Hypovolemic Shock
Shock is a life threatening condition that occurs when the organs and tissues of the body are not receiving an adequate flow of blood. In a sense the circulatory system is failing to effectively deliver oxygen to the cells thus resulting in reduced tissue perfusion. It is characterised by hypoxia and inadequate cellular function that lead to multiple organ failure and potentially death (Kleinpell 2007). This essay will focus on hypovolemic shock in particular, and relate it to patient with complications following gastrointestinal bleeding.
Hypovolemic shock is characterised as the body’s loss of fluids, such cases are haemorrhage due to trauma, dehydration as a result of vomiting and severe diarrhoea or from severe burns (Hand 2001). According to Kleinpell (2007), there are four stages of shock : initial, compensatory, progressive and refractory. In the initial stage signs of shock are minimal with cells switching from aerobic to anaerobic metabolism leading to lactic acidosis, this is the build-up of excess lactic acid in the blood. Taking an arterial blood gas and checking the lactate level in the blood can give clear indication of acidosis. Hypovolemia can manifest when there is about 15% loss of circulatory volume, but the more volume lost the more significant the clinical signs become (Hall, 2010).
The next stage of shock is the compensatory stage, here the body is attempting to stabilise the body’s circulation. This is where body’s compensatory mechanisms fall in to play; the initial compensatory mechanism is the sympathetic nervous response. Here the response is mediated by the decrease in arterial pressure which then stimulates the baroreceptors located in the aortic arch and carotid sinuses (Marieb 1998). The result of the nervous system being stimulated is the release of catecholamines, noradrenaline and adrenaline (Chavez and Brewer 2002). An effect of adrenaline release is it stimulates the beta receptors in the heart increasing myocardial
Hypovolemic shock is characterised as the body’s loss of fluids, such cases are haemorrhage due to trauma, dehydration as a result of vomiting and severe diarrhoea or from severe burns (Hand 2001). According to Kleinpell (2007), there are four stages of shock : initial, compensatory, progressive and refractory. In the initial stage signs of shock are minimal with cells switching from aerobic to anaerobic metabolism leading to lactic acidosis, this is the build-up of excess lactic acid in the blood. Taking an arterial blood gas and checking the lactate level in the blood can give clear indication of acidosis. Hypovolemia can manifest when there is about 15% loss of circulatory volume, but the more volume lost the more significant the clinical signs become (Hall, 2010).
The next stage of shock is the compensatory stage, here the body is attempting to stabilise the body’s circulation. This is where body’s compensatory mechanisms fall in to play; the initial compensatory mechanism is the sympathetic nervous response. Here the response is mediated by the decrease in arterial pressure which then stimulates the baroreceptors located in the aortic arch and carotid sinuses (Marieb 1998). The result of the nervous system being stimulated is the release of catecholamines, noradrenaline and adrenaline (Chavez and Brewer 2002). An effect of adrenaline release is it stimulates the beta receptors in the heart increasing myocardial