Concepts of Cardiovascular and Respiratory Disorders Essay
Myocardial infarction is a consequence of the occlusion of a single or multiple epicardial coronary arteries for at least 20 minutes. The occlusion is ordinarily thrombotic following plaque rupture in coronary arteries. Ischemia results in sarcolemmal disruption, myofibril relaxation, and mitochondrial alteration with subsequent liquefactive necrosis of the myocardial tissue (McCance & Huether, 2019). The alteration in cardiac function is dependent on the region infarcted. However, the limited regeneration capability of the myocardium dictates that healing is by scar formation which results in dilation and segmental hypertrophy of the remaining tissue. Ultimately, cardiac dysfunction ensues.
Endocarditis refers to the inflammation of the endocardial lining of a heart valve, a cardiac chamber, or a great blood vessel with the formation of vegetation. Endocarditis can be infectious or non-infectious. Infective endocarditis results from bacterial invasion and colonization of sterile fibrin-platelet vegetation (Rajani & Klein, 2020). This invasion results in valve destruction and loss of function. In the order of frequency, the mitral valve is affected most followed by the aortic, tricuspid, and pulmonary valves.
Myocarditis denotes the inflammation of the myocardium that is typically seen in young patients. It is mostly viral. Entry of the viral pathogen into myocardial cells initiates a cascade of reactions that leads to activation of the innate immune system and later adaptive immune system. This results in an exaggerated response to the viral destruction of the myocardium causing chronic inflammation, myocardial remodeling, and ventricular dysfunction.
Valvular disorders occur when one or more heart valves do not close or open efficiently. These functional abnormalities include failure to sufficiently open (stenosis), failure to sufficiently close (regurgitation), and slipping out of place (prolapse) (McCance & Huether, 2019). Valvular defects are principally acquired or congenital. The most common valvular defect is aortic stenosis. Finally, valvular diseases can be classified based on severity as mild, moderate, and severe.
A lipid panel is essential for the estimation of cardiovascular risk. Currently, the test is considered routine. A lipid profile highlights four parameters including total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides. Accurate determination of the lipid profile necessitates the deployment of a fasting blood specimen. Clinically, a lipid profile is essential for screening, diagnosis, and disease management.
Coagulation is a dynamic process that entails a cascade of events that result in hemostasis. Physiologically, a delicate balance exists between the thrombogenic and anti-thrombogenic components of the body. Coagulation principally involves an interaction between the blood vessel, platelets, and the coagulation cascade. Finally, coagulation is a sequential process encompassing arteriolar vasoconstriction, primary hemostasis, secondary hemostasis, and clot resorption and stabilization (McCance & Huether, 2019).
Clotting cascade traditionally involves intrinsic and extrinsic pathways which convene at factor X activation. The extrinsic pathway is activated by tissue factor, a substance present in the subendothelial tissue. Tissue factor binds to factor VIIa and calcium resulting in the conversion of factor X to Xa. Meanwhile, the intrinsic pathway commences with factor XII, HMW kininogen, prekallikrein, and factor XI, which results in the activation of factor XI. Factor XIa further activates factor IX, which then acts with factor VIII to activate factor X. Finally, the common pathway involves an interaction factor Xa alongside factor V, phospholipids, and calcium to form prothrombinase complex which converts prothrombin to thrombin.
Deep Vein Thrombosis
DVT is a venous thromboembolic disorder. In DVT, clot formation emanates from the deep calf vein and propagates proximally. Virchow’s triad is the principal pathophysiologic mechanism for DVT. It includes endothelial damage, hypercoagulability, and venous stasis. These three factors interact in various degrees to stimulate cytokine production and leukocyte adhesion that enhance thrombus formation. Nevertheless, thrombus propagation largely depends on the balance between thrombolytic and coagulation pathways.
Hypertension is a condition characterized by persistently elevated systolic blood pressure of 130 mm Hg or more and/or diastolic blood pressure of 80 mmHg or more. The pathophysiology of hypertension is complex and multifactorial entailing volume expansion from enhanced salt absorption, intensified activation of the sympathetic nervous system, and the impaired response of the RAAS. These alterations result in intensified afterload as well as total peripheral resistance leading to hypertension.
Heart failure is a clinical syndrome in which the heart is incapable of pumping enough blood to meet the body’s metabolic requirements (Inamdar & Inamdar, 2016). Cardiac output is a function of stroke volume and heart rate and is dependent o preload, afterload, and ventricular contractility. Heart failure with reduced ejection fraction is a consequence of reduced contractility and systolic dysfunction while heart failure with preserved ejection fraction is a consequence of decreased ventricular compliance and diastolic ventricular dysfunction (Schwinger, 2021). Compensatory mechanisms such as activation of RAAS, myocyte hypertrophy, myocyte regeneration, increased beta-adrenergic activity, and secretion of BNP initially maintain cardiac output but later become maladaptive leading to cardiac remodeling and increased wall stress and subsequent progression of the condition (Schwinger, 2021).
COPD is designated by progressive airflow limitation and tissue destruction. Its pathophysiology mainly entails protease-antiprotease imbalances and oxidative stress. Irritants such as smoking result in an inflammatory response, oxidative stress, and protease-mediated destruction of elastin resulting in loss of elastic recoil and airway collapse during exhalation. Inflammation and airway obstruction causes a reduction in forced expiratory volume (FEV1) while tissue destruction causes airflow limitation and impaired gaseous exchange leading to CO2 retention and hypoxemia. Hyperinflation is usually due to air trapping while acute exacerbation is predominantly due to triggers.
Asthma is a chronic condition of the airway distinguished by airway inflammation and constriction of the airways. Its pathophysiology is complex and entails airway inflammation, intermittent airway obstruction, and bronchial hyperresponsiveness (Gans & Gavrilova, 2020). Following inhalation of an allergen, leads to airway inflammation and enhanced mucus production as a result of bronchial hypersensitivity. Airway obstruction is marked on expiration and occurs due to inflammatory cell infiltration, smooth muscle contraction, and mucus plug formation (Gans & Gavrilova, 2020). Finally, the reversible changes may become irreversible due to airway remodeling characterized by basement membrane thickening, epithelial desquamation, and bronchial smooth muscle hyperplasia.
Pneumonia refers to acute infection of the lung. It is broadly classified as community-acquired, hospital-acquired, and ventilator-associated pneumonia. The pathophysiology of pneumonia involves a disruption of the intricate balance between the host defense forces and the pathogen. Normal local and systemic protective factors of both innate and adaptive immunity prevent microbial invasion and destruction of the lung parenchyma. Overcoming these defense mechanisms leads to inflammation, destruction of the lung parenchyma, impairment of lung compliance, and an increase in the diffusion distance leading and perfusion ventilation mismatch.
Gans, M. D., & Gavrilova, T. (2020). Understanding the immunology of asthma: Pathophysiology, biomarkers, and treatments for asthma endotypes. Pediatric Respiratory Reviews, 36, 118–127. https://doi.org/10.1016/j.prrv.2019.08.002
Inamdar, A. A., & Inamdar, A. C. (2016). Heart failure: Diagnosis, management, and utilization. Journal of Clinical Medicine, 5(7), 62. https://doi.org/10.3390/jcm5070062
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.
Rajani, R., & Klein, J. L. (2020). Infective endocarditis: A contemporary update. Clinical Medicine (London, England), 20(1), 31–35. https://doi.org/10.7861/clinmed.cme.20.1.1
Schwinger, R. H. G. (2021). Pathophysiology of heart failure. Cardiovascular Diagnosis and Therapy, 11(1), 263–276. https://doi.org/10.21037/cdt-20-302
Â· Instructor instructions:
In this exercise, you will complete essay type questions in Knowledge Check to gauge your understanding of this moduleâ€™s content.
Â· Like the discussion question assigned, there are some points to make substantively, do need to cite in KC at least one primary current reference. but each answer is worth 20 points. I would expect about 1 paragraph per answer (a paragraph would include 6-10 sentences).