Cardiogenetic Pulmonary Edema Versus Non-cardiogenic Pulmonary Edema - Paper Example

Introduction

A healthy human lung is a site in which both solute and fluid infiltration occurs across the pulmonary capillary endothelium. The filtrate in the lungs is only restricted to interstitial spaces and pulmonary lymphatic channels through which it moves from formation to removal sites, using inbuilt pressure gradient. The quantity of filtered fluid and the content of protein in the fluid are determined by the protein osmotic and transvascular hydrostatic pressure differences (Sureka, Bansal and Arora, 2015). Another factor contributing to the quantity of fluid is the leakiness of the endothelial barrier to protein and water. When the rate of lymphatic removal is exceeded by that of fluid filtration, then a condition known as pulmonary edema occurs. Pulmonary edema is a condition that comes as a result of increased extravascular water content in human lungs. In simplified terms, the excess fluids in the lungs collect in countless air sacs, creating pressure making it difficult for a patient to breathe (Fujimoto, Morikawa, and Inubushi, 2011). There are two main types of pulmonary edema: the Cardiogenetic Pulmonary Edema (CPE), and the Non-Cardiogenic Pulmonary Edema (NCPE). This paper presents these two conditions in detail and various aspects while also providing their comparisons and differences.

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Etiology

Cardiogenetic pulmonary edema is a condition that comes by as a result of elevated hydrostatic pressure that builds in the pulmonary capillaries. This pressure is caused when the left ventricle of the human heart fails to pump blood to other parts of the body properly. This condition is known as left-sided Congestive Heart Failure (CHF). That is the etiology of CPE. The increased pulmonary venous pressure builds up in the left atrium, then veins and the capillaries (Roguin the et al., 2000).

Consequently, the fluid is forced through the capillary walls and into the surrounding air sacs through transudation. This situation later causes fatal acute respiratory distress (Sureka et al., 2015). On the other hand, Noncardiogenic Pulmonary Edema (NCPE) is a type of pulmonary edema that is not caused by heart-related complications but other factors. Unlike CPE that is caused by heart failure due on the left, NCPE is etiologically caused by injuries to the endothelial and epithelial barriers. The underlying pathogenesis as far NCPE is concerned, include alveolar pressure, neurogenic edema, and high capillary permeability of both endothelial and epithelial walls. As a result of leakage from capillaries in the lungs' air sacs, the fluid can fill other spaces within the gaseous cavity leading to difficulties in breathing (Kollef and Pluss, 1991). Etiologically, the two conditions are not similar in any way because one is heart-related and the other is not, however, they are both associated with difficulties in breathing.

Pathophysiology

The pathophysiology of CPE begins when the left ventricle of the heart can no longer contain the pulmonary venous return. Due to that, the hydrostatic pressure exerted within the pulmonary capillaries elevates to the point that it surpasses pressure in the alveolar interstitial space increasing cardiac preload (Roguin et al., 2000). A self-reinforcing physiological process then initiated, which when it fails, it leads to hypoxia. Hypoxia increases catecholamines which are associated with increased blood pressure and vascular resistance. Diastolic or left ventricular dysfunction can also cause CPE with the presence or absence of cardiac pathologies like valve abnormalities or artery disease (Fujimoto et al., 2011). Other conditions other than heart disease that can cause cardiogenetic pulmonary edema include fluid overload due to blood transfusion, renal artery stenosis, severe renal disease or acute hypertension, and cardiomyopathy (Bosomworth, 2008). The pathophysiology of noncardiogenic pulmonary edema (NCPE) depends on the kind of pathologic insult, whether direct or indirect, that occurs to the permeability of the pulmonary membrane. The primary causes of NCPE include drowning, aspiration, fluid overload, neurogenetic pulmonary edema, inhalation injury, allergic reaction, adult respiratory distress syndrome, acute glomerulonephritis, and acute kidney disease. The cause of permeability of alveolar-capillary membrane can also be attributed to infectious conditions (bacterial, parasitic, viral), trauma, inhalation of smoke or toxic gases, snake venom, and very many others. The pathophysiologies of NCPE and CPE are not so easy to determine. This is why correct diagnosis has to be done relying on both clinical and radiologic findings because notable overlaps have been noted in clinical and imaging outcomes between the various causes. It can be noted that NCPE has numerous possible pathophysiologies than NPE. One of these conditions can lead to the cause of the other (Bosomworth, 2008).

Clinical Presentations

The clinical presentations of CPE include left heart failure, extreme breathlessness, feelings of drowning, and anxiety (Fujimoto, et al., 2011). Pieces of evidence of clinical presentations of CPE also include hypoxia as well as increased sympathetic tone associated with elevated levels of catecholamine. Recorded complaints by patients include profuse diaphoresis, shortness of breath. Other symptoms that have been reported clinically include paroxysmal nocturnal dyspnea, orthopnea, and dyspnea on exertion. Clinical representation of NCPE indicates that most patients having this condition are usually severely ill and immobile as compared to patients of CPE. NCPE patients find it difficult to go to computed tomography (CT) scans and MRI units (Kollef and Pluss, 1991). Readily available for NCPE is the conventional chest radiography that has portability. Unlike NPE, NCPE radiographic findings can be quickly arrived at, but with low specificity of chest radiographs. Patients with NCPE may have clinical features that are similar to those with NPE; however, they often lack jugular venous distention and third heart sound (S3). The pulmonary capillary wedge pressure (PCWP) is often used to measure the pressures in both NPE and NCPE. In NPE patients, the PCWP is generally higher than 18mm Hg while for NCPE patients, it should be less than 18 mm Hg. This reading can be challenging to discern if there is a chronic pulmonary disease. In NCPE, the pulmonary opacities radiate centrifugally and assume a "batwing" pattern (Bosomworth, 2008).

Respiratory Interventions

Respiratory interventions for CPE have been put in place to manage patients suffering from this condition. Part of this management, especially in the initial stages, should include resuscitation (Kollef and Pluss, 1991). This process checks the breathing, clears airways and ensures there is circulation. Patients should be put on oxygen to ensure there is optimal oxygen circulation. Oxygen should be administered through the use of noninvasive pressure support ventilation, continuous positive airway pressure (CPAP) and face masks. Most respiratory interventions of noncardiogenic pulmonary edema patients are similar to those given to CPE patients. They involve administering oxygen and conducting resuscitation because the affected areas mostly are the airways. It is appropriate to ascertain the cause of gas exchange abnormality before initiating the most appropriate inhalation therapeutic measures (Bosomworth, 2008).

Management

Managing CPE has been historically done through medication done by a clinician. Drug therapy has always been used involving drugs like Morphine, Furosemide (Lasix), and Nitroglycerin. To be considered is titrated small doses of intravenous diamorphine. Antiemetic should also be considered. However, opiate should not be administered if the patient feels exhausted, hypotensive or drowsy. CPAP is also effective for managing CPE (Bosomworth, 2008). Managing noncardiogenic pulmonary edema is similar in some aspects, to the management of cardiogenetic pulmonary edema, especially drug therapy. Conservative fluid strategy, diuretics, and albumin can be used on the NCPE patients to keep in check the intravascular osmotic pressure, reduce extravascular water, and minimize capillary leak (Domenighetti, Gayer and Gentilini, 2002). However, for NCPE only and not CPE, mechanical ventilation that involves expansion of lung volume is recommended. This can be done using positive end-respiratory pressure (PEEP) which also requires oxygenation. In both cases, if the conditions are severe, the management should be done in the hospital or critical care setting (Fujimoto et al., 2011).

Outcomes

Treatment outcomes for CPE suggest that standard therapy for patients should be changed together with the adjunctive administration of other medications. According to some medical journals and articles, some treatment modalities for CPE are associated with adverse outcomes especially when the prognosis is not well determined (Fujimoto et al , 2011; Bosomworth, 2008). It is of great importance to diagnose and medically take care of other underlying causes of CPE. The treatment outcomes for NCPE have been so effective when PEEP and oxygenation are used in caregiving. This shows that oxygenation is effective for both CPE and NCPE (Roguin et al., 2000). More modern ventilation techniques like partial fluid ventilation and high-frequency oscillatory ventilation have been tipped to provide more favorable outcomes, especially for NCPE. For both cases, the mortality rates remain high (Fujimoto et al., 2011).

Conclusion

In conclusion, cardiogenetic and noncardiogenic pulmonary edema are two serious conditions that affect millions of patients annually. CPE is caused by heart by heart complications and leads to hydrostatic fluid pressure that builds up causing difficulty in breathing. NCPE is caused by various nonheart complications and factors. It is also associated with fluid build-up in the airways resulting in difficulties in breathing. Treatment and management of these two conditions require a deep understanding of their etiologies, pathophysiologies, clinical presentation, intervention measures, management, and outcomes.

References

Domenighetti, G., Gayer, R., & Gentilini, R. (2002). Noninvasive pressure support ventilation in non-COPD patients with acute cardiogenic pulmonary edema and severe community-acquired pneumonia: acute effects and outcome. Intensive Care Medicine, 28(9), 1226-1232. doi: 10.1007/s00134-002-1373-8

Fujimoto, S., Morikawa, S., & Inubushi, T. (2011). An MR comparison study of cardiogenic and noncardiogenic pulmonary edema in animal models. Journal Of Magnetic Resonance Imaging, 34(5), 1092-1098. doi: 10.1002/jmri.22730

Bosomworth, J. (2008). Rural treatment of acute cardiogenic pulmonary edema: applying the evidence to achieve success with failure. Canadian Journal Of Rural Medicine, 13(3), 121-127. Retrieved from https://www.researchgate.net/publication/23262206_Rural_treatment_of_acute_cardiogenic_pulmonary_edema_applying_the_evidence_to_achieve_success_with_failure

Kollef, M., & Pluss, J. (1991). Noncardiogenic Pulmonary Edema following Upper Airway Obstruction 7 Cases and a Review of the Literature. Medicine, 70(2), 91-98. doi: 10.1097/00005792-199103000-00002

Roguin, A., Behar, D., Ami, H., Reisner, S., Edelstein, S., Linn, S., & Edoute, Y. (2000). Long-term prognosis of acute pulmonary oedema - an ominous outcome. European Journal Of Heart Failure, 2(2), 137-144. doi: 10.1016/s1388-9842(00)00069-6

Sureka, B., Bansal, K., & Arora, A. (2015). Pulmonary Edema Cardiogenic or Noncardiogenic?. Journal Of Family Medicine And Primary Care, 4(2), 290. doi: 10.4103/2249-4863.154684