Acid-Base Physiology & Pathophysiology Flashcards

1
Q

acids - overview

A

*any proton donor
*anything that adds H+ to body fluids

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2
Q

bases - overview

A

*any proton acceptor
*anything that takes H+ from body fluids
*aka alkali

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3
Q

effects of acidosis

A

*physiologic effects:
-systemic vasodilation
-pulmonary vasoconstriction
-hyperventilation
-renal ammoniagenesis

*pathological effects:
-hyperkalemia
-impaired cardiac contractility
-bone demineralization
-cardiac arrhythmia
-drowsiness / coma

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4
Q

effects of alkalosis

A

*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

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5
Q

relationship between pH and [H+]

A

*increased [H+] → low pH (acidosis)
*decreased [H+] → high pH (alkalosis)

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6
Q

relationship between pKa and dissociation of acid

A

*LOWER pKa → HIGHER dissociation of acid into H+ and conjugate base (STRONG ACID)
*HIGHER pKa → LESS dissociation of acid (weaker acid)

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7
Q

HCO3- buffer system

A

*predominant buffer system in humans
*lungs regulate pCO2
*kidneys regulate HCO3-

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8
Q

pH defense mechanisms

A
  1. buffer system - does not remove or add H+ to the body, only ties it up until balance can be re-established
  2. respiratory system - acts in a few minutes to eliminate CO2 and therefore HCO3- from the body
  3. 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
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9
Q

sources of acid & alkali - gains and losses

A

*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

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10
Q

volatile acids

A

*produced from metabolism of carbohydrates & fats into CO2 and H2O
*CO2 produced is eliminated via the lungs

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11
Q

non-volatile acids

A

*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)

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12
Q

net acid excretion by the kidneys

A

net acid excretion = (NH4+ excretion) + (urinary titratable acid) - (HCO3- excretion)

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13
Q

renal regulation of hydrogen ion balance - overview

A

*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

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14
Q

role of proximal nephron in renal regulation of hydrogen ion balance

A

*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)

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15
Q

role of distal nephron in renal regulation of hydrogen ion balance

A

*reabsorbs any remaining HCO3-
*generates “new” HCO3- via H+ secretion and neutralization by urinary buffers (e.g. NH3)

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16
Q

pH relationships to bicarb and pCO2

A

*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)

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17
Q

alkalemia vs. acidemia

A

*alkalemia: pH > 7.40
*acidemia: pH < 7.40

18
Q

anion gap - defined

A

*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

19
Q

effects of albumin on anion gap

A

*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

20
Q

metabolic acidosis - defined

A

*decreased pH (increased [H+])
*DECREASED BICARBONATE

*compensation: hyperventilation → decrease in PCO2

21
Q

metabolic acidosis - 4 primary causes

A
  1. increased acid production
  2. decreased acid excretion
  3. increased HCO3- loss
  4. decreased HCO3- formation

recall: metabolic acidosis is decreased pH due to decreased bicarbonate

22
Q

systemic effects of metabolic acidosis

A

*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

23
Q

2 types of metabolic acidosis

A
  1. high anion gap metabolic acidosis
  2. normal anion gap (hyperchloremic) metabolic acidosis
24
Q

causes of anion gap metabolic acidosis

A
  1. lactic acidosis (type A, type B, or d-lactic acidosis)
  2. ketoacidosis
    -diabetic ketoacidosis
    -alcoholic ketoacidosis
    -starvation ketosis
  3. toxins/drugs (methanol, ethylene glycol, acetaminophen, salicylate)
  4. kidney failure (with severe reduced GFR)
25
Q

osmolar gap

A

*osmolar gap = measured blood osmolality - calculated osmolality
-normal osmolar gap: 10-15

*calculated Osm = 2Na + BUN/2.8 + glucose/18

26
Q

causes of a high osmolar gap

A

*methanol
*ethylene glycol

*isopropyl alcohol (no metabolic acidosis)
*EtOH (no metabolic acidosis)
*infusion of mannitol, sorbitol, or glycine (no metabolic acidosis)

27
Q

causes of normal anion gap (hyperchloremic) metabolic acidosis

A
  1. GI bicarbonate loss: DIARRHEA
  2. renal bicarbonate loss:
    -proximal or distal renal tubular acidoses
    -acetazolamide or topiramate
    -generalized distal nephron dysfunction
    -potassium sparing diuretics
    -ACE inhibitors
28
Q

Winter’s Formula - used to evaluate for respiratory compensation in metabolic acidosis

A

expected PaCO2 = (1.5 x serum HCO3) + (8 +/- 2)

29
Q

metabolic acidosis - compensation

A

*for [HCO3-] decreases of 1.0, PaCO2 decreases by 1.2
*Winter’s Formala: expected pCO2 = (1.5 x HCO3-) + 8 +/- 2

30
Q

metabolic alkalosis - defined

A

*increased pH (decreased [H+])
*INCREASED HCO3-

compensation: hypoventilation → increased pCO2

31
Q

causes of metabolic alkalosis

A

1) net loss of H+ ions via GI tract:
-VOMITING
-NG drainage
-hyperaldosteronism

2) alkali loading

3) disproportionate loss of chloride with increased HCO3- absorption by the kidney

32
Q

maintenance of metabolic alkalosis

A

*normally, metabolic alkalosis is short-lived because the kidneys will dump the extra bicarb
*persists when the kidneys cannot dump the extra HCO3-:
-reduced effective blood volume
-chloride depletion
-hypokalemia

33
Q

systemic effects of metabolic alkalosis

A

*CV: hypotension, arrhythmia
*pulm: hypoventilation
*CNS: obtundation, delirium, decreased seizure threshold
*neuro: tetany hyper-reflexia, muscle cramping, weakness
*metabolic: hypokalemia

34
Q

metabolic alkalosis - compensation

A

*for [HCO3-] increases of 1.0, pCO2 increases by 0.7

35
Q

respiratory acidosis - defined

A

*decreased pH (increased [H+])
*increased pCO2

compensation: increased bicarb (kidneys conserve bicarb)

36
Q

causes of respiratory acidosis

A

*airway obstruction (COPD)
*depression of respiratory control centers (sedatives, opiates)
*neuromuscular disorders
*chest wall restriction
*lung restriction

37
Q

respiratory acidosis - compensation

A

kidneys CONSERVE bicarb (takes 2-3 days)

*acute: for pCO2 increases of 10mmHg, [HCO3-] increases by 1.0
*chronic: for pCO2 increases of 10mmHg, [HCO3-] increases by 4.0

38
Q

respiratory alkalosis - defined

A

*increased pH (decreased [H+])
*decreased PaCO2

compensation: bicarb decreases (kidneys excrete additional bicarb)

39
Q

causes of respiratory alkalosis

A

*CNS: anxiety hyperventilation, tumors
*salicylate drugs
*pulmonary embolism
*high altitude

40
Q

respiratory alkalosis - compensation

A

kidneys EXCRETE additional bicarb (takes 2-3 days)

*acute: for pCO2 decreases of 10mmHg, [HCO3-] decreases by 2.0
*chronic: for pCO2 decreases of 10mmHg, [HCO3-] decreases by 5.0