Acute Pulmonary Oedema (APO) Pathophysiology
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The aim of this paper is to reflect upon the pathophysiology of the acute pulmonary oedema (Apo) and its relation to the patient’s existing condition of chronic renal failure (CRF). The physical assessment of the patients will be discussed accordingly that underpins the presenting symptoms. CKR has four stages from mild damage to the end-stage kidney failure but none of them have been mentioned in the scenario. However, with the interpretation from the serum blood test and presenting signs and symptoms, this will be made clearer later in this paper. Although, there is no cardiac history, this paper will focus more on the cardiogenic Apo as linking renal, cardiovascular and respiratory systems together. In this case scenario, Mr Mario has a history of CRF resulting in acid-base, fluid and electrolyte imbalances which will be discussed in this paper as well (McCance et al 2007, pp.1330). The rhythm strip provided will be assessed and the abnormalities in the electrocardiogram (ECG) will be identified. This will be further discussed linking the ECG with the presenting clinical manifestations. Furthermore, the holistic approach to the patient’s nursing care plan will be delivered with the associated rationales following the conclusion in this paper.
McCance et al (2007, pp.1279) state that the abnormalities in hydrostatic pressure, capillary oncotic pressures, capillary permeability and the lymphatic drainage are the causes of acute Apo. However, on the basis of the case study, we will be focused on the chronic renal failure as being the primary cause of APO. Likewise, Himmelfarb & Mohomed (2010) believe that the patients with CKF will eventually develop cardiovascular diseases and the risk of developing cardiovascular complications begins with the early stages of CKR.
Chronic renal failure (CRF) is the progressive and irreversible loss of renal functions over the period of time and developing complications as manifested in the case study. However, the symptoms occurs when the significant damage to the nephrons (90%) have occurred which indicates the later stages of the CRF.
Accordingly, the nephrons fail to filter waste products such as creatinine and urea from the blood (Lewis, R. 2013 pp.31). Ultimately, the kidney loses its function to regulate sodium and water balance leading to the increased extracellular fluid volume, reduced excretion and oedema (Headley & wall, 2007, pp.19). Nonetheless, the ability to excrete sodium and water differs from one patient to the next and some patients can either develops hypervolemia or hypovolemia as the result. Supporting this, Phipp (2007, pp.1016) suggests, the patients can have oliguria or anuria and hypervolemia due to the disordered fluid and electrolyte balance.
At early stages, as the result of adaptive mechanism, hyperfiltration and hyperpermeabilty leads to proteinuria. This contributes to the tubular injury by accumulating proteins in the tubules and activates the process of inflammation, fibrosis and scarring. Furthermore, this activates the angiotensin II that further increases the glomerular hypertension and ultimately, systemic hypertension which is the major risk factor of cardiovascular disease (McCance et. al, 2007, pp.1392). Zachariah, D., Kalra, P., & Kalra, P. (2009 pp.5) explain that angiotensin II has direct effect on heart promoting left ventricular hypertrophy (LVH). The authors further discusses as LVH is an initially adaptative, however, in long term, diastolic dysfunction occurs as the result of myocytes deaths and left ventricular conductions abnormalities.
Phipp (2007, pp.) states as, “Apo is the accumulation of excess fluid in the extravascular spaces of the lung”. Apo is an emergency condition and can either be cardiogenic or non-cardiogenic originated. Carpenito-moyet, L D (2009, pp.222) states that the hypervolemia and hypertension resulting from chronic renal failure, leads to the increment of the pulmonary vein and pulmonary capillary pressures. Eventually, this increases the blood hydrostatic and interstitial fluid osmotic pressure. Furthermore, the increase in effective filtration pressure to 5mmhg from the normal of 0 causing the shift of fluid from the blood to the interstitial spaces.
Due to fluid overload and diastolic dysfunction, ventricles are unable to pump the blood into the aorta at a rate equal to the blood entering the left ventricles from left atrium( Zachariah, D., Kalra, P., & Kalra, P. 2009 pp.5) Subsequently, this increases the pressure in the left side of the heart and pulmonary system that then pushes fluid to build up in the pulmonary circuit. Initially the lymphatic system combats this by increasing its drainage flow as resulting in no net increase in interstitial volume. However, when the capacity of the lymphatic drainage is exceeded, the fluid initiates to accumulate in the interstitial space that surrounds the lung vasculature. As it continues, the increasing pressure results in reinforcing fluids in the periphery of the alveolar capillary membrane. The surface tension decreases due to the distended surfactant whose functions is to separate the water molecules and finally alveoli gets filled with fluid. Correspondently, the collapsed alveoli prevents gases exchange that causes respiratory symptoms (Phipp 2007 pp. 814).
- Respiratory symptoms
As the results of the increasing hydrostatic pressure and permeability of the plasma membrane , red blood cells moves into the alveoli which then quickly shifts into the bronchioles and bronchi which then forms into productive cough and pink frothy sputum(Phipp 2007, pp. 815).
Phipp (2007 pp. 570) states that the balance between the ventilation (V) and perfusion (Q) determines the efficiency of the gas exchange. Whereas, fluid in alveoli increases the airway resistance and prevent adequate ventilation despite of the adequate perfusion. The mismatch of V/Q ratio decreases the diffusion of oxygen causing impaired gases exchange as lowering down his oxygen saturation as his sp02 is 91% (with Fi02 0.5). As on auscultation, the presence of adventitious sound (crackles) indicates the movement of the air through the fluids in small airways that more commonly heard during inspiration ( Williams & hopper)
- Disturbance in water and electrolyte balance
In CRF, the homeostasis of the body gets disturbed as the volume of fluid and the electrolyte inside the cells, in the interstitial space, and in the blood vessels get imbalanced (Thibodeau GA & Patton K T 2007, 1078). Sodium is the major constituent of the extravascular fluid. Angiotensin II stimulates the secretion of aldosterone which then promotes reabsorbing the sodium and water MCcance pp.110.
- Stress response
Mr Toscana is undergoing physiological stress that have initiated hypothalamus to activate the sympathetic nervous system that then releases the catecholamine. Eventually, this causes increased oxygen demand and diaphoresis in the patient as evident (Craft, Gordon and tiziani 2012, pp. 1064). The loss of sodium through the skin during diaphoresis is common reference. Additionally, hypernatremia occurs during the oliguric renal failure.
- Chest x-ray
Mr Toscana’s chest x-ray shows the presence of bilateral patchy interstitial and alveolar infiltrates predominantly on the mid and lower field lungs displaying uneven distribution of the fluid. The definition of the interstitial markings have diminished and shows the presence of fluffy confluent opacities in various field. However, they can rapidly disappear with the appropriate treatment followed (Burgener, Kormno & Puaus 2008, pp.537).
- Assessment of rhythm strip
McCance( 2007 pp.106) states potassium is the major intracellular electrolyte and plays an important role in action potential in nerve impulses, cardiac rhythm and skeletal muscles contractions. It is excreted through the kidneys and 90% is reabsorbed in the proximal tubule and loop of Henle. On the other hand, the authors also discuss that the changes in pH can affect the potassium balance. Additionally, during acidosis the hydrogen ions moves from the extracellular to the intracellular fluid. Therefore, to balance the cations, potassium moves outside to the extracellular fluid contributing to high level of serum potassium.
Reading above 5.5mEq/L is considered to be potentially fatal (Sánchez, J et. all 2007, 124) and Mr Toscana’s reading is 5.8mEq/L. The characteristic of sinus rhythm is to possess p wave, QRS wave, and PR distance of 3-5 squares and rate of 60-100beats/minute reference As in the ECG, the regularity appears to be regular and with 3 square of PR interval. Find the rate . The ECG provided shows flat P wave, tall and peaked T wave, decreased R wave amplitude and slightly depressed ST segment indicating hyperkalaemia due to the failure of kidney’s function to excrete potassium (Allsopp 2011 pp.12). However, it is a sinus rhythm with the signs of hyperkalaemia. In renal failure, hyperkalaemia becomes the frequent problem when it reached its end-stage as oliguria phase with urine output less than 30mls/hour (Sánchez, J et. all 2007, 124). Therefore, this indicates Mr Toscana to be on this stage of renal impairment.
Arterial blood gas result
- Metabolic acidosis
- pp. 106 mac cance
- PH 10
- Pao2 10 Hypoxia can also cause the shifting of potassium into the extracellular fluid that can result in hyperkalaemia, hypoxia can affect the efficiency of the cell membrane active transport.
- Paco2 100
- Hco3 100
- Metabolic acidosis
- Interpretation of pathology tests 750
- More research pp . 1393 mc
According to Thomas, C., & Thomas, L. (2009), the glomerulus filtration rate (GFR) is the considered to be best marker for the renal impairment. The authors believes the earlier stages are generally silent and are diagnosed by the measurement of the external filtration markers.
In this case study, patient has high level of serum creatinine and blood urea nitrogen (BUN) of 140 umol/L and 35mg/dL respectively. Creatinine and BUN are the metabolic wastes of muscles mechanism and protein breakdown respectively that are excreted into the glomerulus filtrate. The kidneys as in a normal circumstances maintains the level of creatinine and urea within the narrow range. As the disease progresses, GFR declines and plasma concentration of creatinine remains elevated (craft, Gordon & tiziani 2012, pp.926). The normal value of creatinine for the male is 60-110umol/L and the findings indicates the significant kidney impairment (Phipp 2007, pp. 1016). Craft, Gordon and tiziani (2012, pp. 926) believe that the mechanism of the excreting urea is as same as creatinine’s excretion and hence, BUN remains elevated as well while the normal range is 7-2-mg/dL.
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