Acid Base Disorders Flashcards

1
Q
  1. Predict how a body in homeostasis would buffer an acidotic process using bicarbonate.
A

buffering acidotic process with bicarbonate is a response to respiratory acidosis and would consist of increased reabsorption of bicarbonate by the kidneys

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2
Q
  1. Compare and contrast the compensatory mechanisms involved in respiratory acidosis v. metabolic acidosis.
A

compensatory mechanism in respiratory acidosis is reabsorption of HCO3-

compensatory mechanisms in metabolic acidosis is hyperventilation to lower PaCO2

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3
Q
  1. Describe how a COPD exacerbation, vomitting or diarrhea may upset a patient’s acid/base status including compensatory changes.
A

COPD- hypoventaliation leads to hypercapnia and respiratory academia, compensation with increased bicarb

vomitting: loss of H+ causing metabolic alkalosis, compensation with hypoventilation
diarrhea: loss of bicarb, causing metabolic acidosis, compensation with hyperventilation

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4
Q
  1. Explain why a septic patient may be tachypneic in the absence of lung pathology.
A

IL-1 beta stimulates breathing centers to dissipate heat

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5
Q
  1. Estimate the magnitude of compensatory change expected for a defined change in PaCO2.
A

Acute R. Acidosis: change in HCO3= 0.1 x change PaCO2
Acute R. Alkalosis: change HCO3= 0.2 x change PaCO2

Chronic R. Acidosis: change HCO3=0.4 x change PaCO2

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6
Q
  1. Describe the stepwise approach to ABG analysis.
A
  1. What is the primary disorder?
  2. For metabolic acidosis, what is the anion gap?
  3. How much compensation is present?
  4. Is there a secondary process present?
  5. For really sick patients are there hidden problems and are the ABG results reliable?
    5a: is it possible -Henderson Hasselbach
    5b: the delta-delta Change in anion gap minus change in HCO3
    5c: Osmole gap (useful with suspected overdose)
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7
Q
  1. Contrast the physiologies of the disease and conditions typically associated with each primary acid-base disorder.
A

respiratory acidosis: CNS depression, NMJ disorders, airway obstruction, chest wall restriction, sever pulmonary restrictive disorders

respiratory alkalosis: central disorders, hypoxia, pulmonary disease, septicemia, hypotension, hepatic failure , drugs, high altitude, mechanical ventilation

metabolic acidosis: ketoacidosis, lactic acidosis, renal failure, salicylate into, methanol ingestion, loss of bicarb, RTA, villous adenoma, addition of acid to system

metabolic alkalosis: loss of H+ from extracellular fluid, external loss of chloride

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8
Q
  1. Contrast the pattern of changes in acid-base values in acute and chronic reparatory acid-base disorders.
A

acute: change in PaCO2 of 10 should cause pH change of 0.1
chronic: pH is close to normal due to adequate compensation (if there is one process going on)

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9
Q
  1. Describe the pattern of changes in acid-base values in the four primary acid-base disorders.
A

respiratory acidosis: v pH ^PaCO2, ^ HCO3-
respiratory alkalosis: ^pH v PaCO2 v HCO3-
metabolic acidosis: v pH v PaCO2 v HCO3-
metabolic alkalosis: ^pH ^PaCO2 ^HCO3-

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10
Q
  1. Explain how the “delta-delta” may indicate a second underlying acid-base disorder. Additionally, describe when it is applicable.
A

anion gap should match the change in bicarb, if it doesnt, there’s an additional process going on

  1. assess the measured v. normal values for anion gap (Delta) and the HCO3 (delta)
  2. if they are different (+/-2); add the anion gap to the measured HCO3 and assess the calculated HCO3 and the anion gap

if the cal. HCO3 is low, there is a non-gap metabolic acidosis in addition to gap acidosis

if cal HCO3 is high, there is also a metabolic alkalosis in addition to the gapped metabolic acidosis

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11
Q

Define the parameters for acidosis and alkalosis.

A

alkalemia pH>7.44
academia pH< 7.36

note acidosis and alkalosis are processes that cause alkalemia or academia

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12
Q

The changes in HCO3- in acute reparatory acidosis and alkalosis are NOT renal compensatory changes, but are….?

A

physiochemical effect of more or less carbonic acid (dissolved PaCO2) which then dissociates into H2O and HCO3-

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13
Q

Respiratory acidosis is present when PaCO2 is > ____ and pH is < _____

A

respiratory acidosis
PaCO2> 46 mmHg
pH < 7.35

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14
Q

What is the most common cause of respiratory acidosis?

A

acute or chronic airway obstruction

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15
Q
  1. Discuss consequences of respiratory acidosis.
A

CO2 diffuses into cells and CSF resulting cerebral vasodilation and possible cerebral edema (neurologic effects are most pronounced in respiratory acidosis)

increase in circulating catecholamines, resulting in sweating and hypertension and flushing

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16
Q

Respiratory alkalosis is present when PaCO2 is < ____ and pH is > _____

A

respiratory alkalosis:

PaCO2 7.45

17
Q
  1. Discuss the consequences of respiratory alkalosis.
A

reduced cerebral blood flow secondary to cerebral vasoconstriction

reduced calcium bonding and reduced ionized calcium which may lead to parenthesis and tetany

18
Q

Contrast the causes of metabolic acidosis that cause an elevated anion gap and those with normal anion gap.

A

elevated gap (addition of an acid often): ketoacidosis, lactic acidosis, renal failure, salicylate intoxication, methanol , ethylene glycol or paraldehyde ingestion

normal gap: loss of bicarbonate, villous adenoma, renal tubular acidosis, carbonic anhydrase inhibitors, hypreninemic, hypoaldosteronism, addition of acid: hydrochloric, ammonium chord or hyperalmination

19
Q

Discuss mechanisms that maintain a metabolic alkalosis.

A

(mechanisms that impair the ability of the kidneys to excrete excess HCO3-) extracellular fluid volume contraction, mineralocorticoid excess, hypkalemia

20
Q
  1. Discuss the consequences of alkalemia.
A

neuromuscular (hyperexcitability, lethargy and confusion), respiratory (hyperventilation, left shift oxyhemoglobin, increase in 2,3 DPG= right shift)
cardiac (arrhythmias, and enhanced digitalis toxicity)
metabolic (decreased ionized calcium, increased lactate production and slight increase in anion gap)

21
Q

What does apparent “over compensation” likely suggest?

A

there is more than one primary disorder present

additional clues include, change of PaCO2 and HCO3- in opposite directions, compensatory change is too large or small, change in HCO3- differs from change in anion gap

22
Q
  1. What mechanisms could cause increased or decreased CO2 retention?
A

retention: high CO2 production, low minute ventilation, increased dead space (work of breathing overwhelms ventilatory capacity)

increased elimination due to increased minute ventilation

23
Q

Hypoxemia and respiratory _____ very often accompany each other (due to attempts to compensate).

A

alkalosis (ie. pneumonia, pulmonary embolism, mild to moderate asthma, COPD, lung fibrosis and pulmonary edema (CHF)

24
Q

How would you calculate the anion gap?

A

anion gap = Na+ - (Cl- + HCO3-) or = unmeasured anions-unmeasured cations

25
Q

List 3 initiating factors for metabolic alkalosis.

A

loss of H+
loss of K+
increased HCO3- retention or generation

26
Q
  1. How do you estimate the amount of compensation (PaCO2) expected for metabolic acidosis/alkalosis?
A
PaCO2 = 1.5 x HCO3(measured) + 8
PaCO2= 0.7 x HCO3(measured) + 20 (+/-)
27
Q

What lab values are helpful when evaluating acid/base disorder?

A
serum electrolytes (K,Na,Cl, HCO3)
anion gap (Na-(Cl+HCO3)
renal function
glucose
CBC esp. WBC and hematocrit
other lab tests specific to diagnosis under consideration