![[object Object],[object Object],[object Object],[object Object],[object Object],EPOC: Enfermedad Pulmonar Obstructiva Crónica](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
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Prof Héctor Verea
- 1. Fisioterapia Respiratoria en la EPOC Dr Héctor Verea Servicio de Neumología Complejo Hospitalario Universitario A Coruña
- 3. Enfermedades crónicas Mortalidad en USA, 1970-2002 Jemal A, et al. JAMA 2005; 294:1255
- 4. Prevalencia de Epoc en España “ Epi-scan ” Miravitlles M, Thorax 2009; 64:863 Edad (años) 73% no diagnosticados previamente GOLD I: < actividad (ADL) < calidad vida Riesgo de EPOC: > Edad > 30 paq_años < calidad de vida < nivel educación FEV1/FVC < 70%
- 5. Muertes por EPOC y sexo Canada, 1950-2003 (proyección a 2010) Sources: Centre for Chronic Disease Prevention, Public Health Agency of Canada; 2006 using Statistics Canada Data Hospitalización EPOC y sexo Canada, 1979-2003 (proyección 2010 EPOC en mujeres
- 9. Insuficiencia Respiratoria PO 2 PCO 2
- 10. Espirometría * < 50% + IRC FEV1 / FVC < 0,7 Volumen (L) Flujo (L/sec) 4 3 2 1 1 2 3 4 5 0 Epoc predicto 0 Gravedad FEV1 % I Leve > 80 II Moderada < 80 a 50 III Grave < 50 a 30 IV Muy grave < 30 *
- 11. Supervivencia FEV 1 Stage BODE Months 1.0 0.8 0.6 0.4 0.2 0.0 0 4 8 12 16 20 24 28 32 36 40 44 48 52 0 4 8 12 16 20 24 28 32 36 40 44 48 52 Stage I (> 50%) predicted Stage II (36-50%) predicted Stage III ( 35%) predicted Quartile 1 (BODE 0-2) Quartile 2 (BODE 3-4) Quartile 3 (BODE 5-6) Quartile 4 (BODE 7-10) Probability of Survival P < 0.001 P < 0.001 Celli BR, et al. N Engl J Med. 2004;350:1005-1012.
- 12. FEV 1 Disnea Gold I Gold II Gold III-IV
- 13. Garcia-Rio F, AJRCCM 2009; 180:506 EPOC: Limitación en la actividad física e hiperinflacción dinámica Actividad fisica Cambio en End-Expiratory Lung Volume
- 14. Insuflacción Respiración en volumenes altos Aplanamiento diafragmático DISNEA Obstrucción de las vías aéreas > Resistencias
- 15. Historia natural TABACO Obstrucción Exacerbacion Hipersecreción mucosa Inflamación Destrucción alveolar < aclaramiento mucoso Exacerbación Exacerbacion HIPOXEMIA MUERTE 80 70 60 50 40 30 20 10 0 1 2 3 4 5 Normal Fumador EPOC Años FEV 1 Disnea Oxígeno En casa En cama MUERTE
- 17. Masa muscular esquelética y marcadores inflamatorios en EPOC CHI = creatine height index, a measure of skeletal muscle mass Normal CHI 80% predicted, Low CHI <80% predicted Eid AA, et al. Am J Respir Crit Care Med. 2001;164:1414. *P <0.05, † 95% CI * * 3.03-6.81 2.70-3.90 2.00-2.90 3.00-5.90 1.70-2.80 1.86-4.32 †
- 18. Disfunción múscular Normal EPOC Type II 57%
- 19. Apoptosis músculo estriado Sanos EPOC Nucleos de fibras apoptóticas Agusti AG, et al. Am J Resp Crit Care Med. 2002;166:485
- 20. Desacondicionamiento pérdida de la “forma física” Perdida de condición física menos capacidad aerobica Depen-dencia caidas Menos resistencia y fuerza Perdida masa magra SEDENTARISMO ENVEJECIMIENTO Otras ENFERMEDADES TÓXICOS
- 21. La actividad fisica consigue reducir la mortalidad aun cuando se inicie a mediana edad Byberg L, BMJ 2009;338:b688
- 24. Beneficios de la Fisioterapia Respiratoria Capacidad funcional para el ejercicio 6-MWD (n=444) Estado de salud CRQ disnea (n=519) Lacasse Y, et al. Cochrane Database Syst Rev 2002;3:CD003793.
- 25. Niveles de evidencia de la eficacia de la Fisioterapia Respiratoria (ATS, 2004) BENEFICIO NIVEL DE EVIDENCIA Disnea A HRQL A Costes B Supervivencia C
- 27. Niveles de evidencia de la eficacia de la Fisioterapia Respiratoria (ATS, 2004) COMPONENTE NIVEL DE EVIDENCIA Miembros inferiores A Miembros superiores A Músculos respiratorios B Educación B Apoyo psicosocial C
- 32. PCO2 kPa HCO3- mmol/L 6MWT metros Duiverman ML, Resp Res 2011 Fisioterapia Respiratoria y VMNI nocturna * * *
- 33. Neuromuscular electrical stimulation of the lower limbs in patients with chronic obstructive pulmonary disease. Vivodtzey I, Lacasse Y, Matais F. J Cardiopulm Rehabil Prev. 2008; 28(2): 79 Muscle training with repetitive magnetic stimulation of the quadriceps in severe COPD patients. Bustamante V, de Santa Maria EL, Gorostiza A, Jimenez U, Galdiz JB. Resp Med 2010; 104: 237.
Editor's Notes
- Two Models of Parenchymal Airspace Enlargement in Chronic Obstructive Pulmonary Disease. In Panel A, alveolar inflammation leads to the destruction of alveolar walls and the elastic fibers of connective tissue that link the acinus to the terminal airways. In addition to causing airspace enlargement, this allows the terminal bronchioles to recoil and obstruct. In Panel B, inflammation in the terminal bronchioles causes wall thickening, obstruction, and ultimate severing or stretching of the elastic connective- tissue fibers. In addition to allowing the bronchioles to recoil and obstruct, this loss of support for the distal acinus leads to folding and ultimate destruction of unsupported alveolar walls and enlargement of the duct. Although the respiratory bronchioles are omitted for clarity, they must also be involved in the loss of axial tethering in both models.
- En IBERPOC 78% no dx En episcan a pesar de no dx ya tenian deterioro de calidad de vida incluso en fases leves Prevalencia total de epoc: 10,2%; 10,2% de la población española entre 40 y 80 años presenta EPOC Prevalencia: Varones 15.1%, mujeres 5,7% Varones 35,9%, mujeres 10,8% 70 y 79 años Tabaquismo: (> de 30 paq/año) Ex fumadores: 18% Hombres 6% Mujeres Fumadores: 39.9% Hombres 15,4% mujeres. EPISCAN
- Survival in COPD This slide presents the Kaplan-Meier survival curves from the study by Celli and colleagues (2004) for the 3 stages of COPD based on FEV 1 according to the staging system of the American Thoracic Society (on the left) and the 4 quartiles of the BODE index (on the right). As the curves on the left illustrate, survival differed significantly among patients with stage I, stage II, and stage III COPD based on FEV 1 ( P < 0.001 by log-rank test). Survival also differed significantly among patients grouped by BODE index quartiles ( P < 0.001 by log-rank test). Each quartile increase in the BODE score was associated with increased mortality ( P < 0.001). At 52 months, the highest quartile (ie, a BODE score of 7 to 10) was associated with a mortality rate of 80%. Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med . 2004;350:1005-1012.
- Speaker Notes COPD is a progressive disease in which patients experience pulmonary inflammation, mucus hypersecretion, airway obstruction, and exacerbations. This cycle continues ultimately leading to disability and death. Reference From the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease , Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2008. Available from: http://www.goldcopd.org.
- Speaker notes Eighty patients with clinically stable COPD were studied in order to assess the association between body composition and the inflammatory response. Body composition was determined anthropometrically, and skeletal muscle mass was determined as the creatinine-height index (CHI). Additional assessments included nitrogen balance, and circulating concentrations of IL-6, TNF- , and their soluble receptors (SR). Body mass index was normal (>20 kg/m2) in 55 patients, of whom 17 (31%) had a low CHI (<80% predicted). A reduced CHI was associated with significantly increased circulating levels of IL-6 (P=0.001), TNF- ( P =0.032) and their respective SRs (P=0.002 for IL-6 SR, P =0.03 for TNF- SR1, and P =0.001 TNF- SR2). Serum levels of CRP were also increased with low CHI but not significantly. Patients with a normal BMI and low CHI showed levels of inflammatory mediators similar to those in patients with a low BMI and CHI; both were significantly greater than in those with a normal BMI and CHI. Additional Information Skeletal muscle loss in COPD is probably multifactorial in origin, but these data suggest a link with systemic inflammation, even without weight loss. Reference Eid AA, Ionescu AA, Nixon LS, et al. Inflammatory response and body composition in chronic obstructive pulmonary disease. Am J Respir Crit Care Med . 2001;164:1414-1418.
- Speaker Notes Patients with COPD often lose weight during the course of their disease and this may be due to skeletal muscle apoptosis. Quadriceps femoris biopsies in 15 patients with COPD (8 with normal body mass index [BMI] and 7 with low [<20 kg/m 2 ] BMI), 8 healthy volunteers, and 6 sedentary subjects undergoing orthopaedic surgery (both groups with normal BMI) indicated that skeletal muscle apoptosis (as demonstrated by TUNEL staining) was increased in patients with COPD and low BMI as compared with the other three groups ( P =0.005). Reference Agusti AG, Sauleda J, Miralles C, et al. Skeletal muscle apoptosis and weight loss in chronic obstructive pulmonary disease. Am J Respir Crit Care Med . 2002;166:485-489.
- Cumulative mortality from age 50 (Cox regression) according to leisure time physical activity level and total mortality. At end of follow-up, estimated proportions of deaths were 81.4 (95% confidence interval 80.8 to 82.0) for low physical activity, 72.0 (71.5 to 72.5) for medium, and 61.8 (61.4 to 62.2) for high
- CANDIDATOS: Stable symptomatic COPD Reduced activity levels and increased dyspnea despite optimal pharmacological treatment No evidence of active cardiac ischemia, musculo-skeletal, psychiatric or other systemic disease Sufficient motivation Transportation / access
- Años de vida ganados ajustados por la calidad
- Speaker Notes Although pulmonary rehabilitation can produce striking improvements in exercise capacity, general health status, COPD symptoms, and hospital admissions, there are a few limitations as well. Effects of rehabilitation tend to wane over the subsequent 18 months. Patients may drop out of the rehabilitation program, most commonly for exacerbations or lack of motivation. Reference Calverley PM, Walker P. Chronic obstructive pulmonary disease. Lancet . 2003;362:1053-1061.