Acid-Base Disorders Flashcards

1
Q

Acid-Base Balance

A
  • Normal blood pH: 7.4, range of 7.35-7.45
  • Narrow range is necessary to maintain normal physiologic functions
  • pH < 6.7 or >7.7 isn’t compatible with life
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2
Q

Acidosis Complications

A
  • Depress myocardium
  • Depress CNS/respiratory drive
  • Decrease oxygen carrying capacity
  • Decrease threshold for arrhythmia
  • Increase serum potassium
  • Decrease effect of catecholamines
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3
Q

Alkalosis Complications

A
  • Decrease respiratory drive
  • Impair oxygen delivery
  • Increase potential for cardiac arrhythmia
  • Decrease cerebral blood flow
  • Decrease serum potassium
  • Decrease ionized calcium
  • Seizures
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4
Q

Normal Blood Gas Values

A

pH = 6.1 + log[HCO3/0.03 * pCO2]

  • HCO3 typically ~24
  • pCO2 typically ~40
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5
Q

pCO2

A
  • Major acid in body
  • In equilibrium with carbonic acid (H2CO3)
  • Regulated by lungs (ventilation)
  • Disturbances in pCO2 are referred to respiratory
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6
Q

HCO3-

A
  • Serves as a buffer to acids in the body
  • Major base in body
  • Regulated by kidney
  • Disturbances in HCO3 are referred to as metabolic
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7
Q

Component of Analysis

A

Arterial Blood Gas Analysis

  • Measures pH, pCO2, pO2
  • Calculate HCO3-, O2 saturation

Serum Electrolytes

  • Total CO2 content - mainly HCO3, but also pCO2 and H2CO3
  • Total CO2 content ~ HCO3 on ABGs
  • Label vary with lab, some call carbon dioxide or bicarbonate
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8
Q

Compensation

A
  • Non-involved system attempts to move pH back to normal
  • Change in ventilation to compensate for metabolic disorders, occurs rapidly
  • Changes in serum HCO3 to compensate for respiratory disorders, occurs slowly
  • Compensation never completely corrects underlying disorder
  • Amount of compensation is predictable and can be calculated
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9
Q

Metabolic Disorder Compensation

A
  • Compensation by lungs
  • CO2 retention to promote acidosis: hypoventilation, shallow breathing
  • CO2 excretion to promote alkalosis: hyperventilation
  • Effect on pH seen in minutes, 12-24 hours for max effects
  • Expected Acidosis Compensation: pCO2 = (1.5(HCO3) + 8) +/-2
  • Expected Alkalosis Compensation: pCO2 = Increases 0.6 mmHg for each mEq/L increase in HCO3
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10
Q

Respiratory Disorder Compensation

A
  • Metabolic by kidneys
  • Increases HCO3 reabsorption and production by kidney to promote alkalosis
  • Increases HCO3 excretion to promote acidosis
  • Effect takes 12-24 hours and day for max effects
  • Expected Acute Acidosis Compensation: HCO3 - increase 1 mEq/L for every 10 mmHg INCREASE in pCO2
  • Expected Chronic Acidosis Compensation: HCO3 - increase 3.5 mEq/L for every 10 mmHg INCREASE in pCO2
  • Expected Acute Alkalosis Compensation: HCO3 - decrease 2 mEq/L for every 10 mmHg DECREASE in pCO2
  • Expected Chronic Alkalosis Compensation: HCO3 - decrease 5 mEq/L for every 10 mmHg decrease in PCO2
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11
Q

Metabolic Acidosis

A
  • Decrease in pH seen as a result of HCO3 decrease
  • Loss of HCO3 either renally (renal tubular acidosis) or non-renally (diarrhea, intestinal drainage)
  • Consumption from buffering: endogenous acids (lactic/keto) or exogenous acids (salicylates, chloride containing IVs, methanol)
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12
Q

Anion vs Non-Anion Gap

A
  • Two categories of Metabolic Acidosis
  • Anion gap is calculated to help determine etiology of acidosis

AG = Na - (Cl + Total CO2 content)

  • Normal AG ~ 9
  • Elevated AG >= 12, indicates presence of non-chloride containing anions
  • Unmeasured anions include sulfates, phosphates, organic anions, and toxins
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13
Q

Anion Gap Metabolic Acidosis

A

-Due to presence of unmeasured anions

Causes
1. Accumulation of organic acids in renal insufficiency (amino acids, sulfates, phosphate)
2. Ingestion of acid or acid by-product (toxic ingestion, propylene glycol <= avoid in renal impaired/neonates)
EX: Metformin, especially in acutely ill patients

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14
Q

MUDPILES

A
Etiologies of Anion Gap Metabolic Acidosis
M = Methanol
U = Uremia
D = Diabetic Ketoacidosis
P = paraldehyde, Propylene Glycol
I = Iron, Isoniazid (INH)
L = Lactic Acid
E = ethanol, ethylene glycol
S = Salicylates
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15
Q

Non-Anion Gap Metabolic Acidosis

A
  • Occurs when HCO3 deficit is replaced by chloride (to maintain electrical neutrality)
  • Occurs via kidney reabsorption or exogenous sources of chloride (NS, Hypertonic saline, HCl)
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16
Q

Non-Anion Gap Endogenous Causes

A
  • Renal tubular acidosis
  • Diarrhea
  • Intestinal fistula or drainage
  • Carbonic anhydrase inhibitors
  • Potassium-sparing diuretics
  • Hypoaldosteronism
17
Q

Non-Anion Gap Exogenous Causes

A
  • HCl ingestions: bicarbonate buffers acid and Cl remain

- Use of large amounts of Cl containing fluids: usually mild and requires no treatment

18
Q

Treating Acute/Severe Metabolic Acidosis

A
  • pH < 7.2
  • Treat underlying cause if possible
  • Alkali therapy isn’t indicated usually, can be harmful
  • If underlying cause can’t be removed/reversed, consider alkali therapy: IV sodium bicarbonate, tromethamine
19
Q

Sodium Bicarbonate + Severe Metabolic Acidosis

A
  • Unclear when beneficial, may have AE
  • AE: promote intracellular acidosis, shift oxygen satuation to decrease delivery to tissues, hypervolemic hypernatremia, over correct
  • HCO3 Dose = Vd HCO3 * BW (kg) * (Normal HCO3 - actual HCO3), administer 1/2 calculated dose of bicarbonate
  • Vd HCO3 = 0.5
  • Make sure patient is adequately ventilated, goal is to improve not correct to normal
20
Q

Tromethamine + Severe Metabolic Acidosis

A
  • THAM
  • Sodium free organic amine
  • Accepts protons
  • May be able to correct intracellular pH
  • Not shown to be more efficacious than sodium bicarboante
  • Administer slowly
  • AE: respiratory depression, chemical phlebitis, tissue damage
  • Not available in US
21
Q

Chronic Metabolic Acidosis Treatment

A
  • Correct cause
  • Gradual correction over days to weeks
  • Oral admin of bicarbonate (NaHCO3)
  • Oral admin of bicarbonate precursor (citrate, acetate)
22
Q

Metabolic Alkalosis

A
  • Increase pH and HCO3
  • Loss of Cl-rich, bicarbonate poor fluid (loop/thiazide diuretics, emesis, nasogastric suctioning)
  • Excessive bicarbonate intake
  • Volume depletion: enhance reabsorption of bicarbonate
23
Q

Metabolic Alkalosis Categories

A
  • Based on response to saline volume expansion
  • NaCl responsive: urine [Cl] < 10
  • NaCl resistant: urine [Cl] > 20
24
Q

NaCl Responsive Causes

A
  • Vomiting, gastric drainage
  • Some cases of secretory diarrhea that cause chloride loss without proportional bicarbonate loss
  • Excessive diuretic use (loop/thiazide)
  • Have signs of intravascular volume depletion usually
25
Q

NaCl Resistant Causes

A
  • Excess mineralcorticoid activity (Cushings, hyperaldosteroinism, corticosteroids) - increase Na reabsorption in distal tubule, K/H+ secretion into tubule lumen which promotes HCO3 generation/reclamation
  • Alkali ingestion
  • Significant potassium and magnesium deficiency
26
Q

Metabolic Alkalosis Presentation

A
  • No unique signs/symptoms with mild-moderate cases

- Severe (pH > 7.6): cardiac arrhythmia, neuromuscular irritability (tetany, hyperreflexia), mental confusion

27
Q

Metabolic Alkalosis Treatment

A
  • Correct cause/underlying condition
  • Chloride usually responsive to NaCl volume expansion with NS: frequently need to replace with potassium chloride and magnesium too
  • GI losses: antiemetics, H2 blockers, PPI
  • Other treatments: HCl, ammonium chloride, arginine HCl
  • Consider carbonic anhydrase inhibitors (acetazolamide) if not able to tolerate fluid
  • Chloride resistant: correct cause, replace potassium/magnesium if in deficit, treat with spironolactone, amiloride, or triamterene
28
Q

Respiratory Acidosis Causes

A

Acute

  • Pulmonary emboli
  • Severe pneumonia/bronchospasm
  • Airway obstruction
  • Trauma - crash, pneumothorax
  • Narcotic/sedative overdose
  • Increased CO2 production from excess glucose administration

Chronic

  • Neuromuscular abnormalities (MS, polio)
  • Pulmonary abnormalities (COPD)
29
Q

Respiratory Acidosis Treatment

A

Acute: usually with concomitant hypoxia

  • Treat underlying cause
  • Maintain airway and improve oxygen status with supplemental oxygen
  • Ventilation with or without intubation

Chronic

  • Treat underlying disease/cause
  • Cautious use of oxygen since may remove respiratory drive since its hypoxemic dependent
30
Q

Respiratory Alkalosis Causes

A

Central stimulation of Respiration

  • Anxiety, pain, fear
  • Head trauma, brain tumors
  • Pregnancy
  • Progesterone
  • Catecholamines, theophylline, nicotine, salicylates, analeptics
  • Hypoxia
  • Chronic liver disease

Peripheral Stimulation of Respiration

  • Pulmonary emboli
  • CHF, hypotension
  • High altitude

Other Causes

  • Excessive mechanical ventilation
  • Voluntary hyperventilation
31
Q

Respiratory Alkalosis Presentation

A
  • CNS: light-headedness, confusion, syncope, seizures
  • CV: arrhythmia
  • GI: N/V
  • Metabolic: hypocalcemia, hyperchloridemia, hypokalemia, hypophosphatemia
32
Q

Respiratory Alkalosis Treatment

A
  • Correct Cause: pain control, turn down ventilator, breathe into paper bad
  • Oxygen therapy if hypoxemic
  • If asymptomatic, treatment might not be required
33
Q

Compensation Rules

A
  • Primary disturbance always invokes a compensation response to try and normalize pH
  • Never totally corrects pH
  • Degree of compensation is predictable and a greater/lesser response represents a secondary/mixed disorder
34
Q

Mixed Acid-Base Disorders

A
  • Two of the above disorders occurring simultaneously

- Each have their own methods of how to treat and possible causes

35
Q

R Acidosis + M Acidosis

A

Causes

  • Cardiorespiratory arrest
  • Lung disease patients who develop poor tissue perfussion (shock)
  • Unable to compensate
  • Treat both disorders: improve oxygen delivery and give alkali therapy
36
Q

R Alkalosis + M Alkalosis

A

-Commonly occur together
Causes
-Over-aggressive mechanical ventilation and nasogastric sunctioning
-Hyperventilation from hepatic cirrhosis and use of loop diuretics

-Treat by administering NaCl or KCl and correct hyperventilation

37
Q

R Alkalosis + M Acidosis

A

-pH closer to normal values than if either existed alone
Causes
-Salicylate intoxication
-Pulmonary renal syndromes

-Treat by correcting cause