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Chest Pain

A 27-year-old accountant recently drove cross-country to start a new job in Denver, Colorado. A week after her move, she started to experience chest pains. She drove to the emergency department after experiencing 24 hours of right-sided chest pain, which was worse with inspiration. She also experienced shortness of breath and stated that she felt warm. She denied any sputum production, hemoptysis, coughing, or wheezing. She is active and walks daily and never has experienced any swelling in her legs. She has never been treated for any respiratory problems and has never undergone any surgical procedures. Her medical history is negative, and she has no known drug allergies. Oral contraceptives are her only medication. She smokes a pack of cigarettes a day and consumes wine occasionally. She does not use intravenous drugs and has no other risk factors for HIV disease. Her family history is negative for asthma and any cardiovascular diseases.

Physical examination reveals a mildly obese woman in moderate respiratory distress. Her respiratory rate is 24 breaths/min and her pulse is 115 beats/min. Her blood pressure is 140/80 mm Hg, and no jugular vein distension is observed. Heart rate and rhythm are regular, with normal heart sounds and no murmurs. Her chest is clear, and her temperature is 38°C. Her extremities show signs of cyanosis, but no clubbing or edema is detected. Blood gases, obtained while she was breathing room air, reveal a Po2 of 60 mm Hg and a Pco2 of 32 mm Hg; her arterial blood pH is 7.49. Her alveolar-arterial (A-a)o2 gradient is 40 mm Hg. A Gram's stain sputum specimen exhibited a normal flora. A chest X-ray study reveals a normal heart shadow and clear lung fields, except for a small peripheral infiltrate in the left lower lobe. A lung scan reveals an embolus in the left lower lobe.

Case Study Questions

1. What is the cause of a widened alveolar-arterial gradient in patients with pulmonary embolism?

2. What causes the decreased arterial Pco2 and elevated arterial pH?

3. Why do oral contraceptives induce hypercoagulability?

Answers to Case Study Questions for Chapter 20

1. A normal A-ao2 gradient is 5 to 15 mm Hg. A pulmonary embolus will cause blood flow to be shunted to another region of the lung. Because cardiac output is unchanged, the shunting of blood causes overperfusion, which causes an abnormally low A/ ratio in another region of the lungs.

Thus, blood leaving the lungs has a low Po2, resulting in hypoxemia (a low arterial Po2). The decrease in arterial Po2 accounts in part for the increase in the A-aO2 gradient. However, ventilation is also stimulated as a compensatory mechanism to hypoxemia, which leads to hyperventilation with a concomitant increase in alveolar Po2. The A-aO2 gradient is, therefore, further increased because of the increased alveolar Po2 caused by hyperventilation.

2. The decreased Pco2 and increased pH are the result of hyperventilation as a result of the hypoxic drive (low Po2) that stimulates ventilation.

3. The mechanisms by which oral contraceptives increase the risk of thrombus formation are not completely understood. The risk appears to be correlated best with the estrogen content of the pills. Hypotheses include increased endothelial cell proliferation, decreased rates of venous blood flow, and increased coagulability secondary to changes in platelets, coagulation factors, and the fibrinolytic system. Furthermore, there are changes in serum lipoprotein levels with an increase in LDL and VLDL and a variable effect on HDL. Driving cross-country, with long sedentary periods, may have exacerbated the patient's condition.


Cotes JE. Lung Function: Assessment and Application in Medicine. 5th ed. Boston: Blackwell Scientific, 1993.

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Anxiety and Depression 101

Anxiety and Depression 101

Everything you ever wanted to know about. We have been discussing depression and anxiety and how different information that is out on the market only seems to target one particular cure for these two common conditions that seem to walk hand in hand.

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