Acid base disorders Flashcards
Effects of metabolic acidosis
- O2 curve shifts to right = increased O2 delivery to tissues
- CNS depression
- arrhythmias
- decreased cardiac contractility
- hyperkalemia –> due to intracellular buffering
- decreased pulmonary blood flow
Causes of metabolic acidosis
- H gain
- -> Increased H production = multiple causes
- -> Decreased H secretion = Chronic kidney disease, RTA - HCO3 loss
- -> diarrhea
- -> RTA
Differential dx for metabolic diagnosis should ALWAYS start by calculating the anion gap!
Causes of high anion gap metabolic acidsosis
MUDPILES
- Methanol (diethylene glycol)
- Uremia –> build up of sulfates
- Diabetic ketoacidosis
- Propylene glycol
- Ingestions/INH/Infections
- Lactic acidosis
- Ethylene glycol
- Salicylates (late)
Causes of non-anion gap metabolic acidosis
Primarily renal and GI causes
- Renal = RTA –> urine pH is NOT maximally acidic except for late proximal RTA
- GI = diarrhea
HEARTCCU
- Hyperalimentation
- Expansion
- Acetazolimide
- RTA
- Turds –> diarrhea
- Cholestyramine
- Carbonic anhydrase increase
- Uterersigmoidostomy
Effects of metabolic alkalosis
- O2 curve shifts to the left –> decreased O2 delivery to tissues
- decreased cerebral blood flow
- tetany
- seizures
- arrhythmias
Causes of metabolic alkalosis
Gain of HCO3
- citrate –> repeated blood transfusions
- bicarbonate
Loss of H+
- renal –> diuretics
- non-renal
- -> GI = vomiting, NG tube suctioning, HCO3 infestion
- -> hypokalemia –> H+ transcellular shift
Contraction alkalosis
- diuretics –> cause loss of Na, K and Cl and water, but not HCO3 = decreased ECF but same concentration of HCO3- = increased HCO3 concentration
Transient metabolic alkalosis
Metabolic alkalosis resolves after the increased HCO3 load has stopped –> extra HCO3 load lost by the kidney is not reclaimed
Causes
- NaHCO3 loading to prevent tumor lysis syndrome
- Upon correction of acute hypercapnia (hypoventilation) without Cl depletion
- Recovery from organic anion metabolic acidosis
Maintained metabolic alkalosis
Persists after the increased HCO3- load has stopped
- extra HCO3 load is retained by the kidney and H secretion is increased
- occurs because K or Cl depletion occurs simultaneously with HCO3 loading = stimulus that maintains the continued secretion of H in the face of metabolic alkalosis
- K/Cl depletion must be corrected to rectify the metabolic alkalosis
Causes of maintained metabolic alkalosis
Cl/volume depletion
- vomiting, NG tube suctioning (also mild K loss)
- diuretics –> prevent reabsorption of Na,Cl and K, cause volume depletion (mild K loss)
- post hypercapneic alkalosis –> chronic resp acidosis causes a compensatory metabolic alkalosis = increased H + Cl loss by the kidney –> causes Cl depletion –> following correction of the resp acidosis, metabolic alk is maintained by by Cl- depletion
K depletion
- hypokalemia –> transcellular shift = H excretion
- diuretics –> hypokalemia –> transcellular shift
- mineralocorticoid excess –> increased H/K secretion by the kidneys
- -> primary/secondary hyperaldo
- -> apparent mineralocorticoid excess syndrome (licorice)
- renal failure
Cl and K depletion –> Liddles, Barters and Gittlemans
Decreased GFR –> effective volume depletion
Causes of respiratory acidosis
- CNS depressants
- resp muscle dysfunction
- airway obstruction
- poor gas exchange
Causes of respiratory alkalosis
- hypoxemia
- lung disease
- sepsis
- salicylates (early)
- CNS stimulants