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Case details

A 15 year-old boy had numbness and tingling around his mouth and in his finger tips. The problem was intermittent usually occurring during times of great stress. Aside from his problem, he had been in good health. His physical examination was normal, as were his laboratory values, especially his total calcium concentration was 2.5 mM/L, with ionized calcium of 1.2 mM/L(normal 2.1 to 2.6 mM/L and 1.14- 1.30 mM/L respectively). After breathing rapidly for about 3 minutes at 30 breaths per minute, he stated that it provoked the episode. At this time he had increased irritability of his seventh cranial nerve (Chovstek’s sign) and carpal spasm on oxygen deprivation of his hand (trousseau’s sign) both indicating clinical hypocalcemia. His plasma calcium concentration during an episode remained at 2.5 mM/L but his ionized calcium level fell to 0.8 mM/L.

What is the cause for all these symptoms?

A) Stress induced high catecholamine release

B) Stress induced low PTH release

C) Respiratory alkalosis

D) Respiratory acidosis

E) Vitamin D deficiency.

The correct answer is -C) Respiratory alkalosis.

Respiratory alkalosis is a primary decrease in PCO2 with or without compensatory decrease in HCO3 ; pH may be high or near normal.

Alveolar hyperventilation in respiratory alkalosis leads to a decreased partial pressure of carbon dioxide (PCO2). In turn, the decrease in PCO2 increases the ratio of bicarbonate concentration to PCO2 and increases the pH level. The decrease in PCO2 (hypocapnia) develops when a strong respiratory stimulus causes the lungs to remove more carbon dioxide than is produced metabolically in the tissues.

Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PCO2 level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PCO2 level is below the lower limit of normal, but the pH level is normal or near normal.

Acute respiratory alkalosis causes small changes in electrolyte balances. Minor intracellular shifts of sodium, potassium, and phosphate levels occur. A minor reduction in free calcium occurs due to an increased protein-bound fraction.

In the given clinical situation the symptoms of perioral and finger tip paresthesias etc are typical of Hypocalcaemia. When seen intermittently such as this, such symptoms are almost caused by hyperventilation.

In this patient the hyperventilation is related with anxiety.

Effect of hyperventilation on ionic calcium concentration

Normal total serum Calcium concentration ranges from 8.8 to 10.4 mg/dL (2.20 to 2.60 mmol/L). About 40% of the total blood Calcium is bound to plasma proteins, primarily albumin.The remaining 60% includes ionized Ca plus Ca complexed with phosphate (PO4) and citrate.

The circulating calcium binds to plasma proteins via anionic sites that are highly dependent on the pH of blood. Small increase in pH creates more anionic sites for the binding of calcium.

Hyperventilation due to any cause, can acutely raise the pH of blood.

The increased respiratory rate removes carbon dioxide from the lung alveoli and lowers blood CO2, forcing a shift in the indicated equilibrium towards left.

CO2 + H2O <——–> H2CO3 <——–> H+ + HCO3

Carbonic acid (H2CO3) can be ignored because negligible amounts are present at physiological pH, leaving the equilibrium

CO2 + H2O <——-> H+ + HCO3

The leftward shift to replenish exhaled CO2 decreases the hydrogen ion (H+) concentration and increases the pH to produce alkalosis.

The rise in pH promotes binding of ionic calcium to anionic sites on albumin dropping the ionized calcium by up to 30 % without altering the total plasma calcium conc. Since it can occur in just a few seconds, PTH (parathyroid hormone) is unable to compensate for the hypocalcaemia and the symptoms may occur.

PTH is secreted by the parathyroid glands. It has several actions, but perhaps the most important is to defend against hypocalcemia. Parathyroid cells sense decreases in serum Ca and, in response, release preformed PTH into the circulation. PTH increases serum Ca within minutes by increasing renal and intestinal absorption of Ca and by rapidly mobilizing Ca and PO4 from bone (bone resorption).

Since in this case the hyperventilation is due to anxiety the therapy should be directed at lowering the patient’s anxiety. Counseling may be necessary for this.

This respiratory alkalosis is best treated by diminishing the respiratory rate to elevate the blood [CO2], forcing the above equilibrium to the right, elevating the [H+], and decreasing the pH.

The patient can treat his symptoms by preventing the diminished CO2 that accompanies the hyperventilation. He can do this simply by breathing in to paper bag, thereby increasing the CO2 of the inspired air.

As regards other options

A) Stress induced high catecholamine release- Catecholamines have no role to play in calcium homeostasis

B) Stress induced low PTH release- This is also not true, there are no evidences of stress mediated PTH release.

D) Respiratory acidosis by decreasing pH promotes ionization of calcium. Hypocalcemia is not observed in respiratory acidosis.

E) Vitamin D deficiency does not affect only ionic calcium concentration. The total calcium concentration is lowered in vitamin D deficiency.










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Case details-1  

A 45 year-old-female suffering from bronchial asthma was brought to emergency in a critical state with extreme difficulty in breathing.

The blood gas analysis revealed the following

pH- 7.3

PCO2- 46 mm Hg

PO2- 55 mm Hg

HCO3- 24meq/L

What is your Interpretation?


Case discussion-

Low p H – acidosis

Low PO2 and PCO2 excess signify Primary respiratory problem

HCO3:24 -normal

Thus, the patient is suffering from Acute respiratory acidosis.


Case details -2

A 4 day old girl neonate became lethargic and uninterested in breast-feeding. Physical examination revealed tachypnea (rapid breathing) with a normal heart beat and breath sounds. Initial blood chemistry values included normal glucose, sodium, potassium, chloride, and bicarbonate (HCO3-) levels.

Blood gas values revealed a pH of 7.53, partial pressure of oxygen (PO2) was normal (103 mm Hg) but PCO2 was 27 mmHg.

What is the probable diagnosis?


Case discussion

The baby is suffering from Respiratory Alkalosis

Tachypnea in term infants may be due to brain injuries and metabolic diseases that irritate the respiratory center. The increased respiratory rate removes carbon dioxide from the lung alveoli and lowers blood CO2, forcing a shift in the indicated equilibrium towards left

 CO2 + H2O çè H2CO3 çè H+ + HCO3-

Carbonic acid (H2CO3) can be ignored because negligible amounts are present at physiological pH, leaving the equilibrium

 CO2 + H2O çè H+ + HCO3-

The leftward shift to replenish exhaled CO2 decreases the hydrogen ion (H+) concentration and increases the pH to produce alkalosis. This respiratory alkalosis is best treated by diminishing the respiratory rate to elevate the blood [CO2], to force the above equilibrium to the right, elevate the [H+], and decrease the pH.


Case details-3

A new-born with tachypnea and cyanosis (bluish color) is found to have a blood pH of 7.1. Serum bicarbonate is measured as 12 mM  while pCO2 is 40 mm Hg.

What is the probable diagnosis?


Case discussion

Low p H and low bicarbonate indicate metabolic acidosis. Since p CO2 is normal it can not be compensatory respiratory acidosis ( If the baby had respiratory acidosis, the PCO2 would have  been elevated).This is a hypoxia related metabolic acidosis. Hyperventilation is as a compensation to metabolic acidosis.

This condition can be treated  by administration of oxygen to improve tissue perfusion and decrease metabolic acidosis.


Case details -4

A 60-year-old man was brought to hospital in a very serious condition.  The patient complained of constant vomiting containing several hundred mL of dark brown fluid from the previous two days plus several episodes of melaena. Past history of alcoholism, cirrhosis, portal hypertension and a previous episode of bleeding varices was there.

Arterial Blood Gases revealed-

pH – 7.10

pCO2 – 13.8 mmHg

pO2- 103 mmHg

HCO3- 14.1 mmol/l

Laboratory Investigations

Na+ 131 mmol/l., Cl 85 mmol/l. K+ 4.2 mmol/l., “total CO2” 5.1, glucose 52mg/dl, urea 38.6mg/dl, creatinine1.24mg/dl, lactate 20.3 mmol/l  Hb 6.2 G%, and WBC- 18 x103/mm3


Case discussion

The patient is severely ill with circulatory failure and GI bleeding on a background of known cirrhosis with portal hypertension.

The very low pH indicates a severe acidosis. The combination of a low pCO2 and low bicarbonate indicates either a metabolic acidosis or a compensatory respiratory alkalosis (or both). As this patient has a severe acidosis, so the most probable diagnosis is metabolic acidosis. The anion gap is 31 indicating the presence of a high anion gap disorder. The lactate level of 20.3mmol/l is extremely high and this confirms the diagnosis of a severe lactic acidosis. Hb is very low consistent with the history of bleeding and hypovolemia. Urea and creatinine are elevated (renal failure) but at these levels there would not be retention of anions sufficient to result in a renal acidosis. Hence,

Lactic acidosis can be suspected. The respiratory efforts may be due to the distress or as a consequence of a metabolic acidosis (ie compensatory).


Case details-5

A 56- year -old man who smoked heavily for many years developed worsening cough with purulent sputum and was  admitted to the hospital because of difficulty in breathing. He was drowsy and cyanosed. His arterial blood gas analysis was as follows;

 pH –      7.2

p CO2 – 70 mm Hg

HCO3-   26 mmol/L

P O2-  50 mm Hg

What is the likely diagnosis?


Case discussion

The patient is suffering from Respiratory acidosis. Difficulty in breathing, cough and purulent sputum signify the underlying lung pathology. Low p H and raised pCO2 indicate respiratory acidosis. Slightly high HCO3- may be due to compensation as a result of increased reabsorption from the kidney. The low pO2 is due to associated hypoxia. The treatment is based on the treating the primary cause.O2 and mechanical ventilation are often needed.


Case details -6

A 5-year old girl displayed increased appetite, increased urinary frequency, and thirst. Her physician suspected new onset diabetes mellitus and confirmed that she had elevated urine glucose and ketones.

Blood gas analysis revealed


Bicarbonate-12.0 mmol/L

Arterial PCO2- 21


Case discussion

The patient is suffering from Diabetic ketoacidosis

In the presence of insulin deficiency, a shift to fatty acid oxidation produces the ketones that cause metabolic acidosis. The pH and bicarbonate are low, and there is frequently some respiratory compensation (hyperventilation with deep breaths) to lower the PCO2. A low pH with high PCO2 would have represented respiratory acidosis which is not there in the given case.


Case details-7

A 19-year-old boy was brought to the emergency department with loss of consciousness. Apparently the patient was a homeless found on the street.

Arterial blood gases revealed-

pH –     7.33,

pCo2 – 28 mm Hg,

pO2- 117 mmHg and

HCO3- 14 mmol/L

The blood level of methanol was 0.4 mg/dl.

What is your diagnosis?


Case discussion

The patient is suffering from metabolic acidosis as evident from the low p H and low bicarbonate levels. Low p CO2 and high p O2 signify that the patient is in a state of respiratory compensation. Blood methanol level is high, so it might be the case of Methanol poisoning producing metabolic acidosis.


Case details-8

A 66-year-old man had a postoperative cardiac arrest. Past history of hypertension treated with an ACE inhibitor was there. There was no past history of Ischemic heart disease. Following reversal and extubation, myocardial ischemia was noticed on ECG. He was transferred to ICU for overnight monitoring. On arrival in ICU, BP was 90/50, pulse 80/min, respiratory rate was 16/min and S pO2 99%. During handover to ICU staff, he developed ventricular fibrillation which reverted to sinus rhythm with a single 200J counter shock. Soon after, blood gases were obtained from a radial arterial puncture:

Arterial Blood Gases

 pH -7.27

 pCO2 -55.4 mmHg

 pO2- 144 mmHg

 HCO3- 24.3 mmol/l

Biochemistry Results (all in mmol/l): Na+ 138, K+ 4.7, Cl 103, urea 6.4, creatinine 0.07

What is the probable diagnosis?


Case discussion

1) p H– low , Acidosis is present.

2) p CO2- high, hypoventilation(The residual depressant effect of the Anesthetic agents is considered the most likely cause)

3) Bicarbonate– near normal

4) pO 2- high- This is because the patient is breathing a high inspired oxygen concentration. If the patient had been breathing room air (FIO2 = 0.21), then a depression of alveolar pO2 must have occurred. Most ill patients in hospital breathe supplemental oxygen so it is common for the pO2 to be elevated on blood gas results.

5) An acidemia with the pattern of elevated pCO2 and normal HCO3 is consistent with an acute respiratory acidosis.

6) Anion gap– The anion gap is about 11 which is normal so no evidence of a high anion gap acidosis.

Diagnosis- Acute respiratory acidosis

Cause- Resuscitation from postoperative ventricular fibrillation


Case details -9

A 72-year-old male with diabetes mellitus is evaluated in the emergency room because of lethargy, disorientation, and long, deep breaths (Kussmaul respiration). Initial chemistries on venous blood demonstrate high glucose level of 380 mg/dl (normal up to 120 mg/dl) and pH of 7.3. Bicarbonate 15mM and PCO2 30 mmHg, What is the probable diagnosis ?

Case discussion

The man is acidotic as defined by pH lower than normal 7.4. His hyperventilation with Kussmaul respiration can be interpreted as compensation by lungs to blow off CO2 to lower PCO2, to increase [HCO3-]/[CO2] ratio, and to raise pH. Thus the patient has metabolic acidosis due to underlying Diabetic ketoacidosis.


Case details-10

A 24 year female with broken ankle was brought to emergency with acute pain.

Blood gas analysis revealed the following

 pH- 7.55

PCO2- 27

PO2- 105,  

HCO3- 23

What is the probable diagnosis?


Case discussion

 pH:-  7.55 – indicates Alkalosis

PCO2: 27 -low, it is a Primary respiratory disturbance

 PCO2 Deficit = 40-27 = 13

 HCO3 = 23 (Normal)


It is Respiratory alkalosis due to pain related hyperventilation.

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