Resolution
(All information contained here needed for Arizona students to receive full points on this case):
Part 1
Ashen color ? suggests poor blood flow and/or poor oxygenation of blood
Dyspnea ? a problem with breathing. This may be related to: 1) the activation of irritant receptors (due to lung damage or outside irritants), 2) an abnormal work level required for ventilation (due to poor oxygenation of the blood or a stiff lung). In either case the patient is experiencing a perception of abnormal, difficult breathing.
Cough ? probably due to irritation of the airways resulting in activation of irritant receptors. Again, there could be multiple reasons for this.
The history of asthma suggests that his airways may be hyperreactive and that excessive bronchoconstriction could be a problem.
The fact that his condition improved suggests that any asthma-related issues probably resolved, however there is a chance of a delayed response to the inhalation. Bronchoconstriction would increase the resistance to airflow and severe constriction might reduce the effective ventilation, even though the inspiratory and expiratory muscles might be strongly activated. If ventilation is reduced, one would expect an increase in PaCO2 and a decrease in PaO2.
Visibly anxious ? this suggests his sympathetic nervous system output is likely to be increased. That contributes to an increase in blood pressure (SNS activity may increase cardiac output, heart rate and/or total peripheral resistance). All increase pressure! The sympathetic nervous system also dilates airways ? that?s good._ If blood gases are affected, it is possible that chemoreceptors also are stimulating an increase in heart rate,_ blood pressure, and respiratory rate.
The increased respiratory rate could also potentially be related to a decreased lung compliance causing a breathing pattern of rapid, shallow breathing.
Frothy sputum ? sputum indicates enhanced secretions and a frothy nature suggests it may contain surfactant which acts like a detergent and may cause ?suds?. The noted presence of a frothy sputum suggests that there is increased production of fluid in the lungs and that it is coming from the gas exchange areas ? not just mucuc from the conducting airways. This is consistent with damage of the lung.
PART 2
Supplemental oxygen will increase the alveolar PO2 and should improve the oxygenation of the blood. As hemoglobin is oxygenated, it has a red color so that is likely to contribute to the improved color. Also, as the PaO2 increases, the sympathetic drive may decrease. The very fact that something is being done may relieve some of the anxiety, which could have identical effects. The PaO2 of 45 mm Hg while breathing room air suggests that there is a significant barrier for the movement of oxygen, assuming that alveolar ventilation is normal. The fact that the inhaler provided little benefit suggests that the airways are already dilated. With dilated airways, one would suspect that this problem results from problems in the alveolar-capillary membrane leading to decreased diffusion. A decrease in surface area (due to loss of alveolar membrane or reduced capillary blood flow) or an increase in the thickness of the membrane would decrease diffusion. Both of these might be expected after poisoning or damage of the alveolar cells. Giving ZK 100% oxygen improves his PaO2 slightly by increasing the pressure gradient for diffusion of oxygen.
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The threshold for activation of the peripheral chemoreceptors is a PaO2 of about 60 mm Hg. When ZK is breathing room air, his low PaO2 stimulates these receptors, which in turn stimulate increased depth and rate of breathing._ The increased ventilation elevates the alveolar PO2 slightly, but not enough to cause sufficient oxygen diffusion._ Since CO2 is more soluble than O2, its diffusion across the alveolar-capillary membrane is usually not affected as much as O2. Therefore, with the increased ventilation, the alveolar PCO2 falls leading to a decrease in PaCO2._ When the PaO2 improves (with 100% O2), there is reduced stimulation of peripheral chemoreceptors, the patient breathes less and the PaCO2 returns toward normal._
PART 3
Because of the deteriorating blood gases, the patient is hospitalized. Sedation reduces anxiety (and sympathetic nervous system activity) and decreased the metabolic rate. Decreasing the metabolic rate is important to conserve the limited amounts of oxygen carried in the poorly oxygenated blood. Mechanical ventilation also decreases the body metabolism since the respiratory muscles do not have to do any work.
A constant pressure ventilator applies a given pressure and assumes that a reasonable volume will enter the lungs. The need to increase the ventilator pressure suggests that the lung compliance is decreasing. This is consistent with damage to the lung lining leading to inflammation, loss of tissue, pulmonary edema, ?wet lung?. The accumulation of debris and fluid decreases the lung compliance._
This finding of a stiff lung due to pulmonary exudates is consistent with restrictive diseases such as ARDS (adult respiratory distress syndrome). Similar problems were encountered in SARS._
Both decreased surface area and thickened membrane will decrease diffusion of gases.
Heart rate and blood pressure ? At first glance these look borderline normal. However, given that ZK is sedated (or possibly anesthetized), one would expect lower values. The values are probably being increased by drive from the peripheral chemoreceptors. The central chemoreceptor is greatly reduced because of the hyperventilation that is occurring.
The synthetic surfactant was administered to increase lung compliance and prevent further damage to lung tissue by the inflation pressure. It is possible that the endogenous synthesis of surfactant was suppressed by the damage. It is also likely that the edema that was occurring resulted in dilution of the surfactant, thus minimizing its effectiveness. Additional inhaled surfactant would help reduce surface tension and increase lung compliance.
The steroids were presumably anti-inflammatory in nature and represented an attempt to reduce the inflammatory damage. It is also possible that they helped stimulate spontaneous formation of surfactant.
As the required inflation pressure decreased, the lung compliance was obviously increasing. When it approached normal ranges, the chances were good that some healing and restoration had occurred. Reducing the ventilator activity and increasing the metabolic activity (by reducing sedation) helped restore the PaCO2 toward normal. As PaCO2 increased the central chemoreceptor drive to breathe returned and ZK began to attempt to breathe on his own.
Although lung function was adequate to meet resting levels of activity, full lung function had not returned. The caution to avoid exercise was to prevent high respiratory lung pressures associated with stressed ventilation and high blood pressures as well._ It is likely that some damage was done to the pulmonary vasculature as well as the alveolar membrane.
