Hello, my name is Amol and my presentation covers the underlying pathophysiology of heart failure highlighting the case of Mrs Brown. Heart failure is one of the most pressing issues in modern day societal systems, with over 38 million people estimated to be affected globally (Atherton et al. 2018). Australia alone accounted for over 170,000 hospitalisations in 2016 relating to heart failure and cardiomyopathy, where 40% of the cases registered heart failure as the primary diagnosis. The presentation would cover the different clinical manifestations of heart failure referring to the case scenario of Mrs. Brown.
Mrs. Brown was admitted to the Emergency Department in the morning after having complained of severe shortage of breath. She also had a history of heart failure that was diagnosed two years prior. During admission, she was found with several clinical manifestations among which the foremost includes severe dyspnoea and a respiratory rate of 24 breaths per minute. Dyspnoea is essentially the subjective sensation where the breathing pattern becomes abnormal and is caused largely due to the physiological process of the respiration where the problem may exist anywhere between the point of oxygen uptake and the oxygen consumption (Meta-analysis Global Group in Chronic Heart Failure, 2012). Mrs. Brown’s oxygen saturation levels were also very low, ranging in at about 85% on room air. Her blood pressure levels were also moderately high, coming in at BP 170/95mmHg. The heart rate was measured to be 120 beats per minute in atrial fibrillation. The low count for oxygen saturation levels of 85% at room air largely stems from the heart’s inability to receive oxygen rich blood from the lungs. It leads to oxygen de-saturation where the amount of haemoglobin carrying oxygen molecules gradually reduces (Stub et al. 2015).
Moving onto the high blood pressure levels, it has been estimated that over two thirds of cases involving heart failure also involve associated blood pressure abnormalities. While the causes of high blood pressure may be varied and multidimensional, the symptom manifests in patients with heart failure as the haemoglobin carrying the oxygen reduces over time, leading to the heart becoming thicker and stiffer. Doctors generally rely on different measures to control the blood pressure in patients with heart failure, including intravenous vasodilators and even sodium nitroprusside for the more serious cases (Cohn et al. 1982).
Mrs. Brown was also identified to comprise of bilateral basal crackles on auscultation of her lungs. Crackles usually manifest in the form of clicking or crackling noises that take place when the patient engages in inhalation. Basal crackles refer to the crackles that originate near the base of the lung, and bilateral basal crackles occur in both the lungs. In terms of the causes, they primarily occur when small airways in the lungs open explosively owing to infections in either the bronchioles or the alveoli (Silbernagel et al. 2018). Basal crackles are a very common symptom in cases involving heart failure as evident in Mrs. Brown’s initial diagnosis and are usually classified into fine, medium and coarse based on the pitch and intensity of the sounds.
Mrs. Brown’s final diagnosis was an acute exacerbation of chronic heart failure. Myocardial abnormalities in patients with acute heart failure primarily occur due to three different causes with the most prominent relating to neuro hormonal activation. Others recognised causes include inflammatory activation and oxidative stress and are predominantly related to structural abnormalities within the respiratory process (Hartupee & Mann, 2017). The hemodynamic responses also tend to be abnormal, as depicted in the case of Mrs. Brown. Symptoms include decreased cardiac output levels, increase in filling pressures along with augmentations in the afterload (Dickstein et al. 2010).
I would like to conclude my presentation by highlighting the importance of myocardial abnormalities that are associated with heart failure and how they form the basis of pathogenesis for the patients. Low oxygen saturation levels and high blood pressure counts are key aspects in this regard along with dyspnoea. The basal crackles were also an indicator of abnormalities within the respiratory process where explosive opening of the alveoli or bronchioles was identified as the primary cause. To summarise, it is evident that Mrs. Brown’s diagnosis was made based on both the physical as well as the clinical manifestations of her symptoms and was in adherence to the guidelines and recommendations for diagnosing heart failure provided by the National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand.
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Cohn, J. N., Franciosa, J. A., Francis, G. S., Archibald, D., Tristani, F., Fletcher, R., ... & Saunders, R. (1982). Effect of short-term infusion of sodium nitroprusside on mortality rate in acute myocardial infarction complicated by left ventricular failure: results of a Veterans Administration cooperative study. New England Journal of Medicine, 306(19), 1129-1135.
Dickstein, K., Vardas, P. E., Auricchio, A., Daubert, J. C., Linde, C., & van Veldhuisen, D. J. (2010). 2010 Focused Update of ESC Guidelines on device therapy in heart failure: An update of the 2008 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure and the 2007 ESC guidelines for cardiac and resynchronization therapy Developed with the special contribution of the Heart Failure Association and the European Heart Rhythm Association. Europace, 12(11), 1526-1536.
Hartupee, J., & Mann, D. L. (2017). Neurohormonal activation in heart failure with reduced ejection fraction. Nature Reviews Cardiology, 14(1), 30-38.
Meta-analysis Global Group in Chronic Heart Failure (MAGGIC). (2012). The survival of patients with heart failure with preserved or reduced left ventricular ejection fraction: an individual patient data meta-analysis. European heart journal, 33(14), 1750-1757.
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Stub, D., Smith, K., Bernard, S., Nehme, Z., Stephenson, M., Bray, J. E., ... & Meredith, I. T. (2015). Air versus oxygen in ST-segment–elevation myocardial infarction. Circulation, 131(24), 2143-2150.
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