
  • no ion gap

Question 14

causes of metabolic alkalosis

Answer 14

• Prodcues a BASE EXCESS
  
  • loss of protons from the body (comiting, nasogastric suction)
    
    • proton repalcement by body involves generation of bicarbonate
  • volume contraction
    
    • water and NaCl lost through diuretic use but AMOUNT of HCO3- unchanged
      
      • conc of HCO3- INCREASES
    • Aldosterone release promotes Na+ reabsoprtion and H+ secretion
      
      • increased H+ secretion increases HCO3- reabsorption and secretion of acid urine (interferes with effective compnesation for alkalosis)

Question 15

Metabolic alkalsosis compensation

Answer 15

• Decreased ventilation (increased pCO2, decreased pH
• Decreased HCO3- reabsorption, active HCO3- secretion by B-type intercalating cells of collecting duct

Accidental ingestion of excess antacid medication –> common cause of metabolic alkalosis

Question 16

combined acidosis

Answer 16

• patient with respiratory difficulties and renal failure
  
  • cannot effectively BLOW OFF CO2
  • the number of functioning nephrons insufficient to cope with net acid production

Question 17

combined alkalosis

Answer 17

• a patient receiving mechanical ventilation and nasogastric suction
  
  • hyperventilation decreases pCO2
  • removal of gastric acid

Question 18

respiratory acidosis/metabolic alkalosis

Answer 18

• patient with chronic lung disease who is undergoing diuretic therapy
  
  • cannot effectively BLOW OFF CO2
  • volume contraction

Question 19

Metabolic acidosis/respiratory alkalosis

Answer 19

• Salicylate intoxication
  
  • salicylates stimualte respiratory center –> respiratory alkalosis
  • Salicylates INHIBIT various metabolic processes
    
    • increased lactate and ketone body production
    • may produce renal insufficiency –> metabolic acidosis