This case study is intended to explain pulmonary oedema through Mr. Toscanas case. It will discuss the pathophysiology of pulmonary oedema and how Mr. Toscanas chronic renal impairment is related to this specific condition. Also, Mr. Toscana’s ECG, aerial blood gas results and blood tests result will be analysed and explained. Moreover, a nursing plan based on Mr. Toscana’s condition will be made.
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Overview of the Presenting Condition
Pulmonary oedema is a serious condition of the pulmonary system. In simple terms, it is actually excess fluid in the lungs (skinner& Mckinner 2011). To be more specific, it is fluid that moves out from capillaries into the extravascular spaces and causes additional pressure to the lungs (Craft, J 2011). Pulmonary oedema is affecting about 1% of people over the age of 65 (Johnson 2009). It is a worldwide condition and the mortality rate is about 40% within a year of diagnosis (Parissis et al. 2010). The accumulation of the fluid can be in a slow process for patients with chronic renal failure. It can also occur fast for patients who suffer from myocardial infarction (McPhee& Hammer 2010). There are two types of pulmonary oedema, one is cardiogenic pulmonary, and the other in non-cardiogenic pulmonary oedema (Craft, J 2011). Pulmonary oedema is defined as alveolar or interstitial oedema, and such a condition can be identified by chest X-ray (Johnson 2009). And often patients’ oxygen saturation is less than 90% on room air (Johnson 2009). Also severe respiratory distress, with crackles over the lungs and orthopnoea, is often associated with acute pulmonary oedema (Parissis et al. 2010). The most common cause of pulmonary oedema is untreated heart failure (Johnson 2009). The acute respiratory distress syndrome and capillary vessel injury are other common causes of pulmonary oedema (Craft, J et al. 2011). Its signs and symptoms often include dyspnoea, hypoxaemia and increased work of breathing (Skinner& Mckinney 2011). In severe cases of pulmonary oedema, patients often bring up pink frothy sputum when coughing and their carbon dioxide level increases while oxygen level decreases (Craft, J et al. 2011).
Pathophysiology that Underpins the Presenting Condition
As mentioned before, pulmonary oedema is excess fluid in the extravascular space and according to McPhee& Hammer (2010) the extravascular space is constituted by the interstitial space and the airspace (alveoli and airways). The excess fluid can be found in one or both spaces in patients with pulmonary oedema (McPhee& Hammer 2010). Moreover, both spaces have different barriers to stop fluid from entering into them (McPhee& Hammer 2010). The intersitital space is protected by the pulmonary capillary endothelium, i.e. inside layer of capillary and airspaces are protected by alveolar epithelium, namely surface of alveoli (McPhee& Hammer 2010). It is normal for blood vessel to leak and about 0.01% of pulmonary blood flow will leak into interstitial space every hour (McPhee& Hammer 2010). There are several factors that may influence the amount of fluid leaking into interstitial space and the most important one is net pressure (transmural pressure) (McPhee& Hammer 2010). The transmural pressure maintains the balance between the net hydrostatic pressure that moves fluid out of the capillaries, and the colloid osmotic pressure that keeps fluid inside the capillaries (McPhee& Hammer 2010). Any imbalance of these pressures can lead to pulmonary oedema.
Pulmonary oedema can be divided into two types: the cardiogenic and the noncardiogenic. The former is caused by increased transural pressure (hydrostatic or osmotic) while the latter is caused by increased permeability (damaged alveoli and/ or airways) (Copstead& Banasik 2010). Increased pulmonary venous pressure, increased alveolar surface tension, or decreased capillary colloid osmotic pressure can all lead to cardiogenic pulmonary oedema (Copstead& Banasik 2010). Non-cardiogenic pulmonary oedema is normally caused by an acute respiratory distress syndrome, which often results from injury, infection or inhaled toxins (Copstead& Banasik). In this case study, there is no evidence of injury of the lungs nor inhaled toxins, nor infection of any kind. Thus, Mr. Mario Toscana’s condition is more likely to be cardiogenic pulmonary oedema. Although the case study does not address any cardiac problem based on his age and/ or history of chronic renal impairment, Mr. Toscana is prone to cardiac diseases.
In patients with chronic renal diseases, there are damaged nephrons that cannot be regenerated (Craft, J et al. 2011). Due to slow losses of nephrons, the remaining nephrons have to take the burden and try to maintain the normal function of the kidneys (Craft, J et al. 2011). However, over time this compensation will increase the loss of nephrons and the kidney will lose its normal function (Craft, J et al. 2011). This loss of normal function can result in electrolyte imbalance, which leads to various conditions (Craft, J et al. 2011). Fluid over load, hyperkalemia, metabolic acidosis, congestive heart failure and pulmonary oedema are all the common conditions of chronic renal diseases (Craft, J et al. 2011).
Cardiovascular diseases often presents in patients with chronic renal diseases and they have a very high morbidity and mortality rate (McPhee& Hammer 2010). Hypertension can be caused by excess sodium and fluid, and vascular calcification by decreased glomerular filtration rate (Craft, J et al. 2011). Moreover, vascular diseases can lead or contribute to coronary heart disease, left ventricular hypertrophy, heart failure and stroke. Heart failure is defined as a complex syndrome, which comprises of several cardiac dysfunctions and causes inadequate cardiac output (McPhee& Hammer 2010). The common type of heart failure is the left heart failure, also known as congestive heart failure (Craft, J et al. 2011). Additionally, congestive heart failure can result in both systolic and diastolic heart failures, and any of the two can cause pulmonary oedema (Craft, J et al. 2011). In systolic heart failure, the contractility of the heart decreases because of the disease and it can result in the increase of preload (Craft, J et al. 2011). Eventually, the combination will lead to decreased cardiac output and result in increased afterload (Craft, J et al. 2011). Due to the reduced cardiac output, renal perfusion diminishes and plasma volume increases (Craft, J et al. 2011). Patients with systolic heart failure often present with decreased urine output, oedema and pulmonary oedema (Craft, J et al. 2011). And patients with diastolic heart failure can maintain a normal stroke volume and cardiac output (Craft, J et al. 2011). However, left ventricular end-diastolic pressure is still increased by the decreased compliance of the left ventricular, and the abnormal diastolic relaxation (Craft, J et al. 2011). The pressure pushes fluid to go back to the lungs and causes pulmonary oedema (Craft, J et al. 2011).
An ECG can provide information on the electrical movement in the heart and ECG graphs give information such as heart rate, rhythm and any abnormality that may involve the heart (Jevon 2010). With the method proved by Jevon (2009), Mr Toscana’s heart rate can be calculated, which is 120 beats per minute. According to Jevon (2009) heart rate over 90 beats per minute is defined as tachycardia. Based on his other presenting conditions, Mr. Toscana’s tachycardia is most likely caused by hypoxia. Hypoxia is resulted from hypoxemia, which is the decreased level of oxygen in the blood (Craft, J et al. 2011). In order to meet the oxygen demand, the heart is trying to pump harder and faster to bring up cardiac output (Craft, J et al. 2011). On the one hand, hypoxemia can cause dilation of arterioles, capillaries and venules, in order to increase the blood flow through them (Copstead& Banasik 2010). Therefore, peripheral blood flow is increased as well as venous return (Copstead& Banasik 2010). Venous return is a major factor that influences preload and the increased venous return means increased preload (Copstead& Banasik 2010). Preload is one of the factors that determines stroke volume, and when preload increases, stroke volume increases as well (Copstead& Banasik 2010). On the other hand, the cardiovascular system is controlled by medulla oblongata of the brainstem and the neurons communicate with the heart via autonomic nervous system (Craft, J et al. 2011). The Bainbridge reflex causes increased heart rate with increased venous return at the same time (Craft, J et al. 2011).
Mr. Toscana’s ECG shows elevated ST segment and tale T wave as well. They are both signs of hyperkalaemia (Humphreys 2007). This condition can also be confirmed by his potassium level. The normal range of potassium is 3.5-5mEq/L, and his potassium is 5.8mEq/L (Humphreys 2007).
Interpretation of Pathology Tests
Mr. Toscana’s Arterial Blood Gas Result shows that pH is 7.34 and the normal range is 7.35-7.45, which means his pH is lower than normal range. Hasan (2009) states that pH lower than normal range represents acidosis. According to Cowley, Owen& Bion (2013) that high level of blood carbon dioxide means respiratory acidosis, and low level of bicarbonate means metabolic acidosis. The Arterial Blood Gas Result of Mr. Toscana shows blood carbon dioxide and bicarbonate is 51mmHg and 18mmol/L respectively. The normal range of blood carbon dioxide is 35-45mmHg and that for bicarbonate is 22-28mmol/L. Thus, his blood carbon dioxide level is higher and bicarbonate level is lower, which explains that Mr. Toscana is suffering both respiratory and metabolic acidosis (Hasan 2009). Besides, Mr. Toscana’s blood oxygen level is 70mmHg and the acceptability range is 75-100mmHg. According to Hasan (2009) low blood oxygen level indicates hypoxia. SaO2 (saturation of haemoglobin by oxygen) is the most common way to monitor oxygen level in the body. For a healthy person, SaO2 below 95% shows lack of oxygen in the body and can lead to hypoxia (Humphreys 2007).
There are many causes of metabolic acidosis, such as hyperlactataemia, ketoacidosis and renal tubular acidosis (Halperin, Kamel& Goldstein 2010). In this case, based on his history of chronic renal impairment, the cause of his metabolic acidosis is more likely the renal tubular one (Halperin, Kamel& Goldstein 2010). One of the functions of the kidneys is to clear the body’s acid load (Halperin, Kamel& Goldstein 2010). However, for patients with chronic renal impairment, their kidneys are already damaged and they are losing normal renal function (Craft, J et al. 2011). Therefore, kidneys cannot remove acid out of body in an adequate rate. When the acid builds up in the body, it will neutralise with bicarbonate and generate carbon dioxide (Halperin, Kamel& Goldstein 2010). Normally carbon dioxide will be exhaled. However, in this case, because Mr. Toscana suffers from an acute pulmonary oedema, he cannot exhale carbon dioxide effectively (Craft, J et al. 2011).
One of the symptoms of pulmonary oedema is hypoxemia, which is low level of blood oxygen in the body (Craft, J et al. 2011). This occurs as the excess fluid builds up in the extravascular spaces, and impairs normal gas exchange in the lungs (McPhee & Hammer 2010). Moreover, pulmonary oedema can cause dyspnoea, which is a difficulty of breathing and eventually it can damage alveoli (Craft, J et al. 2011). Both dyspnoea and the damaged alveoli can worsen the inadequate gas exchange (Craft, J et al. 2011). Based on Craft, J et al. (2011) when inadequate gas exchange occurs, oxygen in the alveoli cannot get into vessels and the carbon dioxide cannot go in to alveoli to be exhaled. While carbon dioxide accumulates in the body, pH decreases and respiratory acidosis occurs (Halperin, Kamel& Goldstein 2010). In this case, besides the inadequate gas exchange, the chronic renal impairment also contributes to the increase of carbon dioxide in the body.
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The blood test results show both high level of serum creatinine and blood urea nitrogen. Based on Thomas& Thomas (2009) creatinine results from muscular metabolism and will be cleaned out of the body by the kidneys. Urea nitrogen is resulted from protein metabolism and it will also be cleaned out of body by the kidneys (Thomas& Thomas 2009). The reason for the increase in both creatinine and urea nitrogen levels is because of the decreased glomerular filtration rate, which is an indication of chronic renal disease (Craft, J et al. 2011).
Holistic Plan of Nursing Care
The first nursing care for Mr. Toscana is in fact to provide a reassurance to him as he is distressed by the tightness of CPAP mask and his difficulty in breathing. There is a very high chance that he will remove the CPAP mask. If CPAP is removed, it will make it even harder for him to breathe (Ducros et al. 2010). Nurses can educate Mr. Toscana on the use of CPAP and explain to him that by using CPAP, he can breathe more easily (Nehyba 2006). Nurses can also get his family involved to give reassurance to Mr. Toscana.
Then, because Mr. Toscana’s oxygen saturation is lower and he is presenting respiratory acidosis, nurses need to keep his oxygen saturation up (Lemone& Burke 2011). Due to his acute pulmonary oedema, CPAP is a more effective way to deliver oxygen and open up more air ways, which in return improves his gas exchange in the lungs and reduces work of breathing (Ducros, L et al. 2010). Nurses need to remind themselves of a few things while looking after patients breathe with CPAP. First, CPAP mask needs to be sealed properly and tightened to provide a positive pressure air (Ducros, L et al. 2010). Second, nurses need to monitor the patients closely for any change in oxygen saturation and respiratory rate (Ducros, L et al. 2010). Third, they should allow breaks in between sections of the treatment so that patients can cough, drink or eat (Nehyba 2006). Also, breaks can release the pressure caused by CPAP mask and decrease the risk of pressure ulcer. Finally, like any other medical procedure, CPAP also has its adverse effects. When a full mask is used, CPAP therapy can lead to gastric distension (Nehyba 2006). In addition, some air can go into stomach and cause discomfort, splinting of the diaphragm and reduce lung expansion. Therefore, nasogastric tube may be required at some stage (Nehyba 2006)
Monitoring Mr. Toscana’s fluid intake and urine output is also important, as he has a history of chronic renal impairment and presenting pulmonary oedema (Lemone& Burke 2011). A fluid balance chart can be used. If there is a negative balance, doctors need to be notified accordingly (Lemone& Burke 2011). Nurses need to educate Mr. Toscana on adequate fluid intake. His vital signs also need to be monitored, especially his oxygen saturation and respiratory rate (Lemone& Burke 2011). He is presenting signs of hypoxemia and respiratory acidosis, which can lead to respiratory failure (Craft, J et al. 2011). Therefore, closely monitoring his oxygen saturation and respiratory rate can identify any trend towards respiratory failure so as to intervene earlier to prevent it from happening.
Cardiac monitoring is also required for Mr. Toscana because of the following reasons. First, his ECG shows heart rate of 120 which means tachycardia. Second, the most likely cause of his acute pulmonary oedema is heart failure. Third, abnormal potassium level can cause cardiac arrest (Humphreys 2007). Moreover, nurses need to check for any new arterial blood gas results and blood test results to be aware of any changing situation of the patient.
Finally, as Mr. Toscana has a history of chronic renal impairment and both his arterial blood gas results and blood tests result show trend of renal failure, acute dialysis may be needed for him (Daugirdas, Blake, Ing 2012). For patients with chronic renal disease, their renal functions are impaired and some toxic wastes cannot be removed from their bodies (Craft, J et al. 2011). Dialysis is the only effective way to help them to remove these toxic wastes (Daugirdas, Blake, Ing 2012). Nurses cannot order dialysis. However, they can discuss patient’s conditions and tests result with doctors to arrange dialysis if necessary.
Pulmonary oedema is a crucial condition that can lead to respiratory failure. This condition can be caused by heart failure and worsen by chronic renal diseases. Procedures such as ECG, arterial blood gas test and blood tests can help nurses to understand patients’ conditions can identify any trend of deterioration. A detailed, holistic nursing care plan can help nurses to provide better care for patients.
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