Pathophysiology of Hypovolemic Shock - Article Example

Consequently, vasoconstriction takes place as the nervous system tries to contrive the blood away from non-vital organs of the gut and extremities, towards the central core (James & Jonas, 2008).

The renal system initiates other compensatory mechanisms and rennin is released. Accordingly, a cascade of events ensues and with the production and discharge of the angiotensin-angiotensin Il-aldosterone flow. This cycle enhances vasoconstriction as well as the reabsorption of both sodium and water while trying to increase blood volume and these mechanisms can raise blood pressure. In case hypovolemic shock remains untreated for some time he/she becomes unstable and the blood pressure drops significantly.

This is exhibited in Mr. Lee’s diagnosis whereby he has low blood pressure BP 74/40 mmHg (MAP 51 mmHg) (Kelly, 2005). An apical pulse of 120 beats/min (tachycardia) resulted from the increase in the heart rate. The pathophysiology of tachycardia starts with vasoconstriction as a compensatory response to shock. The initial reduction of blood pressure hinders the afferent release of baroreceptors within the aortic arch and also carotid sinus. Consequently, this stimulates sympathetic nervous system output.

The reduction in blood volume as a result of hypovolemic shock hinders the release of stretch receptors within the right atrium in addition to stimulating afferent release from chemoreceptors within the aortic arch and also carotid bodies. As a result, there is increased sympathetic tone that causes the discharge of catecholamines, epinephrine, along with norepinephrine and this intensifies venous tone, increases heart rate resulting in tachycardia (Kelly, 2005). SpO2 90% on a non-rebreather mask at 15L/min.

This is aimed at supporting adequate oxygen delivery through volume loading to treat Mr. Lee’s metabolic acidosis. The pathophysiology of this condition is due to acid-base disturbances. Hypoxic or hypotensive stimulation of both aortic and carotid chemoreceptors, the occurrence of metabolic acidosis as well as painful stimuli activate the respiratory center, resulting in hyperventilation. As the state of shock advances, anaerobic metabolism dominates and this stimulates the production of lactate and successive metabolic acidosis.

The resulting metabolic acidosis further intensifies the shock state and this reduces sensitivity to catecholamines and stress hormones. This results in decreased myocardial contractility, promoting predilection to cardiac dysrhythmias. Lactic acidosis, the physiological deficit ensuing from insufficient perfusion, is indicated in high levels of serum. The quantity of lactate produced compares with the total oxygen debt (James & Jonas, 2008).