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Equation for acidity as it relates to bicarb and CO2

Acidity = [bicarb]/ [CO2]


Describe compensation in metabolic and respiratory acid base disorders

Metabolic: CO2 changes in same direction as the change in bicarb (ie. In metabolic acidosis, bicarb is decreased so CO2 decreases to compensate). Respiratory: bicarb changes in same direction as the change in CO2 (ie. In respiratory alkalosis, CO2 is low, so bicarb decreases to compensate)


How does CO2 change for metabolic acidosis/alkalosis

acidosis: ∆PCO2 = 1 to 1.5 x ∆ HCO3. Alkalosis: ∆PCO2= 0.25 to 1.) x ∆HCO3


How does HCO3 change for respiratory acidosis/alkalosis

Acidosis: ∆ HCO3- = increased 1:10 PCO2 (acute) ∆ HCO3- = increased 4:10 PCO2 (chronic). Alkalosis: ∆ HCO3- = ↓2:10 PCO2 (acute) ∆ HCO3- = ↓4:10 PCO2 (chronic after 3-5 days)

Acidosis: ∆ HCO3- = increased 1:10 PCO2 (acute) ∆ HCO3- = increased 4:10 PCO2 (chronic). Alkalosis: ∆ HCO3- = ↓2:10 PCO2 (acute) ∆ HCO3- = ↓4:10 PCO2 (chronic after 3-5 days)


Causes of respiratory alkalosis

Breathing too much (hyperventilation): anxiety, lung disease, liver disease, sepsis, pregnancy


Causes of respiratory acidosis

Breathing too little: brain stem injury, drugs, hypothyroidism, primary alveolar hypoventilation, muscle fatigue


Causes of generation of metabolic alkalosis

inability to excrete bicarb, loss of H ions (vomiting, severe hypokalemia) contraction alkalosis, excess consumption (in packed RBCs, parenteral nutrition), increased H excretion (cuases bicarb resorption, seen in diureics and mineralocorticoid excess) and hypokalemia


What is contraction alkalosis

Loss of Cl rich and bicarb poor fluid (such as from vomiting, NG suctioning, diuretics) results in a loss of fluid, so bicarb concentration goes up


How does renal H excretion cause alkalosis

H excretion causes bicarb resorption. H excretion is increased with mineralocorticoids and diuretics


Causes of mineralocorticoid excess

Primary hyperaldosteronism, Cushings syndrome, congenital adrenal hyperplasia, hyperreninism, renal artery stenosis


How do diuretics cause metabolic alkalosis

Loop and thiazide diuretics increase the amount of Na in the tubule at the distal segments, so more Na is reabsorbed in these distal segments than normal. This increases the negative charge in the lumen, which enhances secretion of H and consequently the reabsorption of bicarb


Causes of an inability to excrete bicarb

hypovolemia and excess mineralocorticoid acitivity


What causes maintenance of metabolic alkalosis

ALWAYS due to the inability of the kidney to excrete excess bicarb. Chloride depletion, K depletion, increased mineralocorticoid activity, hypovolemia


Chloride responsive vs resistant metabolic alkalosis

Responsive: urine Cl is low (<20mEq) and chloride depletion with hypovolemia is the cause of the metabolic alkalosis. Seen in contraction, addition of bicarb, GI loss, renal H loss. Responds to saline. Resistant: chloride depletion with hypovolemia is NOT the cause of alkalosis. Seen in excess mineralocorticoid activity, intracellular H loss or rare conditions.


How does K depletion maintain metabolic alkalosis

increased aldosterone release


How does increased mineralocorticoid activity maintain metabolic alkalosis

Mineralocorticoids act on the H+-ATPase pump of the intercalated cell in the distal tubule. Stimulation of the H+-ATPase pump leads to secretion of H+ into the tubule lumen which is accompanied by bicarbonate resorption and thus maintains the metabolic alkalosis


How does hypovolemia cause metabolic alkalosis

Hypovolemia causes Na resorption which then causes bicarb and Cl resorption to maintain electroneutrality


Treatment of chloride responseive and resistant metabolic alkalosis

responsive: infusions of NaCl and/or KCl. Chloride resistant: block mineralocorticoid effect with spironolactone


How much acid is produced daily

60mEq. So it consumes 60mEq of bicarb


What parts of the nephron are involved in handling the daily acid load

proximal tubule (reabsorbs bicarb) and distal tubul/collecting duct (secretes H, makes bicarb, acidifies urine, excretes daily acid load)


Cortical vs medullary collecting ducts.

Corticle collecting duct is influenced by the resorption of sodium. Whereas the medullary collecting duct lumen is negative and the H atpase is more under the influence of aldosterone.


Types of cells in distal tubule and functions

Principle cell has apical Na channel and basolateral Na/K pump for Na resorption. Alpha intercalated cell has H ATPase on apical side for H excretion. Beta intercalated cell is responsible for bicarb resorption and has a bicarb/Cl co transporter on the basolateral side


Causes of metabolic acidosis

loss of bicarb( proximal tubule fails to reabsorb) or addition of acid ( distal tubule fails to secrete H)


Calculate serum and urine anion gap

serum: Na-Cl-bicarb (nl is 6-12). Urine: NH4 + Na + K - Cl


What causes positive urine anion gap

Renal loss of bicarbonate (renal tubular acidosis) causes positive urine anion gap . GI loss of bicarb causes negative urine anion gap


Causes of non-anion gap metabolic acidosis

Loss of bicarb from GI tract (diarrhea) or kidney ( renal tubular acidosis)


Types of renal tubular acidosis

Proximal: proximal tubule is damaged so that bicarb resorption can not occur. Distal: Distal tubule is damaged so that H excretion (and bicarb generation) does not occur. urine anion gap is positive. Hyperkalemic: ammonia production is inhibited by hyperkalemia, and ammonia usually binds to H and aids in H excretion. urine anion gap is positive number


Discuss urine pH in metabolic acidosis

Normally, urine pH should be low during metabolic acidosis as the kidneys try to remove H ions. So, in a non-anion gap metabolic acidosis, if the pH is acidic, the kidneys are functioning normally and a GI loss of bicarb is present. If urine is not acidic (ie. >5.3), renal tubular acidosis is occuring


What does urine anion gap tell us?

In metabolic acidosis, urine NH4 should increase (if kidneys are functioning normally), but NH4 is hard to measure, so it is inferred from urine anion gap. If NH4 is increased, urine Cl should also be increased to maintain electroneutrality and as Cl increases, urine anion gap becomes negative. A negative anion gap suggests that kidney function is normal and thus GI loss of bicarb must be occuring.


Causes of anion gap metabolic acidosis

MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acid, ethylene glycol, salicylates


Treatment of metabolic acidosis

Chronic: sodium bicarb therapy. Acute: sodium bicarb therapy is controversial b/c it may cause cardiovascular compromise


Mixed acid base disturbance

Two or more primary acid baste disorders. Compensation will be less than or greater than expected. If CO2 and bicarb differ from normal in opposite direction, a mixed disorder is always present.