A patient taking high doses of barbiturates is at risk for developing which condition due to reduced respiratory function?
Hyperthermia
Hypoxia
Hypocapnia
Hypercapnia
The Correct Answer is D
A. Hyperthermia: Barbiturate toxicity typically leads to central nervous system depression and a decrease in metabolic rate, which can result in hypothermia. While drug reactions vary, the primary life-threatening complication is respiratory failure. It does not typically trigger a primary hyperthermic response.
B. Hypoxia: While hypoxia occurs secondary to hypoventilation, hypercapnia is the direct respiratory acid-base consequence of reduced alveolar ventilation. Barbiturates suppress the medullary respiratory centers, specifically impairing the clearance of carbon dioxide. This leads to a primary elevation in arterial carbon dioxide levels.
C. Hypocapnia: This condition involves abnormally low levels of carbon dioxide in the blood, usually caused by hyperventilation or anxiety. Barbiturates are sedative-hypnotics that slow the breathing rate significantly. They would never cause a decrease in carbon dioxide under standard toxicological conditions.
D. Hypercapnia: Barbiturates depress the drive to breathe, leading to inadequate gas exchange and the systemic retention of carbon dioxide. This elevation in arterial carbon dioxide is the hallmark of respiratory depression. It leads to a concomitant drop in blood pH as carbonic acid levels rise.
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Related Questions
Correct Answer is C
Explanation
A. Aldosterone production increases, promoting sodium retention: Aldosterone is secreted in response to low ECF volume or hypotension to conserve sodium and water. In a volume-expanded state, aldosterone secretion is inhibited. This allows the kidneys to excrete excess sodium and reduce the total fluid volume.
B. ADH secretion is stimulated, increasing water retention: Antidiuretic hormone is suppressed when ECF volume is high to facilitate the excretion of dilute urine. Stimulation of ADH would cause further water retention, worsening the volume overload. The body aims to reduce water reabsorption in the collecting ducts.
C. Natriuretic peptides are released, promoting sodium and water excretion: Atrial natriuretic peptide is secreted by cardiomyocytes in response to increased stretch from high volume. It inhibits renin and aldosterone while increasing the glomerular filtration rate. This promotes the loss of sodium and water to lower blood pressure.
D. Thirst is increased, leading to more fluid intake: High ECF volume suppresses the thirst mechanism to prevent further intake. Increasing thirst would be counterproductive and potentially dangerous in a volume-overloaded patient. The hypothalamus responds to high volume by decreasing the drive to drink.
Correct Answer is B
Explanation
A. equation shifts left, respiratory acidosis, hypoventilation: Respiratory acidosis is caused by the retention of carbon dioxide, not the loss of gastric hydrochloric acid. A leftward shift would occur to consume excess hydrogen ions, which contradicts the loss of acid. Hypoventilation is a response to alkalosis.
B. equation shifts right, metabolic alkalosis, hypoventilation: Loss of gastric protons causes a rise in systemic pH, characterizing metabolic alkalosis. To replace the lost hydrogen ions, the carbonic acid-bicarbonate equation shifts right. The lungs then slow the breathing rate to retain carbon dioxide and lower pH.
C. equation shifts right, metabolic acidosis, hyperventilation: Metabolic acidosis involves an excess of hydrogen ions, which is the opposite of what occurs during vomiting. Hyperventilation is the compensation for acidemia, intended to blow off carbon dioxide. Vomiting specifically depletes acids, leading to an alkaline state.
D. equation shifts left, metabolic alkalosis, hyperventilation: While metabolic alkalosis is the correct diagnosis, a leftward shift would only occur if there were an excess of hydrogen and bicarbonate. Furthermore, hyperventilation would worsen alkalosis by removing more acid. The body compensates by slowing respiration to retain acid.
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