Case Study 1: Case Presentation John, a healthy twenty-eight year old electrical

Question

Case Study 1: Case Presentation

John, a healthy twenty-eight year old electrical engineer, was driving home from work one evening when he experienced sudden stabbing pain in his right pectoral and right lateral axillary regions. He began to feel out of breath and both his respiratory rate and heart rate increased dramatically. As luck would have it, John passed a hospital each day on his way home and was able to get himself to the hospital’s emergency room. The emergency room physician listened to John’s breathing with a stethoscope and requested blood gas analysis and a chest x-ray. John answered a few of the doctor’s questions. The doctor noted that John had no history of respiratory problems but was a heavy smoker.

After viewing the chest radiograph, the doctor informed John that he had experienced a spontaneous pneumothorax, or what is commonly called a collapsed lung. The doctor explained that a hole had opened in John’s right lung and that this hole had allowed air to leak into the cavity surrounding the lung. Then, as a result of the lung’s own elastic nature, the lung had collapsed. The doctor said he could not be certain of the cause of the pneumothorax, but smoking cigarettes had certainly increased the likelihood of it happening. He told John he was fortunate the pneumothorax was small, which meant that relatively little air had escaped from the lung into the surrounding cavity, and it should heal on its own. He instructed John to quit smoking, avoid high altitudes, flying in nonpressurized aircraft, and scuba diving. He also had John make an appointment for a re-check and another chest x-ray.

Case Background

Spontaneous pneumothorax occurs when a blister on the surface of the lung opens, allowing air from the lung to move into the pleural cavity. This occurs because alveolar pressure is normally greater than the pressure in the pleural cavity. As air escapes from the lung, the lung tissues will recoil, and the lung will begin to collapse. The lung will continue to collapse until the difference between the alveolar pressure and pleural pressure disappears or until the collapsing of the lung causes the opening to seal.

The pneumothorax decreases the efficiency of the respiratory system, which in turn results in decreased blood oxygen concentration, increased respiratory rate, and increased heart rate. If the pneumothorax is small, the air that escapes into the pleural cavity can be reabsorbed into the lung once the opening has sealed shut. If the pneumothorax is large, a needle or chest tube may have to be inserted into the pleural cavity to draw the air out and allow for the reexpansion of the lung.

Questions

Define the following terms and explain how they may have been affected by John’s spontaneous pneumothorax.

Visceral pleura

Parietal pleura

Pleural cavity

As a result of a pneumothorax, the lung tissues recoil, and the lung collapses. Explain how recoil and collapse are prevented in a healthy lung?

How does elastic recoil function in breathing?

Why was John instructed to avoid high altitudes and flying in nonpressurized aircraft?

Case Study 2: The Case of the Coughing Housewife

Jessica, a fifty-nine year old mother of four, moved from a ranch in Colorado to Los Angeles, after the death of her husband, to be closer to her oldest son and his family. She has been in Los Angeles for 18 months and has noticed that she is experiencing shortness of breath which has worsened over the last six months. For the last week, she has been coughing and bringing up yellow mucus. She also noticed swelling in her ankles so she decided to visit a physician about her condition.

Jessica's family and medical history include a negative history of asthma or allergies, lack of occupational or home exposure to asbestos, a previous smoking history (one package of cigarettes per day between the ages of 16 and 52), episodes of bronchitis, treated with antibiotics on an outpatient basis, and a positive history of heart disease (father at 52 and brother at 56). Jessica has no history of serious illness, including heart disease, and her weight is within five pounds of her "desired" weight. She usually coughs in the morning to "clear her throat", but there is usually only a small amount of white mucus.

Her nurse practitioner conducts a general physical examination with the following results. Jessica's skin is normal (no rashes or cyanosis) and her nervous system is functioning normally. Her body temperature was 98.4oF while her pulse was regular at 95 beats per minute with an occasional premature beat. Jessica's blood pressure was within normal limits, however her jugular veins were slightly distended. Her respiratory rate was 28 breaths per minute; she breathed with pursed lips and used her accessory respiratory muscles more than would be expected. Jessica presented with a barrel chest and mild dyspnea when climbing onto the examination table. When listening to her breathing, the nurse practitioner noticed that Jessica had prolonged expiration accompanied by expiratory wheezes. Evaluation of her abdomen indicated no masses or tenderness, but she presented with both hepatomegaly and splenomegaly. All of her extremities were normal with the exception of bilaterally pedal edema.

Based on these results, the nurse practitioner suspected a pulmonary disorder and, after consultation with a physician, ordered laboratory tests (blood and sputum), spirometry and chest x-rays. The results of the laboratory tests were as follows: plasma bicarbonate = 38 mEq/L, hematocrit = 49%, white blood cell count = 9000, pH = 7.38; PaCO2 = 56, and PaO2 = 54. Analysis of the sputum sample indicated the presence of epithelial cells, polymorphonucleocytes and gram positive diplococci. Jessica's 1 second forced expiratory volume (FEV1) was 1.5 L/sec and her forced vital capacity (FVC) was 4 L. These values were 40% and 83% of normal, respectively. Results of the chest x-ray indicated scarring and hyperinflation of the lungs.

The results of these tests coupled with the physical examination and history lead to a diagnosis of emphysema. Jessica was prescribed antibiotics for the infection and oxygen by nose as well as a b2-agonist nebulizer as an acute treatment and requested to stay for observation and stabilization. After Jessica's condition was stabilized she was discharged and given a prescription for an inhaler containing a b2-agonist to be used as needed. She was also encouraged to exercise regularly and follow the nutritional guidelines she was given. Jessica was also informed that if the symptoms either worsened or did not lessen within the next week, to return and her treatment would be reevaluated and would possibly include nocturnal oxygen and an inhaler containing corticosteroids.

Answer the following questions about this case

Define the bold terms in the text. (8 points)

What risk factors and symptoms did Jessica present with prior to the physical examination that suggested a pulmonary disorder?

How did the physical examination, chest X-ray and spirometry confirm this hypothesis?

Identify muscles involved in respiration and how these muscles are responsible for the process of ventilation.

How will the b2-agonist in the inhaler help with the respiratory problems Jessica presents with?

Why is it important that a b2-agonist and not simply an b-agonist is used in the inhaler?

If her condition does not progress, why would corticosteroids be used in the inhaler?

Explanation / Answer

CASE 1:

Define the following terms and explain how they may have been affected by John’s spontaneous pneumothorax.

Visceral pleura
The serous membrane that covers the surface of a lung is called the visceral pleura. Pneumothorax involves the rupture of this membrane

Parietal pleura
Each thoracic compartment in the thoracic cavity is lined with a serous membrane called the parietal pleura. This membrane was not directly affected by the pneumothorax

Pleural cavity
The pleural cavity is the potential space between the visceral and parietal pleurae. It is called a potential space because there is normally no actual space between the two membranes. Normally, the membranes come into close contact with one another and are separated only by a thin film of serous fluid. When a pneumothorax occurs, air is allowed into the pleural cavity, which changes from a potential space to an actual air filled cavity.

As a result of a pneumothorax, the lung tissues recoil, and the lung collapses. Explain how recoil and collapse are prevented in a healthy lung?

In a healthy lung, the visceral pleura and parietal pleura are held together by surface tension. Surface tension occurs because the water molecules in the serous fluid between the two membranes are attracted to one another.


How does elastic recoil function in breathing?

Elastic recoil functions during expiration. As the diaphragm and external intercostal muscles relax, the elastic tissues of the lungs recoil and air is forced out of the lungs.

Why was John instructed to avoid high altitudes and flying in nonpressurized aircraft?

At high altitudes, the air pressure is less and the partial pressure of oxygen gas is less. John would have to breathe faster and more deeply in order to supply his tissues with oxygen gas and this could cause another pneumothorax.


CASE 2:

Define the bold terms in the text.
asthma: dyspnea accompanied by spasm of the bronchial tubes or due to swelling of the mucous membranes of the bronchial tubes
bronchitis: inflammation of the bronchial mucous membrane
cyanosis: the bluish discoloration of the skin and mucous membranes due to excessive concentrations of deoxyhemoglobin in the blood.
dyspnea: labored or difficult breathing
edema: the localized or generalized accumulation of interstitial fluid within the interstitial spaces
vital capacity: the maximum volume of air that can be exhaled following a maximum inspiration
emphysema: a pulmonary disease caused by the destruction of alveoli within the lung and subsequent enlargement of remaining alveoli

What risk factors and symptoms did Jessica present with prior to the physical examination that suggested a pulmonary disorder?
The risk factors that Jessica presented with are a history that is positive for smoking, bronchitis and living in a large urban area with decreased air quality. The symptoms that suggest a pulmonary disorder include a productive cough with discolored sputum, elevated respiratory rate, use of the accessory respiratory muscles during quite breathing, exertional dyspnea, tachycardia and pedal edema. The discolored sputum is indicative of a respiratory infection. The changes in respiratory rate, use of respiratory muscles and exertional dyspnea indicate a pulmonary disorder since there is an increased amount of work required for normal breathing. Tachycardia may arise due to the lack of oxygenated blood available to the tissue stimulating an increase in heart rate. The pedal edema most probably results from decreased systemic blood flow.

How did the physical examination, chest X-ray and spirometry confirm this hypothesis?
The physical examination indicated that Jessica had prolonged expiration and wheezes during expiration. These are suggestive of airway obstruction due to the "trapping" of air in the expiratory airway. The normal pH and elevated blood carbon dioxide confirm chronic hypercapnia (elevated carbon dioxide concentrations in the blood) which is being compensated for by elevations in circulating bicarbonate concentrations, suggesting a lack of pulmonary function. The results of the spirometry indicate decreases in both the 1 second forced expiratory volume and 1 second forced vital capacity. These suggest an obstructive pulmonary disease. Finally, the chest X-ray showed scarring and hyperinflation, suggesting an increased lung compliance, which is characteristic of emphysema. The elevation in leukocytes and the presence of polymorphonucleocytes and gram positive diplococci in the sputum sample are indicative of a respiratory tract infection, most probably due to the inability of the pseudostratified ciliated columnar epithelial cells to clear the airway.

Identify muscles involved in respiration and how these muscles are responsible for the process of ventilation.
The respiratory muscles are subdivided based on function. The contraction of the inspiratory muscles increases the volume of the thoracic cavity causing the pressure within the alveoli to decrease and air to flow into the alveoli. During quiet (resting) inspiration, the diaphragm, the external intercostals and the parasternal intercostals contract to stimulate inspiration. During forced inspiration the scalenes and the sternocleidomastoid muscles contract to further expand the thoracic cavity. The pectoralis minor muscles also play a minor role in forced inspiration. During quiet breathing, relaxation of these muscles causes the volume of the thoracic cavity to decrease, resulting in expiration. During a forced expiration, the compression of the chest cavity is increased by contraction of the internal intercostal muscles and various abdominal muscles (the external abdominal oblique, internal abdominal oblique, tranversus abdominis and rectus abdominis muscles).

How will the b2-agonist in the inhaler help with the respiratory problems Jessica presents with?
A b2-agonist will bind to the adrenergic receptors within the respiratory system. Activation of the adrenergic receptors will stimulate dilation of the airway. Dilation will occur due to the relaxation of the smooth muscle within the walls of the bronchioles. This dilation will decrease the resistance to the flow of air and subsequently increase ventilation.

Why is it important that a b2-agonist and not simply an b-agonist is used in the inhaler?

If a generic b-agonist were used rather than a b2-agonist a greater number of side effects would be observed. These side effects would occur when the b-agonist diffused across the alveolar membrane and entered the circulatory system. The circulatory system would then transport the b-agonist to potentially all cells of the body. This could then induce a widespread stimulation of all sympathetic responses within the body. These side effects would include, but not be limited to, elevated heart rate, peripheral vasodilation of b adrenergic responsive blood vessels, decreased gastrointestinal motility and increased apocrine gland secretions. The use of a b2-agonist limits the potential side effects to only those target tissues which have b2-adrenergic receptors. Probably most importantly, this minimizes the cardiovascular side effects that would occur.

If her condition does not progress, why would corticosteroids be used in the inhaler?
Corticosteroids would be used in Jessica's inhaler if her condition does not improve to decrease the immune response. One of the nonspecific immune responses is inflammation. Part of the inflammatory response is the release of histamines. Histamines are potent bronchioconstrictors. By minimizing the inflammatory response there would be minimal histamine secretion and consequently less bronchioconstriction.

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