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Pharmacotherapy 1 > 1 - Acid/Base Disorders > Flashcards

1 - Acid/Base Disorders Flashcards

1
Q

Henderson Hasselbach eqn for physiological pH

A

pH = 6.1 + log (HCO3-/H2CO3)

=(HCO3-/(0.3xpCO2)

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2
Q

normal PaCo2

A

35-45 mmHg

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3
Q

normal HCO3

A

22-26 mEq/L

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4
Q

normal PaO2

A

95-100 mmHg

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5
Q

normal SaO2

A

> =95%

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6
Q

What are the adverse CV effects of acidemia?

A

decr CO
imp’d contractility
incr PVR
arrhythmias

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7
Q

What are the metabolic effects of acidemia?

A

insulin resis
inhib of anaerobic glycolysis
hyperkal

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8
Q

What are the CNS effecs of acidemia?

A

coma or AMS

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9
Q

What are misc effects of acidemia?

A

decr resp musc strength
hypervent
SOB

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10
Q

What are the adverse CV effects of alkalemia

A

decr coronary BF
arteriolar constriction
decr anginal threshold
arrhytmias

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11
Q

What are the metabolic effects of alkalemia?

A

decr K, Ca, Mg

stim of anerobic glycolysis

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12
Q

What are the CNS effects of alkemia?

A

decr cerebral BF

Szs

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13
Q

What are the nonvolatile acids and how are they formed?

A

anaerobic metab: lactic & pyruvic acid

TG ox: acetoacetic and beta-hydroxybutyric acid

AA metb: sulfuric and phosphoric acids

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14
Q

Describe the buggering capacity of bicarb.

A

rapid onset w intermediate capacity

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15
Q

Describe the phosphates as a buffer.

A

intermed onset and capacity.
EC Pi limited actvity
bone relativey inaccessible

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16
Q

Describe proteins as buffer.

A

alb/hbg: rapid onset, limited: more effective IC

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17
Q

What are the mechanisms by which the kidney regulations acid/base status?

A
  • reabsorb filtered bicarb
  • excrete hydrogen ions released from nonvolatile acids
  • ammoniagenesis, titratable acidity
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18
Q

most bicarb is reabosbed at the

A

PCT

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19
Q

limiting H+ secretion into the PCT results in

A

bicarb losses

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20
Q

How can carbonic anhydrase inhibitors affect a/b status?

A

cause metabolic acidosis as HCO3- excretion increases

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21
Q

Where does H+ secretion take place?

A

DCT

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22
Q

H+ secretion in the DCT results in generation of

A

NEW Bicarb

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23
Q

Describe vent reg of a/b status.

A

rapid and large cap

chemoreceptors detect incrin PaCO2 and incr rate and depth of vent.

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24
Q

Which chemoreceptors are activated by arterial acidosis, hypercapnia, and hypoxia?

A

peripheral chemoreceptors in carotid arteries and aorta

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25
Q

Which chemoreceptors are activated by CSF acidosis?

A

central chemoreceptors in medulla

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26
Q

Describe hepatic regulation of A/b status

A

Oxidation of protein generations bicarb and ammonium that can be elim’s via urea synthesis or renal ammoniogenesis.

if liver decr urea synthesis–> incr pH

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27
Q

**comp in met acidosis

A

PaCo2 falls by 1-1.5 x HCO3 fall

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28
Q

**comp in met alk

A

PaCO2 incr by 0.4-0.6 x rise in plasma HCO3-

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29
Q

**comp in resp acid

A

acute: HCO3- rise by 0.1 x incr in PaCO2 +/- 3
chronic: 0.4x +/-4

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30
Q

**comp in resp alk

A

acute: HCO3- fall by 0.1-0.3 x decr in PACO2 but usually not less than 18 mEq/L
chronic: 0.2-0.5, 14 mEq/L

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31
Q

normal anion gap

A

3-11 mEq/L

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32
Q

anion gap eqn

A

AG=Na-Cl-HCO3-

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33
Q

nother name of non-anion gap met acidosis

A

hyperchloremia acidosis

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34
Q

Causes of non-anion gap acidosis

A

GI bicarb loss
renal wasting/imp’d H+ secr
acid/Cl gain

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35
Q

Examples of GI bicarb loss

A

diarrhea
pancreatic fistula
biliary drainage

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36
Q

Explain renal bicarbonate loss

A

type II RTA (PCT)

  • cannot reabs
  • -incr’d Na and fluid loss –> RAAS
  • -2* hyperaldosteronism–>hypokalemia

–> able to acidify urine pH <5.3

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37
Q

what are the causes of reduced renal H+ excretion?

A

type I RTA (hypokalemia)
type IV RTA (hypoaldosteronism / hyperkalemia)
chronic renal failure

38
Q

Explain type I RTA

A

caused by tubule defect, SLE, myeloma, toluene (OD)

H+ cannot be pumped into DCT

  • ->urine cannot be acidified
  • ->incr K+ excretion d/t Na exchange
39
Q

Explain type IV RTA

A

hypoaldosteronism

  • ->decr H+ and K+ excretion
  • ->acidosis and hyperkalemia
40
Q

Explain how CRF can cause a metabolic acidosis.

A

decr H+ secr.

less ammonia production. (less bicarb made)

41
Q

MULEPAK

A 
methanol
uremia
lactic acidosis
ethylene glycol
paraldehyde ingestion
aspirin (salicylates)
ketoacidosis
42
Q

MUDPILES

A 
methanol
uremia
DKA
poisoing/propylene glycol ingestion
intox/infx
lactic acidosis
etylene glycol
salicylate/sepsis
43
Q

delta gap

A

for AG met acidosis add to measured HCO3-

–> if high for HCO3- then mixed disorder (also metabolic alkalosis)

44
Q

What causes lactic acidosis?

A
  • decr clearance of lactate
  • shock (hypoxia, decr hep fxn)
  • DRUGs
45
Q

How does ethanol cause lactic acidosis?

A

incr lactate and hypoglycemia - impaired gluconeogenesis

46
Q

How does metformin cause lactic acidosis?

A

we don’t know

47
Q

How do NRTIs cause lactic acidosis?

A

inhibit DNA Pol for mitochondrial DNA synthesis

48
Q

How do linezolid, isoniazid, and propofol cause lactic acidosis?

A

simply increase lactic acid

49
Q

How do Sz cause lactic acidosis?

A

enhanced met act

self-limiting

50
Q

How does leukemia cause metabolic acidosis?

A

packed porly perfused bone marrow caviity

51
Q

How does hep/RF cause lactic acidosis?

A

imp’d metab and excr

52
Q

How does DM cause lactic acidosis?

A

formation of ketones/lactate; use of metformin

53
Q

How does ketoacidosis cause met acid?

A

increase acetoacetic acid and beta-hydroxy butyric acid (KETONE BODIES)

54
Q

How do salicylates cause AG met acid?

A

resp alkalosis from stim of resp drive

met acid from accumulation of organic acids

55
Q

How do methanol/ethylene glycol cause AG met acid?

A

methanol–>formaldehyde–>formic acid

ethylene glycol–>glycoaldehyde–>glycolate–>glycoxylate–>oxalate

56
Q

Wht are the Sx of lactic acidosis?

A 
Kussmaul respiration
periph vasodil causes flushing and tachycardia --> arrhythmias, decr contractility
hyperkalemia
lethary/coma
N/V
bone demineralization if chronic
57
Q

When to use bicarb therapy?

A

pH <7.1-7.15

ind: hyperkalemia, pH <7.1 w/ cardiac arrest after defib, vent, and meds have been utilized, ODs

58
Q

How to dose bicarb

A

dose (mEq)=[0.5L/kg x IBW] x (goal bicarb - actual bicarb)

use 12 mEq/L for goal

give 1/3-1/2 calc’d dose

monitor ABG

59
Q

Tips for bicarb therapy

A

monitor ABG
supplement K+, if needed
don’t overalk–>left shift hypoxia, hypernatremia, CSF acidosis

60
Q

What electrolyte shifts can bicarb therapy cause?

A

K+ –> shifts IC –> hypokalemia

Ca2+–>decr Cai so decr contractility

61
Q

Dose of chronic bicarb therapy.

A

1-3 mEq/kg/d (up to 10+)

62
Q

What is tromethamine?

A

Tx for acidosis
combines with H+ from H2CO3 to form bicarb

–osmotic diuretic

63
Q

What are some drugs to treat met acidosis?

A

bicarb
tromethamine
carbicarb
dichloroacette (DCA): lactate metab

64
Q

What are the mechanisms of metabolic alk?

A

loss of acid
admin of HCO3- or precursor
contraction alkalosis

65
Q

What the heck does contraction alkalosis mean?

A

loss of Cl- rich, HCO3- poor fluid

66
Q

How do volume and chloride depletion maintain a met alk?

A

decr in blood vol
decr ability to excr bicarb
incr reabs of PCT reabs of bicarb

67
Q

What are the two types of met alkalosis?

A 
saline responsive
saline resistance (Cl in urine >20 mEq/L)
68
Q

What are the causes of saline responsive met alk?

A

diuretic therapy
vomting and NG suction
exogenous HCO3- admin or blood transfusions

69
Q

How is a saline responsive met alk maintained?

A

reduced GFR (incr HCO3 reabs w Na+)

  • incr PCT HCO3- abs w Na+ (hypochloremia)
  • hypokalemia: more H+ secreted and new bicarb
70
Q

How does diuretic therapy cause saline responsive met alk?

A

volume contraction –> ALDOSTERONE –> incr Na reabs in DCT

  • -> incr H+/K+ sec
  • -> incr BICARB made

–>HYPOKALEMIA–> K+ moves EC –> H+ moves IC –> basic EC

–>HYPOCHLOREMIA (d/t diuresis) –> increase bicarb reabs

71
Q

Why do blood products cause alkalosis?

A

contain citrate–>breaks down into bicarb

72
Q

What is the pathology of saline resistant met alk?

A

enhanced renal H+ excr and bicarb reabs

urinary chloride >20 mEq/L
–> no Cl depletion or there is inability to reabsorb Cl

73
Q

What are the causes of saline res mmet alk?

A

incr mineralcorticoid activity
hypokalemia
renal tubular chloride wasting (Bartter’s syndrome)

74
Q

How does increased mineralcorticoid acitivyt cause saline res met alk?

A

stim CD H+ secr

–>incr ammoniagenesis

75
Q

How does hypokalemia cause saline res met alk?

A

incr H+ secr w bicarb reabs and ammoniagenesis

76
Q

How does Bartter’s syndrome cause saline res met alk?

A

chloride wasting:

imp’s NaCl reabs
–>fluid loss –> RAAS –> incr aldosterone

77
Q

What are the Sx of metabolic alkalosis?

A

msucle cramps, weakness, paresthesias
cellular hypoxia, confusion, coma, Sz
myocardial suppression, CV collapse, arrhytmias (low K)

78
Q

How to treat saline responsive alkalosis?

A

fluid/elyte replacement w NaCl or KCl

  • -> less bicarb reabs
  • ->increase volume
  • ->increase K+ –> decr H+ secr

or CAI

79
Q

Example fluid treatment for saline responsive met alk

A

0.9% NaCl w 20-40 mEq/L KCl over 4-6 hrs

80
Q

What to monitor for met alk?

A 
I/O
BP
HR
lung sounds
elyes
edema
81
Q

How do carbonic anhydrase inhibitors help treat saline resp met alk?

A

decr bicarb reabs in PCT

SE: K+ wasting

82
Q

carbonic anhydrase inhibitor dose

A

acetohexamide 250-375 once or bid

83
Q

Rare therapeutic options of met alkalosis

A

HCl acid
Ammonium chloride
arginine monohydrochoride

84
Q

adjunct therapy for pts for met alk d/t NG suctioning or vomitting

A

H2 antagonists or PPIs

85
Q

How to treat saline resistant alkalosis?

A

correct hypokalemia w K-sparing diuretic or KCl supplementation

  • decrease mineralcorticoids
  • spironolactone (mincortR antag, inhib aldosterone-stim of H+ secr)

–correct hyperaldosteronism-> give fluids but not first line

86
Q

What are the causes of respiratory acidosis?

A 
airway obstruction
reduced stimulatus for resp from CNS (OD, sleep apnea, CNS infx)
-failture of heart or lungs
-neuromusc defects (can't breathe)
-mech vent
87
Q

Sx of resp alk?

A

SOB
CNS: HA, drowsy, confusion, coma, Sz
CV: tachycardia, arrhythmias, hypoTN

88
Q

Tx of resp acidosis

A

underlying cause

  • mech vent or O2 (caution in COPD)
  • avoid rapid correction (alk)
  • rarely use bicarb (only high arrhythmia risk)
89
Q

What are the causes of resp alk?

A 
central stim of resp
periph stim of resp
mech vent
pulmonary
salicylate intox
90
Q

What are the Sx of resp alk?

A

CNS: lightheadedness, confusion, Sz
decr cerebral BF
tetany/cramps
N/V

91
Q

How is resp alk treated?

A

correct underlying cause

vent, sedate, paralyze

Pharmacotherapy 1 (26 decks)

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