A patient is brought into the hospital with dyspnea and treated with a 2 agonist

Question

A patient is brought into the hospital with dyspnea and treated with a 2 agonist with the following results:

Before Treatment                                After

Tidal volume

0.5 L

0.5 L

FVC

2.5 L

4.5 L

FEV1

1.2 L

3.5 L

FEV1/FVC

0.48

0.78

(FEV1, volume expired in the first second of forced expiration; FVC, forced vital capacity.)

A. Describe the physiological mechanisms that caused the problem, and how the medicine helped. (remember Ohm’s and Poiseuille’s laws!)

B.What disease do you think the patient had? What effect did this have on their residual volume and functional residual capacity (FRC)?

Tidal volume

0.5 L

0.5 L

FVC

2.5 L

4.5 L

FEV1

1.2 L

3.5 L

FEV1/FVC

0.48

0.78

Explanation / Answer

Explanation:-

The patient had asthma an obstructive pulmonary disease that is characterized by inflammation and narrowing of the airways This narrowing of the airways (i.e., decreased airway radius) led to increased resistance and decreased airflow. The patient wheezes were the sounds produced when he expired forcibly through these narrowed airways.

In asthma, the airways are narrowed for three major reasons:

(1) hyperresponsiveness of bronchial smooth muscle to a variety of stimuli which causes bronchospasm and bronchoconstriction during an attack.

(2) thickening and edema of the bronchial walls secondary to inflammation

(3) increased production of the bronchial mucus that obstructs the airways.

The first mechanism (bronchoconstriction) can be reversed by administering bronchodilator drugs, such as 132-adrenergic agonists (e.g., albuterol). Increases in the airway resistance, such as those seen in asthma lead to decreases in all the expiratory parameters, including FVC, FEV and FEV/FVC. The higher the airway resistance the more difficult it is to expire air from the lungs. Airway resistance is especially increased during the forced expiration, when intrapleural pressure becomes positive and tends to compress, or even closes the airways . Therefore FVC decreases during an asthma attack because the airways close prematurely during expiration. One result of this premature closure of the airways is that air that should have been expired remains in the lungs (air trapping).

The inhaled bronchodilator relaxed patients airways, increasing their radii and decreasing their resistance to airflow. The decrease in airway resistance improved patients expiratory functions increased

1 .EVi and FEVI /FVC. Also, because his airways did not close prematurely, his FVC was increased.

2. Patients asthma was associated with increased airway resistance, which compromised his expiratory functions. As a result, air that should have been expired remained in the lungs, increasing his residual volume and his functional residual capacity (FRC). Because Patients FRC was increased, his normal "tidal" breathing had to occur at higher lung volumes.

The work of breathing is determined by how much pressure change is required to move air into and out of the lungs. In obstructive lung diseases, such as asthma, the work of breathing is increased for two reasons.

(1) During inspiration, a person with asthma must lower intrathoracic pressure more than a healthy person to bring air into the lungs; thus, more work is required during inspiration.

(2) During expiration, because airway resistance is increased, higher pressures must be created to force air out of the lungs; this greater expiratory effort requires the use of accessory muscles. (In healthy people, expiration is passive and does not require the assistance of accessory muscles.) Increased work of breathing is reflected in higher rates of 02 consumption and CO2 production.

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