Cardiovascular and Cardiopulmonary Pathophysiologic Processes

Introduction

Cardiovascular and Cardiopulmonary Pathophysiologic Processes are mainly caused by history of surgery, malignancy, hospitalization and immobility. These pathophysiologic processes can be identified from the symptoms presented by the patient. Below is a case study analysis of a patient presenting various symptoms comprising shortness of breath, pleuritic chest pain and palpitations. A description of pathophysiologic processes beginning at the cellular level is provided to critically understand the symptoms and how these processes interact to affect the patient. Finally, racial variables that may impact physiological functioning are discussed.

Symptoms of Cardiovascular and Cardiopulmonary Pathophysiologic Processes

The cardiovascular and cardiopulmonary pathophysiologic processes that result in the patient presenting these symptoms

The symptoms presented by the patient are a sign of cardiovascular and cardiopulmonary pathophysiologic processes. The EKG results after assessing the patient comprising T wave inversions in the right precordial lead (V1-4) ± the inferior leads (II, III, aVF) are proof of pulmonary embolism. Pulmonary embolism is a venous thromboembolism condition that mainly affects post-op patients (Prisco, Tufano, Cenci, Pignatelli & Santilli, et al., 2019).

The condition is caused by blood clots, often from deep veins, which block one or more lung arteries hindering proper blood flow circulation. Pulmonary embolism can lead to lung tissue damage as well as low blood supply to body organs. It is why the patient is experiencing shortness of breath, pleuritic chest pains, and palpitations. The most common causes of this pathophysiologic process include surgery, hospitalization, immobility, and malignancy. Notably, the patient’s history of surgery and knee replacement has led to immobilization and hospitalization, leading to pulmonary embolism.

Racial/Ethnic Variables That May Impact Physiological Functioning

Venous thromboembolism is greatly dependent on different racial and ethnic variables. Although these racial or ethnic differences play significant roles in impacting physiological functioning, their inheritability, the physiological and clinical basis is not entirely defined. However, research reveals that African-American patients have a considerably high incidence of incident venous thromboembolism. This is because of their increased exposure to inciting risk factors such as operative and accidental traumas. Unlike Asian/Pacific ethnicities, African Americans have numerous diagnoses of pulmonary embolism. The death cases due to pulmonary embolism are 50 percent higher in the latter race than the whites (Khalid, Dasu, Zafar, Suga & et al.,2020). On the other hand, compared to Asians and Native Americans, whites are at a 50 percent higher rate of death.

How These Processes Interact To Affect the Patient

The patient in the study presents the listed signs as a result of interactions from the cardiovascular and cardiopulmonary pathophysiologic processes. Pulmonary embolism occurs when thrombi in deep veins detach and enter the pulmonary circulation. This leads to the blockage or occlusion of oxygen-transporting blood vessels and mainly those carrying blood from the lungs to the heart. Consequently, the gaseous exchange is impaired. More giant emboli wedge in the main pulmonary artery, whereas smaller emboli occlude the peripheral arteries, resulting in pulmonary infarction and interalveolar bleeding. Pulmonary embolism is more commonly found in the lower lobes of the lungs (Velasco & Howard, 2017).

As alveolar ventilation exceeds pulmonary capillary blood flow, emboli obstruct the pulmonary artery, resulting in dead space ventilation and an increase in vascular resistance.

In addition, it causes active platelets to produce serotonin and thromboxane, which causes vasoconstriction and, in turn resulting in right ventricular failure. It can also result in syncope, which is explained as a loss of consciousness caused by a lack of adequate nutrient flow. Pulmonary embolism again causes hypotension because of the low blood pressure triggered by syncope. Among other effects of the interactions of these cardiovascular and cardiopulmonary physiological processes are electromechanical dissociation and risks of sudden death.

Conclusion

Pulmonary embolism can cause lung tissue damage as well as a decrease in blood flow to internal organs. It is a cause of the patient’s shortness of breath, pleuritic chest aches, and palpitations. Surgery, hospitalization, immobilization, and cancer are the most prevalent causes of this pathophysiologic process. Racial and ethnic variations have also been confirmed to have a major effect of physiological functioning. However, their inheritability, as well as the physiological and clinical foundation, are not fully understood.

References

Khalid, Y., Dasu, N., Zafar, R. F., Suga, H., Dasu, K., & Blair, B. (2020). In-Hospital Outcomes of Patients With Pulmonary Hypertension and Cirrhosis: A 6-Year Population Cohort Study of Over One Million PatientsCardiology and Therapy9(2), 479-492.

Prisco, D., Tufano, A., Cenci, C., Pignatelli, P., Santilli, F., Di Minno, G., & Perticone, F. (2019). Position paper of the Italian Society of Internal Medicine (SIMI) on prophylaxis and treatment of venous thromboembolism in patients with cancerInternal and emergency medicine14(1), 21-38.

Velasco, C. E., & Howard, C. (2017). Trouble on Both Sides: Pulmonary Embolism with PneumothoraxThe American journal of medicine130(5), 530-533.