Acid Base JeopardySteve Wood, PhD, UNM School of Medicine

View in slide show mode with speakers on – click on your choice for correct answer to hear if you’re right

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Renal pH Physiology

Clinical

3000

A patient in the ICU has been vomiting. This is expected to cause the following clinical signs:

Respiration Systemic Circulation

Neuro/Muscle

A Hypoventilation Vasoconstriction tetany

B No effect Vasodilation paralysis

C Hyperventilation No effect paralysis

D Hypoventilation Vasodilation arrythmias

explanation

The normal extracellular concentration of hydrogen

ion is ______________nmol/L corresponding to a pH of ________.

[H+] nmol/L pH A 40 7.4 B 100 7.0 C 100 7.4 D 40 7.0

explanation

The normal range of arterial pH is 7.35 to 7.45; the lethal limits of pH are approximately:

A 7.2 – 7.7 B 7.3 – 7.9 C 6.7 – 8.2 D 6.9– 7.8

Kidneys always produce acidic urine.

A True B False

explanation

The daily filtered load of bicarbonate (assume GFR is 180 L/day) in a normal adult is about:

A 4600 mEq B 3200 mEq C 4320 MEq D 80 mEq

explanation

Most or all of the filtered load of bicarbonate is reabsorbed and does not appear in urine. The proximal tubule accounts for about ______ of the

total reabsorption.

A 85% B 10% C 5% D 100%

The total amount of hydrogen ion secreted each day by the renal tubule cells (for adults with a normal mixed diet) is about:

A 80 mEq B 180 mEq C 4320 mEq D 4400 mEq

explanation

One of the reasons that pH regulation is important has to do with the deleterious effects of acidosis on the heart. Cardiac function in a patient with metabolic acidosis and low pH would be expected to show ____________contractility due to _____________.

Contractility Due to A Increased H is beta 2 agonist B Increased Ca++ release from SR C Decreased H+ inhibits slow Ca++

channels D Decreased Activation of R-A2-Ald

explanation

The diuretic acetylzolamide (diamox) inhibits the enzyme carbonic anhydrase. Which of the following data sets shows the expected effects of this drug on pH and renal function?

Urine pH

Blood pH

Urine vol.

Net acid exc.

ABCD

explanation

Acetylzolamide (diamox) is an inhibitor of carbonic anhydrase. Predictable side-effects effects of diamox treatment would include:

A. Diuresis and acidification of urine, decreased blood PCO2

B. Antidiuresis, decreased blood Na+ and PCO2

C. Increased Na+ excretion, diuresis, alkalinization of urine, decreased blood pH

D. Diuresis, increased H+secretion, no change in blood PCO2

explanation

Production of ammonia in renal tubule cells requires a supply of _____________ from amino acid metabolism in the ______________. Buffering of ammonia provides for the excretion of up to __________mEq hydrogen ion per day.

Supply of Source Amount A Glutamine Liver 500 B Phosphate Kidney 50 C Arginine Gut 200 D Glucose Liver 250

A patient using diamox as a diuretic has the following blood chemistry: Na+ = 135 mEq/L; Cl- = 100 mEq/L. Arterial blood gas analysis shows: PaO2 = 89 mm Hg; PaCO2 = 34 mm Hg; HCO3

- = 18 mEq/L; pH = 7.35. The best description of acid base status is ______________with an anion gap of_____________. A) Metabolic acidosis with respiratory compensation; 17

mEq/L B) Metabolic acidosis no compensation; 15 mEq/L C) Respiratory acidosis with renal compensation; 20

mEq/L D) Respiratory acidosis no compensation; 20 mEq/L E) Diabetic ketoacidosis; 40 mEq/L

explanation

A 50 year old man with type 1 diabetes and diabetic nephropathy has the following labs: sodium 130 mEq/l, potassium 6.5 mEq/l, creatinine 180 µEq/l (2.16 mg/dl), chloride 109 µEq/l, pH 7.29, Paco2 27 mm Hg, Pao2 107 mm Hg, bicarbonate 12 mEq/l. What is the acid-base status? A) Metabolic acidosis with respiratory compensation B) Metabolic acidosis no compensation C) Respiratory acidosis with renal compensation D) Respiratory acidosis no compensation

explanation

A cyanotic baby was placed on 65% oxygen by mask. ABG showed pH of 7.30; PaCO2 of 51 mm Hg, PaO2 of 112 mm Hg. What is his acid base status? A) Metabolic acidosis with respiratory compensation. B) Metabolic acidosis, no compensation C) Respiratory acidosis, renal compensation D) Respiratory acidosis, no compensation (Bonus question) What would explain the arterial PO2

being only 112 mm Hg on 65% oxygen? A) diffusion limitation B) right to left shunt (venous admixture) C) hyperventilation D) V/Q mismatch

explanation

Patients with renal failure may have decreased GFR. This would adversely affect the ability of the urine to excrete acid via the _________ buffer.

A. Ammonia B. Phosphate C. Hemoglobin D. Protein tubule

An important physiological effect of metabolic alkalosis is:

A. Increase in intracellular Ca++ leading to coma B. Inhibition of ventilation, pH compensatory but

leading to hypoxia C. Shift of potassium out of cells leading to

hyperkalemia and membrane depolarization D. Vasoconstriction of pulmonary arterioles

leading to pulmonary hypertension

A comatose patient with no medical history available was admitted to the ER. Arterial blood gas and blood chemistry analysis provided the following data:

PaO2 = 100 mm Hg; PaCO2 = 28 mm Hg; pH = 7.3 Plasma Na+ = 140 mEq/L Cl- = 112 mEq/L glucose= 350 mg/dL HCO3

- = 12 mEq/L Which of the following diagnoses is most appropriate?

A. respiratory acidosis with renal compensation and normal anion gap

B. metabolic alkalosis with respiratory compensation and increased anion gap

C. normal pH with hyperventilation driven by arterial hypoxemia with normal anion gap

D. Metabolic acidosis with respiratory compensation and normal anion gap

explanation

A cholera patient with severe diarrhea would be expected to have abnormal acid base status resulting in:

A. Increase of hemoglobin oxygen affinity

B. Inhibition of pulmonary ventilation C. Pulmonary hypotension D. Decreased cardiac contractility

explanation

The effect of hyperkalemia (high extracellular potassium) on neuron resting membrane potential is:

A. Become more negative B. Become less negative C. No change

A buffer system; e.g.,

HA « H ++ A-

is most effective when:A. [HA] > [A-]B. [HA] < [A-]C. [HA] = [A-]D. pH > pK

The defense against acid load with the slowest response time is:A. Chemical bufferingB. Renal compensationC. Respiratory compensationD. Hemoglobin proton coupling

The acid base status of a pregnant woman in the 3rd trimester is best depicted by point___.

A) 3B) 4C) 7D) 2E) 6

pH

PCO2 (mm Hg)

Plas

ma [H

CO3- ]

(mEq

/L)

6.8 7.0 7.2 7.4 7.6 7.8 8.0

40

30

20

10

120 80 60 40 30 20

pH

PCO2 (mm Hg)

Plas

ma [H

CO3- ]

(mEq

/L)

6.8 7.0 7.2 7.4 7.6 7.8 8.0

40

30

20

10

120 80 60 40 30 20

123

45

A normal rate of bicarbonate reabsorption in the renal tubule cells requires the enzyme:

A. Carbonic anhydraseB. Lactate dehydrogenaseC. Tyrosine hydroxylaseD. Carbonate reductase

The most important mechanism of hydrogen secretion in the proximal tubule is:

A. H+ ATPase (electrogenic H pump)

B. H+ - K+ antiporter C. Na+ - H+ antiporterD. diffusion

Lab results for a 24 hour urine sample show: Titratable acid = 20 mEq [NH4

+] = 40 mEq [HCO3

-] = 3 mEqThe patient’s net acid excretion is:

A. 63 mEq/dayB. 20 mEq/dayC. 57 mEq/dayD. 23 mEq/day

The inhibition of ventilation by metabolic alkalosis is countered (partially reversed) by the stimulation of ventilation due to:

A. pH increasesB. hypercapniaC. hypoxiaD. low bicarbonate

PaO2 = 35 mm HgPaCO2 = 64 mm HgpH = 7.2 Hb = 10 g/dLSat. = 60 %HCO3- = 26 mEq/LBase excess = 0 mEq/L

Acid base status is most accurately described as:

A.Uncompensated metabolic acidosisB.Uncompensated respiratory acidosisC.Compensated respiratory acidosisD.Compensated metabolic acidosis

COPD patient in respiratory failure. ABG report:

explanation

Room Air 100% oxygen

PO2 mm Hg 43 mm Hg 452 mm Hg

PCO2 mm Hg 16 mm Hg 34

pH

HCO3-

7.50

15

7.32

17

The patient’s acid base status on room air is: A.Compensated respiratory alkalosis

B.Uncompensated respiratory alkalosisC.Uncompensated metabolic alkalosisD.Compensated metabolic alkalosis

4. COPD patient with with cyanosis and marked peripheral edema. ABG report:

explanation

The patient’s acid base status is:

A. NormalB. Respiratory + metabolic acidosisC. Respiratory acidosisD. Metabolic acidosis + resp. alkalosisE. Metabolic alkalosis

pH = 7.2PCO2 = 52 mm HgHCO3

- = 18 mmEq/LPaO2 = 81 mm Hg

A COPD patient who is an alcoholic is admitted to the ER after losing consciousness at home. ABG shows

During an operation, the arterial PCO2 and pH of an anesthetized patient are monitored. The patient is being ventilated by a mechanical respirator, and the initial values are normal (PCO2 = 40 mm Hg; pH = 7.41). If the ventilation is increased, which of the following is most likely to occur?

Arterial PCO2

A. DecreaseB. DecreaseC. DecreaseD. IncreaseE. IncreaseF. Increase

Arterial pHDecreaseIncreaseNo changeDecreaseIncreaseNo change

explanation

A patient excretes 3 L of urine with a pH of 7.6 with a [HCO3

-] = 24 mEq/L. What is the net acid excretion?

A. 24 mEq/LB. 48 mEq/LC. NegativeD. Can not tell from these data

explanation

Lab results for a patient with DKA show a [HCO3-] = 10 mEq/L, PCO2 = 33 mm

Hg. You forgot your calculator and impress the chief resident by telling her that you used the Henderson-Hasselbalch equation to calculate a pH = _______.

A. 7.4B. 6.8C. 6.1D. 7.1

explanation

Lab results for a patient with respiratory failure and cholera show a [HCO3-] = 2 mEq/L,

PCO2 = 66 mm Hg. You forgot your calculator and impress the chief resident by telling her that you used the Henderson-Hasselbalch equation to calculate a pH = _______.

A. 7.4B. 6.8C. 6.1D. 7.1

explanation

Daily Double

Daily Double

Daily Double

Final Jeopardy

Use a bicarb – pH diagram to plot the course of a triple disorder in an alcoholic with ketoacidosis who develops hyperventilation from liver failure and then starts to vomit.

The diagram above shows plasma bicarbonateas a function of pH at different PCO2 levels.The two points that represent “mixed” acid basedisorders are:

A. 2 and 6B. 4 and 7C. 8 and 10D. 8 and 9

explanation

pH

PCO2 (mm Hg)

Pla

sma

[HC

O 3- ]

(mE

q/L)

6.8 7.0 7.2 7.4 7.6 7.8 8.0

40

30

20

10

120 80 60 40 30 20

15

1

2

3

4

5

6 7

8

9

10

pH

PCO2 (mm Hg)

Pla

sma

[HC

O 3- ]

(mE

q/L)

6.8 7.0 7.2 7.4 7.6 7.8 8.0

40

30

20

10

120 80 60 40 30 20

15

pH

PCO2 (mm Hg)

Pla

sma

[HC

O 3- ]

(mE

q/L)

6.8 7.0 7.2 7.4 7.6 7.8 8.0

40

30

20

10

120 80 60 40 30 20

15

1

2

3

4

5

6 7

8

9

10

Filtered load = GFR x plasma concentration

= 180 L/day x 24 mEq/L

= 4320 mEq/day

Alkalosis will inhibit the central and peripheral Chemoreceptors causing hypoventilation and increasedPCO2, which will cause alveolar and arterial PO2 to Decrease. This will stimulate the carotid body PO2 receptorWhich will oppose the inhibition by alkalosis. Also, the Increased PCO2 will compensate the alkalosis.

Systemic alkalosis causes vasoconstriction in most vascularBeds. This may be countered by the hypoxia in some bedsBut normally there is cerebral and coronary vasoconstriction.

Alkalosis caused decreased extra and intracellular calciumLeading to prolonged action potentials and muscle spasm (tetany).

urine may be alkaline as well as acidic, depending on dietand/or compensation for alkalosis. citrus fruits, due to highamounts of citrate will produce alkaline urine. citrate ismetabolized to citric acid by adding a hydrogen ion. this makes blood, and urine, more alkaline.

compensation for metabolic alkalosis is both respiratory and by renal excretion of bicarbonate.

Acidosis inhibits the slow calcium channels which are activated during phase 2 of the cardiac action potential. in addition, tissueacidosis causes hydrogen in and potassium out of cells leading tohyperpolarization (more negative membrane potential).

The force of contraction is directly dependent on the magnitude of the initial calcium influx, therefore acidosis decreases the force of contraction.

For more http://www.accessmedicine.com/content.aspx?aID=889838Used id = rossmed password = rossmed

http://www.accessmedicine.com/content.aspx?aID=943477&searchStr=acetazolamide

CA is present in both the brush border of the luminal membrane and in the cytoplasm. nahco3uptake from filtrate is inhibited so hco3- reabsorptionis blocked leading to higher urine ph and lower blood ph

anion gap = NA – (CL + HCO3-) = 135 – 118 = 17 mEq/lpH = 7.35 so acidosis. what kind? has to be metabolic

since pco2 is low, not high. PCO2 is down by 6 to partially compensate for HCO3- being down by 6 (which wouldpredict that ph would be 7.3 and instead it is 7.35 due to partial

respiratory compensation

pH = 7.29 = acidosisPCO2 = 27 mmHg, so you know it’s metabolic acidosis and hyper

Ventilation is compensatoryHCO3

- = so you also know it is metabolic acidosis

The concentration of free hydrogen ion is so small it ismeasured in nanomoles (a nanomole is a billionth of a mole)

A pH of 7.4 = 40 nmoles/L (extracellular)A pH of 7.0 is 100 nmoles/L (typical intracellular)

The renal tubule cells normally secrete enough hydrogen ion to completely reabsorb all the filtered bicarb (4320 mEq/L) PLUS

enough extra to produce new bicarb to replace that lost in buffering fixed acid from metabolism (80 mEq/L) for a total

of

4400 mEq/L

because pco2 is increased from 40 to 51(11 mm hg), you would expect the pH to be decreasedby about 0.1 units, which it is. so, you have uncompensated respiratory acidosis.

the pao2 increases to only 112 mm hg on 65% oxygen. this probably means there is a fairly large right to leftshunt where venous blood entering the lungs does notcome into contact with the high oxygen levels in thealveoli.

Most of the acidification of urine takes place In the:

A) Proximal tubuleB) Descending loop of HenleC) Ascending loop of HenleD) Distal tubule/collecting duct

explanation

A patient in the ICU has diarrhea and metabolic acidosis. This is expected to cause the following clinical signs:

Respiration Systemic Circulation

Neuro/Muscle

A Hypoventilation Vasoconstriction tetany

B No effect Vasodilation paralysis

C Hyperventilation Vasoilation Muscle weakness

D Hypoventilation Vasodilation arrythmias

explanation

acidosis stimulates the carotid body ph receptor and causes systemic vasodilation. acidosis causes hyper-kalemia and this lowers resting membrane potential. sustained depolarization lead to muscle weakness.

Diarrhea cause metabolic acidosis. HbO2 affinity decreases. Acidosis stimulates the carotid body pH receptor and causes systemic vasodilation. Acidosis inhibits the slow calcium channels which are activated during phase 2 of the cardiac action potential. in addition, tissue acidosis causes hydrogen in and potassium out of cells leading to hyperpolarization (more negative membrane potential).

The force of contraction is directly dependent on the magnitude of the initial calcium influx, therefore acidosis decreases the force of contraction.For more http://www.accessmedicine.com/content.aspx?aID=889838Used id = rossmed password = rossmed

“…the distal part of the nephron exchanges cellular hydrogen and/or potassium ions for sodium ions in the tubular urine. Ammonia diffuses into acid urine and is trapped as ammonium ion. Diamox, by interfering with the supply of cellular hydrogen ions, reduces exchange of hydrogen for sodium and favors the

exchange of potassium for sodium.”

Am J Physiol 194: 125-134, 1958; Localization of Acidification of Urine, Potassium and Ammonia Secretion and Phosphate Reabsorption in the Nephron of the Dog Robert F. Pitts 1, Ruth S. Gurd 1, Richard H. Kessler 1, and Klaus Hierholzer 1 1 From the Department of Physiology, Cornell University Medical College, New York City

Point 8 indicates a combination of respiratory (high PCO2) and metabolic (lowered bicarb) acidosis. This might happen in a patient with lung disease who has diarrhea.

Point 10 shows a combination of respiratory (low PCO2) and metabolic (high bicarb) alkalosis. This might happen in a patient with liver failure who starts vomiting.In liver failure toxins may stimulate the respiratory ctr. Causing hyperventilation (respiratory alkalosis) and low potassium may also cause a metabolic alkalosis.

pH = pK + log [HCO3-]/(PCO2 x )

pH = 6.1 + log 2/(66 x 0.03) = 6.1 + log 2/1.98 6.1 (log 1 = 0)

pH = pK + log [HCO3-]/(PCO2 x )

pH = 6.1 + log 10/(33 x 0.03) = 6.1 + log 10/1 7.1 (log 10 = 1)

Net acid excretion = (titratable acid + ammonia) – urine bicarb

If urine has pH > 7.4 net acid excretion is always negative.

Increased ventilation will lead to decreased PCO2 and, as a result, increased pH

Uncompensated respiratory acidosis because PCO2 is increased from 40 to 64 = + 24. this predicts that pH should be decreased by about 0.2 units, which it is (7.2). If there were any renal compensation, pH would be higher than 7.2 as bicarbonate is produced by the kidneys and there would be a positive base excess.

Compensated respiratory alkalosis because PCO2 is decreased from 40 to 16 = - 24. This predicts that pH should be increased by 0.2 units, to 7.6. With renal compensation, bicarb is decreased to 15, so the actual pH is 7.5 (partial compensation).

The pH is acidosis. The low bicarb means it’s metabolic. The low PCO2 means the expected respiratory compensation (hyperventilation) has occurred. The anion gap is 140 – (112 + 12) = 16 mEq/L (normal range 8 – 16)

Filtered sodium enters the proximal tubule by way of several co-transporters (see figure) but most of the reabsorption is via the Na-H antiporter.