According to Dehler, Zessin, Bartsch, and Mairbaurl (2006), cardiac pulmonary edema also known as congestive cardiac failure (CCF) or congestive heart failure (CHF) occurs in alveolar hypoxia pathological because of an increase in pulmonary capillary pressure. Cardiac pulmonary edema is directly linked to high capillary pressure by alveolar fluid reabsorption, disruption of endothelial barrier function, alveolar epithelial permeability, reduction in plasma oncotic pressure, and increases in lung vascular endothelial and transmicrovascular filtration mechanisms (Diseases and Conditions Pulmonary Edema, 2014). Dehler, Zessin, Bartsch, and Mairbaurl (2006) argue that the asymmetry of cardiac efficiency leads to ejection fraction with a low volume of blood or the heart’s failure to pump sufficient blood, which comes from the lungs. The resulting increase in pressure in the left atrium and vein capillaries (cardiac myocytes) causes blood to engorge into the veins and the tissues leading to the swelling of the feet and legs (Dehler, Zessin, Bartsch & Mairbaurl, 2006). In summary, the direct causes of CHF include heart failure, intrapulmonary pressure (cardiac preload) in the pulmonary artery at the diastole just before systole, and chronic lung diseases, which lead to increases in interstitial fluids or extravascular lung water.
The medical condition resulting in CHF includes coronary heart disease which is caused by the accumulation of plaque and the consequent heart attack. Cardiomyopathy is another factor that causes edema, which is a result of damaged heart muscles and heart valve problems (Dehler, Zessin, Bartsch & Mairbaurl, 2006).
Essential hypertension is another risk factor that causes edema. Clinical trials show that when high blood pressure remains uncontrolled, it causes the thickening of the left ventricular muscle, which is the direct cause of coronary artery disease or idiopathic cardiomyopathy. The symptoms of hypertension include shortness of breath swollen feet, fatigue, sudden death, and frequent coughing. Essential hypertension, which is associated with transmicrovascular, remains elevated because of the transcapillary escape of proteins (Diseases and Conditions Pulmonary Edema, 2014). The presence of efferent (postglomerular) arteriolar resistance causes the transmission of oncotic pressure, which decreases peritubular capillary pressure. The resistance of both ultrafiltration coefficient and renal plasma flow underpins the increase in glomerular capillary pressure. A high heart rate combined with high stroke volume leads to cardiac output and high peripheral resistance of essential hypertension.
According to Diseases and Conditions Pulmonary Edema (2014), non-cardiac pulmonary is another direct cause of edema, which is directly linked to heart disease in elderly people (Diseases and Conditions Pulmonary Edema, 2014). Investigations show that an increase in the permeability of vascular endothelium, pulmonary vascular resistance and pressure, interstitial and alveolar edema fluid high in protein content (inflammatory cytokines and leukocytes in bronchoalveolar lavage), fluid leakages in the pulmonary arterial walls (endothelial permeability), damaged capillary walls and peripheral arteries, and over perfumed to be the direct causes of heart failure (Dehler, Zessin, Bartsch & Mairbaurl, 2006). Other causes include acute respiratory distress syndrome (hypoxia) as a result of high altitudes. Clinical investigations show that increases in edema and protein leaks are directly caused by a combination of hypoxia and viral infections of the tract (Dehler, Zessin, Bartsch & Mairbaurl, 2006).
In conclusion, the syntheses of the differences between the three causes of edema provide an excellent basis for further research in controlling the disease.
References
Dehler, M., Zessin, E., Bartsch, P. & Mairbaurl, H(2006) Hypoxia causes permeability oedema in the constant-pressure perfused rat. European respiratory journal, 27(3), 1-7.
Diseases and Conditions Pulmonary Edema (2014). Web.