Acid/Base

Question 1

What is the difference between acidosis and acidemia? Alkalosis and alkalemia?

Answer 1

Acidosis/alkalosis are processes.

Acidemia/alkalemia are states of increased or decreased H+.

Question 2

1. (decrease in CO2 resulting in a increase in pH)
2. (increase in CO2 resulting in a decrease in pH)
3. (increase in HCO3 resulting in an increase in pH)
4. (decrease in HCO3 resulting in decrease in pH)

Answer 2

1. Respiratory alkalosis (decrease in CO2 resulting in a increase in pH)
2. Respiratory acidosis (increase in CO2 resulting in a decrease in pH)
3. Metabolic alkalosis (increase in HCO3 resulting in an increase in pH)
4. Metabolic acidosis (decrease in HCO3 resulting in decrease in pH)

Question 3

Primary respiratory alkalosis is ALWAYS caused by______. It can occur due to _______ (many).

Answer 3

Breathing too much (aka hyperventilation).

pulmonary diseases, hypoxemia, voluntary, mechanical ventilation, and miscellaneous causes that directly simulate the respiratory center such as fever, liver disease, pregnancy, head injuries, salicylate toxicity (salicylate toxicity results in a concomitant metabolic acidosis)

Question 4

In acute respiratory alkalosis, the bicarbonate is expected to fall by ______ fall in PCO2; in chronic respiratory alkalosis, the bicarbonate is expected to fall by ______ fall in PCO2.

Answer 4

2 mEq/L for every 10 mmHg

4 mEq for every 10 mmHg

Question 5

Potential lab abnormalities, symptoms, and consequences of respiratory alkalosis:

Answer 5

Lab abnormalities: decreased potassium (small); decreased phosphorus (may be large).

Symptoms: neurologic (paresthesias, carpopedal spasms).

Consequences: decreased intracranial pressure, cardiac arrhythmias.

Question 6

Treatment of respiratory alkalosis

Answer 6

Treat the underlying cause. If alkalemia is severe (pH >7.55), then depressing ventilation with a sedative could be considered to prevent arrhythmias, tetany, etc.

Question 7

Primary respiratory acidosis is ALWAYS from____.

Answer 7

inadequate respiration

Question 8

Name the four broad categories of respiratory acidosis and some specific disease states that fall within each.

Answer 8

1) Sensing and signalling refers to processes that impair the medullary control center (e.g., sedatives, obesity hypoventilation syndrome) or impair neurologic signals to the muscle of respiration (e.g., amyotrophic lateral sclerosis, Guillian-Barre syndrome
2) Muscles and motion refers to processes that impair function of the respiratory muscles (e.g., hypokalemia, periodic paralysis)
3) Free flow refers to processes that impair the free flow of air resulting in airway obstruction (e.g., foreign body)
4) Gas exchange refers to processes that impair the exchange of CO2 and O2 in the alveoli (e.g., pneumonia, acute lung injury, COPD)

Question 9

What is the compensation for respiratory alkalosis?

Answer 9

Compensation for respiratory alkalosis is by a decrease in HCO3 which occurs in two steps:

1) buffering from cells (H+ release from cells) and
2) renal H+ retention.

In both cases the H+ binds HCO3, consuming and lowering HCO3, and driving the Henderson-Hasselbalch equation toward the formation of CO2 and H2O. Renal compensation takes 3-5 days.

Question 10

What is the compensation for respiratory acidosis?

Answer 10

As with respiratory alkalosis, cell buffering occurs first, this time H+ is absorbed by cell buffers resulting in the generation of HCO3. Renal compensation occurs by the renal excretion of H+ which results in the generation of new HCO3. Renal excretion takes 3-5 days.

Question 11

In acute respiratory acidosis, the bicarbonate is expected to increase by _____ increase in PCO2; in chronic respiratory acidosis, the bicarbonate is expected to increase by _____ rise in PCO2.

Answer 11

1 mEq/L for every 10 mmHg

4 mEq for every 10 mmHg

**The pH does not fall below 7.20 in appropriately compensated chronic respiratory acidosis.

Question 12

Potential symptoms and consequences of respiratory acidosis:

Answer 12

Symptoms: Neurologic: headache, decreased arousal/sleepiness (aka CO2 narcosis)

Consequences: Increased intracranial pressure, cardiac arrhythmias, hypotension from peripheral vasodilatation

Question 13

Tx for respiratory acidosis:

Answer 13

Treat underlying causes and pay attention to the PO2. In patients with COPD, titrate oxygen saturation to about 88 to 92%. In the chronic state, no specific treatment of the acid-base disorder is indicated.

Question 14

What is the most generic definition of metabolic alkalosis?

Answer 14

Any process that increases the total amount of HCO3

Question 15

A primary increase in plasma bicarbonate leading to metabolic alkalosis is classically considered to be two step process that requires generation and maintenance. What are the 5 broad categories of generation, and what maintains the imbalance (or is responsible).

Answer 15

1) Removal of H+
2) Addition of HCO3
3) Loss of fluids rich in Cl-
4) Post-hypercapnea
5) Hypokalemia

Maintenance of metabolic alkalosis is ALWAYS the kidney’s fault and is due to factors that impair the ability of the kidney to excrete the excess HCO3; maintenance is most often due to chloride depletion or potassium depletion which affects ion channels in the kidney and impairs bicarbonate excretion.

Question 16

Please name as many specific causes of each of the 5 broad categories which generate a metabolic alkalosis as you can remember.

Answer 16

1) Addition of HCO3- can occur due to:
- Direct administration of bicarbonate
- Direct administration of a substrate that is metabolized to bicarbonate (e.g.,lactated ringers which
contains lactate, which is metabolized to bicarbonate).

2) Loss of H+ can occur due to:
GI loss: vomiting, nasogastric suctioning
Renal loss: Loop and thiazide diuretics, mineralocorticoid excess

3) Loss of chloride rich fluid (formerly known as contraction alkalosis) can be due to: Loop diuretics, possibly also congenital chloride diarrhea, sweat loss in cystic fibrosis.
4) Post-hypercapnia is the development of metabolic alkalosis in a patient with chronic respiratory acidosis
5) Hypokelemia. Incompletely understood. Hypokalemia can both generate and maintain metabolic alkalosis.

Question 17

How can loop and thiazide diuretics generate a loss of H+ and subsequent metabolic alkalosis?

Answer 17

Diuretics inhibit Na+ resorbtion in the thick ascending loop of Henle (loop diuretics) or distal tubule (thiazides) resulting in an increased delivery of Na+ to the distal nephron. The distal nephron resorbs some of the Na+, generating a negatively charged tubular lumen which favors H+ secretion.

Question 18

Describe how post-hypercapnic metabolic alkalosis develops.

Answer 18

Post-hypercapnia is the development of metabolic alkalosis in a patient with chronic respiratory acidosis (low pH; high CO2 and high bicarbonate to compensate) who has received mechanical ventilation with a rapid lowering of CO2; in this setting the CO2 is newly normal but the bicarbonate remains high as it takes longer for the kidneys to excrete the bicarbonate. Chloride depletion is a feature of chronic respiratory acidosis as retention of bicarbonate by the kidneys occurs with secretion and excretion of chloride. Thus, after mechanical ventilation and the development of metabolic alkalosis, the alkalosis is maintained by chloride depletion which prevents excretion of the excess HCO3-.

Question 19

Metabolic alkaloses must be generated, then maintained. What are the mechanisms (4) that help perpetuate a metabolic alkalosis?

Answer 19

1) Chloride depletion (see further flashcard)
2) K+ depletion (increased aldosterone release)
3) Mineralocorticoid deficiency (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)
4) Hypovolemia (release of aldosterone and other factors in order to correct volume contraction by increasing renal Na+ resorption; as a consequence, HCO3- resorption also increases to maintain electroneutrality)

Question 20

Clinically, metabolic alkalosis is divided into 2 categories:

1) chloride responsive (also known as saline responsive)
2) chloride unresponsive (also known as saline resistant)

To differentiate between these categories:

Answer 20

Urine [Cl-] is measured.

Urine [Cl-] is the metabolic alkalosis is categorized as chloride responsive (aka saline responsive). The low urine chloride reflects chloride depletion as the major maintenance factor. Chloride responsive metabolic alkalosis is typically associated with a loss of intravascular volume (which is also responsive to an infusion of saline – i.e., 0.9% NaCl). Urine chloride may also be low in the setting of intravascular volume depletion due to renal resorption of Na+, which is accompanied by the resorption of Cl-.

If the urine [Cl-] is > 20 mEq/L, metabolic alkalosis is categorized as chloride resistant (aka saline resistant).

Question 21

What are 6 causes of Chloride responsive metabolic alkaloses?

Answer 21

1) Diuretics
2) Vomiting/gastric drainage
3) Villous adenomas
4) Congenital chloride-losing diarrhea
5) Cystic fibrosis
6) Post-hypercapnea

Question 22

What are two causes of chloride resistant metabolic alkaloses?

Answer 22

1) Mineralocorticoid excess (Generated and maintained by renal H+ loss from aldosterone action)
2) Licorice ingestion (Generated and maintained by renal H+ loss from glycyrrhetinic acid contained in some licorice. Glycyrrhetinic inhibits the enzymatic breakdown of aldosterone and cortisol thus increasing aldosterone action.)

Question 23

What is the compensation for metabolic alkalosis?

Answer 23

The rise in pH from the increase in [HCO3-] is sensed by respiratory system chemoreceptors which leads to a decrease in ventilation, retention of CO2, and a rise in CO2.
The expected increase in CO2 in metabolic alkalosis is predicted by the following:

ΔCO2 (in mmHg) = (0.25 – 1.0) X Δ HCO3

OR just use winter’s formula (expPco2 = HCO3(1.5) + 8 +/-2) –> if memory serves correctly.

Question 24

There are two main reasons to consider urgent treatment a metabolic alkalemia:

Answer 24

(1) Cardiac arrhythmias. Alkalemia increases sensitivity to catecholamines and may precipitate life- threatening arrhythmias.
(2) Hypocalcemia. Calcium circulates in two forms: free and active ionized calcium and ‘bound’ which refers primarily to inactive calcium bound to albumin. Alkalosis increases the binding of free calcium to albumin, thereby lowering plasma ionized calcium concentration. This may increase neuromuscular irritability with the possibility of tetany.

Question 25

Tx for metabolic alkalemia:

Answer 25

In an emergency, any acid-base state may be altered quickly with mechanical ventilation, thus hypoventilation may be considered to correct alkalemia if adequate oxygenation is maintained. Chloride responsive--> Infusions of NaCl and/or KCl. Chloride resistant --> In some cases, blocking mineralocorticoid effect with spironolactone or amiloride will be effective. In general, will need to identify specific cause to identify the appropriate therapy.

Question 26

What is the broad definition of a metabolic acidosis, and what are the two generic causes?

Answer 26

Metabolic acidosis is a metabolic process that causes a primary decrease in the HCO3. A primary decrease in plasma HCO3- leading to metabolic acidosis occurs in two major ways: 1) Loss of bicarbonate 2) Addition of acid (anion gap)

Question 27

If the serum anion gap is normal, metabolic acidosis is due to a ______; if the serum anion gap is increased, metabolic acidosis is due to the _____, thus, the differential diagnosis of metabolic acidosis is based on whether it is a non-anion gap metabolic acidosis (normal serum anion gap) or an anion gap metabolic acidosis (increased serum anion gap).

Answer 27

loss in bicarbonate addition of acid **Loss of HCO3- results in a normal anion gap because the loss of bicarbonate is replaced by an increase in chloride (but not “other anions”) to maintain electroneutrality as shown below. Since the Cl- concentration increases but the anion gap does not change, this form of acidosis is often referred to as a hyperchloremic acidosis.

Question 28

Non-anion gap (or hyperchloremic) metabolic acidosis is due to the loss of bicarbonate which can either be from the ___ or ____. GI loss of bicarbonate causing a non-anion gap metabolic acidosis is most commonly due to ____, although certain surgical procedures such as bowel resection can also result in significant loss of HCO3- from the body. Renal loss of bicarbonate causing a non-anion gap metabolic acidosis is due to a defect in renal bicarbonate or hydrogen ion handling resulting in a renal tubular acidosis (RTA). There are three major forms of RTAs: _____, _____, and _____

Answer 28

GI tract or kidney diarrhea a) proximal, b) distal, and c) hyperkalemic.

Question 29

Renal bicarbonate and hydrogen ion handling. Normal acid base balance is maintained by the kidney in two steps:

Answer 29

1) Bicarbonate reabsorption (performed primarily in the proximal tubule) 2) H+ excretion (performed primarily in the distal tubule) which generates new bicarbonate. * *1. Bicarbonate resorption is necessary to reclaim all of the filtered bicarbonate, if the proximal tubule is damaged in a way that this cannot occur, bicarbonate is lost in the urine and a proximal RTA is present. Normally, the proximal tubule reabsorbs about 90% of filtered HCO3-. 2. H+ excretion. Every day, about 60 mEq of H+ is generated via metabolism, and is known as the daily acid load (estimated to be approximately 1 mEq/kg/day). The 60 mEq of H+ consumes 60 mEq of bicarbonate, thus, new bicarbonate needs to be generated every day by the distal tubule, generation of new bicarbonate occurs by the excretion of H+.

Question 30

H+ excretion (bicarbonate generation) is accomplished through 3 mechanisms:

Answer 30

1) Excretion of ‘titratable’ acids. Titratable acids are anions that are filtered at the glomerulus and then bind to H+. The primary anion in this process is phosphate which binds hydrogen to form H2PO4. The amount of anion filtered by the glomerulus is relatively constant and does not increase when the H+ level in the body increases. 2) Excretion of nontitratable acid (NH4+). Ammonia (NH3+) is produced by the proximal tubule and binds to H+ to form ammonium (NH4+). Ammonia production (and therefore ammonium generation) can be increased in response to an increase in H+ level in the body. As you will see, this method of H+ excretion is measured clinically using the urine anion gap. Ammonia production is inhibited by hyperkalemia, thus hyperkalemia can inhibit ammoniagenesis and cause an RTA. 3) Free hydrogen excretion by the distal tubule (measured by pH).

Question 31

The ______ can be used to determine if renal acid excretion (new bicarbonate generation) is appropriate.

Answer 31

urine pH and the urine anion gap ***Normally, if a metabolic acidosis is present, urine H+ excretion should increase. Thus, if the urine pH is not acidic (i.e., is greater than 5.3) in the setting of a non-anion gap metabolic acidosis, this suggests that an RTA is present. If the urine pH is acidic (i.e., is less than 5.3), this suggests that the kidneys are functioning normally, and that a GI loss of bicarbonate (e.g., diarrhea) is present. ****If a metabolic acidosis is present, NH4+ production should increase. Unfortunately, NH4+ is difficult to measure directly; to indirectly assess whether NH4+ is present, the urine anion gap is calculated. The urine anion gap is = urine [Na+] + urine [K+] - urine [Cl-]. If NH4+ production is increased, then urine chloride (Cl-) should also increases to maintain electroneutrality; as chloride increases, the urine anion gap becomes a negative number. Thus, a negative urine anion gap suggests that ammonia production in the kidney is occurring and that the non-anion gap metabolic acidosis is due to GI loss. If the urine anion gap is a positive number, is suggests that renal ammonia production is impaired and that an RTA is present.

Question 32

What is the mnemonic for causes of an anion gap metabolic acidosis?

Answer 32

K - Ketoacidosis (Increased oxidation of fatty acids yielding acetoacetic and beta hydroxybutyric acids) A - Aspirin and other toxicities R - Renal Failure (Retention of sulfate, phosphate, and organic anions and failure to generate NH3) L - Lactic Acidosis (OR can use MUDPILES which is more specific and less broad)

Question 33

Please give specific examples of each of the four anion gap acidoses.

Answer 33

Ketoacidosis--> Diabetic (insufficient insulin) Alcoholic (mixture of ketoacids, lactic acids, acetic acids), and Starvation Aspirin/tox--> Methanol (formic acid), ASA, Ethylene glycol Renal failure --> Retention of sulfate, phosphate and failure to generate NH3 Lactic acidosis --> Type A (Ischemia - L-type), Type B (Mitochondrial derangement - L type), D lactic acidosis (gut bacteria)

Question 34

What is the six-step process to evaluating acid-base disorders? What should be checked at each step?

Answer 34

1) Is the patient acidemic or alkalemic? --> Determine blood pH. 2) Is the disturbance respiratory or metabolic? -->Assess carbon dioxide tension (PCO2) and serum bicarbonate level. 3) If a respiratory disturbance is present, is it acute or chronic? --> Compare measured pH with expected change in pH. 4) If a metabolic disturbance is present, is there an increased anion gap? --> If the serum anion-gap is normal, calculate urine anion-gap. Measure serum sodium, chloride, and bicarbonate levels to assess anion gap. 5) If a metabolic disturbance is present, is the respiratory system compensating adequately? --> Compare measured PCO2 with expected PCO2 to assess whether a respiratory acidosis or alkalosis is also present. 6) If a metabolic disturbance is present, is the respiratory system compensating adequately? (Are there any other hidden acid base disturbances present?) --> Determine the change in bicarbonate level and compare with change in serum anion gap.** **To uncover a hidden underlying acid-base disorder, one compares the “delta HCO3-” or change in bicarbonate with the “delta serum anion gap”. If there is only one disorder present, then the change in serum bicarbonate should equal the change in serum anion gap. (see notes)

Question 35

What is the calculation for the compensation of metabolic acidosis?

Answer 35

Winters formula: Expected pCO2 = 1.5[HCO3) + 8 +/-2

Question 36

What is the calculation for the compensation of metabolic alkalosis?

Answer 36

Δ pCO2 = (0.25-1) x Δ [HCO3-]

Question 37

What is the compensation of an acute respiratory acidosis? State both the change in HCO3- and pH.

Answer 37

HCO3 increases by 1 for every 10mmHg increase in pCO2. In general, the pH will change by 0.08 for every 10 mmHg change in PCO2 in acute situations

Question 38

What is the compensation of a chronic respiratory acidosis? State both the change in HCO3- and pH.

Answer 38

HCO3 increases by 4 for every 10mmHg increase in pCO2. In general, the pH will change by 0.03 for every 10 mmHg change in PCO2 in chronic conditions.

Question 39

What is the compensation of an acute respiratory alkalosis? State both change in HCO3- and pH.

Answer 39

HCO3 increases by 2 for every 10mmHg decrease in pCO2. pH decreases by 0.08 for every 10mmHg decrease in pCO2.

Question 40

What is the compensation of a chronic respiratory alkalosis? State both change HCO3- and pH.

Answer 40

HCO3 increases by 4 for every 10mmHg decrease in pCO2. pH decreases by 0.03 for every 10mmHg decrease in pCO2.

Question 41

What is the equation for determining the urine anion gap? What does the result mean?

Answer 41

Na+k-Cl Negative number = kidney works Positive number = RTA present and kidney not work so good.