Oferta e utilização de oxigênio na musculatura esquelética durante o exercício dinâmico em pacientes com a sobreposição da doença pulmonar obstrutiva crônica com a insuficiência cardíaca
Data
2015-06-24
Tipo
Tese de doutorado
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Resumo
A insuficiência cardíaca (IC) com fração de ejeção (FE) reduzida é uma comorbidade comum e incapacitante da doença pulmonar obstrutiva crônica (DPOC). As interações cardiopulmonares negativas em ambas doenças, DPOC e IC, podem prejudicar a oferta de oxigênio (O2) para a musculatura periférica em atividade. A hipótese deste estudo foi a de que o fluxo sanguíneo periférico e o débito cardíaco estariam mais comprometidos nos pacientes com DPOC+IC comparativamente ao observado nos pacientes com DPOC ou IC. Respostas fisiológicas e sensoriais ao exercício de 16 pacientes com associação da DPOC e IC (VEF1= 56,9 ± 15,9% previsto e FE= 32 ± 6%), 16 pacientes com DPOC (VEF1= 54,1 ± 13,9% e FE= 64 ± 10%), 15 pacientes com IC (VEF1= 79,3 ± 11,2%; FE= 31 ± 8%), e 12 controles saudáveis sedentários (VEF1= 94,1 ± 8,2%; FE= 66 ± 10%) foram avaliados. Os pacientes realizaram teste cardiopulmonar descontínuo de carga constante e os dados foram reportados a 20% e 80% da carga de pico. Débito cardíaco por cardioimpedância, fluxo sanguíneo (BFI) e extração muscular periférica por espectroscopia por raios quasi-infravermelhos, capacidade inspiratória, lactato,gasometria arterializada e percepção de esforço foram mensurados. Os grupos não apresentaram diferenças nas características demográficas e antropométricas (p>0.05). Pacientes com associação DPOC e IC apresentaram menor variação do BFI e do débito cardíaco em comparação com os demais grupos (p<0,05). Reduções do BFI foram diretamente proporcionais aos déficits de incremento do débito cardíaco. Deficiências no fluxo sanguíneo muscular periférico foram também relacionadas à maiores níveis de desoxigenação muscular e lactato no grupo DPOC+IC (r= -0,64; p<0,01) e IC (r= -0,73; p<0,01). O grupo DPOC apresentou maior sensação de dispneia durante o exercício enquanto o grupo DPOC+IC apresentou maior desconforto de membros inferiores (p<0.05). Análise de regressão múltipla revelou que apenas ?BFI/?consumo de O2 (r = 0,49) e, secundariamente,escores de desconforto nos membros inferiores (r= 0,26) relacionaram-se de forma independente com o tempo de tolerância ao exercício neste grupo (r2= 0,75; p<0,01).Concluindo, pacientes com a coexistência da DPOC e IC apresentaram maior redução da perfusão muscular esquelética e do débito cardíaco durante o exercício comparativamente aos pacientes com DPOC ou IC. Essas anormalidades foram intimamente relacionadas à menor capacidade de exercício, podendo responder a intervenções que melhorem o equilibrio entre oferta e demanda periférica de O2.
Background: Improving exercise tolerance remains an unmet clinical need in patients with chronic obstructive pulmonary disease (COPD) and coexistent heart failure. Negative cardiopulmonary interactions have been found to impair peripheral muscle perfusion during exercise in COPD without overt cardiac disease. Heart failure might lead to further decrements in cardiac output and muscle blood flow in COPD which could contribute to patient's intolerance to exertion. Objectives: To investigate the role of impaired central and peripheral hemodynamics in limiting endurance exercise tolerance in COPD-heart failure overlap. Methods: Cycle ergometer exercise tests at 20% and 80% peak work rate were performed by overlap (FEV1= 56,9 ± 15,9 % predicted, ejection fraction= 32 ± 6%; N= 16), FEV1-matched COPD (FEV1= 54,1 ± 13,9% redicted, ejection fraction= 64 ± 10 %; N= 16), ejection fraction-matched heart failure (FEV1= 79,3 ± 11,2% predicted, ejection fraction= 31 ± 8%; N=15) and sedentary controls (FEV1= 94,1 ± 8,2% predicted, ejection fraction= 66 ± 10%; N=12). Measurements and main results: Changes (delta from 20% and 80% peak work rate) in cardiac output (impedance cardiography) and vastus lateralis blood flow and oxygenation (intra-venous indocyanine green and near infrared spectroscopy) were expressed relative to deltaO2 uptake. Despite similar end-exercise Borg dyspnea scores, overlap had approximately 30% lower endurance exercise capacity than COPD or heart failure. In contrast, larger leg effort - dyspnea diferences at exercise cessation were found in overlap (p<0,01). Delta Blood flow was closely commmensurate to delta cardiac output in all groups (p<0,01). Overlap showed the largest impairment in delta cardiac output / deltaO2 uptake and delta blood flow / deltaO2 uptake (p<0,05). Blood arterial oxygenation, however, was better preserved in this group. Impairments in limb perfusion were related to greater muscle de-oxygenation and lactate levels in overlap (r= -0,64; p<0,01) and heart failure (r= -0,73; p<0,01). Limb blood flow and, secondarily, leg effort scores were the only independente predictors of endurance exercise capacity in these patients (r2= 0,75; p<0,01). Conclusion: Impaired central and peripheral hemodynamics with consequent decrease in limb muscle oxygenation assume a prominent role in limiting xercise tolerance in COPDheart failure overlap. Novel rehabilitive strategies aimed at increasing muscle O2 delivery and/or decreasing O2 demands are likely to be particularly useful in this patient population.
Background: Improving exercise tolerance remains an unmet clinical need in patients with chronic obstructive pulmonary disease (COPD) and coexistent heart failure. Negative cardiopulmonary interactions have been found to impair peripheral muscle perfusion during exercise in COPD without overt cardiac disease. Heart failure might lead to further decrements in cardiac output and muscle blood flow in COPD which could contribute to patient's intolerance to exertion. Objectives: To investigate the role of impaired central and peripheral hemodynamics in limiting endurance exercise tolerance in COPD-heart failure overlap. Methods: Cycle ergometer exercise tests at 20% and 80% peak work rate were performed by overlap (FEV1= 56,9 ± 15,9 % predicted, ejection fraction= 32 ± 6%; N= 16), FEV1-matched COPD (FEV1= 54,1 ± 13,9% redicted, ejection fraction= 64 ± 10 %; N= 16), ejection fraction-matched heart failure (FEV1= 79,3 ± 11,2% predicted, ejection fraction= 31 ± 8%; N=15) and sedentary controls (FEV1= 94,1 ± 8,2% predicted, ejection fraction= 66 ± 10%; N=12). Measurements and main results: Changes (delta from 20% and 80% peak work rate) in cardiac output (impedance cardiography) and vastus lateralis blood flow and oxygenation (intra-venous indocyanine green and near infrared spectroscopy) were expressed relative to deltaO2 uptake. Despite similar end-exercise Borg dyspnea scores, overlap had approximately 30% lower endurance exercise capacity than COPD or heart failure. In contrast, larger leg effort - dyspnea diferences at exercise cessation were found in overlap (p<0,01). Delta Blood flow was closely commmensurate to delta cardiac output in all groups (p<0,01). Overlap showed the largest impairment in delta cardiac output / deltaO2 uptake and delta blood flow / deltaO2 uptake (p<0,05). Blood arterial oxygenation, however, was better preserved in this group. Impairments in limb perfusion were related to greater muscle de-oxygenation and lactate levels in overlap (r= -0,64; p<0,01) and heart failure (r= -0,73; p<0,01). Limb blood flow and, secondarily, leg effort scores were the only independente predictors of endurance exercise capacity in these patients (r2= 0,75; p<0,01). Conclusion: Impaired central and peripheral hemodynamics with consequent decrease in limb muscle oxygenation assume a prominent role in limiting xercise tolerance in COPDheart failure overlap. Novel rehabilitive strategies aimed at increasing muscle O2 delivery and/or decreasing O2 demands are likely to be particularly useful in this patient population.
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Citação
OLIVEIRA, Mayron Faria de. Oferta e utilização de oxigênio na musculatura esquelética durante o exercício dinâmico em pacientes com a sobreposição da doença pulmonar obstrutiva crônica com a insuficiência cardíaca. 2015. 122 f. Tese (Doutorado em Pneumologia) - Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), São Paulo, 2015.