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Patho-physiology

Discuss about the Case Study Of Robert Holden Suffering From Cardiac Health Adversities.

This case study represents the case of a patient named Robert (Bobby) Holden who is a 62 year old man suffering from various cardiac health adversities which ultimately resulted into the incidence of an acute pulmonary oedema. There can be various different course of pathophysiology that can lead to the cardiac complications that has been indicated in the case study. First and foremost, it has to be mentioned that acute pulmonary oedema is associated with fluid accumulation in the lung parenchyma and alveoli that leads to chronic and frequent episodes of shortness of breath and impaired gas exchange; enhancing the chances of mortality of the patient (Vital, Ladeira & Atallah, 2013). Now, the preliminary diagnosis of the buddy nurse attending the patient under consideration indicated at acute pulmonary oedema and the most plausible reason behind the diagnosis can be congestive heart failure. The underlying pathophysiology behind the manifestation of acute pulmonary oedema is centered on the excessive fluid backup. According to the Norhammar, Johansson, Thrainsdottir and Rydén (2017), one of the prime contributors of congestive heart failure is the inability of the left ventricle to pump enough blood satisfy the need for fresh oxygenated blood to reach the entire body, which leads to oxygen deficiency. In such conditions the heart is not able to remove the pulmonary circulation out at a sufficient rate which causes blood back up (Huh et al., 2012). This phenomenon enhances the wedge pressure effectively, and facilitated by the cumulative impact of left ventricular failure, fluid overload in the kidney and arrhythmia, it leads directly to pulmonary oedema. On a more elaborative note, it has to be mentioned that the ability of the lymphatic system to remove the fluid from the interstitial space depends critically on the systemic venous pressure. In case of the congestive heart failure, the decreased cardiac output and deficiency of oxygenated blood contributes to the pulmonary congestion and acutely increased after-load, indirectly facilitating pulmonary oedema (Al Deeb, Barbic, Featherstone, Dankoff & Barbic, 2014).


In this case scenario, the patient had been a active smoker for 44 years and also had a habit of drinking two bottles of VB every night. Hence these two factors can have a significant impact on the respiratory apparatus and the cardiac muscles, enhancing the vulnerability of the patent going through the resent clinical manifestations. Along with that the patient had been slightly obese and had been diagnosed with diabetes as well, both of which enhance the risk of congestive heart failure due to excessive blood sugar and cholesterol deposition leading to blockages (Caudrillier et al., 2012). The patient had the symptoms of cool to touch extremities and distended jugular veins; both of which is a clear indication of a oxygen deficiency leading to congestive heart failure and pulmonary embolism. It has to be mentioned that in congestive heart failure the lack of proper oxygenated blood flow to the vital organs result into blood being pulled off from the accessory organs like the extremities causing it to appear cool to touch; and it enhances the central nervous pressure. Hence the most plausible reason behind the acute pulmonary oedema is the congestive heart failure and its deterioration (Davison, Terek & Chawla, 2012).

Contributing Factors

The first symptom that the patient under case study which can relate excellently to the congestive heart failure, is the shortness of breath. It has to be mentioned that systolic heart failure, the left ventricle is unable to pump enough oxygenated blood to satisfy the need of the entire body. Due to the inefficiency of the heart to pump and remove the blood from the pulmonary veins, the blood backs up into the pulmonary veins causing a congestion that increases the blood pressure in the veins. As a direct result of this phenomenon the fluid is pushed into the surrounding alveoli, which in turn reduces the normal oxygen movement through the lungs as well. The cumulative result of both of the phenomenon together cause shortness of breath, and this is the most likely pathophysiology behind the shortness of breath experienced in case of the patient as well (Mammoto et al., 2013).

The second symptom exhibited by the patient had been the accelerated heart rate at 126 beats per minute. It has to be mentioned that this symptom exhibited by the patient as well is a very common clinical manifestation of the heart failure and is most frequently observed as well. Exploring the underlying pathophysiology, it can be mentioned that congestive heart failure is associated with inability of the left ventricle of the heart which performs the greatest blood circulating burden throughout the body. As a result there is a significant deficiency of oxygen rich blood throughout the body (Miniati, Cenci, Monti & Poli, 2012). There is significant threat to the various metabolic and physiological processes that keep the human body functional. Hence, there is enhanced burden on the heart and in order to satisfy the demand of the body, it overcompensates the amount of blood pumped. This overcompensation to meet the demands of the rest of the body leads directly to higher heart rate and tachypnoea. In this case as well the patient had a more or less sedentary lifestyle and with the added burden of diabetes, smoking, and alcohol addiction, enhanced the arterial blockages of the patient and damaged the cardiac muscles which led to congestive heart failure (Gavrilovskaya, Gorbunova, Koster & Mackow, 2012).

Investigative assessments are a key decisive factor associated with adequate care and management of cardiac emergencies. In this case, that needs to be performed for the patient under focus in the case study is the arterial blood gas assessment. It has to be understood in thos context that the interruption of the blood flow after a cardiac arrest can lead to intense hypercarbic and metabolic acidosis which results into accumulation of CO2, lactate and the hydrogen anions. According to the research, there are a few dominant blood gas abnormalities in the patients going through a cardiac arrest episode, such as the hypoxemia, heypercarbic acidosis and lactic acidosis. The arterial blood gases provide critical information regarding the pCO2 and pO2 levels as well (von Auenmueller, Christ, Sasko & Trappe, 2017). The pCO2 levels assessment within the first 5 minutes oif the arrival of the patient to the emergency department has been considered an independent predictor of the chances of sustained ROSC in the patient and the status if the ischemic insult as well. On amore elaborative note, it has to be mentioned that pH level assessment marks the duration and severity grade of the no-flow-interval and high lactate levels indicate poor outcome and increased chances of mortality. Hence, it can be safely concluded that the te arterial blood gases parameters correlate exceptionally well with the mortality of the patients. Hence, arterial blood gas assessment is the first line of assessment needed to be done for the patient (Kim et al., 2016).

Symptoms

The next assessment that has been ordered is the 12 lead ECG, which is another highly crucial assessment for the patients going through a severe cardiac arrest. It has to be understood in this context that electrocardiogram has been a breakthrough in health care which has improved the mortality status for cardiac patients effectively, and according to the American heart association, 12 lead ECG assessment is central for the clinical decision making framework for the cardiac arrest patients. This particular assessment is recommended right after the Return of spontaneous circulation tests. This test identifies whether the patient is having a STEM or non STEM myocardial infarction. According to the research, each of the different steps of the 12 lead ECG allows the health care professionals to identify whether and to what extent the patient will be benefitted from coronary reperfusion interventions. Hence, it has been undoubtedly the second most necessary investigative assessment used in the study (James et al., 2015).

Acute pulmonary oedema is a very common yet very risky complication that arises from the congestive heart failures and has the possibility of causing further complications leading to fatal consequences (Mebazaa et al., 2015). Hence, it is very important for the nursing professionals caring for the patient must take into consideration immediate and prompt emergency care initiatives to stabilize the patient and prevent any further exacerbations. It has to be mentioned in this context that the most important care priority in this case is to improve the oxygenation and reduce the pulmonary congestion leading to the shortness of breath and troubled breathing as well. Although, in this case the external breathing support is the most frequently opted measure to manage the patient however, it is not sufficient by any means (Kushimoto et al., 2012). Decreasing fluid overload and blood back up is a primary concern for the patient which will have lasting effects on reducing the wheezing and shortness of breath. Pharmacological interventions that can be employed in this case include administration of medications, like diuretic lasix which will significantly reduce the fluid overload by facilitating dieresis in his body. It will gradually reduce the level of pulmonary congestion and will help the patient breathe better and will reduce the symptoms of pulmonary oedema (De Boer et al., 2016). It has to be understood that for the patients with congestive heart failure extending towards pulmonary oedema reducing the fluid volume is crucial. This loop diuretic helps in triggering the kidneys to remove water more efficiently from the rest of body, reducing mortality of the patient and facilitating normal physiological functions of the body. (Bahloul et al., 2013). Along with that, Lasix will help in reducing the fluid back up from the lungs and hence will reduce the shortness of breath that he had been feeling. The diuretic effect of the drug helps in reducing swelling from the rest of the body as well (Hodson et al., 2017).

Investigations

References:

Al Deeb, M., Barbic, S., Featherstone, R., Dankoff, J., & Barbic, D. (2014). Point?of?care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta?analysis. Academic Emergency Medicine, 21(8), 843-852. Doi: org/10.1111/acem.12435

Bahloul, M., Chaari, A., Dammak, H., Samet, M., Chtara, K., Chelly, H., ... & Bouaziz, M. (2013). Pulmonary edema following scorpion envenomation: mechanisms, clinical manifestations, diagnosis and treatment. International journal of cardiology, 162(2), 86-91. Doi: 10.1016/j.ijcard.2011.10.013

Caudrillier, A., Kessenbrock, K., Gilliss, B. M., Nguyen, J. X., Marques, M. B., Monestier, M., ... & Looney, M. R. (2012). Platelets induce neutrophil extracellular traps in transfusion-related acute lung injury. The Journal of clinical investigation, 122(7), 2661-2671. Doi: 10.1172/JCI61303

Davison, D. L., Terek, M., & Chawla, L. S. (2012). Neurogenic pulmonary edema. Critical care, 16(2), 212. doi.org/10.1186/cc11226

De Boer, R. A., ter Maaten, J., Damman, K., Muntendam, P., Sica, D. A., van Veldhuisen, D., & Pitt, B. (2016). PHARMACOKINETIC AND PHARMACODYNAMIC RESPONSE TO ORAL AND SUBCUTANEOUS FUROSEMIDE ADMINISTRATION: FIRST EXPERIENCES WITH A NOVEL BUFFERED FUROSEMIDE FORMULATION IN PATIENTS WITH CHRONIC HEART FAILURE. Journal of the American College of Cardiology, 67(13 Supplement), 1474. DOI: 10.1016/S0735-1097(16)31475-9

Gavrilovskaya, I., Gorbunova, E., Koster, F., & Mackow, E. (2012). Elevated VEGF levels in pulmonary edema fluid and PBMCs from patients with acute hantavirus pulmonary syndrome. Advances in virology, 2012. Doi: 10.1155/2012/674360

Hall, M. J., Levant, S., & DeFrances, C. J. (2012). Hospitalization for congestive heart failure: United States, 2000–2010. age, 65(23), 29. Retrieved from https://www.researchgate.net/profile/Carol_DeFrances/publication/232718240_Hospitalization_for_Congestive_Heart_Failure_United_States_2000-2010/links/0f317535869223eaea000000.pdf

Hodson, D., Jackson, K., Chunara, Z., Rao, V., Mahoney, D., Thomas, D., ... & Ahmad, T. (2017). Urine Sodium Content is Highly Variable in Hospitalized Acute Heart Failure Patients: Lasix Urine is Not Necessarily “Half-Normal Saline”. Journal of Cardiac Failure, 23(8), S7. DOI: https://doi.org/10.1016/j.cardfail.2017.07.013

Huh, D., Leslie, D. C., Matthews, B. D., Fraser, J. P., Jurek, S., Hamilton, G. A., ... & Ingber, D. E. (2012). A human disease model of drug toxicity–induced pulmonary edema in a lung-on-a-chip microdevice. Science translational medicine, 4(159), 159ra147-159ra147. DOI: 10.1126/scitranslmed.3004249

James, S., Murphy, T., Waterhouse, D. F., Gallagher, J., O’Connell, E., Barton, D., & McDonald, K. (2015). 22 Role of 12-lead electrocardiography in predicting heart failure in the community. Retrieved from https://heart.bmj.com/content/101/Suppl_5/A12.1

Karinda, M., Eff, A. R. Y., & Ramatillah, D. L. DRUG RELATED PROBLEM ASSOCIATED WITH TREATMENT FOR CONGESTIVE HEART FAILURE PATIENT IN MINTOHARDJO HOSPITAL. International Journal of Pharmacy Teaching & Practices (IJPTP), 1491. Retrived from file:///C:/Users/absas/Downloads/SUPPLEMENT%20angkatan%2031.pdf

Kim, Y. J., Lee, Y. J., Ryoo, S. M., Sohn, C. H., Ahn, S., Seo, D. W., ... & Kim, W. Y. (2016). Role of blood gas analysis during cardiopulmonary resuscitation in out-of-hospital cardiac arrest patients. Medicine, 95(25). doi:  10.1097/MD.0000000000003960

Kushimoto, S., Taira, Y., Kitazawa, Y., Okuchi, K., Sakamoto, T., Ishikura, H., ... & Yoshikawa, K. (2012). The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome. Critical Care, 16(6), R232. Doi: 10.1186/cc11898

Mammoto, A., Mammoto, T., Kanapathipillai, M., Yung, C. W., Jiang, E., Jiang, A., ... & Ingber, D. E. (2013). Control of lung vascular permeability and endotoxin-induced pulmonary oedema by changes in extracellular matrix mechanics. Nature communications, 4, 1759. doi:10.1038/ncomms2774

Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., ... & McDonagh, T. (2015). Recommendations on pre?hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. European journal of heart failure, 17(6), 544-558. Doi: 10.1002/ejhf.289

Miniati, M., Cenci, C., Monti, S., & Poli, D. (2012). Clinical presentation of acute pulmonary embolism: survey of 800 cases. PloS one, 7(2), e30891. Doi: 10.1371/journal.pone.0030891

Norhammar, A., Johansson, I., Thrainsdottir, I. S., & Rydén, L. (2017). Congestive heart failure. Textbook of Diabetes, 659-672. Doi:10.1002/9781118924853.ch45

Swedberg, K., Komajda, M., Böhm, M., Borer, J., Robertson, M., Tavazzi, L., ... & Shift Investigators. (2012). Effects on outcomes of heart rate reduction by ivabradine in patients with congestive heart failure: is there an influence of beta-blocker dose?: findings from the SHIFT (Systolic Heart failure treatment with the If inhibitor ivabradine Trial) study. Journal of the American College of Cardiology, 59(22), 1938-1945. Doi: 10.1016/j.jacc.2012.01.020

Vital, F. M., Ladeira, M. T., & Atallah, Á. N. (2013). Non?invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. The Cochrane Library. DOI: 10.1002/14651858.CD005351.pub3

von Auenmueller, K. I., Christ, M., Sasko, B. M., & Trappe, H. J. (2017). The value of arterial blood gas parameters for prediction of mortality in survivors of out-of-hospital cardiac arrest. Journal of emergencies, trauma, and shock, 10(3), 134.

von Auenmueller, K. I., Christ, M., Sasko, B. M., & Trappe, H. J. (2017). The value of arterial blood gas parameters for prediction of mortality in survivors of out-of-hospital cardiac arrest. Journal of emergencies, trauma, and shock, 10(3), 134. doi:  10.4103/JETS.JETS_146_16

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