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Emergency Critical Care VTS > Acid/Base > Flashcards

Acid/Base Flashcards

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1
Q

What is the equation of PAO2?

A
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2
Q

Anticipated Compensation for Acid-Base Disorders

A
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3
Q

Herderson-Hasselbalch

A

Used to estimate the pH of a buffer solution

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4
Q

Anion Gap equation

A

(Na+K+) - (HCO3 + Cl-)

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5
Q

pH normal

A

7.35 - 7.45

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6
Q

PaCO2 normal range

A

35-45

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7
Q

HCO2 normal range

A

20-28

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8
Q

Rule of 4 for pH, PaCO2, HCO3

A

Averages
pH: 7.4
PaCO2: 40
HCO3: 24

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9
Q

Normal anion gap

A

12-24meq/L

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10
Q

What does high anion gap indicate?

A

Cations > anions
If Na and K are normal, likely to indicate other cations are high
- lactic acidosis
- ketoacidosis
- renal failure (uremic - sulphates and phosphates)
- toxin (ethylene glycol, sialcyates - aspirin/sunscreen)

Pneumonic: DUEL
DKA
Uremic
Ethylene glycol
lactic acidosis

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11
Q

Indications for metabolic acidosis with normal anion gap

A

GI or renal bicarb loss
impaired renal excretion

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12
Q

What are four causes of Metabolic Alkalosis?

A

Bicarbonate concentration increases
examples:
- GI outflow obstruction
- hypokalemia (K+ shifts out of cells in exchange for H+ ions into the cells increasing blood pH)
- bicarbonate administration
- excessive loss of Chloride (Cl-)
- volume depletion
- loop diuretics and thiazide diuretics
- vomiting (loss of acid in stomach)
- Excessive NGT suctioning (removing the stomach acid)

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13
Q

What are four methods of developing metabolic acidosis?

A
  1. Loss of bicarbonate (e.g. small bowel diarrhea)
  2. Inability to excrete H+ (e.g. chronic renal failure)
  3. Increase acid production (e.g. increased cellular metabolism causing an increase in formation of biproducts (lactate, CO2, H+), DKA - build up of ketone bodies –> Kussamaul breathing - large quick breaths to get rid of CO2)
  4. Addition of exogenous acids to the body.
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14
Q

What are clinical signs of hypernatremia

A

nonspecific central nervous system signs
* lethargy
* weakness
* behavioral or postural changes
* ataxia
* seizures
* altered level of consciousness
* coma
* death

clinical signs not observed until sodium concentrations > 170mEq/L

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15
Q

What are idiogenic osmoles? When and why are they produced?

A

The body makes intracellular osmolytes when hypernatremia persists for more than a few hours to help restore the osmolality of the intracellular space. Full compensation occurs in roughly 24 hours.

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16
Q

Explain why rapid sodium correction is detrimental?

A

Because the idiogenic osmoles allowed for intracellular fluid and extracellular fluid to be in equilibrium. Rapid fluid administration will reduce extracellular osmolality. The intracellular fluid is hyperosmolar compared to the extracellular fluid, so water will travel back into cells resulting in cellular swelling, cerebral edema and life-threatening neurological dysfunction.

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17
Q

What is the free water deficit equation?

A
18
Q

What is the maximum rate of sodium correction?

A

no more than 0.5mEq/L/hr

19
Q

What do nursing staff have to monitor for when patient is undergoing sodium correction?

A
  • changes in mentation
  • level of consciousness
  • pupil size
  • seizures
  • changes in breathing pattern as indicator of cerebral edema
  • Cushing’s reflex
20
Q

What is central pontine myelinolysis and when does it occur?

A

neurological injury to the myelin sheath covering the nerve cells in the middle of the brainstem (pons) resulting from rapid hyponatremia correction.

Effects are permanent

21
Q

How fast should hypokalemia be corrected?

A

No more than 0.5-1mEq/L/hr

22
Q

What direction will potassium go with pH correction?
What are considerations for normal potassium levels and acidosis?

A

Plasma potassium concentrations increase with acidosis as the H+ moves intracellularly in place of K+. Therefore K+ will go in the direction of pH.

Indications: if patient has normal potassium values and is acidotic, the K+ values will drop as pH is corrected.

23
Q

What are the effects of potassium on resting membrane potential?

What are indications for hyperkalemia?

A

Potassium will move resting membrane potential closer to threshold action potential.

If resting membrane potential exceeds the threshold action potential, in case of hyperkalemia, the cell will be unable to repolarize and therefore cannot depolarize.

24
Q

What are three causes of hyperkalemia?

A
  1. cellular shifting or translocation
  2. decrease urine excretion
  3. increase intake of potassium
25
Q

What is the course of treatment for severe hyperkalemia?

A
  1. evaluate ECG
  2. Dilute with IVF therapy
  3. IV calcium to move threshold potential away from altered resting membrane potential.
  4. Shift potassium intracellularly.
26
Q

What are three approaches to drive potassium intracellulary?

A
  1. insulin and supplement with glucose to maintain normoglycemia
  2. beta 2 adrenergic antagonist (albuterol, terbutaline)
  3. Administer bicarbonate –> has side effects, not commonly used
27
Q

What are three causes for hypokalemia?

A
  1. Redistribution of potassium from ECF to ICF
  2. Excessive losses
  3. Inadequate intake
28
Q

What are 4 ways redistribution of potassium from ECF to ICF can occur?

A
  1. secondary to insulin therapy
  2. metabolic acidosis
  3. refeeding syndrome
  4. beta-adrenergic agonist therapy
29
Q

What are some ways to have excessive potassium losses?

A
  1. Osmotic or post obstructive diuresis following urethral obstruction
  2. loop diuretic therapy
  3. Chronic kidney disease
  4. hyperaldosteronism
  5. diabetes mellitus
  6. renal tubular acidosis
  7. vomiting
  8. diarrhea
30
Q

What are clinical symptoms of hypokalemia?

A
  1. generalized skeletal muscle weakness
  2. hypoventilation to impared ventilation
  3. ventroflexion of neck in cats with severe hyperkalemia
31
Q

What changes to the ECG are associated with hypokalemia?

A

atrioventricular dissociation, wide Q-T bradycardia

32
Q

What regulates calcium excretion and absorption?

A

Parathyroid hormone released from the parathyroid gland

33
Q

HARDIONS-G

Causes for hypercalcemia

A

H: hyperparathyroidism
A: Addison’s disease (hypoadrenocorticism)
R: renal disease
D: vitamin D toxicities (generally for rodenticide toxicity or calcium supplementation)
I: Idiopathic hypercalcemia of flines
O: Osteolytic disease
N: Neoplascia
S: spurious (lab error)
G: granulomatous disease

34
Q

How does hypercalcemia affect ECG readings?

A

QT shortening
PR interval elongation

bradyarrhythmias; rarely see ventricular fibrillation

35
Q

What are clinical signs of hypecalcemia?

A

polyuria/polydipsia
anorexia
weakness
lethargy
seizures

36
Q

What are some causes for hypocalcemia?

A

CKD/AKI
Eclampsia (calcium utilized by neonates)
hypoparathyroidism
ethylene glycol toxicity
GI disease that cause malabsorption
protein losing enteropathy
massive blood transfusion with citrate
hypomagnesmia
acute tremor lysis syndrome

37
Q

What is the correlation of calcium with albumin

A

large portion of calcium is protein bound, therefore hypoalbinemia will reduce serium calcium levels (not iCal)

38
Q

What is the corrected calcium equation?

A

measured Ca - albumin (g/dL) + 3.5

39
Q

What are clinical signs of hypocalcemia?

A

muscle fasciculations
seizures
muscle cramping
facial rubbing
panting
pyrexia
pu/pd
rare seen: hypotension and death

40
Q
A

Emergency Critical Care VTS (21 decks)

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