Pulmonary edema (PE) is failure in the left ventricle characterized by high pressure in the capillaries and flooding of fluid in the interstitium and the alveolar within the lungs. Flooding of the alveoli leads to deprivation of oxygen which leads to shortness of breath, a common characteristic of PE. PE is also caused by damages on the membrane barrier between the alveolar and the capillaries and the presence of an obstruction in the lymphatic system. The different causes of PE give forth to the different types of PE. Cardiogenic or hydrostatic pulmonary edema (CPE) is caused by an increase in capillary pressure due to failure within the left ventricles and non-cardiogenic pulmonary edema is caused by damage on the endothelial and epithelial lining (Chioncel et al., 2015).
Demographics from different sources portray PE as a disease that is widespread across the globe. The Acute Heart Failure Global Survey of Standard Treatment puts the global prevalence rate of PE at 37% with 25.3 % of these cases being caused by a left ventricular ejection fraction (LVEF) that goes beyond 45%. The mortality rate of the reported cases in the global survey was at 7.4% in the period covering 2006 to 2007 (Parissis et al., 2010). The European Heart Failure Survey II conducted between 2004 and 2005 records a European prevalence rate of 16.2% with the most affected age at 71.2 years. Of the reported cases, 59.4% were male with an overall mortality rate of 9.1% (Nieminen et al., 2006). The Acute Heart Failure Database puts PE prevalence at 18.4% with a peak age of 73.8 years. The database indicates that men are more prone to suffer from PE at 55.9% (Spinar et al., 2011).
Delegate your assignment to our experts and they will do the rest.
Normal anatomy
The heart, lungs and the lymphatic system work concurrently in the transportation, oxygenation of the blood and fluid clearance. The ventricles are responsible for the pumping of blood out of the heart. The left ventricle, after receiving oxygenated blood from the lungs, pumps it to the rest of the body for circulation. The right ventricle, after receiving non-oxygenated blood from the rest of the body, pumps it to the lungs for oxygenation. Both processes are controlled by systematic pressures created by systolic and diastolic movements. Enroute to the lungs, non-oxygenated blood flows through the pulmonary arteries that subdivide into finer capillaries in the lungs. It's at the alveoli and the capillary level where the exchange occurs. The two are separated by a fused basement membrane. During the oxygen-carbon (IV) oxide exchange, hemoglobin releases carbon (IV) oxide which dissolves in the blood plasma and diffuses into the alveoli via the membrane. The alveoli, simultaneously, releases oxygen via the membrane to the blood plasma, where it gets dissolved and picked up by hemoglobin.
The lymphatic system has a role in the alveolar-capillary exchange process. During the oxygenation of the blood, body fluid finds its way into the alveolar. Alveolar fluid clearance takes place courtesy of the lymphatic system. Balancing of the sodium ions and chloride ions in the alveolar enable their drainage into a venous pool that channels them to the lymphatic system. Aquaporins also take part in the fluid clearance process. They are minute membrane proteins responsible for water movement via the epithelial and endothelial cells of the alveolar. The flow of water follows an osmotic gradient created by the sodium and chloride ions (Chioncel et al., 2015).
Normal physiology
In a normal blood circulation process, the left ventricle contracts and creates a regulated pressure capable of pumping oxygenated blood to the rest of the body. The pressure created in the ventricle is transmitted evenly up to the capillary level thus dictating the plasma oncotic and the interstitial pressure. A positive interstitial pressure leads to the elimination of fluids that accumulates in the alveolar. An intact alveolar-capillary barrier creates a vital boundary that prevents excessive flow and accumulation of fluid in the alveolar. A lymphatic system takes up any fluid that is eliminated from the alveolar through the alveolar fluid clearance process. With no obstruction, the fluid flows to the right lymphatic duct and the thoracic duct, where the fluid is delivered to the blood through the subclavian veins.
Mechanism of Pathophysiology
Hydrostatic edema is caused by failure in the left ventricle of the heart. A failure in the left ventricle of the heart results in a sudden increase in the pressure within the capillaries. An increase in pressure implies that the capillary filtration rate increases thus more fluid is delivered into the neighboring tissues. When the rate of capillary filtration surpasses the rate of lymphatic drainage, both the interstitial tissues and the alveolar become flooded with body fluid thus leading to hydrostatic edema (Mutlu & Sznajder, 2005).
Non-cardiogenic edema or permeability edema occurs due to physical damage on the micro-vascular membrane. The micro-vascular is a semipermeable membrane that allows only macro-molecules to pass through from the blood to the interstitium. When this barrier is interfered with, the pore sizes increase thus letting through large volumes of body fluid resulting in non-cardiogenic edema.
Another form of edema is lymphedema that results from a disruption of the lymph pump. An infected or impaired lymph pump reduces drainage rate thus leading to flooding. The lymphatic system responsible for fluid drainage works optimally on an increase in capillary pressure. An increase in capillary pressure increases interstitial tissue pressure thus pushing more fluid into the lymphatic system. However, further elevation of the capillary pressure overwhelms the drainage system leading to edema. Additionally, blockage within the lymphatic system derails the drainage flow. A slowed flow implies excessive accumulation of fluid thus worsening the formation of edema. Physical damage on the lumen of the lymphatic system also increases its permeability thus allowing a flow of proteins back into the tissues leading to edema (Mutlu & Sznajder, 2005).
Prevention
Prevention of PE to a certainty of zero occurrences is a feat yet to be achieved. It is advised that those with a history of PE should always be on a high alert and seek medication whenever symptoms are felt. There are, however, several measures capable of minimizing the occurrence of PE. First off, consistent regular body exercise strengthens heart muscles thus lowering the probability of experiencing left ventricular heart failure. Taking of flu and pneumonia vaccine also minimizes the chances of PE. Both pneumonia and flu are known to potentially increase the quantity of fluid in the lungs. Any other lifestyle activities that accelerate the risk of heart failure should be avoided. The activities include smoking, drug abuse and eating of high cholesterol foods. This helps in maintaining a healthy body mass index thus reducing the chances of heart failure. Persons with a history of PE should also avoid high altitudes and deep diving as the two interfere with internal body pressure. Lastly, persons who have had past episodes of PE should remain on diuretics to minimize the chances of a reoccurrence.
Treatment
Treatment of PE involves the administration of drugs or therapies that enhance blood oxygenation, maintain normal heart functioning and minimize flooding in the lungs. One such treatment is the administration of nitrates in form glyceryl trinitrate via sublingual or intravenous infusion. Dosage for sublingual tablets varies from 300 to 600 micrograms per minute to a limit of 1800 micrograms. The limit for the intravenous administration is capped at 200 micrograms. Low doses of nitrates relax heart muscles thus minimizing the severity of left ventricular heart failure. Higher doses dilate the arteries thus decreasing blood pressure and reducing the accumulation of fluids in the interstitial tissues. Dilation within the coronary arteries improves oxygenation within the heart muscles leading to improved performance in the ventricles. Nitrates are, however, linked to hypotension and monitoring of blood pressure is essential. Use of nitrates may also lead to tachycardia, bradycardia, and tachyphylaxis (Purvey & Allen, 2017).
Diuretics, such as furosemide, are also intravenously administered in patients with PE. A dosage of four milligrams per minute is sufficient to reduce preload and may be repeated after 20 minutes for better results. Morphine is also useful n the treatment of PE as it reduces the effects of dyspnea, symptomized by difficulty in breathing. It also reduces anxiety in patients which helps reduce blood pressure. Side effects of morphine include depression of the nervous system and hypotension. Inotropes, such as dobutamine and milrinone are mostly prescribed for patients with acute PE but they may worsen hypotension in patients and are contraindicated in patients with atrial fibrillation. Lastly, PE patients may need ventilation support. Ventilation support is attained through proper sit up the positioning of patients but oxygen may be administered only if the oxygen saturation level is below 92 percent (Purvey & Allen, 2017).
Clinical Relevance
Most PE prescriptions lack efficacy and research data to qualify their mechanism. In “ Managing acute pulmonary oedema” , Purvey and Allen (2017) note that there is insufficient evidence to demonstrate the efficacy of nitrates and diuretics in the treatment of PE. The use of morphine has been traditional but has adverse side effects that may affect the quality of life when routinely used. Inotrope, such as milrinone, is known to increase mortality rate thus not relevant to a majority of patients.
Conclusion
At a prevalence rate of 37%, it's conclusive that PE is globally widespread. Left ventricular heart failure remains the main cause of this condition, with other causes such as atrial fibrillation, injury in lungs, and obstruction in the lymphatic drainage system also contributing to its occurrence. The available clinical procedures are mostly symptomatic with numerous side effects. The use of inotropes such as milrinone is associated with a high mortality rate thus making it, arguably, clinically inefficient. Other medications, such as nitrates, diuretics, and morphine are efficient in managing symptoms of PE but their side effects may cause lifelong medical conditions. The Acute Heart Failure Global Survey of Standard Treatment puts the global mortality rate of PE patients at 7.4%, an indication that there exists a gap in research on the treatment of PE. More emphasize needs to be put on lifestyle activities such as physical exercise, less smoking, and avoiding drug abuse as prevention measures against PE.
References
Chioncel, O., Ambrosy, A. P., Filipescu, D., Bubenek, S., Vinereanu, D., Petris, A., … Gheorghiade, M. (2015). Patterns of intensive care unit admissions in patients hospitalized for heart failure. Journal of Cardiovascular Medicine , 16 (5), 331-340. doi:10.2459/jcm.0000000000000030
Mutlu, G. M., & Sznajder, J. I. (2005). Mechanisms of pulmonary edema clearance. American Journal of Physiology-Lung Cellular and Molecular Physiology , 289 (5), L685-L695. doi:10.1152/ajplung.00247.2005
Nieminen, M. S., Brutsaert, D., Dickstein, K., Drexler, H., Follath, F., & Harjola, V. (2006). EuroHeart Failure Survey II (EHFS II): a survey on hospitalized acute heart failure patients: description of population. European Heart Journal , 27 (22), 2725-2736. doi:10.1093/eurheartj/ehl193
Parissis, J. T., Nikolaou, M., Mebazaa, A., Ikonomidis, I., Delgado, J., Vilas-Boas, F., … Follath, F. (2010). Acute pulmonary oedema: clinical characteristics, prognostic factors, and in-hospital management. European Journal of Heart Failure , 12 (11), 1193-1202. doi:10.1093/eurjhf/hfq138
Purvey, M., & Allen, G. (2017). Managing acute pulmonary oedema. Australian Prescriber , 40 (2), 59-63. doi:10.18773/austprescr.2017.013
Spinar, J., Parenica, J., Vitovec, J., Widimsky, P., Linhart, A., Fedorco, M., … Jarkovsky, J. (2011). Baseline characteristics and hospital mortality in the Acute Heart Failure Database (AHEAD) Main registry. Critical Care , 15 (6), R291. doi:10.1186/cc10584
