Number 1 post: RW
According to WHO, pneumonia is an acute respiratory infection that affects the lungs. When an individual has pneumonia, the alveoli are filled with pus and fluid, which makes breathing painful and limits oxygen intake. Pneumonia is caused by several infectious agents, including viruses, bacteria, and fungi. Pneumonia is transmitted is a number of ways; it can be either viral or bacterial. They can be inhaled through the nose or throat, be spread via air-borne from a cough or sneeze or spread through blood. (2022). Pneumonia is the leading cause if morbidity and mortality worldwide, especially among the elderly population and those patients with comorbidities. (Htun et al., 2019).
Hospital acquired vs Community acquitted
Both hospital acquired and community acquired pneumonia are major causes of death. Hospital acquired pneumonia is classified as a respiratory tract infection which develops 48 hours after hospital admission. Hospital acquired and community acquired pneumonia display differences in the spectrum of bacteria, the susceptibility of the bacteria to antibiotics and the fact that with hospital acquired pneumonia, the patient’s host resistance is affected by concomitant disease and therapy effects. Patients suffering from hospital acquired pneumonia might have reduced inflammatory responses and a restricted intrinsic response. (Tschernig, 2016). Community acquired pneumonia is an acute infection whereby a patient acquired the infection in the community, as distinguished from hospital-acquired pneumonia. Community acquired pneumonia is a common and potentially serious illness associated with considerable need for therapy targeting multi-drug resistant pathogen being considered on a case by case basis. (File, 2021).
One of the major roles of the lungs is to facilitate gas exchange between circulatory system and the external environment. For effective gas exchange to occur, alveoli must be ventilated and perfused. Ventilation refers to the flow of air into and out of the alveoli, while perfusion refers to the flow of blood to alveolar capillaries. Changes in the ventilation and perfusion ratio can effect gas exchange and can contribute to hypoxemia. Gas exchange occurs in the respiratory zone of the lung, where alveoli are present. According to Fick’s law of diffusion, diffusion of a gas across the alveolar membrane increases with increased surface area of the membrane, increased alveolar pressure difference, increased solubility of the gas, and decreased membrane thickness. Deoxygenated blood from the pulmonary arteries has a PVO2 of 40mmHg, and alveolar air has a PAO2 of 100 mmHg, resulting in a movement of oxygen into capillaries until arterial blood equilibrates at 100 mmHg (PaO2). Meanwhile, carbon dioxide partial pressure decreases from a PVCO2 of 46 mmHg to a PaCO2 of 40 mmHg in alveolar capillaries due to a PACO2 of 40 mmHg. (Powers, 2021).
Hypoxia is a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis; this can result from inadequate oxygen delivery to the tissues either due to low blood supply or low oxygen content in the blood (hypoxemia). FiO2 is fraction of the inspired O2. This is indicated for low PaO2 less than 60 or SaO2 less than 90, and this can be achieved by increasing the percentage of oxygen in the inspired air that reaches the alveoli. If the FiO2 drops this may indicate a deterioration in gas exchange. (Bhutta et al., 2021).
Emphysema vs Pneumonia
Emphysema is a progressive lung disease. Unlike pneumonia, it’s a chronic condition. It is a form of chronic obstructive pulmonary disease (COPD). Emphysema is defined as a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitations that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases. (Pahal et al., 2021).
Number 2 post: AL
1) List three symptoms the patient exhibits and the pathophysiology principles.
There are several risk factors and subsequent symptoms a patient may exhibit with a diagnosis of heart failure. Depending on whether the heart failure has been determined as systolic heart failure (not pumping hard enough) or diastolic heart failure (not filling enough) is how the patient will present (Dlugasch & Story, 2021). For this case we will look at left sided diastolic heart failure. Our patient reports pink frothy sputum, wheezing when he breathes in, and shortness of breath (dyspnea) with exertion. All of these symptoms lead us to believe there is left sided heart failure. Left sided heart failure presents with pulmonary complications from blood overfilling the ventricle causing ineffective left ventricular contractility (Left Heart Failure Assessment, 2021; Dlugasch & Story, 2021). In left sided heart failure, cardiac output falls and blood is not being pumped into the body as it should be (Dlugasch & Story, 2021). The blood backs up in the left atrium and then, eventually, backs up in pulmonary circulation (Dlugasch & Story, 2021). Endothelial cell dysfunction can be said to contribute to 60% of non-cardiomyocyte cells that impact the function and structure of the heart (Simmonds et al., 2020). HFrEF (heart failure reduced ejection fraction) and HFpEF (heart failure preserved ejection fraction) are two categories that need more patient information to categorize (Dlugasch & Story, 2021).
2) What role does hypertrophy play in heart failure?
Hypertrophy in the heart muscle occurs for many reasons and is typically due to comorbidities such as hypertension, diabetes, kidney disease, and obesity (Dlugasch & Story, 2021). In any of these cases, there is increased workload on the heart to push blood out. Over time, the myocardial tissue in the ventricles increases to compensate for the extra work being performed. The hypertrophied cells in the ventricular walls become stiff due to this remodeling and there can also be the loss of functional cardiomyocytes (Dlugasch & Story, 2021). Simmonds et al., (2020) compared the cardiomyocyte cell death in two cardiac hypertrophy categories, eccentric and concentric. Cardiomyocytes cell death was present in HFrEF and absent in HFpEF and heart structure was thickened in the HFpEF and normal for HFrEF,(Simmonds et al., 2020). These changes lead to a decrease in cardiac output. Ultimately, compensatory mechanisms, such as the release of ADH, do not end up working long term and the heart muscle will continue to weaken. As a result, the person with a hypertrophied heart muscle will end up in heart failure due to dysfunction of the systolic or diastolic contractions (Dlugasch & Story, 2021).
3) Does this patient have Ischemic disease? Why or why not?
Ischemic heart disease (IHD) is normally associated with coronary artery disease (CAD) and the presence of atherosclerotic plaque, but this is not always true (Severino et al., 2020). There is literature supporting the pathological mechanisms of coronary microvascular dysfunction (CMD) as a central role in heart failure (HF) and IHD specifically of the left sided diastolic dysfunction (Severino et al., 2020). Without further diagnostic testing we cannot know if our patient’s heart has IHD but we can suspect there is a high probability. Though coronary artery disease and hypertension account for about 75% of heart failure instances, there are many other reasons why someone may have heart failure (Dlugasch & Story, 2021). Other instances leading to heart failure include valvular dysfunction, myocarditis, chronic dysrthythmias, chronic lung disease, thyroid disorders, or even medications such as anticancer drugs and antidiabetic drugs (Dlugasch & Story, 2021).
4) What is Virchow’s Triad?
Virchow’s Triad is what describes the mechanisms leading to the formation of venous thrombosis (Kushner & William, 2021). The triad depicts three conditions that predispose a person to the development of venous thrombosis and thromboembolic events such as DVTs, CVAs, or PEs (Kushner & William, 2021). The triad is as follows: 1) endothelial injury, 2) sluggish blood flow (stasis), and 3) increased coagulopathy (hypercoagulability) (Dlugasch & Story, 2021). Virchow’s Triad principles were originally aimed at peripheral vascular disease (PVD) but can also lend explanation to abnormal arterial blood flows too (Severino et al., 2020). Venous thrombosis usually arises from a combination of Virchow’s Triad.