An 80-year-old man had a bad cold. After two weeks he said,
“It went in to my chest; I am feeling tightness in my chest,
I am coughing, suffocated and unable to breathe!” (Figure)
Figure- The gaseous exchange is impaired in pulmonary diseases
What could be the possible reason?
A. Metabolic Acidosis
B. Metabolic Alkalosis
C. Respiratory Acidosis
D. Respiratory Alkalosis
E. None of the above.
Answer- C- Respiratory acidosis is the correct answer.
Respiratory acidosis is CO2 accumulation (hypercapnia) from a decrease in respiratory rate, respiratory volume (hypoventilation), or both. It can be due to severe pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control and is recognized by an increase in PaCO2 and decrease in pH.
Respiratory acidosis may be acute or chronic. Distinction is based on the degree of metabolic compensation.
In acute respiratory acidosis, there is an immediate compensatory elevation (due to cellular buffering mechanisms) in HCO3–, which increases 1 mmol/L for every 10-mmHg increase in PaCO2.
In chronic respiratory acidosis (>24 h), renal adaptation increases the [HCO3–] by 4 mmol/L for every 10-mmHg increase in PaCO2. The serum HCO3– usually does not increase above 38 mmol/L. Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur in calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.
The clinical manifestations include-
- A rapid increase in PaCO2 may cause anxiety, dyspnea, confusion, psychosis, and hallucinations and may progress to coma.
- Lesser degrees of dysfunction in chronic hypercapnia include sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor and myoclonic jerks etc.
- Headaches and other signs that mimic raised intracranial pressure are also there.
Acute respiratory acidosis can be life threatening, and measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation. This may necessitate tracheal intubation and assisted mechanical ventilation.
Chronic respiratory acidosis is frequently difficult to correct, but measures aimed at improving lung function can help some patients and forestall further deterioration in most.
As regards other options
Metabolic acidosis is a primary decrease in serum HCO3 – concentration and, in its pure form, manifests as acidemia (pH <7.40). Metabolic acidosis is acid accumulation from increased acid production or acid ingestion; decreased acid excretion; or GI or renal HCO3 − loss. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation.
Metabolic alkalosis is primary increase in HCO3 − with or without compensatory increase in PCO2; pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 − excretion must be present to sustain 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.
Since the levels of pH, pCO2 and bicarbonate are not provided , it is difficult to comment on the acid base status, but based on the clinical manifestations and the history provided the most likely cause is respiratory acidosis, there is difficulty to blow out excess CO2.Please help Biochemistry for Medics by "CLICKING ON THE ADVERTISEMENTS" every time you visit us. Thank you!