9. Explain the mechanism for the edema in the patient.

Upon admission at the ER, the patient was noted to have a generalized edema with a grade III bipedal edema and weak peripheral pulses. He had crackles in his mid lung fields with decreased breath sounds mid to base bilateral lung fields. His abdomen is slightly globular and symmetrically enlarged with everted umbilicus and a palpable liver. Edema can be a localized or a generalized condition in which the body tissues contains an excessive amount of body fluid in the interstitial space or in one or more of the cavities of the body. Edema is not a disease itself but a sign of an underlying cause or problem. It may result from a lot of factors. The patients blood chemistry results showed a reduction in his plasma proteins. There was a significant drop in his albumin level and a slight decrease in his globulin level. Albumin, being the major plasma protein of the body, is the one responsible for maintaining the intravascular oncotic pressure which retains the fluids inside the blood vessels. With a low albumin level, there would be a decrease in the intravascular oncotic pressure causing the fluid to escape or seep out from the intravascular to the extravascular compartment. These fluids may build up in the interstitium first but may later cause a third space shifting causing the fluid to enter in the peritoneal cavity, pleural cavity, pericardium or even the alveoli. The presence of crackles and the enlargement of abdomen may be indicative of this third space shifting. 10. Explain the mechanism for dyspnea in the patient. Dyspnea, the sensation of feeling breathless, is a symptom experienced under conditions in which there is an inordinately high ventilatory demand relative to the ability to breathe. Its major physical sign is tachypnea which is evident on the patients respiratory rate of 40. There are no known universal theory on the mechanism of dyspnea because this symptom may be caused by a lot of factors. The patients ABG profile for one, can be a basis on why the patient is gasping for breath. The result showed a decrease in pH, p02, HCO3 and O2 sat. Considering this blood gas abnormalities, the lowered pH and HCO3 specifically, is already suggestive of the condition called metabolic acidosis where the concentration of H+ in the blood is increased. This acid base imbalance then stimulates the central chemoreceptors located on the ventral surface of the medulla which in turn causes an increase in ones respiration. This rapid respiration which was evident on the patient is indicative of his bodys attempt to compensate and expel the excess CO2 to bring the bloods ph and HCO3 to normal again. On the other hand, considering also the presence a generalized edema and the presence of fluids in the patients lungs, suggestive of the crackles and the decreased breath sounds, we can assume that the alveoli is already accumulating fluid, thereby increasing the distance in which CO2 and O2 needs to cross and limiting the amount of O2 it can accommodate because of the already occupied alveoli in the lungs. This may result to an impaired gas exchange and inadequacy of O2 delivery to the tissues and the lungs. Another factor to consider is the drop in the patients haemoglobin level. The oxygen carrying capacity of the blood depends on the amount of haemoglobin present because O2 binds and depends on haemoglobin for its transport. So a decrease in Hgb would also mean a decrease in oxygenation.

The low Hgb level, together with the fact that the blood pH is low and the lungs is drowning in fluids, and although his body tries to compensate by increasing the respiration and heart rate, the patient is still not getting enough oxygen making breathing difficult for him putting him in a severe respiratory distress.

New developments in monitoring ventilation during exercise have improved our ability to evaluate the symptom of dyspnea and to understand pathophysiological mechanisms contributing to the symptom. We briefly describe the range of mechanisms that determine exercise ventilation and their possible relationship to dyspnea. Questionnaires and psychophysical testing have been used to quantify dyspnea, but there is variability in dyspnea grade from these methods. Dyspnea-producing stimuli and the mechanisms by which they act are reviewed. Disorders producing dyspnea and the pathophysiological mechanisms underlying each are discussed. Perception of dyspnea is obviously through the central nervous system, where dyspnea-producing stimuli are integrated. The specific integration site is probably in the region of the brain stem, since occasional patients with brain stem lesions do not experience dyspnea despite the presence of a number of dyspnea-producing stimuli.control