Acid-Base Disorders Flashcards
Acid-Base Balance
- 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
Acidosis Complications
- Depress myocardium
- Depress CNS/respiratory drive
- Decrease oxygen carrying capacity
- Decrease threshold for arrhythmia
- Increase serum potassium
- Decrease effect of catecholamines
Alkalosis Complications
- Decrease respiratory drive
- Impair oxygen delivery
- Increase potential for cardiac arrhythmia
- Decrease cerebral blood flow
- Decrease serum potassium
- Decrease ionized calcium
- Seizures
Normal Blood Gas Values
pH = 6.1 + log[HCO3/0.03 * pCO2]
- HCO3 typically ~24
- pCO2 typically ~40
pCO2
- Major acid in body
- In equilibrium with carbonic acid (H2CO3)
- Regulated by lungs (ventilation)
- Disturbances in pCO2 are referred to respiratory
HCO3-
- Serves as a buffer to acids in the body
- Major base in body
- Regulated by kidney
- Disturbances in HCO3 are referred to as metabolic
Component of Analysis
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
Compensation
- 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
Metabolic Disorder Compensation
- 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
Respiratory Disorder Compensation
- 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
Metabolic Acidosis
- 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)
Anion vs Non-Anion Gap
- 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
Anion Gap Metabolic Acidosis
-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
MUDPILES
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
Non-Anion Gap Metabolic Acidosis
- 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)