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PHRM 864 Module 3 > Acid-Base > Flashcards

Acid-Base Flashcards

1
Q

Acid base normal ranges

A

normal physiological pH: 7.35-7.45
pH < 6.7 or < 7.7 is considered incompatible with life

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2
Q

Acidemia pH

A

pH < 7.35

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3
Q

Alkalemia pH

A

pH > 7.45

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4
Q

Carbonic acid/bicarbonate buffer system

A

H+ + HCO3- <–> H2CO3 <–> CO2 + H2O
left side occurs in “kidney” metabolic side; right side occurs in “lungs”
metabolic disorders involve changes in H+ or HCO3- levels, while repsiratory disorders involve changes in CO2
compensation for a particular disorder involves the opposite part (lungs compensate metabolic disorders, kidneys compensate respiratory disorders)

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5
Q

Henderson-Hasselbach equation

A

the relationship between pH and the concentration of acid-base pairs in buffer system
pH = pKa + log (base/acid)
pH = 6.1 + log (HCO3-/H2CO3)
pH = 6.1 + log (HCO3-/0.03 x pCO2) - pH of blood determined by ratio of HCO3- to pCO2

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6
Q

Normal blood gas values

A

PaCO2: 40 mmHg
HCO3: 24 mmHg
arterial blood is the best source for obtaining these readings

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7
Q

Adverse consequences: acidemia

A

cardiovascular, metabolic, CNS, others

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8
Q

Acidemia - cardiovascular AEs

A

decreased cardiac output, impairment of cardiac contractility, increase in pulmonary vascular resistance and arrhythmias

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9
Q

Acidemia - metabolic AEs

A

insulin resistance, inhibition of anaerobic glycolysis, hyperkalemia

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10
Q

Acidemia - CNS AEs

A

coma or altered mental status

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11
Q

Acidemia - other AEs

A

decreased respiratory muscle strength, hyperventilaion, dyspnea

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12
Q

Adverse consequences: alkalemia

A

cardiovascular, metabolic, CNS, others

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13
Q

Alkalemia - cardiovascular AEs

A

decreased coronary blood flow from arteriolar constriction
decreased anginal threshold; arrhythmias

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14
Q

Alkalemia - metabolic AEs

A

decrease in K+, Ca, and Mg (all important for electrical activity of the heart)
stimulation of anaerobic glycolysis

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15
Q

Alkalemia - CNS AEs

A

decrease cerebral blood flow
seizures

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16
Q

Alkalemia - other AEs

A

decrease respirations

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17
Q

Acid generation - diet

A

~1mEq/kg/day of acid consumed/day; from oxidation of proteins + fats
aerobic metabolism of glucose produces 15-20K mmol of CO2/day
nonvolatile acids also formed

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18
Q

Nonvolatile acids formed

A

anaerobic metabolism produces lactic acid and pyruvic acid
triglyceride oxidation produces acetoacetic acid and beta-hydroxybutyric acid
metabolism of sulfur-containing amino acids and phospholipids result in sulfuric and phosphoric acids
0.8 mEq H+ from nonvolatile acids/kg of body weight must be excreted daily

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19
Q

Acid regulation: 3 standard mechanisms

A

buffering, renal regulation, ventilatory regulation

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20
Q

Extracellular/intracellular buffering systems

A

first line defense
buffer: ability of a weak acid and its anion (base) to resist change in pH with addition of strong acid or base
buffers: bicarbonate/carbonic acid, phosphate, and protein

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21
Q

Extracellular/intracellular buffering systems -Bicarbonate principle buffer

A

rapid onset with intermediate capacity to control acid level
HCO3- buffer present in largest concentration extracellulary: supply of CO2 is unlimited, acidity can be controlled by HCO3- or the pCO2
ability of the kidneys + lungs to excrete and retain HCO3- and CO2 respectively
when acid is added, large quantities of CO2 can be exhaled very rapidly; body needs need HCO3- added to system in amount equivalent to H+ load ingested each day

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22
Q

Extracellular/intracellular buffering systems - phosphates

A

intermediate onset and capacity
extracellular inorganic phosphates limited activity
intracellular organic phosphates
calcium phosphates in bone relatively inaccessible

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23
Q

Extracellular/intracellular buffering systems - proteins

A

albumin/hemoglobin: rapid onset, limited capacity
more effective intracellular buffer vs extracellular buffer

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24
Q

Renal system regulation

A

kidney serves 2 main purposes: reabsorb filtered HCO3- and excrete H+ ions released from nonvolatile acids (help generate new HCO3-)

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25
Q

Renal system regulation - bicarbonate reabsorption

A

most is reabsorbed by proximal tubule, rest is reabsorbed via distal tubule or collecting duct
virtually no HCO3- in urine

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26
Q

Bicarbonate reabsorption

A

filtered HCO3- combines with a secreted H+ to form H2CO3 –> through the action of carbonic anhydrase (acts in urine), dissasociation occurs to form H2O and CO2 –> H2O and CO2 are reabsorbed into tubular cell (proximal tubule) to form H2CO3 –> H2CO3 dissociates into HCO3-, which is reabsorbed into peritubular capillary (back in bloodstream), and H+ which is secreted into tubular lumen in exchange for Na+
net effect: filtered HCO3- is reabsorbed without net loss of H+!

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27
Q

Anything limiting H+ secretion into proximal tubule lumen results in

A

urinary bicarbonate losses
ex. carbonic anhydrase inhibitors: inhibit activity of carbonic anhydrase –> decrease entry of CO2 and H2O (decrease HCO3- for reabsorption) –> metabolic acidosis occurs with increased HCO3- excretion secondary to increased urine Na+

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28
Q

Bicarbonate generation/H+ excretion

A

H+ excretion takes place primarily in the distal tubule

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29
Q

2 processes for bicarb generation

A

ammonium excretion
titratable activity

30
Q

Ammonium excretion

A

secreted H+ combines with NH3 to form NH4+ –> NH4+ can’t cross membranes and ultimately is excreted –> intracellular HCO3- formed during the processed is also reabsorbed in the peritubular capillaries
ammoniagenesis

31
Q

Titratable acidity

A

filtered HPO4- combines with secreted H+ and is excreted as H2PO4- –> intracellular HCO3- formed from dissociation of H2CO3 is reabsorbed as new HCO3-
capacity cannot be increased (limited by plasma concentration of HPO4- buffer and by GFR)

32
Q

Distal tubular hydrogen ion secretion

A

~50% of net acid excretion
CO2 combines with water in presence of carbonic anhydrase to form H2CO3 which breaks down H+ and HCO3- –> H+ transported back into tubular lumen by ATPase –> HCO3- freely crosses distal tubular membrane and enters peritubular capillary absorption

33
Q

Acid regulation - ventilatory regulation

A

rapid onset and large capacity
chemoreceptors detect increase in PaCO2 and increase rate and depth of ventilation
peripheral chemoreceptors in carotid arteries and aorta, and central chemoreceptors in medulla

34
Q

Hepatic regulation

A

oxidation of proteins generates HCO3- and NH4+ –> NH4+ can be eliminated via urea synthesis or renal ammoniagenesis; therefore if liver dimishes hepatic urea synthesis, metabolic alkalosis may occur or an acidotic state will be corrected
decrease urea synthesis: more bicarb sitting around

35
Q

Compensation characteristics for acid-base disorders

A

respiratory compensation very rapid
renal compensation takes 3-5 days for max effect
compensation moves pH towards normal, but rarely corrects pH to normal

36
Q

Metabolic acidosis

A

change: decreased HCO3-
compensation: decreased PaCO2

37
Q

Metabolic alkalosis

A

change: increased HCO3-
compensation: increased PaCO2

38
Q

Respiratory acidosis

A

change: increased PaCO2
compensation: increased HCO3-

39
Q

Respiratory alkalosis

A

change: decreased PaCO2
compensation: decreased HCO3-

40
Q

1 treatment for all metabolic disorders

A

fix the cause

41
Q

Metabolic disorders - metabolic acidosis

A

low pH (<7.35), low serum HCO3- (<24 mEq/L) and a compensatory decrease in PaCO2 from hyperventilation
classified as either non-anion gap or anion gap metabolic acidosis

42
Q

If metabolic acidosis present, LOOK AT

A

anion gap
anion gap = Na - (Cl + HCO3)
normal: 3-11 mEq/L
normal or low: non-anion gap
high: anion gap

43
Q

Pathophysiology of non-anion gap acidosis (hyperchloremic acidosis)

A

loss of plasma HCO3- replaced by Cl-
causes: gastrointestinal biacarb losses; renal bicarb loss; reduced renal H+ excretion (distal tubule RTAs); acid and chloride administration

44
Q

Gastrointestinal bicarb losses

A

diarrhea very common cause
pancreatic fistulas/biliary drainage

45
Q

Renal bicarb losses: type II renal tubular acidosis

A

problem within the proximal tubule (can’t reabsorb bicarb) - can result from various diseases or toxins; reabsorptive threshold for HCO3- is reduced in the proximal tubule
with enhanced bicarb loss –> increase in Na+ and fluid loss –> activates renin-angiotension system leading to secondary hyperaldosteronism –> increased aldosterone –> increased K+ excretion –> hypokalemia

46
Q

Reduced renal H+ excretion (distal tubule RTAs - most common)

A

type I RTA (hypokalemia RTA): H+ can’t be pumped into tubule lumen by cells of collecting duct/distal tubule –> urine can’t be maximally acidified –> increase in K+ excretion b/c Na gets interchanged with K+, H+ can’t be secreted in repsonse to Na+ reabsorption
type IV RTA (hypoaldosteronism or hyperkalemia RTA): aldosterone stimulates H+ excretion, with less aldosterone = H+ retention; hyperkalemia also leads to increased H+ retention
chronic renal failure: decreased H+ secretion; less ammonia production ( decreased ability to make new HCO3- via process of ammonium excretion)

47
Q

Acid and chloride administration

A

just give too much acid: in TPN or HCl/ammonium Cl adminisitration

48
Q

Pathophysiology of anion gap acidosis

A

pts have elevated anion gap
overall HCO3- losses are replaced with another anion besides Cl-
calculate delta gap: difference between pts anion gap and normal anion gap; then add delta gap to pts measured HCO3- –> if you get elevated HCO3-, mixed disorder

49
Q

Causes of anion gap metabolic acidosis

A

MUDPILES
methanol intoxication, uremia, diabetic ketoacidosis, poisoning/propylene glycol ingestion, intoxication/infection, lactic acidosis, salicylate/sepsis

50
Q

Lactic acidosis

A

increased levels almost always result from decreased clearance vs overproduction
possible causes: shock, drugs/toxins (ethanol, metformin, propylene glycol, linezolid, isoniazid, propofol, topiramate) , seizures, leukemia, hepatic/renal failure, DM, malnutrition, rhadbomyolysis

51
Q

Drug intoxications

A

salicylate toxicity: respiratory alkalosis from stimulation of respiratory drive; metabolic acidosis from accumulation of organic acids

52
Q

Treatment of anion gap acidosis

A

treat underlying cause!
acute bicarb therapy: consider if pH <7.10-7.15
dose (mEq) = [0.5 L/kg (IBW)] x (desired HCO3 - actual HCO3)
use 12 mEq/L for desired HCO3-
give 1/3-1/2 the calculated dose
during cardiac arrests, ~1 mEq/kg may be given
chronic bicarb therapy for chronic metabolic acidosis: 1-3 mEq/kg/day

53
Q

Hazards of bicarb therapy

A

overalkanization can impair oxygen release from Hgb to tissues
hypernatremia/hyperosmolality
CSF acidosis
electrolyte shifts: hypokalemia and hypocalcemia

54
Q

Metabolic alkalosis

A

increased pH (>7.45), increased HCO3- (>30 mEq/L) and a compensatory hypoventilation resulting in increased PaCO2

55
Q

Metabolic alkalosis pathophysiology

A

primary rise in plasma HCO3- from: loss of acid from GI tract or urine; administration of HCO3- or a bicarb precursor; contraction alkalosis

56
Q

Saline responsive alkalosis (urinary chloride < 10-20 mEq/L)

A

diuretic therapy
vomiting and NG suction
exogenous HCO3- administration or blood transfusions (contain citrate, which is broken down to HCO3-)
maintenance of alkalosis

57
Q

Diuretic therapy

A

enhances excretion of sodium chloride and water –> volume contraction –> aldosterone release –> aldosterone increased distal tubular Na+ reabsorption and induces H+ and K+ secretion (H+ secreation associated with HCO3- reabsorption in proximal tubule and HCO3- generation in distal tubule)
in response to the hypokalemia –> H+ moves intracellularly and K+ moves extracellularly –> in exchange for the K+, Na+ gets reabsorbed
hypochloremic: without Cl-, Na+ is reabsorbed with HCO3-

58
Q

Saline resistant alkalosis (urinary chloride > 20 mEq/L)

A

enhanced renal H+ excretion and HCO3- reabsorption
key difference: no chloride depletion or inability to reabsorb chloride

59
Q

Causes of saline resistant alkalosis

A

increased mineralcorticoid activity: stimulates H+ secretion and increases ammoniagenesis by causing hypokalemia
hypokalemia
renal tubular wasting: impaired NaCl reabsorption –> volume depletion activates RAA system –> increase aldosterone which leads to H+ secretion and hypokalemia

60
Q

Treatment of saline resistant alkalosis

A

correct underlying cause!

61
Q

Treatment of saline responsive alkalosis

A

treat with saline (fluid electrolyte replacement with NaCl or KCl) - allows more Na+ to be reabsorbed with Cl- vs getting exchanged with H+ or reabsorbed with HCO3-; caution in pts with HF or hepatic/renal failure
carbonic anhydrase inhibitors for pts who can’t tolerate excess fluids or sodium (acetohexamide)

62
Q

Persistent metabolic alkalosis

A

HCl acid in either D5W or NS: indicated for pts with contraindication to Na replacement (HF, renal failure), failure of previous therapies, or confirmed severe metabolic alkalosis
ammonium chloride: avoid in hepatic/renal failure
arginine monohydrochloride

63
Q

Adjunct therapy:

A

H2 antagonists or PPIs in pts with vomiting or NG suction

64
Q

Saline resistant alkalosis

A

urinary chloride concentration > 20 mEq/L
correct hypokalemia with potassium sparing diuretic or KCl supplementation; decrease dose of mineralcorticoid; administer spironolactone; correct hyperaldosteronism

65
Q

Respiratory disorders - respiratory acidosis

A

characterized by low pH (<7.35), hypercapnia (>45 mmHg) and a compensatory increase in HCO3- concentration

66
Q

Pathophysiology of respiratory acidosis

A

results from a failure of excretion versus overproduction
causes: airway obstruction, reduced stimulus for respiration from CNS, failure of heart or lungs, neuromuscular defects affecting nerves or skeletal muscles required for ventilation, mechanical ventilation

67
Q

Treatment of respiratory acidosis

A

correct underlying cause
mechanical ventilation or oxygen (caution giving O2 in COPD pt)
avoid rapid correction to prevent alkalemia

68
Q

Respiratory disorders - respiratory alkalosis

A

increased pH (>7.45), decreased PaCO2 (<40 mmHg), and a compensatory decrease in HCO3- concentration

69
Q

Respiratory alkalosis pathophysiology

A

causes: central/peripheral stimulation of respiration, mechanial ventilation, pulmonary, salicylate intoxication

70
Q

Treatment of respiratory alkalosis

A

correct the underlying cause!
ventilation, sedation, paralysis

PHRM 864 Module 3 (9 decks)

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