Acid Base Disorders

often caused by respiratory stimulus

caused by primary depression of consciousness and respiration

measurement of acidity or alkalinity of arterial blood circulation, measures gases

Recommended to determine acid-base disorder associated with a change in ventilation

7.35-7.45

35-45 mmHg

80-100 mmHg

22-26 mEq/L

-2 to +2

Arterial pH below the normal range (pH<7.35)
pH= -log[H+] $\rightarrow$↓pH=acidemia

Arterial pH above the normal range (pH>7.45)
pH= -log[H+] $\rightarrow$↑pH=alkalemia

Process lowering pH, may be caused by a ↓ in serum
bicarbonate and/or a rise in the partial pressure of carbon dioxide ($PaCO_2$)

Process raising pH, may be caused by a rise in serum bicarbonate and/or a ↓ in $PaCO_2$

Maintained by various chemical buffer systems
• Primarily HCO3/CO2 buffer system
• CO2 via alveolar ventilation in the lungs
• HCO3 via excretion/reabsorpon in the kidney

• Poor vascular tone $\longrightarrow$ Hypotension
• Myocardial pump failure $\longrightarrow$↓Cardiac Output
• Altered Mental Status
• Reduced responsiveness to catecholamines
• Arrhythmias

Chemical Buffering
Respiratory Regulation
Renal Regulation

• Intracellular: proteins (albumin, globulins), phosphate
• Extracellular: bicarbonate, phosphate, ammonia, proteins
• Immediate effect (within minutes)

• Adjust $CO_2$ excretion (increase or decrease $PCO_2$)
• Over minutes to hours

• Adjust $HCO_3$ - excretion and reabsorption
• Over hours to days

the arterial pH is less than 7.35 and serum bicarbonate concentration ([HCO3−]) is less than 22 mEq/L

the arterial pH is greater than 7.45 and serum [HCO3−] is greater than 26 mEq/L

if the arterial pH is less than 7.35 and partial pressure of carbon dioxide (PCO2) is > 45 mm Hg (PaCO2 is high, ie. Hypoventilation)

If the arterial pH is greater than 7.45 and PCO2 is less than 35 mm Hg (PaCO2 is low, ie hyperventilation)

pH is in the normal range

only used in metabolic acidosis
$Expected pCO_2 = 1.5 x HCO_3 + 8 ∓ 2$

A primary metabolic disorder will result in respiratory compensaion
A primary respiratory disorder will result in metabolic compensation

Compensation does not return pH to normal

Patients never overcompensate

is the difference between extracellular cations and anions in the blood
$AG=Na^+ - (Cl^- + HCO_3)$

• Methanol
• Uremia
• DKA
• Paraldehyde
• Isoniazid, Iron, Ibuprofen (massive OD)
• Lactic acidosis (most common)
• Ethylene glycol
• Salicylates

$(AG-12)/(24-HCO_3^-)= DG$

If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure)
• Toxic ingestion is suspected!!

AG = < 12 (NAGMA)
H = hyperchloridemia/ hyperalimenta on (e.g., starting TPN).
A = acetazolamide use (causes loss of HCO3 by kidneys)
R = renal tubular acidosis
D = diarrhea (loose HCO3)
U = uretosigmoid fistula (because the colon will waste bicarbonate).
P = pancreatic fistula (because of alkali loss–the pancreas secretes a
bicarbonate-rich fluid)

• Correct underlying disorder
• Give sodium bicarbonate (only in severe cases)

Who gets sodium bicarbonate?
• Only in severe metabolic acidosis when pH < 7.15
• Toxin excretion
• Life-threatening hyperkalemia

Why doesn’t everyone get it?
• Worsen intracellular acidosis through CO2 production
• Overcorrection
• Hypernatremia or hypokalemia
• Alteration of O2-Hgb dissociation

low urine chloride (<10 mEq/L) are those that have chloride-responsive alkalosis,

normal or high urine chloride (>10 mEq/L) have chloride unresponsive alkalosis