Cardiogenic Pulmonary Oedema (CPO) - Lungs Disease - Case Study Assessment Answer

TITLE CASE STUDY

Introduction

Acute pulmonary oedema is the medical condition that is caused due to the accumulation of fluid in the lungs. The fluid accumulates in the numerous air sacs present in the lungs due to which the person finds difficulty in breathing (Gillenwater, amp Garner, 2017). Such condition may arise in the patient due to impaired heart functioning or appearance of other condition like pneumonia, exposure to toxins, aggressive medication, trauma to the chest wall, and so on (Coccia et al., 2016). This case study represents the clinical condition of Mrs X, 49-year-old, female who was presented at the local hospital due to chest pain, rapid heartbeat, and increasing shortness in breadth. Mrs X also has a medical history of type 2 diabetes mellitus (T2DM), hypertension, and rheumatic fever when she was a child. She has no history of allergy and at present consumes 20 cigarettes and drinks three to six beers every day. She has been experiencing shortness in breadth from last few months and has noticed swelling of ankles from last few weeks. She was present at the local hospital as she looked quite unwell and has grown weak. This study will further describe Mrs X pathophysiology of the existing problems and investigate appropriate treatment for recovering her condition. Additionally, the pharmacological intervention that can be implemented for improving the patients condition will be discussed followed by the conclusion.

Pathophysiology

Cardiogenic pulmonary oedema (CPO) is a fatal condition that causes acute respiratory distress. Many times CPO is the result of acute decompensated heart failure (ADHF). In healthy human lungs, the fluid and the solute gets filtered in the lungs across the pulmonary capillary endothelium. The filtration procedure occurring in the lungs gets confided anatomically adjacent tointerstitial spaces. Here the in-pressure gradient is developed from the site of formation to the site of removal by the help of pulmonary channels (Purvey amp Allen, 2017). Moreover, the quantity of the fluid and the protein depends on the difference in transvascular hydrostatic pressure and protein osmotic pressure and leakiness of the endothelial barrier for water as well as protein. Additionally, the lymphatic drainage can be increased up to several folds which is a clear indication of pulmonary edema. In the appearance of such condition, the increase in extravascular water content of the lungs is restricted until the filtration of the fluid exceeds the rate of the lymphatic removal (Platz et al., 2015). Generally, there is two types of oedema recognized by the researcher which includes cardiogenic also known as hydrostatic pulmonary edema and noncardiogenic pulmonary oedema. In cardiogenic pulmonary oedema the capillary pressure becomes elevated at the left side of the heart while in case of noncardiogenic oedema the injury is caused in the endothelial tissues and the epithelial barriers. Each of these types of oedema occurs due to distinct differences in clinical condition and thus has distinct prognosis (Harjola et al., 2017).
In this case study, Mrs X was experiencing several signs of shock which can be also referred to as cardiogenic shock. This type of shock is caused due to vasoconstriction. Moreover, Mrs X was a currently heavy smoker and smokes atleast 20 cigarettes per day and drinks 3 to 6 beers daily. Both of these condition increases the risk for development of respiratory distress syndrome. Moreover, heavy smoking and alcoholism may result in acute respiratory failure as fluids start accumulating in the air sacs of the lungs. In such a situation, the lungs are unable to release oxygen into the bloodstream (Arrigo et al., 2016). The deficiency of oxygen in the bloodstream restricts adequate functioning of the organs which leads to shock. Cardiogenic shock is associated with inadequate tissue perfusion due to cardiac dysfunction caused due to a myocardial infarction. The formation of vicious spiral circle ischemia causes myocardial infarction which in turn provokes myocardial ischemia. Moreover, the myocardial stunning aggravates this condition and worsens it. Ischemia and reperfusion results may result in systemic inflammation (Mentz amp Oconnor, 2016). In this condition, patient has elevation in left ventricular filling pressure despite depressed left ventricular ejection.
Mrs X has several signs and symptoms of heart failure as her reports show additional sound in her heartbeat and her respiratory rate is quite high that is, 32 breaths per minutes. These two problems note were quite significant in nature. In normal condition patient generally shows two heart sounds referred to as S1 and S2 respectively. These sounds are caused due to the closing of the atrioventricular valves and semilunar valves. In addition to the normal sound additional gallop rhythm, S3 and S4 may appear in patients that are referred to as heart murmurs and adventitious sound respectively. In this case, the patient has shows heart murmurs that are generated by the turbulent flow of blood due to the pressure difference of 30 mm of Hg. The abnormal murmurs in the heart are caused due to stenosis that restricts the heart valves from the opening which lead to the turbulence of the blood flow through it. Moreover, S3 sound is caused due to the oscillation of blood back and forth between the ventricles walls. The common pathologic condition in case of adults for S3 sound is related to congestive heart failure. Moreover, the increased respiratory rate is an indicator of abnormal condition as is also associated with congestive heart failure.

Investigation

The medical officer has ordered differential diagnosis test related to acute pulmonary oedema which includes Chest X-ray (CXR), Arterial Blood Gas (ABG), Full blood examination (FBE), and urea and electrolyte test (UampE). The chest X-Ray report showed an enlarged heart alone with interstitial and alveolar oedema. The vital recorded showed GCS 15 (E4, V5, M6), pulse rate to be 150 bpm, respiratory rate to be 32 per minutes, blood pressure to be 90/70 mmHg, and SpO2 to be 92 on room air. These vitals clearly indicate that Mrs X has altered respiratory rate, poor oxygen content, and lower blood pressure than optimal range (Koulouras et al., 2016). However, two other appropriate tests for investigating the patient condition would include physical examination and electrocardiogram (ECG).

The physical examination will include four distinct stages such as inspection, palpitation, percussion, and auscultation. The inspection will involve examining of feet and hand of Mrs X, the appearance of decreased perfusion will be visible by the appearance of bluish or grayish skin. Secondly, elevated venous pressure and thoracic expansion is an indication of congestion of the heart (Coccia et al., 2016). Mrs X also showed higher breathing rate i.e. 32 per minute. The second physical test will involve taking note of the palpitation. The Holter monitoring is useful in the recording of heart palpitation which will show the patients heartbeat rhythm. The third examination will involve percussion. This test will enable the nurse to test the lung field and can be done through the fluid collection. In the case of Mrs X decreased air entry is evident for the cause of pulmonary oedema. The fourth physical examination will include auscultation which indicates the air entry in the lung field. Auscultation test will enable the nurse to listen to the internal sound of the body with the help of a stethoscope. The distinct sound produced is due to the movement of the gas or liquid inside the body (Shah et al., 2017).

The second important test will include taking of patients ECG test. This is a non-invasive test that records the abnormal electrical activity of the heart that usually occurs in case of a heart attack. The heart muscles are generally in oxygen-deprived condition. The test confirms the incidence of heart attack in 90 of the cases. The ST elevation detected during the test confirms the severity of the blockage in the blood flow in the heart. The ST elevation is detected when J-point is recorded to 0.15 mV in case of women, the depression in ST and change in T-waves are identified when new horizontal or down-sloping gt0.05 mV in case of contiguous leads. The appearance of the abnormal electrical reading of the heartbeat is a clear indication of myocardial infarction (Blondonnet et al., 2016).

Pharmacology

Mrs X has identified to have renal impairment and the suitable medication that could be prescribed to her will be Erythropoietin (EPO). EPO is the growth factor that is produced in the kidney which stimulates the production of red blood cells. This promotes the division and differentiation of erythroid progenitors in the human bone marrow. Epoetin alfa is 165 amino acid erythropoiesis-stimulating glycoprotein which is used for the treatment of chronic renal failure inpatient, antiviral drug therapy, reduce the risk of blood loss due to the surgical procedure, etc.( Park et al., 2018). This medication contains identical amino acids sequence that has been isolated from natural erythropoietin. The EPO binds with the erythropoietin receptor present in the body and activates intracellular signal transduction pathway. On binding to the receptor a conformational change in introduced which brings EOP-R-associated Janus family tyrosine-protein kinase 2 (JAK 2) molecules close to each other. The JAK 2 molecules are activated due to the action of phosphorylation. Then the phosphorylated tyrosine residue acts as the docking site for Src homology 2-domain-containing intracellular signaling proteins. The STAT5 on phosphorylation gets dissociated from EPO-R and translocates to the nucleus where they act as a transcription factor. Ultimately the inhibition of apoptosis due to activation of EPO-Activated JAK2/STAT5/Bcl-x pathway is crucial. Moreover, the binding of the EPO results in cellular internalization which involves degradation of the ligand. Moreover, after their action, they get degraded by reticuloendothelial scavenging pathway. However, a very small amount of the unchanged epoetin alfa is found in the urine sample. The side effect associated with the drug overdose includes a rapid increase in the concentration of hemoglobin. The patient may have other hematologic abnormalities. Moreover, the condition like polycythemia requires to be managed accurately with phlebotomy (Ji et al., 2017). Thus the introduction of this drug should be done with close monitoring of the patients condition.

One of the important pharmacological intervention that could be applicable for management of Mrs X medical condition includes administration of vasodilators. This is a suitable treatment that could be introduced in case of hypertensive patient and the patient suffering from pulmonary oedema. The higher dose of the nitrate could be administered as the patient shows a lower heart rate, higher oxygen saturation, and low respiratory rate (Domingo, Magdo, amp Day, 2018). Vasodilator helps in the widening of the blood vessels and relaxes the smooth muscles cells and vessels walls. Moreover, vasodilation directly affects the relationship between the mean arterial pressure, total peripheral resistance, or cardiac output. This process occurs during the cardiac systole and the cardiac output seems to improve. The relaxation of the muscle helps in removing the stimulus that promotes contraction (Powell et al, 2016). There is various therapeutic importance of the introduction of this treatment. The vasodilatation aid in drug treatment by enhancing the drug delivery target. Additionally, the certain drug has shown to diffuse easily in dilated vessels which increase the bioavailability of the drug in case of surrounding tissue. The dilated blood vessels are able to carry a large volume of blood that potentially improves the amount of the drug absorbed by the tissue. Moreover, this is very efficient in providing the targeted delivery of the drug (Montani et al., 2016). The non-invasive nature of this treatment also has the advantage of causing no harm to the blood vessels.

Conclusion

This case study analysed the pathophysiology of the patients condition in details and also focused on various test results. Moreover, the study also highlighted the additional investigation that could be beneficial for the patient and also provided a scientific rationale for it. Additionally, the study also focused on the prescribing of suitable medication for the patient and also discussed the drugs mechanism of action, interaction with the patient and possible side effects. Further, the study also discussed the immediate management plan and appropriate pharmacological intervention for managing the condition of Mrs X. Overall the study discussed the various clinical aspect of the patient suffering from acute pulmonary oedema and heart failure.

References

Arrigo, M., Parissis, J. T., Akiyama, E., amp Mebazaa, A. (2016). Understanding acute heart failure pathophysiology and diagnosis.European Heart Journal Supplements,18(suppl_G), G11-G18.
Blondonnet, R., Constantin, J. M., Sapin, V., amp Jabaudon, M. (2016). A pathophysiologic approach to biomarkers in acute respiratory distress syndrome.Disease markers,2016.
Coccia, C. B., Palkowski, G. H., Schweitzer, B., Motsohi, T., amp Ntusi, N. A. B. (2016). Dyspnoea Pathophysiology and a clinical approach.SAMJ South African Medical Journal,106(1), 32-36.
Domingo, L., Magdo, H. S., amp Day, R. W. (2018). Acute Pulmonary Vasodilator Testing and Long-Term Clinical Course in Segmental Pulmonary Vascular Disease.Pediatric cardiology,39(3), 501-508.
Gillenwater, J., amp Garner, W. (2017). Acute Fluid Management of Large Burns Pathophysiology, Monitoring, and Resuscitation.Clinics in plastic surgery,44(3), 495-503.
Harjola, V. P., Mullens, W., Banaszewski, M., Bauersachs, J., BrunnerLa Rocca, H. P., Chioncel, O., amp Fuhrmann, V. (2017). Organ dysfunction, injury and failure in acute heart failure from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).European journal of heart failure,19(7), 821-836.
Ji, M. H., Tong, J. H., Tan, Y. H., Cao, Z. Y., Ou, C. Y., Li, W. Y., amp Zhu, S. H. (2016). Erythropoietin pretreatment attenuates seawater aspiration-induced acute lung injury in rats.Inflammation,39(1), 447-456.
Koulouras, V., Papathanakos, G., Papathanasiou, A., amp Nakos, G. (2016). Efficacy of prone position in acute respiratory distress syndrome patients a pathophysiology-based review.World journal of critical care medicine,5(2), 121.
Mentz, R. J., amp Oconnor, C. M. (2016). Pathophysiology and clinical evaluation of acute heart failure.Nature Reviews Cardiology,13(1), 28.
Montani, D., Lau, E. M., Dorfmller, P., Girerd, B., Jas, X., Savale, L., amp Fadel, E. (2016). Pulmonary veno-occlusive disease.European Respiratory Journal,47(5), 1518-1534.
Park, B. H., Shin, M. H., Douglas, I. S., Chung, K. S., Song, J. H., Kim, S. Y., amp Kim, Y. S. (2018). Erythropoietin-Producing Hepatoma Receptor Tyrosine Kinase A2 Modulation Associates with Protective Effect of Prone Position in Ventilator-induced Lung Injury.American journal of respiratory cell and molecular biology,58(4), 519-529.
Platz, E., Jhund, P. S., Campbell, R. T., amp McMurray, J. J. (2015). Assessment and prevalence of pulmonary oedema in contemporary acute heart failure trials a systematic review.European journal of heart failure,17(9), 906-916.
Powell, J., Graham, D., OReilly, S., amp Punton, G. (2016). Acute pulmonary oedema.Nursing Standard (2014),30(23), 51.
Purvey, M., amp Allen, G. (2017). Managing acute pulmonary oedema.Australian prescriber,40(2), 59.
Shah, P., Pellicori, P., Cuthbert, J., amp Clark, A. L. (2017). Pharmacological and Non-pharmacological Treatment for Decompensated Heart Failure What Is New.Current heart failure reports,14(3), 147-157.

You Might Also Like:

Human Lung Function and Oxygen Consumption Under Different Exercise Conditions ‑ Nursing Assessment Answers

Looking For Complete Assignment Sample Get It On WhatsApp