Acid-Base Physiology & Pathophysiology Flashcards
acids - overview
*any proton donor
*anything that adds H+ to body fluids
bases - overview
*any proton acceptor
*anything that takes H+ from body fluids
*aka alkali
effects of acidosis
*physiologic effects:
-systemic vasodilation
-pulmonary vasoconstriction
-hyperventilation
-renal ammoniagenesis
*pathological effects:
-hyperkalemia
-impaired cardiac contractility
-bone demineralization
-cardiac arrhythmia
-drowsiness / coma
effects of alkalosis
*physiologic effects:
-peripheral vasoconstriction
-pulmonary vasodilation
-hypoventilation
-renal bicarbonate secretion
*pathological effects:
-hypokalemia
-reduced coronary blood flow
-reduced cerebral blood flow
-decreased ionized plasma calcium
-paresthesias and muscle cramps
relationship between pH and [H+]
*increased [H+] → low pH (acidosis)
*decreased [H+] → high pH (alkalosis)
relationship between pKa and dissociation of acid
*LOWER pKa → HIGHER dissociation of acid into H+ and conjugate base (STRONG ACID)
*HIGHER pKa → LESS dissociation of acid (weaker acid)
HCO3- buffer system
*predominant buffer system in humans
*lungs regulate pCO2
*kidneys regulate HCO3-
pH defense mechanisms
- buffer system - does not remove or add H+ to the body, only ties it up until balance can be re-established
- respiratory system - acts in a few minutes to eliminate CO2 and therefore HCO3- from the body
- kidneys - most powerful line of defense; reacts slower (over several hours to several days); kidneys are able to eliminate excess acid or base from the body
sources of acid & alkali - gains and losses
*dietary intake (acid gain)
*metabolism / catabolism (acid gain)
*GI H+ or HCO3- loss
*renal HCO3- filtration (potential loss)
*renal HCO3- reabsorption and generation
*renal H+ secretion
volatile acids
*produced from metabolism of carbohydrates & fats into CO2 and H2O
*CO2 produced is eliminated via the lungs
non-volatile acids
*produced from metabolism of proteins (amino acids)
*primary mechanism of removal of these acids is renal excretion (phosphate buffer & ammonium)
*kidneys must replenish the bicarb lost by neutralization of non-volatile acids
*related to renal net acid excretion (RNAE) and net endogenous acid production (NEAP)
net acid excretion by the kidneys
net acid excretion = (NH4+ excretion) + (urinary titratable acid) - (HCO3- excretion)
renal regulation of hydrogen ion balance - overview
*kidneys must:
1. conserve all existing HCO3-
2. generate new HCO3- to replete the alkali deficit secondary to 1 mEq/kg/day of H+ input
role of proximal nephron in renal regulation of hydrogen ion balance
*reclaims 80-90% of filtered HCO3-
*secretes acid (H+)
*generates NH3 (which is important for subsequent generation of “new” HCO3- via H+ secretion and NH4+ production)
role of distal nephron in renal regulation of hydrogen ion balance
*reabsorbs any remaining HCO3-
*generates “new” HCO3- via H+ secretion and neutralization by urinary buffers (e.g. NH3)
pH relationships to bicarb and pCO2
*pH is directly proportional to bicarb:
-increased [HCO3-] → increased pH (alkalosis)
-decreased [HCO3-] → decreased pH (acidosis)
*pH is inversely proportional to pCO2:
-increased pCO2 → decreased pH (acidosis)
-decreased pCO2 → increased pH (alkalosis)
alkalemia vs. acidemia
*alkalemia: pH > 7.40
*acidemia: pH < 7.40
anion gap - defined
*the difference between the measured cations sodium (Na+) and the measured anions chloride (Cl-) and bicarbonate (HCO3-)
*anion gap = sodium - (bicarb + chloride)
*normal anion gap is 10 +/- 2
*if elevated > 20, then can have a hidden metabolic acidosis
effects of albumin on anion gap
*normal anion gap: 10 +/- 2
*for every 1mg/dl drop in albumin (below 4 mg/dl), decrease the “normal range” anion gap by 2.5
metabolic acidosis - defined
*decreased pH (increased [H+])
*DECREASED BICARBONATE
*compensation: hyperventilation → decrease in PCO2
metabolic acidosis - 4 primary causes
- increased acid production
- decreased acid excretion
- increased HCO3- loss
- decreased HCO3- formation
recall: metabolic acidosis is decreased pH due to decreased bicarbonate
systemic effects of metabolic acidosis
*CV: hypotension, arrhythmia
*pulm: hyperventilation, reduced O2 delivery
*GI: hypomotility, decreased absorption
*renal: Na+ and K+ wasting, uric acid retention
*metabolic: protein catabolism; altered catecholamine, aldosterone, PTH, vitamin D production and response
2 types of metabolic acidosis
- high anion gap metabolic acidosis
- normal anion gap (hyperchloremic) metabolic acidosis
causes of anion gap metabolic acidosis
- lactic acidosis (type A, type B, or d-lactic acidosis)
- ketoacidosis
-diabetic ketoacidosis
-alcoholic ketoacidosis
-starvation ketosis - toxins/drugs (methanol, ethylene glycol, acetaminophen, salicylate)
- kidney failure (with severe reduced GFR)
