Use of Electrocardiographic Analysis for Investigation of Ascites Syndrome in Broiler Chickens

Odom, T.W.; Hargis, Billy M.; López, Carlos Martínez; Arce, Mauricio; Ono, Yasuhiro; Avila, Gustavo

doi:10.2307/1591604

Cited by 36 publications

(13 citation statements)

References 15 publications

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“…When the RV wall hypertrophies the right atrioventricular valve also hypertrophies, leading to valvular insufficiency and RVF Qulian, 1987). Genetic or congenital differences in the RV wall or valve may make some broilers even more susceptible to PH-induced RVF as suggested by structural and electrocardiographic studies (Asson-Batres et al, 1989;Odom et al, 1989Odom et al, , 1991Odom et al, , 1992cMartinez et al, 1992).…”

Section: Pathogenesis Of Pulmonary Hypertensionmentioning

confidence: 99%

Ascites in poultry

1993

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SUMMARYResearch on ascites occurring in meat-type chickens reared at moderate and low altitude has shown that the pathogenesis is similar to that of the high altitude disease. Pulmonary hypertension (PH) caused by increased blood flow or increased resistance to flow in the lung results in right ventricular hypertrophy (RVH), valvular insufficiency, increased venous pressure and ascites. The structure of the avian heart, with its thin-walled right ventricle and muscular right atrioventricular valve, allows PH to induce heart failure quickly. The sudden increase in pulmonary hypertension syndrome (PHS) in meat-type chickens in the 1980s was associated with a rapid increase in growth rate and feed conversion. This was a result of a combination of genetic selection for fast-growing, heavy broilers with low feed conversion and a more dense, high caloric, pelleted food that supplied all the nutrients required for rapid growth and encouraged a high nutrient intake. PHS in meat-type chickens is usually primary pulmonary hypertension, that is, PH that occurs without evidence of prior heart or lung disease that could account for the increase in blood flow or resistance to flow that results in the increased pressure in the pulmonary arteries. The lungs of birds are firm and fixed in the thoracic cavity and they do not expand to draw air into the lung. The blood and air capillaries form a rigid network that allows only minimal expansion of the blood capillaries when more blood flow is required. Air is moved through the lung by abdominal movement which draws air in and out of the air sacs. The anatomy and physiology of the avian respiratory system are important in the susceptibility of meat-type chickens to PHS. The small stature of the modern meat-type chicken, the large, heavy breast mass, the pressure from abdominal contents on air sacs, and the small lung volume compared to body weight, may all be involved in the increased incidence of PHS. There is limited space for blood flow in the avian lung. Factors that increase blood flow or increase resistance to flow are additive. Increased blood viscosity caused by the polycythaemia of hypoxia, or increased erythrocyte rigidity of high Na + , are more likely to produce PH in fast-growing than in slow-growing birds. Increased flow due to cold exposure is also additive. Ascites caused by PH is a production-related disease at low altitude. It can be prevented easily by restricting growth rate. It is possible that some meat-type chickens of the phenotype we have created have reached the limit of blood flow through their lungs and that future improvements in growth rate will only be possible if the lung and abdominal cavity capacities are enlarged.

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Section: Pathogenesis Of Pulmonary Hypertensionmentioning

confidence: 99%

Ascites in poultry

1993

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“…Standard electrocardiogram (ECG) limb lead configurations, typical ECG wave segments, and standard degree-vector alignments for the frontal plane mean electrical axis (MEA; degrees) and mean resultant vector amplitude (MRV, millivolts) have been described for mammals and birds (Sturkie, 1986;Guyton, 1991;Odom et al, 1991;Conover, 1992). Owen et al (1990) first reported increased ECG lead II RS wave amplitudes when pulmonary hypertension and cardiac hypertrophy were triggered by exposing broilers to hypobaric hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Electrocardiographic Evaluation of Broilers During the Onset of Pulmonary Hypertension Initiated by Unilateral Pulmonary Artery Occlusion

Wideman

Kirby

1996

Poultry Science

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Electrocardiography previously has been used as a noninvasive method for detecting cardiac hypertrophy associated with pulmonary hypertension syndrome (PHS, ascites). In the present study, 36 of 100 male broiler chicks were selected for inclusion in the experiment based on their hatch weight (> or = 40 g), Day 1 to 14 BW gain (upper 50% of population distribution), and the normalcy of their Day 14 electrocardiogram (ECG). On day 16, 10 chicks were assigned to the unoperated control group (CONTROL), sham operations were performed on 10 chicks (SHAM), and pulmonary hypertension was initiated by clamping the left pulmonary artery in 16 chicks (PA-CLAMP). Electrocardiogram leads I, II, III, and aVF were recorded daily until Day 27, when 6 of the 12 birds surviving in the PA-CLAMP group had developed clinical ascites. The right: total ventricular weight ratio (RV:TV) was higher and BW was lower in the PA-CLAMP group than in the CONTROL and SHAM groups on Day 27. The RS, R, and S wave amplitudes in lead II for the CONTROL and SHAM groups did not change, whereas in lead II for the PA-CLAMP group the S wave attained a more negative amplitude by Day 21, the RS wave attained a more negative amplitude by Day 22, and the R wave declined to a less positive amplitude by Day 23 when compared with presurgery values. Similar differences were observed for the RS and S waves for leads III and aVF. The mean electrical axis (MEA) and mean resultant vector (MRV) of the CONTROL and SHAM groups did not change; however the PA-CLAMP group the MEA rotated significantly from +3 degrees to -72 degrees and to -88 degrees on Days 14, 22 and 27, respectively, and the MRV amplitude increased from 0.052 to 0.108 mV and then to 0.179 mV on Days 14, 22, and 27, respectively. When data from all treatment groups were combined, higher absolute and BW-normalized RV:TV ratios were inversely correlated (r = 0.859 to -0.880) with increasingly negative S wave amplitudes in leads II and aVF. Higher absolute and BW-normalized RV:TV ratios were directly correlated (r = 0.786 to 0.789) with increasing MRV amplitudes. These ECG characteristics constitute accurate, noninvasive predictive criteria suitable for detecting cardiac changes occurring early during the onset of primary pulmonary hypertension.

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“…Electrocardiography (ECG) has been shown to be an effective tool for determining if a bird is developing ascites. Reports have indicated that speci®c ECG changes, such as negative Lead II S-wave amplitudes are predictive of elevated right ventricle to total ventricle ratios (Owen et al, 1990(Owen et al, , 1995aOdom et al, 1991Odom et al, , 1992cKirby, 1995, 1996;Wideman et al, 1997Wideman et al, , 1998b. Pulmonary arterial pressure can be measured directly through the use of a venous catheter (Guthrie et al, 1987;Owen et al, 1995c;.…”

Section: Genetic Selection Methodsmentioning

confidence: 99%

Ascites Syndrome (Pulmonary Hypertension Syndrome) in Broiler Chickens: Are We Seeing the Light at the End of the Tunnel?

Balog¹

2003

Avian & Poul. Biolog. Rev.

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Ascites syndrome in broilers is a cascade of events that result in cardiac anomalies including an enlarged, flaccid heart, and right ventricular hypertrophy, as well as an accumulation of fluid in the abdominal cavity. Ascites was first noticed as a problem for commercial poultry producers, at farms that were located at high altitudes. Within the last 3 decades, however, ascites has become a significant problem for producers everywhere. Ascites fluid accumulation can be caused by many different factors. There are four general categories of dysfunctions that will result in ascites fluid build-up: (1) vascular damage that allows capillaries to leak; (2) blockage of the lymphatic system that prevents drainage; (3) decreased plasma oncotic pressure; and the most frequently seen dysfunction, (4) increased vascular hydraulic pressure. Increased vascular hydraulic pressure can be caused by several types of pathologies including hepatic, cardiac or right atrioventricular, and the most significant, pulmonary hypertension. Pulmonary hypertension accounts for most cases of ascites seen in commercial broilers, yet the hypertension can originate from many different causes. Environmental causes such as altitude, cold stress and incubator environment will affect the incidence of ascites. Management also plays a significant role in ascites development, for example; feed, lighting, air quality and ventilation have all been implicated in ascites development. Anatomy and physiology of the modern broiler also influences the incidence of ascites. Growth rate, oxygen requirements, organ size and capacity, hematological parameters and cellular responses can all determine how resistant or susceptible a broiler is to ascites. All of these factors cause ascites by inducing hypoxia in the bird (Julian, 1987(Julian, , 1988.The bird's demand for oxygen exceeds its cardiopulmonary capacity resulting in pulmonary hypertension. One final area that not only greatly influences, but also has potential to end ascites syndrome, is the area of genetic selection. In the past, a lot of the blame for our current ascites situation has been placed on poultry breeding and genetic selection for rapid growth, high meat yield and good feed conversion.While genetic selection may have exacerbated the ascites problem, it is also our best solution for eliminating this disorder in the near future.The selection of ascites resistant lines of broilers not only provides birds that can be raised at their maximal growth rate, it also provides a population in which to determine the exact molecular basis for ascites and pulmonary hypertension.

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Use of Electrocardiographic Analysis for Investigation of Ascites Syndrome in Broiler Chickens

Cited by 36 publications

References 15 publications

Ascites in poultry

Ascites in poultry

Electrocardiographic Evaluation of Broilers During the Onset of Pulmonary Hypertension Initiated by Unilateral Pulmonary Artery Occlusion

Ascites Syndrome (Pulmonary Hypertension Syndrome) in Broiler Chickens: Are We Seeing the Light at the End of the Tunnel?

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