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Which arterial blood gas result reflects respiratory acidosis?

A.

pH 7.48, PaCO2 37 mm Hg, HCO3 30 mEq/L

B.

pH 7.28, PaCO2 31 mm Hg, HCO3 20 mEq/L

C.

pH 7.39, PaCO2 38 mm Hg. HCO3 23 mEq/L

D.

pH 7.30, PaCO2 50 mm Hg, HCO3 24 mEq/L

Answer and Explanation

The Correct Answer is D

A. pH 7.48, PaCO2 37 mm Hg, HCO3 30 mEq/L: This ABG shows alkalemia with normal PaCO2 and slightly elevated bicarbonate, consistent with metabolic alkalosis. It does not indicate respiratory acidosis because PaCO2 is within normal limits.

B. pH 7.28, PaCO2 31 mm Hg, HCO3 20 mEq/L: This reflects acidemia with low PaCO2 and low HCO3, suggestive of metabolic acidosis with respiratory compensation. The low CO2 indicates hyperventilation to compensate, not primary respiratory acidosis.

C. pH 7.39, PaCO2 38 mm Hg, HCO3 23 mEq/L: These values are within normal physiologic ranges, representing a normal ABG with no evidence of acid-base disturbance.

D. pH 7.30, PaCO2 50 mm Hg, HCO3 24 mEq/L: This ABG indicates acidemia (low pH) with elevated PaCO2 and normal bicarbonate, which is consistent with respiratory acidosis. The elevated CO2 reflects hypoventilation or impaired gas exchange leading to CO2 retention and decreased pH.


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Related Questions

Correct Answer is D

Explanation

A. Afterload:Afterload is the resistance the left ventricle must overcome to eject blood during systole. It is influenced by systemic vascular resistance and arterial pressure, not the volume of blood in the ventricles at the end of diastole.

B. Stroke volume:Stroke volume is the amount of blood ejected by a ventricle with each contraction. While stroke volume depends in part on end-diastolic volume, it measures output per beat rather than the volume present before contraction.

C. Cardiac reserve:Cardiac reserve is the difference between resting cardiac output and the maximum output achievable during increased demand. It reflects functional capacity, not the baseline ventricular volume at end-diastole.

D. Preload:Preload refers to the volume of blood in the ventricles at the end of diastole, immediately before contraction. It stretches the ventricular myocardium, influencing the force of contraction according to the Frank-Starling law and directly affecting cardiac output.

Correct Answer is {"A":{"answers":"A"},"B":{"answers":"A"},"C":{"answers":"B"},"D":{"answers":"A"},"E":{"answers":"A"},"F":{"answers":"B"}}

Explanation

Risk Factors

Modifiable

Non-Modifiable

Smoking

✔

Obesity

✔

Ethnicity

✔

Hypertension

✔

Diabetes

✔

Family history

✔

• Smoking: Smoking damages the vascular endothelium, promotes inflammation, and increases platelet aggregation, accelerating atherosclerosis. Because tobacco use is a behavior, cessation significantly reduces coronary artery disease (CAD) risk. Risk declines progressively after quitting. Therefore, smoking is considered a modifiable lifestyle factor.

• Obesity: Excess body weight contributes to dyslipidemia, insulin resistance, and increased cardiac workload. Weight reduction through diet and physical activity can improve lipid profiles and blood pressure. Since body weight can be altered through lifestyle interventions, it is categorized as modifiable. Managing obesity lowers overall cardiovascular risk.

• Ethnicity: Certain ethnic groups have a higher prevalence of coronary artery disease due to genetic predisposition and inherited metabolic traits. Individuals cannot change their ethnic background. While lifestyle modifications can reduce overall risk, ethnicity itself remains unalterable.

• Hypertension:Elevated blood pressure causes endothelial injury and accelerates plaque formation within coronary arteries. Blood pressure can be controlled through medications, diet, exercise, and stress management. Because treatment and lifestyle changes can significantly improve control, hypertension is modifiable. Effective management reduces CAD progression.

• Diabetes: Poorly controlled diabetes promotes vascular inflammation and accelerates atherosclerosis through chronic hyperglycemia. Glycemic control through medication adherence, dietary changes, weight management, and exercise lowers cardiovascular complications. Although genetic predisposition exists, blood glucose levels can be managed.

• Family history: A family history of premature coronary artery disease reflects inherited genetic risk factors. These genetic influences may affect lipid metabolism, clotting tendencies, and inflammatory responses. Although lifestyle interventions can mitigate overall risk, inherited predisposition cannot be changed.

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