Acid-Base Disorders Flashcards
Major types of acid-base disorders
- Respiratory alkalosis (decrease in CO2 resulting in a increase in pH)
- Respiratory acidosis (increase in CO2 resulting in a decrease in pH)
- Metabolic alkalosis (increase in HCO3 resulting in an increase in pH)
- Metabolic acidosis (decrease in HCO3 resulting in decrease in pH)
Respiratory alkalosis: Definition/differenital dx
- respiratory process caues primary decrease in PCO2
- DDx:
- always due to hyperventilation
- pulmonary disease
- hypoxemia
- mechanical ventilation
Respiratory alkalosis: compensation
- decreased HCO3 due to:
- H+ release from cells (acute)
- renal H+ retention (chronic)
- takes 3-5 days to complete
- compensation rules:
- ##### Acute: ΔHCO3- = ↓ 2 meq/L for every 10 mmHg ↓ in PCO2 [↓(2:10)]
- ##### Chronic (3 to 5 days): ΔHCO3- = ↓4 meqL for every 10 mmHg ↓ in PCO2 [↓(4:10)]
Respiratory alkalosis: Signs, Sx, Tx
- Lab abnormalities: decreased potassium (small); decreased phosphorus (may be large).
- Symptoms: neurologic (paresthesias, carpopedal spasms).
- Consequences: decreased intracranial pressure, cardiac arrhythmias.
- Tx: treat underlying cause; can depress ventilation w/sedative
Respiratory acidosis: definition, DDx
- respiratory process causes a primary increase in the PCO2
- DDx:
- always due to inadequate respiration @ 4 steps of respiration: sensing/signaling, muscles, free flow, gas exchange
Respiratory acidosis: compensation
- increased HCO3 due to:
- cell buffering (acute)
- H+ reabsorbed by intracellular buffers
- renal H+ excretion (chronic)
- 3-5 days
- cell buffering (acute)
- pH should not fall below 7.20 in appropriately compensated chronic respiratory acidosis
- compensation rules:
- Acute: ΔHCO3- = ↑ 1 meq/L for every 10 mmHg ↑ in PCO2 [↑ (1:10)]
- Chronic (3 to 5 days): ΔHCO3- = ↑4 meqL for every 10 mmHg ↑ in PCO2 [↑ (4:10)]
Respiratory acidosis: Signs, Sx, Tx
- Symptoms: Neurologic: headache, decreased arousal/sleepiness (aka CO2 narcosis)
- Consequences: Increased intracranial pressure, cardiac arrhythmias, hypotension from peripheral vasodilatation
- **Treatment: **
- Treat underlying cause
- Pay attention to PO2
Metabolic alkalosis: definition, DDx
- metabolic process causes primary increase in HCO3
- DDx:
- generation of bicarb increase
- addition of HCO3
- loss of H+
- loss of fluid w/chloride
- post-hypercapneia
- hypokalemia
- maintenance of met alk is always due to renal inability to excrete excess HCO3
- generation of bicarb increase
Main mechanisms that generate metabolic alkalosis
- Added HCO3 via:
- direct admin of bicarb
- direct admin of substrate metabolized to bicarb
- Loss of H+ via:
- GI loss: vomiting
- Renal loss: loop, thiazide diuretics, mineralcorticoid excess
- Loss of chloride rich fluid
- loop diuretics
- cystic fibrosis
- post-hypercapnia
- metabolic alkalosis in patient w/chronic respiratory acidosis + mechanical ventilation
- hypokalemia
Mechanisms of maintenance of metabolic alkalosis
- chloride depletion ==> increased resorption of bicarb (chloride vs. non-chloride responsive met alk)
- potassium depletion
- increased mineralocorticoid activity ==> stimulate H+ ATPase to secrete H+ into tubule ==> bicarb resorption
- hypovolemia ==> release of aldosterone ==> increased Na resorption + bicarb (to maintain electroneurtrality)
Definition/causes of chloride responsive metabolic alkalosis
- [UCl] < 20 mEq/L => chloride depletion is major maintence factor
- major causes:
- diuretics
- vomiting, gastric drainage
- villous adenomas
- congenital chloride-losing diarrhea
- cystic fibrosis
- post-hypercapnia
Definition/causes of chloride resistant metabolic alkalosis
- [UCl] > 20 mEq/L
- causes:
- excess mineralocorticoids
- hyperaldosteronism
- cushing’s syndrome
- licorice ingestion
- excess mineralocorticoids
Metabolic alkalosis: compensation
- rise in pH ==> decrease in ventilation ==> rise in CO2
- compensation rules:
- ΔCO2 (in mmHg) = 0.25 – 1.0 XΔHCO3
Metabolic alkalosis: treatment
- possible severe consequences:
- cardiac arrhythmias
- hypocalcemia => neuromuscular irrability => tetany
- hypoventilation via mechanical vent
- Chloride responsive = Infusions of NaCl or KCl
- Chloride resistant = block mineralocorticoid effect w/sprionolactone
Metabolic acidosis: definition, DDx
- metabolic process causes primary decrease in HCO3
- DDx/major mechanisms:
- loss of bicarbonate = normal anion gap
- addition of acid = increased anion gap
- anion gap = [Na] - [Cl] - [HCO3]
- normal = 9 +/- 3
Characteristics of non-anion gap metabolic acidosis
- caused by loss of bicarb
- loss of bicarb is replaced by an increase in chloride
Characteristics of anion gap metabolic acidosis
- caused by addition of acid ==> decrease in bicarb/loss of anion from plasma
- anions other than chloride increase to maintain electroneutrality
- anion gap is “increased” when > 18
Causes of non-anion gap metabolic acidosis
- loss of bicarb
- GI loss: diarrhea
- urine pH < 5.3
- urine anion gap < 0
- renal loss: renal tubular acidosis = due to defect in renal bicarbonate or hydrogen ion handling
- proximal, distal, hyperkalemic
- urine pH > 5.3
- urine anion gap > 0
Causes of anion gap metabolic acidosis
- MUD PILES:
- Methanol
- Uremia (renal failure)
- DKA
- propylene Glycol
- INH (isoniazid)
- Lactate
- Ethylene Glycol
- Salicylates
Physiologic effects of metabolic acidosis
- myocardial contractility decreases + peripheral resistance falls ==>
- hypotension, pulmonary edema, vfib
- respirations = deep and rapid (Kussmaul’s)
- chronic ==> hypercalcuira + bone disease
Metabolic acidosis: compensation
- increased ventilation ==> fall in PCO2
- = incomplete compensation
- appropriate compensation:
- Δ PaCO2 (in mmHg) = 1.0 – 1.5 x Δ **[HCO3-] (in mEq/L) **
- quick approximation: PCO2 = last 2 digits of pH
- both HCO3 and PCO2 should be decreased; if this does not occur likely a mixed disorder__
Mixed disorder: primary respiratory alkalosis + metabolic acidosis
- Δ PaCO2 (in mmHg) > 1.0 – 1.5 x Δ [HCO3-] (in mEq/L)
Metabolic acidosis: Tx
- correct underlying disorder
- chronic = oral sodium bicarbonate
Characteristics of mixed disorders
- coexistence of two+ primary acid-base disorders
- expected compensation will be less than or greater than expected
- PCO2 and HCO3 differ from normal in opposite direction