Introduction
This essay will endeavour to analyse the case study of Mr Mario Toscana, a 63 year old man transferred to HDU post MET call for an acute pulmonary oedema (APO). Firstly, the author will explain the pathophysiology that underpins Mr Toscana’s presenting condition. Furthermore, the provided ECG strip, the arterial blood gases (ABGs) and blood test results will be examined and their significance in relation to the presenting medical condition described. To conclude, the specific assessment criteria and essential nursing interventions required will be discussed.
Pathophysiology
The term oedema defines the collection of excess fluids within the interstitial spaces in the body (). Therefore, acute pulmonary oedema (APO) refers to the accumulation of extra fluid in the lung interstitium, with a sudden onset of its symptoms (). In order to maintain homeostasis, at capillary level, the fluids shift between the body fluid compartments is maintained via the balance of two opposing pressures namely hydrostatic and colloid osmotic pressure (). The hydrostatic pressure is the pressure exerted by a fluid (blood) against the walls of its container (capillary), and being the capillary walls semi-permeable, the blood is pushed out of it (). The colloid osmotic pressure, also known as oncotic pressure, constitutes the pulling force that draws the fluid back into the capillary due to the difference of solute (salt, plasma proteins and blood cells) concentration between the intravascular and the extravascular space (). Moreover, any excess fluid that leaks into the interstitial space gets removed and returned to the circulation via the lymphatic system (). Having said so, any changes in one of the two pressures will create an imbalance in homeostasis that can lead to oedema (). Generally, pulmonary oedema can be caused by increased hydrostatic pressure in the pulmonary circulation, damage of the capillary walls that consents proteins to escape from the plasma, or blocked lymphatic drainage (). Pulmonary oedema is categorised as cardiogenic (as a result of cardiac conditions) or non-cardiogenic (as a result of other pathological processes such as infection, injury or inhaled toxins) ().
The excess fluid deposited in the lungs goes to increase the distance that exists between the pulmonary capillaries and the air in the alveoli, which will result in impaired gas exchange (). Mr Toscana is exhibiting common signs and symptoms of APO including sudden onset of breathlessness followed by anxiety, cough with presence of pink frothy sputum (blood tinged), and diaphoresis; however it is complex to determine whether Mr Toscana’s APO has cardiogenic or non-cardiogenic origin (). In the scenario there is no mentioning of any significant history that could lead to a non-cardiogenic APO, but it is important to notice that he also has a medical history of chronic renal impairment (CRI). CRI is best defined as the gradual loss of kidney functions due to the presence of...
