Abordagem à Síndrome de Insuficiência Cardíaca no cão e no gato
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2009
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Em Medicina Veterinária, tal como em Medicina Humana, a insuficiência cardíaca (IC) tem despertado um maior interesse nos últimos anos, pelo facto de ser uma importante causa de morbilidade e mortalidade tanto em cães como em gatos. Por este motivo, as doenças cardiovasculares, como causa de IC, assumem, cada vez mais, um papel importante na clínica de animais de companhia. A IC é uma síndrome na qual o coração não é capaz de responder às necessidades metabólicas do organismo, ou só o consegue fazer a pressões de enchimento elevadas. A fisiopatologia da IC assenta na cronicidade e “má adaptação” de mecanismos homeostáticos de defesa, fenómenos compensadores desencadeados para tentarem corrigir a diminuição do débito cardíaco e da pressão de perfusão de órgãos nobres. Estes mecanismos conduzem à estimulação cardíaca (inotropismo, cronotropismo e lusitropismo), à vasoconstrição arteriolar periférica e à retenção hidrossalina. Estes efeitos resultam da activação de diferentes agentes neuro-humorais que, a curto prazo, ajudam a manter a homeostasia cardíaca, sendo a sua activação crónica deletéria, contribuindo para o ciclo vicioso de auto-agravamento que caracteriza esta síndrome. Clinicamente, a IC pode manifestar-se por sinais de baixo débito cardíaco (depressão, letargia ou hipotensão) ou sinais de congestão (edema pulmonar, ascite ou derrame pleural). Nas últimas duas décadas a compreensão da fisiopatologia da IC tem evoluído, o que permitiu alterar o seu tratamento de forma a modular os mecanismos compensatórios que promovem a exacerbação da sintomatologia. É objectivo deste trabalho fazer uma revisão bibliográfica sobre esta síndrome, dando particular ênfase ao seu tratamento, seguida da apresentação de casos clínicos observados durante o período de estágio no Small Animal Teaching Hospital em Liverpool.
In Veterinary Medicine, as in Human Medicine, heart failure (HF) has been of great interest in the last years for its morbidity and mortality in dogs and in cats. For this reason, cardiovascular diseases, as a cause of HF, have an important role in small animal practice. HF is a syndrome in which the heart is not able to respond to the metabolic needs of the body, or can only do it at high filling pressures. The pathophysiology of HF is based on chronic and "poor adjustment" of homeostatic defense mechanisms, compensating phenomena triggered to try to correct the decrease in cardiac output and noble organ perfusion pressure. These mechanisms lead to cardiac stimulation (inotropism, chronotropism and lusitropism), peripheralarteriolar vasoconstriction and water and salt retention. These effects result from the activation of various neurohumoral agents that, in the short term, help to maintain cardiac homeostasis, but its chronic activation is deleterious, contributing to the vicious cycle of self-deterioration that characterizes this syndrome. Clinically, HF may manifest itself by signs of low cardiac output (depression, lethargy or hypotension) or signs of congestion (pulmonary edema, ascite or pleural effusion). In the last two decades the understanding of the pathophysiology of HF has evolved, enabling the exchange of its treatment in order to adjust the compensation mechanisms that promote the exacerbation of symptoms. The aim of this thesis is to do a review of this syndrome, with particular interest on its treatment, followed by a presentation of clinical cases observed during the training period at the Small Animal Teaching Hospital in Liverpool.
In Veterinary Medicine, as in Human Medicine, heart failure (HF) has been of great interest in the last years for its morbidity and mortality in dogs and in cats. For this reason, cardiovascular diseases, as a cause of HF, have an important role in small animal practice. HF is a syndrome in which the heart is not able to respond to the metabolic needs of the body, or can only do it at high filling pressures. The pathophysiology of HF is based on chronic and "poor adjustment" of homeostatic defense mechanisms, compensating phenomena triggered to try to correct the decrease in cardiac output and noble organ perfusion pressure. These mechanisms lead to cardiac stimulation (inotropism, chronotropism and lusitropism), peripheralarteriolar vasoconstriction and water and salt retention. These effects result from the activation of various neurohumoral agents that, in the short term, help to maintain cardiac homeostasis, but its chronic activation is deleterious, contributing to the vicious cycle of self-deterioration that characterizes this syndrome. Clinically, HF may manifest itself by signs of low cardiac output (depression, lethargy or hypotension) or signs of congestion (pulmonary edema, ascite or pleural effusion). In the last two decades the understanding of the pathophysiology of HF has evolved, enabling the exchange of its treatment in order to adjust the compensation mechanisms that promote the exacerbation of symptoms. The aim of this thesis is to do a review of this syndrome, with particular interest on its treatment, followed by a presentation of clinical cases observed during the training period at the Small Animal Teaching Hospital in Liverpool.
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Dissertação de Mestrado em Medicina Veterinária