Brisket disease

Hecht, Hans H.; Kuida, Hiroshi; Lange, Ramon L.; Horne, J L; Brown, Aileen

doi:10.1016/0002-9343(62)90288-7

Cited by 98 publications

(13 citation statements)

References 11 publications

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“…Despite a 2‐fold increase in RHF mortality, the number of cattle that died of RHF in 2012 was relativity minor when compared to DD: approximately 4‐5 times more cattle died of DD than RHF. Although death loss from RHF was relatively minor, the occurrence of RHF in feedlot cattle is noteworthy for 2 reasons: First, before the 1970s, RHF was only reported in cattle at altitudes over 2,130 m;3, 4, 9 therefore, a 2‐fold increase in RHF over a 12 year period in feedlots located at low (657 m) to moderate (1,145 m) elevations deserves attention. Second, although RHF occurred throughout the feeding period, half of all cases occurred after 19 weeks; this makes death loss from RHF particularly costly.…”

Section: Discussionmentioning

confidence: 99%

“…Cattle exposed to the hypobaric hypoxia of high altitude have a greater baseline risk of alveolar hypoxia and, consequently, are at greater risk of RHF than cattle at lower altitudes. Before the 1970s, RHF had only been reported in cattle at altitudes over 2,130 m3, 4; it has since been reported at lower altitudes, however. In 1974, a study of 4 US feedlots located at an altitude of 1,600 m reported the attack risk of RHF to be 2.85 cases per 10,000 cattle entering the feedlot 5.…”

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Right‐Sided Congestive Heart Failure in North American Feedlot Cattle

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Booker

Wildman

et al. 2015

Veterinary Internal Medicne

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BackgroundAnecdotal reports suggest the incidence of right‐sided congestive heart failure (RHF) in feedlot cattle is increasing; however, the rate of occurrence and risk factors are largely unknown.ObjectiveThe purposes of this study were to evaluate the risk of RHF over time and among feedlots, to characterize some of the risk factors for RHF, and to investigate how risk factors may affect the timing of RHF occurrence.AnimalsThe population at risk consisted of 1.56 million cattle that were placed in 10 Canadian feedlots during the years 2000, 2004, 2008, and 2012, and 5 US feedlots during the year 2012.MethodsA retrospective observational study was conducted. Variables, including year of feedlot entry, were evaluated for association with RHF using zero‐inflated negative binomial and logistic regression models. Factors affecting time to RHF were evaluated using Cox proportional hazard regression analyzes. Death from digestive disorders (DD) served as a control.ResultsThe risk of RHF in Canadian feedlots doubled from the year 2000 to the year 2012 (P = .003). For every 10,000 cattle entering US feedlots in 2012, 11 cattle died from RHF and 45 cattle died from DD. The median time to RHF was 19 weeks. Cattle treated for bovine respiratory disease were 3 times more likely to die from RHF, and they died earlier in the feeding period.ConclusionsA doubling of the incidence of RHF over a short time period is concerning, particularly for US feedlots situated at moderate altitudes in the High Plains.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Right‐Sided Congestive Heart Failure in North American Feedlot Cattle

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Booker

Wildman

et al. 2015

Veterinary Internal Medicne

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“…Lowlanders with a brisk hypoxic vasoconstriction traveling to high altitudes may also be exposed to the risk of right heart failure. This complication of high altitude exposure has been reported in high altitude cattle (85), infants of Chinese Han brought to high altitudes in Tibet (208), Indian soldiers transported to high altitude borders with China (3) and occasional Europeans travelling to the South American altiplano (98). …”

Section: Exercise In Hypoxiamentioning

confidence: 92%

Pulmonary Circulation at Exercise

Naeije¹,

Chesler

2012

Comprehensive Physiology

154

164

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The pulmonary circulation is a high flow and low pressure circuit, with an average resistance of 1 mmHg.min.L−1 in young adults, increasing to 2.5 mmHg.min.L−1 over 4–6 decades of life. Pulmonary vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary pressures, up to a 20–25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40–50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher pulmonary vascular pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of pulmonary vascular tone have little effect on pulmonary vascular pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with pulmonary hypertension is associated with sharp increases in pulmonary artery pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint pulmonary vascular pressures-flow relationships may uncover early stage pulmonary vascular disease.

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“…The structural changes in small pulmonary arteries and veins appear to reflect this genetically based and adaptive process [3][4][5] in humans and animals. Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude.…”

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases. M. Maggiorini, F. Léon-Velarde. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a hallmark of high-altitude pulmonary oedema (HAPE) and of congestive right heart failure in subacute mountain sickness (SMS) and chronic mountain sickness (CMS) in the Himalayas and in the end-stage of CMS (Monge9s disease) in the Andes.There are studies to suggest that transmission of excessively elevated pulmonary artery pressure and/or flow to the pulmonary capillaries leading to alveolar haemorrhage is the pathophysiological mechanism of HAPE.In the Himalayas, HAPE was successfully prevented by extending the acclimatisation period from a few days to 5 weeks, however, this did not prevent the occurrence of congestive right heart failure after several weeks of stay at 6,000 m. This leads to the concept that rapid remodelling of the small precapillary arteries prevents HAPE but not the development of right heart failure in SMS and CMS.Unresponsiveness of pulmonary hypertension to oxygen at high altitude and its complete resolution only after weeks of stay at low altitude suggest that structural rather than functional changes are its pathophysiological mechanism. Since pulmonary hypertension at high altitude is the driving force leading to high-altitude pulmonary oedema and "high-altitude right heart failure" in newcomers and residents of high altitude, the authors propose to adjust current terminology accordingly. The physiological response of the pulmonary circulation to hypobaric and normobaric hypoxia is to increase pulmonary arteriolar resistance. The magnitude of hypoxic pulmonary vasoconstriction is highly variable between humans, probably based on genetics and adaptive mechanisms. Sites of hypoxic pulmonary vasoconstriction are small pulmonary arterioles and veins of a diameter of v900 mm, the veins accounting for y20% of the total increase in pulmonary vascular resistance caused by hypoxia [1,2]. The structural changes in small pulmonary arteries and veins appear to reflect this genetically based and adaptive process [3][4][5] in humans and animals. Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude. An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9]. The results of these studies suggest that an excessive rise in PAP is a common denominator in HAPE [9], the syndrome described by SUI et al. [8] in infants and by ANAND et al. [7] in adults at 6,700 m and termed "subacute...

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Brisket disease

Cited by 98 publications

References 11 publications

Right‐Sided Congestive Heart Failure in North American Feedlot Cattle

Right‐Sided Congestive Heart Failure in North American Feedlot Cattle

Pulmonary Circulation at Exercise

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

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