The Author

Dr. Frank Jones Extension Section Leader

Introduction

This increase in pulmonary arterial pressure (hypertension) triggers the accumulation of fluid in the abdominal cavity (ascites). Since several seemingly independent factors contribute to the overall incidence of ascites, attempts to manage ascites can be confusing unless we are able to focus on a unifying strategy. The objectives of this article are to summarize the progression leading from pulmonary hypertension to terminal ascites, to provide an understanding of how pulmonary hypertension can begin and to suggest ways to reduce the chances of your flock getting the disease.

How Birds Breath

While some may already understand, before beginning our discussion of ascites, it is important to have a basic understanding of how respiration (breathing) takes place in birds. The process of respiration in birds is similar in some ways to respiration in mammals. Blood in need of oxygen is brought from the tissues through the veins (venous blood) to the heart and pumped to the lungs for oxygenation. Oxygen rich blood leaves the lungs and returns to the heart and pumped to body tissues. Arteries carry blood (arterial blood) from the heart to other organs or tissues.

Although birds have lungs, they are small and rigid in comparison to those of mammals. Birds have no true diaphragm. Instead, birds have a series of thin walled pouches called air sacs connected to their lungs. Respiratory muscles move the keel bone to push air in and out of the birds in a manner similar to a bellows. The exchange of oxygen and carbon dioxide occurs only in the lungs and avian lungs are much less capable of expansion than are mammalian lungs. Yet avian lungs are more efficient than mammalian lungs at gas exchange and air sacs effectively move large volumes of air through the respiratory system. Thus, any condition that interferes with the air sacs hinders respiration. In addition to their role in respiration, air sacs help remove excess heat from the bird’s body and can act as shock absorbers, protecting internal organs.

How Pulmonary Hypertension progresses to Ascites

Venous blood from the bird’s body first enters a collecting chamber of the heart called the right atrium and then passes through a simple flap-like valve into a pumping chamber called the right ventricle. The right ventricle normally pumps at a low pressure that is just sufficient to push all of the returning venous blood through the blood vessels of the lungs. Maintaining this low pumping pressure reduces the work load of the heart and prevents swelling and fluid accumulation in the lungs (pulmonary edema). When excessive blood flow causes the heart to increase pressure to the lung (pulmonary hypertension), the relative inflexibility of the lungs causes fluid from the blood vessels to begin to move into the lung tissues.

Soon after it begins, pulmonary hypertension causes the wall of the right ventricle to thicken, indicating it is performing increased work to pump blood through the lungs. Research has demonstrated that increases in the relative weight of the right ventricle are directly correlated with increases in blood pressure in the arteries leading to the lungs (pulmonary arteries). In addition, recent experiments have shown that elevations in pulmonary arterial pressure can cause blood to flow so rapidly through the lungs of healthy broilers that insufficient time elapses for adequate oxygen uptake. This rapid blood flow causes blood oxygen levels to gradually decline in affected broilers which can be detected visually as a slight darkening of the normally bright red comb and wattles. Pulmonary edema also may contribute to reduced blood oxygenation as pulmonary hypertension progresses.

After initially thickening, the wall of the right ventricle then begins to stretch and enlarge. This enlargement indicates that in spite having increased the pulmonary arterial pressure, the right ventricle still cannot pump all of the blood through the lungs. The volume within the right ventricle must increase when an excessive amount of blood remains within the pumping chamber at the completion of contraction. This enlargement physically reduces the pumping efficiency of the right ventricle, and extensive enlargement may prevent the valve between the right atrium and right ventricle from sealing properly, allowing blood to regurgitate back into the right atrium during each ventricular contraction.

The reduced blood oxygen levels accompanying pulmonary hypertension may contribute to a generalized weakening of heart muscle. These events mark the beginning of right-sided congestive heart failure, which is characterized by the engorging of veins throughout the body with blood that cannot be efficiently pumped through the lungs. The accumulated blood congests the blood channels within the liver and causes plasma leakage through the surface of the liver. This plasma is the source of the fluid which accumulates in the abdominal cavity and eventually kills the bird by compressing the abdominal air sacs so that respiration can not occur. As the syndrome enters its terminal stages, large reductions in blood oxygen cause the comb and wattles of affected broilers to exhibit a dark blue “cyanotic” appearance.

What Causes Pulmonary Hypertension?

Since ascites starts with pulmonary hypertension, strategies to reduce the incidence of ascites in fast growing broilers must focus on the underlying causes of pulmonary hypertension. Broilers that are susceptible to ascites are capable of outgrowing the capacity of their lungs to accept and oxygenate blood at a sufficiently low pulmonary arterial pressure. Detailed anatomical studies have shown that, on a body weight basis, the process of domestication has reduced the pulmonary gas exchange capacity of both chickens and turkeys. Selection for improved feed efficiency and rapid body weight gain may have unintentionally contribute to a marginal pulmonary capacity making birds less capable of sustained activity.

The metabolic demands associated with fast growth in broilers constantly challenge the heart to pump higher volumes of blood as a source of nutrient and oxygen delivery. Recent research clearly demonstrates that broiler lungs maintain an essentially constant resistance during large increases in blood flow. This means that broiler lungs can only expand so much and are functionally inelastic. This inelasticity means that pulmonary blood pressure must increase in order to propelled the increased blood flow through the lungs. When the volume of blood pumped by the heart per minute (known as the cardiac output) increases in fast growing broilers, pulmonary hypertension must occur since resistance in the lungs (pulmonary vascular resistance) can not be reduced to accommodate the increased volume of blood returning to the heart.

Factors that Trigger Pulmonary Hypertension and Ascites

Ascites mortality tends to be highest in the fastest growing flocks, and that incidence can be lowered by any strategy that slightly slows the overall flock growth rate. This slightly slower growth rate reduces the demand on the heart, pulmonary hypertension and ascites. The incidence of ascites increases whenever broilers are exposed to cool temperatures. Cool temperatures increase cardiac output since the bird’s metabolic rate must increase to meet the demand for body heat production. Exposing broilers to low oxygen immediately triggers an increase in pulmonary arterial pressure since the efficiency of respiratory process is reduced. When birds are chronically exposed to low oxygen levels, it tend to lead to a high incidence of ascites. The respiratory damage associated with disease, dust, or poor air quality can reduce respiratory efficiency. In addition, these conditions can partially obstruct the airways, reduce the number of vascular channels available for blood flow, thereby reducing blood oxygen, increasing pulmonary vascular resistance and pulmonary arterial pressure, and causing ascites in broilers.

Lowering the Odds of for Pulmonary Hypertension and Ascites

In contrast to the known triggers for ascites outlined above, the incidence of ascites can be lowered by any strategy that reduces the metabolic demand for oxygen and thus reduces cardiac output. Slightly restricting broiler growth rates and providing thermoneutral temperatures fall into this category. The incidence of ascites also can be reduced by treatments that reduce pulmonary vascular resistance by dilating the pulmonary vasculature. Although a number of chemical are capable of reducing pulmonary vascular resistance, none are approved for use in birds destined for human consumption. However, the amino acid arginine is utilized by cells lining the pulmonary blood vessels to facilitate pulmonary vascular dilation during high pressure and flow conditions. Our research has shown that adding supplemental arginine to broiler diets effectively reduces pulmonary vascular resistance and the incidence of ascites in broilers exposed to cool temperatures. Nonetheless, it is important to remember that increased use dietary arginine have been shown to influence lysine requirements.

Conclusion

Broilers susceptible to ascites are capable of outgrowing the capacity of their lungs to oxygenate blood. Factors that increase oxygen demand include: exposure to cool temperatures, low oxygen levels, and respiratory damage associate with disease, dust or poor air quality. Pulmonary hypertension and ascites in modern broiler strains may be reduced by any strategy that reduces the metabolic demand for oxygen and thus reduces cardiac output. Slight restrictions in broiler growth and providing a thermoneutral environment are two strategies that work.

Further Information

This article was largely abstracted from a 1999 Hubbard Farms Technical Report by R. F. Wideman (“Understanding pulmonary hypertension syndrome (ascites)”). This article is published with the permission of the author and Hubbard Farms.

Source: Avian Advice - Fall 2005 - Volume 7, Number 3