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From Flashcardlet > Acid Base, Fluids, Elytes > Flashcards

Acid Base, Fluids, Elytes Flashcards

1
Q

Define COP

A

Force generated when 2 solutions with different concentrations of colloids are separated by a semipermeable membrane

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2
Q

What is albumin’s contribution to COP?

A

65-80%

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3
Q

What is the Gibbs-Donnan effect?

A

Sodium’s constribution to COP b/c they are noncovalently bound to negatively charged albumin

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4
Q

What besides albumin and sodium contribute to COP?

A

globulins, fibrinogen, hemoglobin, RBC (<5%)

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5
Q

Odunayo, JVECC, 2011. COP in WB vs. plasma. Main findings?

A

plasma COP * lower than whole blood COP with mean difference 0.5 mm Hg; regardless both in reference range (21-25 mm Hg); no diff in sex, decreased slightly when frozen, hemolysis had no effect

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6
Q

Hayes, JVECC, 2011. What significantly affected TPP readings?

A

hypercholesterolemia and hyperglycemia

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7
Q

An increase in serum glucose by ___ assc’d with increase in refractometer TPP of ____. Hayes, JVECC, 2011

A

10 mmol/L

0.23 g/dL

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8
Q

An increase in serum cholesterol of 38.6 mg/dL (1 mmol/L) assc’d with increase in refractometer TPP of ____.

A

0.14 g/dL

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9
Q

TPP < 58 g/L was highly specific for serum hypoalbuminemia and hypoproteinemia. T/F Hayes, JVECC, 2011

A

T - 84% specificity

nonlinear relationship

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10
Q

What formula predicted toal protein by refractometer?

A

serum protein (g/L) = 0.3 + 0.84(refractometer TP)

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11
Q

How does refractometer work?

A

measures angle of refraction b/t air and aqueous solution

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12
Q

Mechanisms of iHCa in trauma patients.

A 
Calciuresis
Dilution following fluids
Cellular uptake of calcium
Chelation with citrate in blood products
Aberrations in hormones and electrolytes that regulate iCa
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13
Q

Holowaychuk, JVECC, 2011. Significant differences in iHCa trauma patients.

A

higher HR, lower SBP, higher ATT, higher systems score, lower HCO3, higher BE, higher lac, higher creat, higher mortality, longer in hospital, needed more transfusion, colloid, oxygen, vasopressor

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14
Q

The trauma system scores uses what 6 body systems?

A

skin, appendage, thorax, head, abdomen, spine

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15
Q

iHCa (<1.25) found in __% trauma patients. Holowaychuck, 2011, JVECC

A

16%

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16
Q

What are the 3 independent variables in Stewart AB?

A

Atot, pCO2, SID

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17
Q

What is Atot?

A

total plasma concentration of nonvolatile weak buffers such as albumin, globulins, and phosphate

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18
Q

What is SID?

A

Difference in charge between fully dissociated and therefore nonreactive or nonbuffering strong cations and strong anions at physiologic pH

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19
Q

What is the strong ion gap?

A

SIDa - SIDe

SIDa: Na, K, Ca, Mg, Cl, lactate
SIDe: HCO3, albumin, phosphate

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20
Q

SIG increased by ______ and decreased by ______.

A

unmeasured anions, unmeasured cations

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21
Q

What was the mean and derived ref range for SIG using SIDa-SIDe? Fettig, JVECC, 2012

A

mean 7.13; RR: 1.85-10.61

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22
Q

What was the mean and derived reference range for SIG using (alb) x 4.9-AG? This formula derived from Atot and Ka on healthy dogs. Fettig, JVECC, 2012

A

mean -0.22, RR: -5.36-5.18

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23
Q

SIG in vivo is usually…

A

positive due to an excess of unmeasured anions compared to unmeasured cations

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24
Q

BE takes into account…

A

free water, chloride, protein, and phosphate concentrations

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25
Q

T/F. A simple conversion factor can convert SIG1 to SIG2.

A

F - values are not interchangable and conversion factor cannot be used

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26
Q

What are the two methods to correct hyponatremia?

A
  1. Sodium deficit [(desired change)] x TBW
  2. Adrogue-Madias to determine estimation of effect of infusing a 1 L bag of fluids:
    (desired change) = (infusate Na - serum Na) / (TBW +1)
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27
Q

How do you calculate free water deficit?

A

TBW x (serum Na/normal sodium - 1)

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28
Q

For every 100 mg increase in glucose, sodium decreases…

A

1.6 - pseudohyonatremia

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29
Q

How much sodium does 23.4% have in mEq/ml

A

4

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30
Q

Myelinolysis lesions in dogs are typically found where?

A

thalamus (pons in humans)

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31
Q

What are the most common reasons for a Na/K less than 27:1

A

renal failure, hypoadrenocorticism, GI dz (whips, salmonella, duodenal perforation)

also chronic chylothorax, lung lobe torsion, neoplastic pleural effusion, pregnancy in greyhounds

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32
Q

What is the most notable adverse metabolic effect of hypokalemia?

A

glucose intolerance, insulin release impaired

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33
Q

Cardiac effects of hypokalemia.

A

High intracellular to extracellular K induces state of electrical hyperpolarization leading to prolongation of the the action potential. This may predispose to atrial and ventricular tachyarrhythmias, AV dissociation, and ventricular fibrillation

Predisposes to dig induced cardiac arrhythmias and causes myocardium to be refractory to class 1 antiarrhythmics

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34
Q

How do you treat a normovolemic, hyponatremic patient in an emergency setting of hyponatremia (chronic)?

A

mannitol along with furosemide to ensure that electrolyte free water is excreted along with the mannitol; goal = increase sodium no more than 10 mEq/L during first 24 hours

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35
Q

Causes of pseudohyperkalemia

A

thrombocytosis, leukocytosis, Akita dogs (their RBC have a fxnal Na-K ATPase so have high intracellular K),

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36
Q

Drugs that promote hyperkalemia

A

ACE inhibitors, Beta blockers, K sparing diuretics

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37
Q

Complexed calcium is bound to…

A

phosphate, bicarbonate, lactate, citrate, oxalate

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38
Q

Principle actions of PTH

A

increased tubular reabsorption of calcium, increased osteoclastic bone resorprtion, increased production of 1,25(OH)2D3

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39
Q

Calcitonin

A

Produced by thyroid gland in response to hypercalcemia, acts on bone to inhibit osteoclastic bone resorption activity

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40
Q

Effects of alkalosis and acidosis on ionized calcium?

A

alkalosis decreases iCa (b/c more bound to protein)

acidosis increases iCa (b/c less bound to protein)

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41
Q

Clinical signs of hypercalcemia

A

PU/PD (dogs only), anorexia, constipation, lethargy, weakness, ataxia, obtundation, listlessness, muscle twitching, seizures, coma

42
Q

ECG findings of hypercalcemia

A

prolonged PR interval, widened QRS, shortened QT, shortened or absent ST, widened T wave, bradyarrhythmias that progress to complete heart block, asystole, cardiac arrest

43
Q

Most common cause of hypercalcemia in dogs vs cats?

A

dogs cancer

cats idiopathic

44
Q

Why is 0.9% saline the fluid of choice for hypercalcemia?

A

Additional sodium ions present competition for calcium and result in reduced renal tubular calcium reabsorption

Furosemide enhances urinary calcium loss

45
Q

Mechanism of hypercalcemia in fungal disease

A

due to dysregulated production of 1,25-(OH2)D3 (calcitriol) by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation.

46
Q

Steroid MOA for hypercalcemia

A

reduces bone resorption, increases urinary loss, decreases intestinal calcium absorption

47
Q

Calcitonin MOA for hypercalcemia

A

decreases osteoclast bone resorption

48
Q

Bisphosphonates MOA for hypercalcemia

A

Decreases osteoclast activity and bone resorption

Ex: pamidronate, zoledronate, alendronate (oral)

49
Q

Calcimimetic MOA

A

Activate the calcium sensing receptor and therefore decrease PTH

50
Q

ECG abnormalities of hypocalcemia

A

decreased inotropy and chronotropy (bradycardia), prolonged QT interval (d/t proloned ST segment), deep, wide T waves, or AV block

51
Q

Serum magnesium breakdown

A

66% (cats) 63% (dogs) ionized, 4-6% complexed to anions, 30-31% protein bound

52
Q

Where is most Mg absorbed in GI tract?

A

jejunum and ileum

53
Q

Where is most Mg absorption in kidney?

A

LoH

54
Q

ECG changes of hypomagnesemia

A

prolongation of PR interval, widening of QRS, depression of ST, peaking of T wave

55
Q

What effect does magnesium have on acetylcholine release?

A

Hypomagnesemia increases acetylcholine release and enhances the excitatiblity of nerve and muscle membranes; also increases intracellular content of skeletal muscle

56
Q

Mg relationship to Ca

A

Hypomagnesemia impairs PTH release and enhances calcium movement from extracellular fluid to bone

57
Q

Endocrinopathies associated with hypermagnesemia

A

hypoadrenocorticism, hyperparathyroidism, hypothyroidism

58
Q

ECG findings of hypermagnesemia

A

prolonged PR and widened QRS

59
Q

Hypermagnesemia results in varying degrees of….

A

neuromuscular blockade

60
Q

How do you treat hypermagnesemia

A

Stop exogenous sources
Calcium salts are direct antagonists of Mg at NM jxn
Saline diuresis +/- furosemide
Severe signs - anticholinesterase

61
Q

How do glucose and insulin affect Ph

A

shifts intracellular and trapped as glucose-6-phosphate

62
Q

Endocrinopathies associated with hyperphosphatemia

A

Hypoparathyroidism, GH excess (acromegaly, hyperthyroidism)

63
Q

What is base excess?

A

the amt of strong acid or base needed to restore plasma pH of iL of blood to 7.4 at a PaCO2 of 40 mm Hg and temperature of 37 C

provides a measure of metabolic component independed of changes in PCO2

64
Q

What is the expected compensation for metabolic acidosis?

A

PCO2 decreases by 0.7 mm Hg for every 1 mEq/L decrease in bicarb +/-3

65
Q

What is the expected compensation for metabolic alkalosis?

A

PCO2 increases by 0.7 mm Hg for every 1 mEq/L increase in bicarb +/- 3

66
Q

What is the expected compensation for acute vs. chronic respiratory acidosis?

A

Bicarb increases 0.15 (acute) or 0.35 (chronic) per 1 mm Hg increase in PCO2

67
Q

What is the expected compensation for acute vs. chronic respiratory alkalosis?

A

Bicarb decreases 0.25 (acute) or 0.55 (chronic) per 1 mm Hg decrease in PCO2

68
Q

What is TCO2?

A

sum of bicarb, carbonic acid, and dissolved CO2 in the system

69
Q

When acidosis occurs without an increase in AG, the cause is

A

hyperchloremia

So, hyperchloremic metabolic acidosis = normal AG acidosis whereas a normochloremic metabolic acidosis = high AG acidosis

70
Q

Increased SID =

A

alkalosis

71
Q

Decreased SID =

A

acidosis

72
Q

SID estimated by…

A

Na - Cl

73
Q

SID really ….

A

Na+K+Ca+Mg-Cl-other strong anions

74
Q

Causes of hyponatremia

A

sodium loss thru vomiting or diarrhea, 3rd space loss, nephrotic syndrome, hypoadrenocorticism, CHF, psychogenic polydipsia, diuretic administration, hypotonic fluid use, SIADH

75
Q

Sodium contribution to A/B

A

Hyponatremia is acidifying
Hypernatremia is alkalinizing

Change BE = 0.25 (dog sodium-normal sodium)
Change BE = 0.22 (cat sodium-normal sodium)

Hyponatremia decreases BE (more negative)
Hypernatremia increases BE (less negative)

76
Q

Chloride contribution to A/B

A

Hypochloridemia is alkalinizing
Hyperchloridemia is acidifying

Corr Cl / pet Cl = Normal Na / pet Na

Change BE = Normal Cl - pet’s Cl

Hypochloridemia will increase BE (less negative)
Hyperchloridemia will decrese BE (more negative)

77
Q

Protein’s contribution to A/B

A

Hyperproteinemia is acidifying
Hypoproteinemia is alkalizing

Change BE = 3 (Normal protein - Pet’s protein)
Change BE = 3.7 (Normal albumin - Pet’s albumin)

Hyperproteinemia increases BE (more negative)
Hypoproteineia decreases BE (less negative)

78
Q

Phosphorus’s contribution to A/B

A

Hyperphosphatemia is acidifying
Hypophosphatemia is alkalinizing

Change BE = 0.6 (Normal Ph - Pet’s Ph)

Hyperphosphatemia increases BE (more negative)
Hypophosphatemia decreases BE (less negative)

79
Q

d-lactate

A

metabolic product of bacterial metabolism, also reported to be clinically significant in humans with short bowel syndrome, cats with propylene glycol, DM cats, EPI cats

80
Q

l-lactate

A

isomer produced metabolically in dogs and cats
many hospital analyzers only measure l-lactate, so d-lactate would be recognized as a metabolic acidosis w/ an increased AG not accounted by routine lactate measurement

81
Q

What is the purpose of lactate synthesis in aerobic metabolism?

A

to regenerate nicotinamide adenine dinucleotide (NAD) so that glycolysis can procede

NAD essential reducing agent for glycolysis

Lactate can also be transported to liver under aerobic conditions for energy storage via gluconeogenesis and glycogen synthesis –> Involves conversion of lactate to pyruvate in liver (cori cycle) under aerobic conditions to drive Kreb’s cycle

82
Q

What is the difference between A and B lactate?

A

Type A = true hypoxic form

Type B = nonhypoxic form, occurs in face of adequate oxygen delivery when mitochondrial oxidative fxn is abnormal

83
Q

Causes of Type A lactic acidosis

A

Hypoxemia, anemia, poor perfusion, increased tissue demand (exercise, convulsions, heat stroke)

84
Q

Causes of Type B lactic acidosis

A

Drugs, toxins, hypoglycemia, DM, liver failure, renal failure, LSA, sepsis, inborn errors in metabolism

85
Q

What toxins cause type B lactic acidosis?

A

cyanide, ethanol, ethylene glycol

86
Q

What drugs cause type B lactic acidosis?

A

salicylate, lactulose, beta agonists, nitroprusside, acetaminophen, propylene glycol, phenformin

87
Q

What (other than drugs and toxins) cause type B lactic acidosis?

A 
SIRS
DM
Malignancy (hematologic)
Thiamine deficiency
Liver failure
Hypoglycemia
Inborn errors or metabolism
Mitochondrial myopathies
88
Q

What are the metabolic complications of TLS?

A

hyperphosphatemia, hyperkalemia, hypocalcemia, metabolic acidosis

89
Q

When would you expect to hear a mill weed murmur?

A

air embolism

90
Q

What variables decreased in Muir’s study on LRS to anesthetized dogs, JAVMA 2011?

A

PCV, total protein, albumin, hemoglobin, whole blood viscosity

91
Q

Crystalloids with SID of ___ maintain base excess near zero and are considered balanced.

A

24

92
Q

Conclusions of Muir’s study…JAVMA, 2011

A

Conventional rates of LRS to healthy iso’d dogs increase plasma volume and CO and decrease blood viscosity and protein but do not increase rate urine prod’n or produce consistent and significant alterations in mean CVP or arterial BP

93
Q

Boag, JVIM, 2005. Dogs with linear FBs were more likely to have what e-lyte abnormality?

A

Hyponatremia.

Study also found hypochloremic metabolic alkalosis found in most regardless of GI or jejunal FB. 25% hypokalemic

94
Q

i-hypoCalc in critically ill dogs (Holowaychuk, 2009, JVIM). Findings?

A

16% critically ill dogs hypocalcemic
ihypo Ca assc’d with longer ICU and hospital stays, but not with decreased survival. Septic dogs (>3 SIRS criteria and positive culture) more likely to have ihypo Ca

95
Q

Normal value for Atot in dogs vs. cats

A
  1. 4 +/- 8.6 mmol/L (equivalent to 0.273 mmol/g total protein or 0.469 mmol/g albumin) DOGS
  2. 3 +/- 4.6 mmol/L cats
96
Q

Normal Ka dogs vs. cats

A
  1. 17 +/- 0.11 x 10^-7 DOGS
  2. 67 +/- 0.4 x 10^-7 CATS

Ka = dissociation constant for plasma nonvolatile buffers

97
Q

Normal pKa dogs

A

7.77

98
Q

Normal SID in dogs vs. cats

A

27 mEq/L dogs

30 mEq/L cats

99
Q

Net protein charge for normal canine plasma

A
  1. 25 mEq/g total protein

0. 42 mEq/g albumine

100
Q

What are the 6 primary acid-base disturbances in the strong ion approach?

A
  1. respiratory acidosis
  2. respiratory alkalosis
  3. strong ion acidosis (decreased SID)
  4. strong ion alkalosis (increased SID)
  5. nonvolatile buffer ion acidosis (increased albumin, globulin, or phosphate)
  6. nonvolatile buffer ion alkalosis (decreased albumin, globulins, or phosphate)

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