<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.1 20151215//EN" "https://jats.nlm.nih.gov/publishing/1.1/JATS-journalpublishing1.dtd">
<article xmlns:xlink="http://www.w3.org/1999/xlink" specific-use="sps-1.9" dtd-version="1.1" xml:lang="pt" article-type="research-article">
  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
        <publisher-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">N8DNgvpb8QHJkfGvXNWJ8mr</article-id>
      <article-id pub-id-type="other">00005</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2007000600005</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(07)08800605</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2007000600005</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Modifica&#231;&#227;o do padr&#227;o respirat&#243;rio melhora o controle cardiovascular na hipertens&#227;o essencial</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Pinheiro</surname>
            <given-names>Carlos Hermano da Justa</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Medeiros</surname>
            <given-names>Renato Ant&#244;nio Ribeiro</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Pinheiro</surname>
            <given-names>Denise Gon&#231;alves Moura</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Marinho</surname>
            <given-names>Maria de Jesus Ferreira</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Fortaleza</named-content>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Universidade de Fortaleza</institution>
        <institution content-type="orgdiv1">Escola de Sa&#250;de P&#250;blica do Estado do Cear&#225; </institution>
        <institution content-type="orgdiv2">Laborat&#243;rio de Cardiopneumologia e Fisiologia do Exerc&#237;cio</institution>
        <country country="BR">Brazil</country>
      </aff>
      <aff id="aff02">
        <addr-line>
          <named-content content-type="city">London</named-content>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Imperial College London</institution>
        <institution content-type="orgdiv1">Imperial College of Science Technology and Medicine </institution>
        <country country="GB">United Kingdom</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>06</month>
        <year>2007</year>
      </pub-date>
      <volume>88</volume>
      <issue>6</issue>
      <fpage>651</fpage>
      <lpage>659</lpage>
      <history>
        <date date-type="rev-recd">
          <day>08</day>
          <month>11</month>
          <year>2006</year>
        </date>
        <date date-type="received">
          <day>03</day>
          <month>09</month>
          <year>2006</year>
        </date>
        <date date-type="accepted">
          <day>14</day>
          <month>12</month>
          <year>2006</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>FUNDAMENTO: Estudos recentes apontam os benef&#237;cios do controle da respira&#231;&#227;o na melhoria do barorreflexo, variabilidade da freq&#252;&#234;ncia card&#237;aca e redu&#231;&#227;o da press&#227;o arterial em pacientes hipertensos. OBJETIVO: Avaliar os efeitos do treinamento com t&#233;cnica de respira&#231;&#227;o lenta na modula&#231;&#227;o dos sistemas cardiovascular e respirat&#243;rio de pacientes (n=10, homens e mulheres, com 45 a 60 anos de idade) com hipertens&#227;o arterial essencial, assistidos em ambulat&#243;rio. M&#201;TODOS: No delineamento do estudo, cada paciente foi utilizado como controle de si mesmo, sendo a coleta de dados realizada antes e ap&#243;s o per&#237;odo de interven&#231;&#227;o. Foram avaliados par&#226;metros como variabilidade da freq&#252;&#234;ncia card&#237;aca, press&#227;o arterial sist&#243;lica, press&#227;o arterial diast&#243;lica, press&#227;o arterial m&#233;dia, ventilometria, cirtometria tor&#225;cica e an&#225;lise estat&#237;stica dos dados. O treinamento respirat&#243;rio utilizou exerc&#237;cios de baixa freq&#252;&#234;ncia e foi realizado duas vezes por semana durante um m&#234;s. Cada sess&#227;o teve dura&#231;&#227;o de 30 minutos. RESULTADOS: Os resultados demonstraram redu&#231;&#227;o da press&#227;o arterial sist&#243;lica, da press&#227;o arterial diast&#243;lica e da press&#227;o arterial m&#233;dia (p &lt; 0,05 vs controle), aumento da variabilidade da freq&#252;&#234;ncia card&#237;aca evidenciado pelo aumento da vari&#226;ncia dos intervalos RR e &#237;ndice SDNN, redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria (p &lt; 0,01 vs controle), aumento do volume corrente (p &lt; 0,01 vs controle), e aumento da expansibilidade tor&#225;cica apical (p &lt; 0,01 vs controle). CONCLUS&#195;O: A reeduca&#231;&#227;o respirat&#243;ria com a t&#233;cnica de respira&#231;&#227;o lenta parece ser um bom recurso complementar para o controle tanto cardiovascular como respirat&#243;rio em pacientes hipertensos.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Respira&#231;&#227;o</kwd>
        <kwd>press&#227;o arterial</kwd>
        <kwd>hipertens&#227;o</kwd>
        <kwd>exerc&#237;cios respirat&#243;rios</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>23</day>
        <month>07</month>
        <year>2007</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>ARTIGO ORIGINAL </bold>
    </p>
    <p>Modifica&#231;&#227;o do padr&#227;o respirat&#243;rio melhora o controle cardiovascular na hipertens&#227;o essencial </p>
    <p>
      <bold>Carlos Hermano da Justa Pinheiro; Renato Ant&#244;nio Ribeiro Medeiros; Denise Gon&#231;alves Moura Pinheiro; Maria de Jesus Ferreira Marinho </bold>
    </p>
    <p>Laborat&#243;rio de Cardiopneumologia e Fisiologia do Exerc&#237;cio da Universidade de Fortaleza, Escola de Sa&#250;de P&#250;blica do Estado do Cear&#225; - Fortaleza, CE - Brasil </p>
    <p> Imperial College of Science Technology and Medicine - IC &#150; London - England</p>
    <p>
      <xref ref-type="corresp" rid="corr1">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> Estudos recentes apontam os benef&#237;cios do controle da respira&#231;&#227;o na melhoria do barorreflexo, variabilidade da freq&#252;&#234;ncia card&#237;aca e redu&#231;&#227;o da press&#227;o arterial em pacientes hipertensos. </p>
    <p><bold>OBJETIVO:</bold> Avaliar os efeitos do treinamento com t&#233;cnica de respira&#231;&#227;o lenta na modula&#231;&#227;o dos sistemas cardiovascular e respirat&#243;rio de pacientes (n=10, homens e mulheres, com 45 a 60 anos de idade) com hipertens&#227;o arterial essencial, assistidos em ambulat&#243;rio. </p>
    <p><bold>M&#201;TODOS:</bold> No delineamento do estudo, cada paciente foi utilizado como controle de si mesmo, sendo a coleta de dados realizada antes e ap&#243;s o per&#237;odo de interven&#231;&#227;o. Foram avaliados par&#226;metros como variabilidade da freq&#252;&#234;ncia card&#237;aca, press&#227;o arterial sist&#243;lica, press&#227;o arterial diast&#243;lica, press&#227;o arterial m&#233;dia, ventilometria, cirtometria tor&#225;cica e an&#225;lise estat&#237;stica dos dados. O treinamento respirat&#243;rio utilizou exerc&#237;cios de baixa freq&#252;&#234;ncia e foi realizado duas vezes por semana durante um m&#234;s. Cada sess&#227;o teve dura&#231;&#227;o de 30 minutos. </p>
    <p><bold>RESULTADOS:</bold> Os resultados demonstraram redu&#231;&#227;o da press&#227;o arterial sist&#243;lica, da press&#227;o arterial diast&#243;lica e da press&#227;o arterial m&#233;dia (p &lt; 0,05 <italic>vs </italic>controle), aumento da variabilidade da freq&#252;&#234;ncia card&#237;aca evidenciado pelo aumento da vari&#226;ncia dos intervalos RR e &#237;ndice SDNN, redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria (p &lt; 0,01 <italic>vs </italic>controle), aumento do volume corrente (p &lt; 0,01 <italic>vs</italic> controle), e aumento da expansibilidade tor&#225;cica apical (p &lt; 0,01 <italic>vs</italic> controle). </p>
    <p><bold>CONCLUS&#195;O: </bold> A reeduca&#231;&#227;o respirat&#243;ria com a t&#233;cnica de respira&#231;&#227;o lenta parece ser um bom recurso complementar para o controle tanto cardiovascular como respirat&#243;rio em pacientes hipertensos. </p>
    <p><bold>Palavras-chave:</bold> Respira&#231;&#227;o, press&#227;o arterial, hipertens&#227;o, exerc&#237;cios respirat&#243;rios. </p>
    <p>
      <bold>Introdu&#231;&#227;o </bold>
    </p>
    <p>A hipertens&#227;o arterial sist&#234;mica &#233; um dos principais fatores de risco para doen&#231;a cardiovascular e constitui problema de sa&#250;de p&#250;blica no Brasil, onde sua preval&#234;ncia &#233; de cerca de 22% na popula&#231;&#227;o sem vi&#233;s de sexo<sup>1</sup>. No mundo, e de acordo com o <italic>Seven Countries Study</italic><sup>2 </sup><italic>, </italic>cada incremento de 10 mmHg resulta na duplica&#231;&#227;o do risco de &#243;bito em pacientes hipertensos. Por ser um fator de risco independente para as duas principais causas de &#243;bito no Brasil, o infarto do mioc&#225;rdio e o acidente vascular cerebral<sup>3</sup>, sua preven&#231;&#227;o prim&#225;ria por meio de interven&#231;&#245;es farmacol&#243;gicas e n&#227;o-farmacol&#243;gicas reduz a morbidade e a mortalidade resultantes da doen&#231;a<sup>4,5</sup>. Dentre as terapias n&#227;o-farmacol&#243;gicas, as modifica&#231;&#245;es do estilo de vida, como redu&#231;&#227;o do peso corporal, restri&#231;&#227;o de sal na dieta, restri&#231;&#227;o do consumo de &#225;lcool e exerc&#237;cio f&#237;sico de intensidade moderada, s&#227;o indicadas como recurso no controle cl&#237;nico da doen&#231;a<sup>6</sup>. Nesse contexto, surgem evid&#234;ncias recentes de que a redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria pelo uso de dispositivos eletr&#244;nicos que interagem com o paciente, orientando-o a respirar de maneira mais lenta, diminui a press&#227;o arterial em pacientes com hipertens&#227;o arterial de graus leve e moderado e naqueles com hipertens&#227;o resistente e sem mudan&#231;as no uso da medica&#231;&#227;o<sup>7,8</sup>. </p>
    <p>Em trabalho recente, o incentivo a um padr&#227;o respirat&#243;rio lento pelo aumento da expansibilidade tor&#225;cica mostrou-se eficaz em reduzir a press&#227;o arterial e a freq&#252;&#234;ncia card&#237;aca em um caso de hipertens&#227;o arterial no p&#243;s-operat&#243;rio de revasculariza&#231;&#227;o do mioc&#225;rdio<sup>9</sup>. Evid&#234;ncias cient&#237;ficas apontam que a pr&#225;tica de um padr&#227;o respirat&#243;rio lento melhora a sensibilidade do barorreflexo em sujeitos saud&#225;veis<sup>10 </sup>e em hipertensos<sup>11</sup>. Assim, a modula&#231;&#227;o da respira&#231;&#227;o teria valor terap&#234;utico no controle da hipertens&#227;o arterial. De acordo com Scheinecols.<sup>7</sup>, essa melhora est&#225; associada &#224; modifica&#231;&#227;o do padr&#227;o respirat&#243;rio do paciente, que passaria a respirar com menor freq&#252;&#234;ncia e com maior amplitude. No entanto, os poucos trabalhos descritos na literatura internacional relatam somente altera&#231;&#245;es agudas ou de uma &#250;nica sess&#227;o no sistema respirat&#243;rio, com repercuss&#245;es no sistema cardiovascular. Diante desse problema, este estudo se prop&#244;s a testar os efeitos do treinamento com a t&#233;cnica de respira&#231;&#227;o lenta na reeduca&#231;&#227;o respirat&#243;ria e na modula&#231;&#227;o do controle tanto cardiovascular como respirat&#243;rio de pacientes com hipertens&#227;o arterial essencial. </p>
    <p>
      <bold>M&#233;todos </bold>
    </p>
    <p>A pesquisa foi realizada no Laborat&#243;rio de Cardiopneumologia e Fisiologia do Exerc&#237;cio da Universidade de Fortaleza, ap&#243;s aprova&#231;&#227;o pelo Comit&#234; de &#201;tica em Pesquisa da institui&#231;&#227;o. Todos os sujeitos do estudo deram seu consentimento livre e esclarecido para a participa&#231;&#227;o, tendo sido respeitados todos os princ&#237;pios da Declara&#231;&#227;o de Helsinki de 1974<sup>12</sup>, revisada em 1983<sup>13</sup>. </p>
    <p>Foram estudados 10 pacientes (5 homens e 5 mulheres, com idade entre 45 e 60 anos) com diagn&#243;stico m&#233;dico de hipertens&#227;o arterial essencial submetidos a tratamentos cl&#237;nico e farmacol&#243;gico (<xref ref-type="fig" rid="a05fig01">fig. 1</xref>) e atendidos no N&#250;cleo de Assist&#234;ncia M&#233;dica Integrada (NAMI) da Universidade de Fortaleza. Nenhum paciente da amostra era obeso (&#237;ndice de massa corporal m&#233;dio de 26 &#177; 1,4) ou possu&#237;a outras co-morbidades associadas &#224; hipertens&#227;o, com exce&#231;&#227;o de dislipidemia (<xref ref-type="table" rid="tab1">tab. 1</xref>). O crit&#233;rio de inclus&#227;o na pesquisa compreendia ter diagn&#243;stico m&#233;dico de hipertens&#227;o arterial essencial e estar sob tratamento cl&#237;nico. Os pacientes do estudo foram selecionados a partir de suas fichas de acompanhamento cl&#237;nico; ap&#243;s a sele&#231;&#227;o, cujos crit&#233;rios de inclus&#227;o e exclus&#227;o ser&#227;o descritos adiante, foram realizadas entrevistas para coleta de dados referentes ao tipo de tratamento (cl&#237;nico e farmacol&#243;gico) e ao perfil epidemiol&#243;gico dos sujeitos. Foram utilizadas, como crit&#233;rio de exclus&#227;o: causas secund&#225;rias de hipertens&#227;o arterial; insufici&#234;ncia renal, card&#237;aca ou hep&#225;tica; e pacientes que tiveram evento cardiovascular recente. Tamb&#233;m foram exclu&#237;dos casos de doen&#231;a pulmonar, usu&#225;rios de bebidas alco&#243;licas, tabagistas, usu&#225;rias de contraceptivos orais, portadores de afec&#231;&#245;es como diabetes melito, neuropatias, doen&#231;as auto-imunes, doen&#231;a de Chagas, arritmias card&#237;acas e outras doen&#231;as que afetam o controle neuroauton&#244;mico, assim como usu&#225;rios de antidepressivos, neurol&#233;pticos, antiarr&#237;tmicos e l&#237;tio. </p>
    <p content-type="asset">
      <fig id="a05fig01">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf01.jpg"/></fig>
    </p>
    <table-wrap id="tab1">
      <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gt01.jpg"/></table-wrap>
    <p><italic>Delineamento da pesquisa</italic> - No in&#237;cio do estudo, foi realizada coleta de dados a fim de mensurar os valores da press&#227;o arterial sist&#243;lica, da press&#227;o arterial diast&#243;lica e da variabilidade da freq&#252;&#234;ncia card&#237;aca. As vari&#225;veis respirat&#243;rias monitoradas foram: volume corrente, freq&#252;&#234;ncia respirat&#243;ria, volume-minuto, e expansibilidade tor&#225;cica tanto apical como basal. No final do estudo, ap&#243;s um m&#234;s de treinamento com t&#233;cnica de respira&#231;&#227;o lenta, todas essas mensura&#231;&#245;es foram novamente realizadas para coleta final de dados e an&#225;lise estat&#237;stica. </p>
    <p><italic>Mensura&#231;&#227;o da press&#227;o arterial e an&#225;lise do equil&#237;brio auton&#244;mico card&#237;aco </italic>- A press&#227;o arterial foi aferida, ambulatorialmente, em tr&#234;s momentos distintos, calculando-se a m&#233;dia entre as aferi&#231;&#245;es. Foi utilizado, para a aferi&#231;&#227;o, esfigmoman&#244;metro do tipo aner&#243;ide devidamente calibrado e de acordo com as instru&#231;&#245;es contidas nas IV Diretrizes para Hipertens&#227;o Arterial da Sociedade Brasileira de Cardiologia<sup>14 </sup>e no <italic>Joint National Committee</italic><sup>15</sup>. </p>
    <p>Para a an&#225;lise do equil&#237;brio auton&#244;mico ou equil&#237;brio simp&#225;tico/parassimp&#225;tico card&#237;aco, foi utilizado o m&#233;todo de estudo da variabilidade da freq&#252;&#234;ncia card&#237;aca, calculada por meio da m&#233;dia dos intervalos RR, da vari&#226;ncia dos intervalos RR e do m&#233;todo no dom&#237;nio do tempo (&#237;ndices SDNN e PNN50) em todas as 12 deriva&#231;&#245;es eletrocardiogr&#225;ficas. Para a tabula&#231;&#227;o dos dados foi utilizado o <italic>software </italic>Microsoft Excel vers&#227;o 2003, e para a avalia&#231;&#227;o estat&#237;stica foi utilizado SPSS vers&#227;o 10. </p>
    <p><italic>An&#225;lise da mec&#226;nica respirat&#243;ria</italic> - O volume-minuto e a freq&#252;&#234;ncia respirat&#243;ria foram mensurados por ventil&#244;metro da marca Wright e o volume corrente foi calculado por meio da raz&#227;o volume-minuto/freq&#252;&#234;ncia respirat&#243;ria. </p>
    <p>A expansibilidade tor&#225;cica foi analisada por meio de cirtometria tor&#225;cica tanto apical (medidas tomadas nas axilas) como basal (medidas tomadas no final do ap&#234;ndice xif&#243;ide). </p>
    <p><italic>Protocolo de reeduca&#231;&#227;o respirat&#243;ria </italic>- Foi aplicado protocolo de treinamento de controle respirat&#243;rio, utilizando-se, inicialmente, a pr&#225;tica dos padr&#245;es respirat&#243;rios diafragm&#225;tico, intercostal e apical, com o objetivo de conscientizar o paciente sobre seus movimentos respirat&#243;rios. Durante a execu&#231;&#227;o dessas t&#233;cnicas, os pacientes foram orientados a deitar em dec&#250;bito dorsal, com os joelhos flexionados e os p&#233;s apoiados no solo, enquanto levavam as m&#227;os &#224;s &#225;reas do t&#243;rax relacionadas a cada tipo de respira&#231;&#227;o: diafragma, m&#250;sculos intercostais e regi&#227;o clavicular (<xref ref-type="fig" rid="a05fig02">fig. 2</xref>). Em cada padr&#227;o respirat&#243;rio, os pacientes foram orientados a sentir e a identificar o movimento da caixa tor&#225;cica e sua amplitude. Em seguida, foram orientados a reduzir, gradativamente, a freq&#252;&#234;ncia respirat&#243;ria, &#224; medida que tamb&#233;m aumentavam a amplitude respirat&#243;ria. Esse procedimento foi repetido 10 vezes para cada tipo de respira&#231;&#227;o. </p>
    <p content-type="asset">
      <fig id="a05fig02">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf02.jpg"/></fig>
    </p>
    <p>Depois da execu&#231;&#227;o das t&#233;cnicas descritas, os pacientes, em postura sentada, realizaram a t&#233;cnica de respira&#231;&#227;o lenta, cujo objetivo &#233; realizar respira&#231;&#227;o mais tranq&#252;ila por meio do aumento da amplitude respirat&#243;ria e da redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria durante a execu&#231;&#227;o simult&#226;nea dos tr&#234;s padr&#245;es respirat&#243;rios descritos. A t&#233;cnica foi realizada por 30 minutos di&#225;rios, duas vezes por semana, durante um m&#234;s. </p>
    <p><italic>An&#225;lise estat&#237;stica </italic>- Todos os dados foram submetidos a an&#225;lise estat&#237;stica descritiva e as m&#233;dias inicial e final foram submetidas ao teste <italic>t </italic>de <italic>Student </italic>e &#224; an&#225;lise do p-valor. As vari&#225;veis ventilom&#233;tricas e os n&#237;veis de press&#227;o arterial foram submetidos ao teste de correla&#231;&#227;o de Pearson e &#224; an&#225;lise de regress&#227;o linear (<italic>R-square</italic>). Foram consideradas significantes as an&#225;lise com p &lt; 0,05. </p>
    <p>
      <bold>Resultados </bold>
    </p>
    <p>N&#227;o houve mudan&#231;as na medica&#231;&#227;o utilizada e no estilo de vida relatado pelos pacientes no in&#237;cio do estudo (dados n&#227;o demonstrados). Os resultados est&#227;o apresentados a seguir. </p>
    <p><italic>Reeduca&#231;&#227;o respirat&#243;ria e press&#227;o arterial</italic> - Na amostra de pacientes com hipertens&#227;o deste estudo foi observada redu&#231;&#227;o da press&#227;o arterial (<xref ref-type="fig" rid="gr1">gr&#225;fico 1</xref>). Houve redu&#231;&#227;o das press&#245;es sist&#243;lica, m&#233;dia e diast&#243;lica: de 135 &#177; 14,32 mmHg para 123 &#177; 14,29 mmHg (p &lt; 0,05), de 99 &#177; 7,8 mmHg para 91 &#177; 7,5 mmHg (p &lt; 0,05), e de 81 &#177; 8,75 mmHg para 74 &#177; 6,1 mmHg (p &lt; 0,05), respectivamente. </p>
    <fig id="gr1">
      <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf03.jpg"/></fig>
    <p><italic>Reeduca&#231;&#227;o respirat&#243;ria e modula&#231;&#227;o auton&#244;mica cardiovascular</italic> - Houve melhora da variabilidade da freq&#252;&#234;ncia card&#237;aca (<xref ref-type="fig" rid="a05gr02">gr&#225;fico 2</xref>). No entanto, n&#227;o foi observada altera&#231;&#227;o significativa da freq&#252;&#234;ncia card&#237;aca em repouso (74 &#177; 8 bpm para 72 &#177; 9,1 bpm, p &gt; 0,05) e da m&#233;dia dos intervalos RR (1.002 &#177; 3,4 ms para 1.004 &#177; 3,2 ms, p &gt; 0,05). A melhora da variabilidade da freq&#252;&#234;ncia card&#237;aca foi constatada pelo aumento da vari&#226;ncia dos intervalos RR e &#237;ndice estat&#237;stico SDNN, enquanto o &#237;ndice PNN50 permaneceu inalterado. </p>
    <p content-type="asset">
      <fig id="a05gr02">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf04.jpg"/></fig>
    </p>
    <p><italic>Reeduca&#231;&#227;o respirat&#243;ria e mec&#226;nica respirat&#243;ria </italic>- Foram observadas altera&#231;&#245;es do padr&#227;o respirat&#243;rio ap&#243;s o per&#237;odo de treinamento (<xref ref-type="fig" rid="a05gr03">gr&#225;fico 3</xref>). Os pacientes hipertensos demonstraram redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria de repouso (de 14,60 &#177; 1,6 incurs&#245;es respirat&#243;rias por minuto [irpm] para 10,10 &#177; 1,1 irpm, p &lt; 0,01). N&#227;o foram observadas altera&#231;&#245;es significativas do volume-minuto, o que foi atribu&#237;do ao aumento compensat&#243;rio do volume corrente (de 419,75 &#177; 60,93 ml para 560,30 &#177; 60,76 ml, p &lt; 0,01). O aumento do volume corrente foi atribu&#237;do ao aumento da expansibilidade tor&#225;cica apical (de 1,9 &#177; 0,56 cm para 2,33 &#177; 0,49 cm, p &lt; 0,01), enquanto a expansibilidade basal permaneceu inalterada (<xref ref-type="fig" rid="a05gr03">gr&#225;fico 3</xref>). Tamb&#233;m foi constatada correla&#231;&#227;o negativa moderada (coeficiente de Pearson, -0,5; p &lt; 0,05) entre o volume corrente e os n&#237;veis de press&#227;o arterial sist&#243;lica e de press&#227;o arterial m&#233;dia na amostra estudada (n&#227;o demonstrada), representada pela an&#225;lise de regress&#227;o linear (<xref ref-type="fig" rid="a05gr04">gr&#225;fico 4</xref>). </p>
    <p content-type="asset">
      <fig id="a05gr03">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf05.jpg"/></fig>
    </p>
    <p content-type="asset">
      <fig id="a05gr04">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf06.jpg"/></fig>
    </p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>O presente estudo teve como objetivo avaliar a efici&#234;ncia de um programa de treinamento com a t&#233;cnica de respira&#231;&#227;o lenta no controle cardiovascular e da press&#227;o arterial em uma amostra de pacientes com hipertens&#227;o arterial essencial. Foi demonstrado que a reeduca&#231;&#227;o do padr&#227;o respirat&#243;rio pode melhorar o controle cardiorrespirat&#243;rio e reduzir a press&#227;o arterial em hipertensos. Os dados deste estudo est&#227;o em concord&#226;ncia com os dos estudos de Joseph e cols.<sup>11</sup>, Kaushik e cols.<sup>16</sup>, Bernardi e cols.<sup>17 </sup>e Goso e cols.<sup>18</sup>. Esses estudos avaliaram os efeitos de uma &#250;nica sess&#227;o de exerc&#237;cio com a t&#233;cnica de respira&#231;&#227;o lenta em sujeitos saud&#225;veis, hipertensos e com insufici&#234;ncia card&#237;aca e demonstraram os benef&#237;cios que a modula&#231;&#227;o volunt&#225;ria da respira&#231;&#227;o pode promover no controle cardiovascular e na redu&#231;&#227;o da press&#227;o arterial. </p>
    <p>Os autores deste estudo decidiram avaliar o impacto de um programa de reeduca&#231;&#227;o respirat&#243;ria com a t&#233;cnica de respira&#231;&#227;o lenta ao longo de um m&#234;s em pacientes com hipertens&#227;o arterial. Os autores acreditavam que a pr&#225;tica regular desses exerc&#237;cios respirat&#243;rios poderia exercer algum efeito psicofisiol&#243;gico com o objetivo de modificar o padr&#227;o respirat&#243;rio em repouso. Embora com amostra de poucos pacientes, por causa da grande quantidade de crit&#233;rios de exclus&#227;o adotados no estudo, a estat&#237;stica dos dados foi determinante. Em futuros estudos, &#233; preciso que sejam avaliados mais pacientes, se poss&#237;vel com amostra probabil&#237;stica para an&#225;lise da efici&#234;ncia e do impacto desse tipo de interven&#231;&#227;o na popula&#231;&#227;o. </p>
    <p>O controle da press&#227;o arterial &#233; considerado a melhor estrat&#233;gia para diminuir o impacto das doen&#231;as cardiovasculares em pacientes com hipertens&#227;o arterial, o que pode ser feito por meio de campanhas de preven&#231;&#227;o, tratamento dos fatores de risco, diagn&#243;stico precoce e tratamento efetivo da doen&#231;a<sup>19</sup>. Algumas evid&#234;ncias cient&#237;ficas sugerem que altera&#231;&#245;es do controle respirat&#243;rio tamb&#233;m podem ser consideradas fator de risco associado ao estilo de vida em pacientes com hipertens&#227;o arterial<sup>20</sup>. </p>
    <p><italic>Dist&#250;rbios respirat&#243;rios como fator de risco para hipertens&#227;o arterial </italic>- A rela&#231;&#227;o entre anormalidades respirat&#243;rias e hipertens&#227;o arterial ganhou destaque na comunidade cient&#237;fica pelos relatos de aumento da preval&#234;ncia de doen&#231;as cardiovasculares em indiv&#237;duos com dist&#250;rbios respirat&#243;rios do sono<sup>21</sup>. O mecanismo pelo qual os dist&#250;rbios respirat&#243;rios do sono exercem influ&#234;ncia sobre a press&#227;o arterial e a hipertens&#227;o ainda n&#227;o est&#225; claro<sup>22</sup>. No entanto, Ehlenz e cols.<sup>23 </sup>demonstraram altera&#231;&#245;es da regula&#231;&#227;o da press&#227;o arterial em pacientes hipertensos quando comparados a indiv&#237;duos saud&#225;veis. Estudos experimentais com animais tamb&#233;m demonstraram que a apn&#233;ia obstrutiva do sono, um dos principais dist&#250;rbios respirat&#243;rios relacionados ao sono, possui forte associa&#231;&#227;o com mudan&#231;as da press&#227;o arterial tanto sist&#234;mica como pulmonar<sup>24</sup>. Segundo Brooks e cols.<sup>25</sup>, essas mudan&#231;as do controle da press&#227;o arterial ocorreriam durante o sono e durante o per&#237;odo diurno, indicando, desse modo, papel causal dos dist&#250;rbios respirat&#243;rios do sono no desenvolvimento e na manuten&#231;&#227;o da hipertens&#227;o arterial. Al&#233;m disso, estudos epidemiol&#243;gicos demonstram grande preval&#234;ncia de dist&#250;rbios respirat&#243;rios do sono em pacientes hipertensos<sup>26,27 </sup>e que cerca de 50% a 80% dos pacientes com essas altera&#231;&#245;es s&#227;o hipertensos<sup>20</sup>. Nesse contexto, a rela&#231;&#227;o causal dos dist&#250;rbios respirat&#243;rios poderia se tornar confusa ou se perder ao se considerar a idade, a preval&#234;ncia de obesidade, o tabagismo e o etilismo em pacientes hipertensos. No entanto, Grote e cols.<sup>20</sup>, em estudo cl&#237;nico transversal e controlado com 1.190 pacientes, demonstraram que os dist&#250;rbios respirat&#243;rios do sono s&#227;o fatores de risco para hipertens&#227;o arterial e s&#227;o independentes de &#237;ndice de massa corporal, idade, tabagismo, etilismo, n&#237;veis de colesterol e press&#245;es parciais de oxig&#234;nio e di&#243;xido de carbono. Assim, os dados cient&#237;ficos demonstram a exist&#234;ncia de rela&#231;&#227;o de causa e manuten&#231;&#227;o da hipertens&#227;o arterial por altera&#231;&#245;es do controle respirat&#243;rio. </p>
    <p><italic>Modula&#231;&#227;o volunt&#225;ria da respira&#231;&#227;o e redu&#231;&#227;o da press&#227;o arterial</italic> - Em pacientes com hipertens&#227;o arterial essencial, essas mudan&#231;as da press&#227;o arterial correlacionam-se com a mudan&#231;a do padr&#227;o respirat&#243;rio, conforme evidenciado neste estudo por meio da correla&#231;&#227;o estat&#237;stica e da regress&#227;o linear. De acordo com Joseph e cols.<sup>11</sup>, a redu&#231;&#227;o da press&#227;o arterial durante a execu&#231;&#227;o de padr&#227;o respirat&#243;rio lento, mais precisamente abaixo de 10 irpm, estaria associada a melhora da sensibilidade do barorreflexo, o que indica altera&#231;&#227;o do equil&#237;brio auton&#244;mico resultante de redu&#231;&#227;o absoluta ou relativa da atividade simp&#225;tica ou aumento do t&#244;nus parassimp&#225;tico. Uma das dificuldades enfrentadas neste estudo refere-se &#224; n&#227;o mensura&#231;&#227;o do barorreflexo, pois esse m&#233;todo demanda custos elevados e laborat&#243;rio equipado para tal. No entanto, a an&#225;lise da variabilidade da freq&#252;&#234;ncia card&#237;aca &#233; um m&#233;todo com significante valor cl&#237;nico e bem caracterizado na literatura, tendo a vantagem de possibilitar avalia&#231;&#227;o n&#227;o-invasiva e seletiva da fun&#231;&#227;o auton&#244;mica<sup>28 </sup>. Na amostra de pacientes deste estudo, observou-se que, paralelamente &#224; redu&#231;&#227;o da press&#227;o arterial, tamb&#233;m houve melhora da variabilidade da freq&#252;&#234;ncia card&#237;aca. Isso sugere que a melhora decorre do efeito da modula&#231;&#227;o respirat&#243;ria no sistema nervoso aut&#244;nomo. Bernardi e cols.<sup>17 </sup>estudaram o efeito de uma sess&#227;o com t&#233;cnica de respira&#231;&#227;o lenta em sujeitos saud&#225;veis e pacientes com hipertens&#227;o, em que se observou melhora da sensibilidade do barorreflexo com conseq&#252;ente redu&#231;&#227;o da press&#227;o arterial e da freq&#252;&#234;ncia card&#237;aca. Neste estudo, n&#227;o houve modifica&#231;&#227;o da freq&#252;&#234;ncia card&#237;aca, o que se op&#245;e aos efeitos cronotr&#243;picos agudos citados na literatura<sup>17 </sup>e observados previamente pelos autores deste estudo em um paciente com infarto agudo do mioc&#225;rdio e hipertens&#227;o arterial<sup>9</sup>. Isso pode ter ocorrido pela falta de m&#233;todos mais apurados para detectar as altera&#231;&#245;es cronotr&#243;picas. Em estudos futuros, seria recomend&#225;vel a utiliza&#231;&#227;o de registro eletrocardiogr&#225;fico mais longo por Holter para melhor an&#225;lise dessas altera&#231;&#245;es da freq&#252;&#234;ncia card&#237;aca e de monitoriza&#231;&#227;o ambulatorial da press&#227;o arterial (MAPA) para se analisar a magnitude do efeito anti-hipertensivo proporcionado por essa t&#233;cnica respirat&#243;ria. </p>
    <p><italic>Desequil&#237;brio auton&#244;mico na hipertens&#227;o arterial e respira&#231;&#227;o </italic>- O sistema nervoso aut&#244;nomo desempenha papel fundamental no controle da press&#227;o arterial e da freq&#252;&#234;ncia card&#237;aca, sendo importante fator fisiopatol&#243;gico no desenvolvimento da hipertens&#227;o arterial<sup>29</sup>. A exist&#234;ncia de hiperatividade simp&#225;tica tem sido freq&#252;entemente associada &#224; hipertens&#227;o arterial, em que a sensibilidade do controle baroceptor est&#225; prejudicada, comprometendo a fun&#231;&#227;o auton&#244;mica<sup>30</sup>. Esse estado de hiperexcita&#231;&#227;o com aumento das descargas simp&#225;ticas &#233; bem caracterizado na literatura, que tamb&#233;m demonstra os benef&#237;cios de sess&#245;es de relaxamento mental associado ou n&#227;o a exerc&#237;cios respirat&#243;rios em pacientes com hipertens&#227;o arterial<sup>16</sup>. Na hipertens&#227;o arterial essencial, a hiperatividade simp&#225;tica n&#227;o se restringe apenas &#224; vasoconstri&#231;&#227;o arteriolar, mas o estado excitat&#243;rio &#233; distribu&#237;do de maneira generalizada por outros &#243;rg&#227;os e sistemas, al&#233;m de ativar o quimiorreflexo, importante mecanismo de regula&#231;&#227;o da respira&#231;&#227;o<sup>31</sup>. Pacientes hipertensos geralmente apresentam sinais de hiperventila&#231;&#227;o em repouso, sugerindo que as anormalidades cardiovasculares e respirat&#243;rias podem estar relacionadas a padr&#227;o excitat&#243;rio comum do sistema nervoso aut&#244;nomo, o qual poderia ser modulado pela ado&#231;&#227;o de padr&#227;o respirat&#243;rio mais lento<sup>11</sup>. Nesse contexto, o padr&#227;o hiperexcitat&#243;rio generalizado poderia explicar os sinais de hiperventila&#231;&#227;o observados em pacientes com hipertens&#227;o arterial essencial<sup>11</sup>, e sendo a respira&#231;&#227;o pass&#237;vel de controle volunt&#225;rio a pr&#225;tica de determinado padr&#227;o respirat&#243;rio, em longo prazo, tamb&#233;m poderia induzir modifica&#231;&#245;es do controle cardiovascular. </p>
    <p>A variabilidade da freq&#252;&#234;ncia card&#237;aca est&#225; reduzida em pacientes hipertensos se comparados a indiv&#237;duos normotensos. No m&#233;todo de an&#225;lise no dom&#237;nio do tempo, os &#237;ndices PNN50 e SDNN est&#227;o reduzidos, refletindo diminui&#231;&#227;o do t&#244;nus vagal (parassimp&#225;tico) e aumento do t&#244;nus simp&#225;tico, respectivamente<sup>32</sup>. No presente estudo, observou-se melhora da variabilidade da freq&#252;&#234;ncia card&#237;aca pelo aumento da vari&#226;ncia dos intervalos RR e o &#237;ndice SDNN, enquanto o &#237;ndice PNN50 n&#227;o sofreu altera&#231;&#227;o significativa (p &gt; 0,05). Isso sugere que a reeduca&#231;&#227;o respirat&#243;ria com a t&#233;cnica de respira&#231;&#227;o lenta melhorou a fun&#231;&#227;o auton&#244;mica n&#227;o por aumento do t&#244;nus parassimp&#225;tico, mas sim pela diminui&#231;&#227;o da atividade simp&#225;tica. Os dados deste estudo ratificamos dados dos estudos de Josephecols.<sup>11 </sup>e de Bernardi e cols.<sup>17</sup>, que tamb&#233;m observaram melhora da variabilidade da freq&#252;&#234;ncia card&#237;aca. </p>
    <p>Segundo Kaushik e cols.<sup>16</sup>, o estado de hiperexcita&#231;&#227;o por aumento de descargas simp&#225;ticas pode ser modulado por sess&#245;es de relaxamento e exerc&#237;cios de respira&#231;&#227;o, de forma associada ou isolada. Entretanto, segundo esses autores, os exerc&#237;cios respirat&#243;rios e o relaxamento modulariam o sistema nervoso aut&#244;nomo por diferentes mecanismos que ainda precisam ser mais bem caracterizados. No presente estudo, n&#227;o se pode descartar a hip&#243;tese de que os exerc&#237;cios respirat&#243;rios tenham proporcionado algum grau de relaxamento nos pacientes. Entretanto, pela exist&#234;ncia de correla&#231;&#227;o estat&#237;stica negativa e significante (p &lt; 0,05) entre o volume corrente e a press&#227;o arterial, acredita-se que a modula&#231;&#227;o da mec&#226;nica respirat&#243;ria tenha papel-chave nesse efeito anti-hipertensivo. </p>
    <p><italic>Integra&#231;&#227;o do controle cardiovascular e benef&#237;cios da reeduca&#231;&#227;o respirat&#243;ria</italic> - Os sistemas cardiovascular e respirat&#243;rio mant&#234;m estreita rela&#231;&#227;o em seus mecanismos de controle neural, cuja fisiologia n&#227;o &#233; objetivo da discuss&#227;o desteartigo. No entanto, vale salientar que, nesse mecanismo de controle tanto cardiovascular como respirat&#243;rio, o n&#250;cleo do tracto solit&#225;rio possui papel-chave, uma vez que recebe afer&#234;ncia de baroceptores localizados no cora&#231;&#227;o e nos vasos sangu&#237;neos, quimioceptores e receptores de estiramento no pulm&#227;o<sup>33</sup>. Dessa maneira, o barorreflexo, o quimiorreflexo e o reflexo de Hering-Breur parecem ter vias neuroanat&#244;micas comuns, o que pode embasar biologicamente os efeitos da modula&#231;&#227;o da respira&#231;&#227;o no controle cardiovascular e a redu&#231;&#227;o da press&#227;o arterial. </p>
    <p>Diante dessas evid&#234;ncias, os achados deste estudo poderiam ser explicados de v&#225;rias maneiras. Durante a execu&#231;&#227;o de um padr&#227;o respirat&#243;rio lento, o volume corrente aumenta para compensar a redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria e manter a ventila&#231;&#227;o-minuto<sup>34,35</sup>, o que pode ser respons&#225;vel pelas mudan&#231;as auton&#244;micas por meio da redu&#231;&#227;o da atividade simp&#225;tica ou da ativa&#231;&#227;o do reflexo de Hering-Breuer<sup>18</sup>. De acordo com Bernardi e cols.<sup>17</sup>, essa melhora do barorreflexo dependeria somente da redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria e n&#227;o do controle da respira&#231;&#227;o; desse modo, uma freq&#252;&#234;nciade 6 irpm melhora o barorreflexo, o mesmo n&#227;o ocorrendo com freq&#252;&#234;ncia similar &#224; taxa de respira&#231;&#227;o espont&#226;nea, como 15 irpm, de forma controlada. Para Joseph e cols.<sup>11</sup>, as mudan&#231;as de amplitude respirat&#243;ria, isto &#233;, de expansibilidade tor&#225;cica, podem aumentar as flutua&#231;&#245;es dos intervalos RR, melhorar a efici&#234;ncia do barorreflexo e reduzir a press&#227;o arterial. Por outro lado, o aumento do volume corrente e a ativa&#231;&#227;o do reflexo de Hering-Breuer, que reduz a sensibilidade do quimiorreflexo, poderiam real&#231;ar a efici&#234;ncia do barorreflexo e reduzir a press&#227;o arterial e a atividade simp&#225;tica<sup>36</sup>. </p>
    <p>Esses resultados tamb&#233;m poderiam ser explicados pela diminui&#231;&#227;o do quimiorreflexo, cujo aumento &#233; bem conhecido por elevar a atividade simp&#225;tica e a press&#227;o arterial<sup>37</sup>. Para Bernardi e cols.<sup>17</sup>, o treinamento com a t&#233;cnica de respira&#231;&#227;o lenta melhorou a satura&#231;&#227;o de oxig&#234;nio e a regula&#231;&#227;o do quimiorreflexo hipox&#234;mico, com melhora da capacidade de exerc&#237;cio em pacientes com doen&#231;a cardiovascular. Embora n&#227;o tenham sido mensuradas as trocas gasosas na amostra deste estudo, o aumento do volume corrente atribu&#237;do ao aumento da expansibilidade tor&#225;cica pode ter proporcionado melhor oxigena&#231;&#227;o nesses pacientes. Outros estudos devem atentar para esse par&#226;metro metab&#243;lico por meio de an&#225;lise do volume m&#225;ximo de oxig&#234;nio (VO<sub>2</sub>) e do volume de di&#243;xido de carbono (VCO<sub>2</sub>). No entanto, os dados deste estudo demonstraram que a redu&#231;&#227;o da freq&#252;&#234;ncia respirat&#243;ria n&#227;o induz hiperventila&#231;&#227;o nesses pacientes ap&#243;s a t&#233;cnica, uma vez que o volume-minuto n&#227;o sofre altera&#231;&#227;o e o volume corrente sofre aumento compensat&#243;rio. Esses dados tamb&#233;m foram confirmados no estudo realizado por Joseph e cols.<sup>11</sup>, em que a pr&#225;tica da t&#233;cnica de respira&#231;&#227;o lenta n&#227;o alterou o volume-minuto e a taxa de di&#243;xido de carbono exalado (CO<sub>2 </sub>et). Pelo fato de o CO<sub>2 </sub>manter-se dentro de valores de repouso, a t&#233;cnica de respira&#231;&#227;o lenta &#233; bem tolerada pelos pacientes. </p>
    <p>A manipula&#231;&#227;o do padr&#227;o respirat&#243;rio parece ser um recurso bem razo&#225;vel, uma vez que seria utilizado est&#237;mulo volunt&#225;rio para se induzir mudan&#231;as reflexas no sistema cardiovascular. A exist&#234;ncia de bases neuroanat&#244;micas comuns na modula&#231;&#227;o do controle tanto cardiovascular como respirat&#243;rio &#233; considerada a base biol&#243;gica dessa interven&#231;&#227;o. No entanto, o mecanismo exato de tal integra&#231;&#227;o deve ser mais bem caracterizado em futuros estudos. A t&#233;cnica de respira&#231;&#227;o lenta n&#227;o &#233; um m&#233;todo novo. Sua pr&#225;tica &#233; bastante antiga no mundo oriental, em pr&#225;ticas do ioga<sup>38</sup>. Por causa dos benef&#237;cios proporcionados pelo ioga a pacientes com doen&#231;as cardiovasculares, seus componentes (alongamento, relaxamento e t&#233;cnicas de respira&#231;&#227;o) ganharam o interesse da comunidade cient&#237;fica<sup>39 </sup>. Alguns estudos demonstram a melhora do controle cardiorrespirat&#243;rio em pacientes hipertensos e praticantes de ioga que utilizam uma t&#233;cnica conhecida por <italic>Pranayama Bramari, </italic>a qual envolve padr&#245;es respirat&#243;rios lentos, enquanto as pr&#225;ticas que envolvem exerc&#237;cios respirat&#243;rios de alta freq&#252;&#234;ncia apresentam efeitos antag&#244;nicos<sup>40</sup>. </p>
    <p><italic>Limita&#231;&#245;es e considera&#231;&#245;es finais </italic>- No presente estudo, foi utilizada uma amostra de pacientes com hipertens&#227;o arterial bem controlada. Uma pr&#243;xima etapa seria analisar a reprodutibilidade desses achados em pacientes com graus mais elevados de hipertens&#227;o arterial com ou sem preval&#234;ncia de outras co-morbidades. </p>
    <p>Os autores conclu&#237;ram, com base nos presentes achados, que a corre&#231;&#227;o das anormalidades do controle respirat&#243;rio em pacientes hipertensos melhoraria o controle tanto cardiovascular como respirat&#243;rio, atuando como um recurso complementar aos tratamentos cl&#237;nico e farmacol&#243;gico da hipertens&#227;o arterial. A t&#233;cnica de respira&#231;&#227;o lenta &#233; um m&#233;todo simples, sem contra-indica&#231;&#245;es e cujo custo-benef&#237;cio &#233; bastante v&#225;lido para a melhoria do balan&#231;o auton&#244;mico, para o controle respirat&#243;rio e para a redu&#231;&#227;o da press&#227;o arterial em pacientes com hipertens&#227;o arterial essencial. No entanto, h&#225; necessidade de novos estudos com casu&#237;sticas maiores e amostras probabil&#237;sticas para se avaliar o impacto dessa interven&#231;&#227;o em uma popula&#231;&#227;o maior de pacientes com hipertens&#227;o arterial. </p>
    <p>
      <bold>Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflitos de interesses pertinentes. </p>
    <p>
      <bold>Refer&#234;ncias </bold>
    </p>
    <p>
      <fn id="corr1" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Carlos Hermano da Justa Pinheiro </p>
        <p> Avenida Jaguar&#233;, 249/124 </p>
        <p> 05346-000 - S&#227;o Paulo, SP - Brasil </p>
        <p> E-mail:</p>
        <p>
          <email xlink:href="fisiologia_carlos@yahoo.com.br">fisiologia_carlos@yahoo.com.br</email>
        </p>
      </fn>
    </p>
    <p> Artigo recebido em 03/09/06; revisado recebido em 08/11/06; aceito em 14/12/06. </p>
  </body>
  <back>
    <ref-list>
      <ref id="B1">
        <mixed-citation>1. Souza MFM, Timerman A, Serrano CV Jr, Santos RD, Mansur AP. Tend&#234;ncia    do risco de morte por doen&#231;as circulat&#243;rias nas cinco regi&#245;es    do Brasil de 1979 a 1996. Arq Bras Cardiol. 2001; 77: 562-8. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Tend&#234;ncia do risco de morte por doen&#231;as circulat&#243;rias nas cinco regi&#245;es do Brasil de 1979 a 1996</article-title>
          <source>Arq Bras Cardiol</source>
          <date>
            <year>2001</year>
          </date>
          <fpage>562</fpage>
          <lpage>8</lpage>
          <volume>77</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Souza</surname>
              <given-names>MFM</given-names>
            </name>
            <name>
              <surname>Timerman</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Serrano</surname>
              <given-names>CV Jr</given-names>
            </name>
            <name>
              <surname>Santos</surname>
              <given-names>RD</given-names>
            </name>
            <name>
              <surname>Mansur</surname>
              <given-names>AP</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B2">
        <mixed-citation>2. Keys A. The Seven Countries Study: a multivariate analysis of death and    coronary heart disease. Cambridge (MA): Harvard University Press; 1980. </mixed-citation>
        <element-citation publication-type="book">
          <source>The Seven Countries Study: a multivariate analysis of death and coronary heart disease</source>
          <date>
            <year>1980</year>
          </date>
          <person-group person-group-type="author">
            <name>
              <surname>Keys</surname>
              <given-names>A</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B3">
        <mixed-citation>3. Diretrizes Brasileiras de Hipertens&#227;o Arterial. Sociedade Brasileira    de Hipertens&#227;o, Sociedade Brasileira de Cardiologia e Sociedade Brasileira    de Nefrologia. Hipertens&#227;o. 2002; 6: 1-2. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Diretrizes Brasileiras de Hipertens&#227;o Arterial: Sociedade Brasileira de Hipertens&#227;o, Sociedade Brasileira de Cardiologia e Sociedade Brasileira de Nefrologia</article-title>
          <source>Hipertens&#227;o</source>
          <date>
            <year>2002</year>
          </date>
          <fpage>1</fpage>
          <lpage>2</lpage>
          <volume>6</volume>
        </element-citation>
      </ref>
      <ref id="B4">
        <mixed-citation>4. Stamler J, Stamler R, Neaton JD. Blood pressure, systolic and diastolic,    and cardiovascular risks: U.S. population data. Arch Intern Med. 1993; 153:    598-615. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Blood pressure, systolic and diastolic, and cardiovascular risks: U.S. population data</article-title>
          <source>Arch Intern Med</source>
          <date>
            <year>1993</year>
          </date>
          <fpage>598</fpage>
          <lpage>615</lpage>
          <volume>153</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Stamler</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Stamler</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Neaton</surname>
              <given-names>JD</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B5">
        <mixed-citation>5. MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, et al. Blood    pressure, stroke, and coronary heart disease: part 1. Prolonged differences    in blood pressure: prospective observational studies corrected for the regression    dilution bias. Lancet. 1990; 335: 765-74. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Blood pressure, stroke, and coronary heart disease: part 1: Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias</article-title>
          <source>Lancet</source>
          <date>
            <year>1990</year>
          </date>
          <fpage>765</fpage>
          <lpage>74</lpage>
          <volume>335</volume>
          <person-group person-group-type="author">
            <name>
              <surname>MacMahon</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Peto</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Cutler</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Collins</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Sorlie</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Neaton</surname>
              <given-names>J</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B6">
        <mixed-citation>6. Suzuki S, Ohta T. Non-pharmacological treatment of hypertension in the elderly.    Nippon Rinsho. 2005; 63 (6): 1010-5. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Non-pharmacological treatment of hypertension in the elderly</article-title>
          <source>Nippon Rinsho</source>
          <date>
            <year>2005</year>
          </date>
          <fpage>1010</fpage>
          <lpage>5</lpage>
          <issue>6</issue>
          <volume>63</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Suzuki</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Ohta</surname>
              <given-names>T</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B7">
        <mixed-citation>7. Schein MH, Gavish B, Herz M, Rosner-Kahana D, Naveh P, Knishkowy B, et al.    Treating hypertension with a device that slows and regularises breathing: a    randomised, double-blind controlled study. J Hum Hypertens. 2001; 15 (4): 271-8. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Treating hypertension with a device that slows and regularises breathing: a randomised, double-blind controlled study</article-title>
          <source>J Hum Hypertens</source>
          <date>
            <year>2001</year>
          </date>
          <fpage>271</fpage>
          <lpage>8</lpage>
          <issue>4</issue>
          <volume>15</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Schein</surname>
              <given-names>MH</given-names>
            </name>
            <name>
              <surname>Gavish</surname>
              <given-names>B</given-names>
            </name>
            <name>
              <surname>Herz</surname>
              <given-names>M</given-names>
            </name>
            <name>
              <surname>Rosner-Kahana</surname>
              <given-names>D</given-names>
            </name>
            <name>
              <surname>Naveh</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Knishkowy</surname>
              <given-names>B</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B8">
        <mixed-citation>8. Grossman E, Grossman A, Schein MH, Zimlichman R, Gavish B. Breathingcontrol    lowers blood pressure. J Hum Hypertens. 2001; 15 (4): 263-9. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Breathingcontrol lowers blood pressure</article-title>
          <source>J Hum Hypertens</source>
          <date>
            <year>2001</year>
          </date>
          <fpage>263</fpage>
          <lpage>9</lpage>
          <issue>4</issue>
          <volume>15</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Grossman</surname>
              <given-names>E</given-names>
            </name>
            <name>
              <surname>Grossman</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Schein</surname>
              <given-names>MH</given-names>
            </name>
            <name>
              <surname>Zimlichman</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Gavish</surname>
              <given-names>B</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B9">
        <mixed-citation>9. Pinheiro CHJ, C&#233;zar ID, Marinho MJF, Ara&#250;jo FCS. Efeitos dos    exerc&#237;cios de controle respirat&#243;rio sobre a p&#243;s-carga card&#237;aca    em pacientes hipertensos no p&#243;s-operat&#243;rio tardio de revasculariza&#231;&#227;o    do mioc&#225;rdio. [Resumo]. In: 11&#351; Encontro de Inicia&#231;&#227;o    &#224; Pesquisa da Universidade de Fortaleza. Fortaleza; 2005. </mixed-citation>
        <element-citation publication-type="confproc">
          <source>Resumo</source>
          <date>
            <year>2005</year>
          </date>
          <person-group person-group-type="author">
            <name>
              <surname>Pinheiro</surname>
              <given-names>CHJ</given-names>
            </name>
            <name>
              <surname>C&#233;zar</surname>
              <given-names>ID</given-names>
            </name>
            <name>
              <surname>Marinho</surname>
              <given-names>MJF</given-names>
            </name>
            <name>
              <surname>Ara&#250;jo</surname>
              <given-names>FCS</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B10">
        <mixed-citation>10. Radaelli A, Raco R, Perfetti P, Viola A, Azzellino A, Signorini MG, et    al. Effects of slow, controlled breathing on baroreceptor control of heart rate    and blood pressure in healthy men. J Hypertens. 2004; 22 (7): 1361-70. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Effects of slow, controlled breathing on baroreceptor control of heart rate and blood pressure in healthy men</article-title>
          <source>J Hypertens</source>
          <date>
            <year>2004</year>
          </date>
          <fpage>1361</fpage>
          <lpage>70</lpage>
          <issue>7</issue>
          <volume>22</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Radaelli</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Raco</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Perfetti</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Viola</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Azzellino</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Signorini</surname>
              <given-names>MG</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B11">
        <mixed-citation>11. Joseph CN, Porta C, Casucci G, Casiraghi N, Maffeis M, Rossi M, et al.    Slow breathing improves arterial baroreflex sensitivity and decreases blood    pressure in essential hypertension. Hypertension. 2005; 46 (4): 714-8. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Slow breathing improves arterial baroreflex sensitivity and decreases blood pressure in essential hypertension</article-title>
          <source>Hypertension</source>
          <date>
            <year>2005</year>
          </date>
          <fpage>714</fpage>
          <lpage>8</lpage>
          <issue>4</issue>
          <volume>46</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Joseph</surname>
              <given-names>CN</given-names>
            </name>
            <name>
              <surname>Porta</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Casucci</surname>
              <given-names>G</given-names>
            </name>
            <name>
              <surname>Casiraghi</surname>
              <given-names>N</given-names>
            </name>
            <name>
              <surname>Maffeis</surname>
              <given-names>M</given-names>
            </name>
            <name>
              <surname>Rossi</surname>
              <given-names>M</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B12">
        <label>12</label>
        <mixed-citation>12. World Medical Association (WMA). Declaration of Helsinki. Somerset West: (South Africa) 1996. In: 48th General Assembly-WMA. 2000 October 6. Acessado em 2006 nov. 10. Dispon&#237;vel em: &lt;<ext-link ext-link-type="uri" xlink:href="http://www.wma.net">http://www.wma.net</ext-link>&gt;.</mixed-citation>
        <element-citation publication-type="confproc">
          <date>
            <month>10</month>
            <day>06</day>
            <year>2000</year>
          </date>
        </element-citation>
      </ref>
      <ref id="B13">
        <label>13</label>
        <mixed-citation>13. World Medical Association (WMA). Declaration of Helsinki. Edinburgh (Scotland) 2000. In: 52nd General Assembly. 2000 October 13. Acessado em 2006 nov 10. Dispon&#237;vel em: &lt;<ext-link ext-link-type="uri" xlink:href="http://www.wma.net">http://www.wma.net</ext-link>&gt;.</mixed-citation>
        <element-citation publication-type="confproc">
          <date>
            <month>10</month>
            <day>13</day>
            <year>2000</year>
          </date>
        </element-citation>
      </ref>
      <ref id="B14">
        <mixed-citation>14. IV Diretrizes Brasileiras de Hipertens&#227;o Arterial. Arq Bras Cardiol.    2004; 82 (supl. 4): 2-22. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>IV Diretrizes Brasileiras de Hipertens&#227;o Arterial</article-title>
          <source>Arq Bras Cardiol</source>
          <date>
            <year>2004</year>
          </date>
          <fpage>2</fpage>
          <lpage>22</lpage>
          <volume>82</volume>
        </element-citation>
      </ref>
      <ref id="B15">
        <mixed-citation>15. Joint National Committee on Detection, Evaluation and Treatment of High    Blood Pressure (JNC). Seventh Report of Joint National Committee onPrevention,    Detection, Evaluation and Treatment of High Blood Pressure: The JNC 7 report.    JAMA. 2003; 299: 2560-72. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Seventh Report of Joint National Committee onPrevention, Detection, Evaluation and Treatment of High Blood Pressure: The JNC 7 report</article-title>
          <source>JAMA</source>
          <date>
            <year>2003</year>
          </date>
          <fpage>2560</fpage>
          <lpage>72</lpage>
          <volume>299</volume>
        </element-citation>
      </ref>
      <ref id="B16">
        <mixed-citation>16. Kaushik RM, Kaushik R, Mahajan SK, Rajesh V. Effects of mental relaxation    and slow breathing in essential hypertension. Complement Ther Med. 2006; 14    (2): 120-6.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Effects of mental relaxation and slow breathing in essential hypertension</article-title>
          <source>Complement Ther Med</source>
          <date>
            <year>2006</year>
          </date>
          <fpage>2</fpage>
          <volume>14</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Kaushik</surname>
              <given-names>RM</given-names>
            </name>
            <name>
              <surname>Kaushik</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Mahajan</surname>
              <given-names>SK</given-names>
            </name>
            <name>
              <surname>Rajesh</surname>
              <given-names>V</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B17">
        <mixed-citation>17. Bernardi L, Porta C, Spicuzza L, Bellwon J, Spadacini G, Frey AW, et al.    Slow breathing increases arterial baroreflex sensitivity in patients with chronic    heart failure. Circulation. 2002; 105: 143-5. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Slow breathing increases arterial baroreflex sensitivity in patients with chronic heart failure</article-title>
          <source>Circulation</source>
          <date>
            <year>2002</year>
          </date>
          <fpage>143</fpage>
          <lpage>5</lpage>
          <volume>105</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Bernardi</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Porta</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Spicuzza</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Bellwon</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Spadacini</surname>
              <given-names>G</given-names>
            </name>
            <name>
              <surname>Frey</surname>
              <given-names>AW</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B18">
        <mixed-citation>18. Goso Y, Asanoi H, Ishise H, Kameyama T, Hirai T, Nozawa T, et al. Respiratory    modulation of muscle sympathetic nerve activity in patients with chronic heart    failure. Circulation. 2001; 104: 418-23. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Respiratory modulation of muscle sympathetic nerve activity in patients with chronic heart failure</article-title>
          <source>Circulation</source>
          <date>
            <year>2001</year>
          </date>
          <fpage>418</fpage>
          <lpage>23</lpage>
          <volume>104</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Goso</surname>
              <given-names>Y</given-names>
            </name>
            <name>
              <surname>Asanoi</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Ishise</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Kameyama</surname>
              <given-names>T</given-names>
            </name>
            <name>
              <surname>Hirai</surname>
              <given-names>T</given-names>
            </name>
            <name>
              <surname>Nozawa</surname>
              <given-names>T</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B19">
        <mixed-citation>19. Gus I, Harzheim E, Zaslavsky C, Medina C, Gus M. Prevalence, awareness,    and control of systemic arterial hypertension in the state of Rio Grande do    Sul. Arq Bras Cardiol. 2004; 83 (5): 424-8. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Prevalence, awareness, and control of systemic arterial hypertension in the state of Rio Grande do Sul</article-title>
          <source>Arq Bras Cardiol</source>
          <date>
            <year>2004</year>
          </date>
          <fpage>424</fpage>
          <lpage>8</lpage>
          <issue>5</issue>
          <volume>83</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Gus</surname>
              <given-names>I</given-names>
            </name>
            <name>
              <surname>Harzheim</surname>
              <given-names>E</given-names>
            </name>
            <name>
              <surname>Zaslavsky</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Medina</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Gus</surname>
              <given-names>M</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B20">
        <mixed-citation>20. Grote L, Ploch T, Heitmann J, Knaack L, Penzel T, Peter JH. Sleep-related    breathing disorder is an independent risk factor for systemic hypertension.    Am J Respir Crit Care Med. 1999; 160 (6): 1875-82. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Sleep-related breathing disorder is an independent risk factor for systemic hypertension</article-title>
          <source>Am J Respir Crit Care Med</source>
          <date>
            <year>1999</year>
          </date>
          <fpage>1875</fpage>
          <lpage>82</lpage>
          <issue>6</issue>
          <volume>160</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Grote</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Ploch</surname>
              <given-names>T</given-names>
            </name>
            <name>
              <surname>Heitmann</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Knaack</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Penzel</surname>
              <given-names>T</given-names>
            </name>
            <name>
              <surname>Peter</surname>
              <given-names>JH</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B21">
        <mixed-citation>21. He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index    in obstructive sleep apnea: experience in 385 male patients. Chest. 1988; 94:    9-14. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Mortality and apnea index in obstructive sleep apnea: experience in 385 male patients</article-title>
          <source>Chest</source>
          <date>
            <year>1988</year>
          </date>
          <fpage>9</fpage>
          <lpage>14</lpage>
          <volume>94</volume>
          <person-group person-group-type="author">
            <name>
              <surname>He</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Kryger</surname>
              <given-names>MH</given-names>
            </name>
            <name>
              <surname>Zorick</surname>
              <given-names>FJ</given-names>
            </name>
            <name>
              <surname>Conway</surname>
              <given-names>W</given-names>
            </name>
            <name>
              <surname>Roth</surname>
              <given-names>T</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B22">
        <mixed-citation>22. Wright J, Johns R, Watt I, Melville A, Sheldon T. Health effects of obstructive    sleep apnoea and the effectiveness of continuous positive airways pressure:    a systematic review of the research evidence. Br Med J. 1997; 314: 851-60. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Health effects of obstructive sleep apnoea and the effectiveness of continuous positive airways pressure: a systematic review of the research evidence</article-title>
          <source>Br Med J</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>851</fpage>
          <lpage>60</lpage>
          <volume>314</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Wright</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Johns</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Watt</surname>
              <given-names>I</given-names>
            </name>
            <name>
              <surname>Melville</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Sheldon</surname>
              <given-names>T</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B23">
        <mixed-citation>23. Ehlenz K, Peter JH, Kaffarnik H, von Wichert P. Disturbances in volume    regulating hormone system  a key to the pathogenesis of hypertension in    obstructive sleep apnea syndrome? Pneumologie. 1991; 45 (Suppl. 1): 239-45. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Disturbances in volume regulating hormone system: a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome?</article-title>
          <source>Pneumologie</source>
          <date>
            <year>1991</year>
          </date>
          <fpage>239</fpage>
          <lpage>45</lpage>
          <volume>45</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Ehlenz</surname>
              <given-names>K</given-names>
            </name>
            <name>
              <surname>Peter</surname>
              <given-names>JH</given-names>
            </name>
            <name>
              <surname>Kaffarnik</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>von Wichert</surname>
              <given-names>P</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B24">
        <mixed-citation>24. Schneider H, Schaub CD, Andreoni KA, Schwartz AR, Smith PL, Robotham JL,    et al. Systemic and pulmonary hemodynamic responses to normal and obstructed    breathing during sleep. J Appl Physiol. 1997; 83: 1671-80. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep</article-title>
          <source>J Appl Physiol</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>1671</fpage>
          <lpage>80</lpage>
          <volume>83</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Schneider</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Schaub</surname>
              <given-names>CD</given-names>
            </name>
            <name>
              <surname>Andreoni</surname>
              <given-names>KA</given-names>
            </name>
            <name>
              <surname>Schwartz</surname>
              <given-names>AR</given-names>
            </name>
            <name>
              <surname>Smith</surname>
              <given-names>PL</given-names>
            </name>
            <name>
              <surname>Robotham</surname>
              <given-names>JL</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B25">
        <mixed-citation>25. Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive    sleep apnea as a cause of systemic hypertension: evidence from a canine model.    J Clin Invest. 1997; 99: 106-9. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Obstructive sleep apnea as a cause of systemic hypertension: evidence from a canine model</article-title>
          <source>J Clin Invest</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>106</fpage>
          <lpage>9</lpage>
          <volume>99</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Brooks</surname>
              <given-names>D</given-names>
            </name>
            <name>
              <surname>Horner</surname>
              <given-names>RL</given-names>
            </name>
            <name>
              <surname>Kozar</surname>
              <given-names>LF</given-names>
            </name>
            <name>
              <surname>Render-Teixeira</surname>
              <given-names>CL</given-names>
            </name>
            <name>
              <surname>Phillipson</surname>
              <given-names>EA</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B26">
        <mixed-citation>26. Lavie P, Ben-Yosef R, Rubin AE. Prevalence of sleep apnea syndrome among    patients with essential hypertension. Am Heart J. 1984; 108 (2): 373-6. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Prevalence of sleep apnea syndrome among patients with essential hypertension</article-title>
          <source>Am Heart J</source>
          <date>
            <year>1984</year>
          </date>
          <fpage>373</fpage>
          <lpage>6</lpage>
          <issue>2</issue>
          <volume>108</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Lavie</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Ben-Yosef</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Rubin</surname>
              <given-names>AE</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B27">
        <mixed-citation>27. Fletcher EC, DeBehnke RD, Lovoi MS, Gorin AB. Undiagnosed sleep apnea in    patients with essential hypertension. Ann Intern Med. 1985; 103: 190-5.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Undiagnosed sleep apnea in patients with essential hypertension</article-title>
          <source>Ann Intern Med</source>
          <date>
            <year>1985</year>
          </date>
          <fpage>190</fpage>
          <lpage>5</lpage>
          <volume>103</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Fletcher</surname>
              <given-names>EC</given-names>
            </name>
            <name>
              <surname>DeBehnke</surname>
              <given-names>RD</given-names>
            </name>
            <name>
              <surname>Lovoi</surname>
              <given-names>MS</given-names>
            </name>
            <name>
              <surname>Gorin</surname>
              <given-names>AB</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B28">
        <mixed-citation>28. Task Force of the European Society of Cardiology and the North American    Society of Pacing and Electrophysiology. Heart rate variability: standards of    measurement, physiological interpretation and clinical use. Circulation. 1996;    93: 1043-65. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Heart rate variability: standards of measurement, physiological interpretation and clinical use</article-title>
          <source>Circulation</source>
          <date>
            <year>1996</year>
          </date>
          <fpage>1043</fpage>
          <lpage>65</lpage>
          <volume>93</volume>
        </element-citation>
      </ref>
      <ref id="B29">
        <mixed-citation>29. Julius S. Autonomic nervous system dysregulation in human hypertension.    Am J Cardiol. 1991; 67: 3B-7B. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Autonomic nervous system dysregulation in human hypertension</article-title>
          <source>Am J Cardiol</source>
          <date>
            <year>1991</year>
          </date>
          <fpage>3B</fpage>
          <lpage>7B</lpage>
          <volume>67</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Julius</surname>
              <given-names>S</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B30">
        <mixed-citation>30. Guzzetti S, Piccaluga E, Casati R, Cerutti S, Lombardi F, Pagani M, et    al. Sympathetic predominance in essential hypertension: a study employing spectral    analysis of heart rate variability. J Hypertens. 1988; 6: 711-7.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Sympathetic predominance in essential hypertension: a study employing spectral analysis of heart rate variability</article-title>
          <source>J Hypertens</source>
          <date>
            <year>1988</year>
          </date>
          <fpage>711</fpage>
          <lpage>7</lpage>
          <volume>6</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Guzzetti</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Piccaluga</surname>
              <given-names>E</given-names>
            </name>
            <name>
              <surname>Casati</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Cerutti</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Lombardi</surname>
              <given-names>F</given-names>
            </name>
            <name>
              <surname>Pagani</surname>
              <given-names>M</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B31">
        <mixed-citation>31. Somers VK, Mark AL, Abboud FM. Potentiation of sympathetic nerve responses    to hypoxia in borderline hypertensive subjects. Hypertension. 1988; 11: 608-12. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects</article-title>
          <source>Hypertension</source>
          <date>
            <year>1988</year>
          </date>
          <fpage>608</fpage>
          <lpage>12</lpage>
          <volume>11</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Somers</surname>
              <given-names>VK</given-names>
            </name>
            <name>
              <surname>Mark</surname>
              <given-names>AL</given-names>
            </name>
            <name>
              <surname>Abboud</surname>
              <given-names>FM</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B32">
        <mixed-citation>32. Menezes AS Jr, Moreira HG, Daher MT. An&#225;lise da variabilidade da    freq&#252;&#234;ncia card&#237;aca em pacientes hipertensos, antes e depois    do tratamento com inibidores da enzima conversora da angiotensina II. Arq Bras    Cardiol. 2004; 83 (2): 165-8. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>An&#225;lise da variabilidade da freq&#252;&#234;ncia card&#237;aca em pacientes hipertensos, antes e depois do tratamento com inibidores da enzima conversora da angiotensina II</article-title>
          <source>Arq Bras Cardiol</source>
          <date>
            <year>2004</year>
          </date>
          <fpage>165</fpage>
          <lpage>8</lpage>
          <issue>2</issue>
          <volume>83</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Menezes</surname>
              <given-names>AS Jr</given-names>
            </name>
            <name>
              <surname>Moreira</surname>
              <given-names>HG</given-names>
            </name>
            <name>
              <surname>Daher</surname>
              <given-names>MT</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B33">
        <mixed-citation>33. Spyer KM. Central nervous integration of cardiovascular control. J Exp    Biol. 1982; 100: 109-28. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Central nervous integration of cardiovascular control</article-title>
          <source>J Exp Biol</source>
          <date>
            <year>1982</year>
          </date>
          <fpage>109</fpage>
          <lpage>28</lpage>
          <volume>100</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Spyer</surname>
              <given-names>KM</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B34">
        <mixed-citation>34. Bernardi L, Spadacini G, Bellwon J, Hajric R, Roskamm H, Frey AW. Effect    of breathing rate on oxygen saturation and exercise performance in chronic heart    failure. Lancet. 1998; 351: 1308-11. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Effect of breathing rate on oxygen saturation and exercise performance in chronic heart failure</article-title>
          <source>Lancet</source>
          <date>
            <year>1998</year>
          </date>
          <fpage>1308</fpage>
          <lpage>11</lpage>
          <volume>351</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Bernardi</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Spadacini</surname>
              <given-names>G</given-names>
            </name>
            <name>
              <surname>Bellwon</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Hajric</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Roskamm</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Frey</surname>
              <given-names>AW</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B35">
        <mixed-citation>35. Spicuzza L, Gabutti A, Porta C, Montano N, Bernardi L. Yoga and chemoreflex    response to hypoxia and hypercapnia. Lancet. 2000; 356: 1495-6. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Yoga and chemoreflex response to hypoxia and hypercapnia</article-title>
          <source>Lancet</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>1495</fpage>
          <lpage>6</lpage>
          <volume>356</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Spicuzza</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Gabutti</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Porta</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Montano</surname>
              <given-names>N</given-names>
            </name>
            <name>
              <surname>Bernardi</surname>
              <given-names>L</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B36">
        <mixed-citation>36. Bernardi L, Gabutti A, Porta C, Spicuzza L. Slow breathing reduces chemoreflex    response to hypoxia and hypercapnia, and increases baroreflex sensitivity. J    Hypertens. 2001; 19: 2221-9. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Slow breathing reduces chemoreflex response to hypoxia and hypercapnia, and increases baroreflex sensitivity</article-title>
          <source>J Hypertens</source>
          <date>
            <year>2001</year>
          </date>
          <fpage>2221</fpage>
          <lpage>9</lpage>
          <volume>19</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Bernardi</surname>
              <given-names>L</given-names>
            </name>
            <name>
              <surname>Gabutti</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Porta</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Spicuzza</surname>
              <given-names>L</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B37">
        <mixed-citation>37. Francis DP, Coats AJS. Chemoreflex-baroreflex interactions in cardiovascular    disease. In: Bradley TD, Floras JS, eds. Sleep apnea: implications in cardiovascular    and cerebrovascular disease. New York: Marcel Dekker; 2000. p. 33-60. </mixed-citation>
        <element-citation publication-type="book">
          <source>Sleep apnea: implications in cardiovascular and cerebrovascular disease</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>33</fpage>
          <lpage>60</lpage>
          <person-group person-group-type="author">
            <name>
              <surname>Francis</surname>
              <given-names>DP</given-names>
            </name>
            <name>
              <surname>Coats</surname>
              <given-names>AJS</given-names>
            </name>
            <name>
              <surname>Bradley</surname>
              <given-names>TD</given-names>
            </name>
            <name>
              <surname>Floras</surname>
              <given-names>JS</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B38">
        <mixed-citation>38. Schell FJ, Allolio B, Schonecke OW. Physiological and psychological effects    of Hatha-Yoga exercise in healthy women. Int J Psychosom. 1994; 41: 46-52. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Physiological and psychological effects of Hatha-Yoga exercise in healthy women</article-title>
          <source>Int J Psychosom</source>
          <date>
            <year>1994</year>
          </date>
          <fpage>46</fpage>
          <lpage>52</lpage>
          <volume>41</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Schell</surname>
              <given-names>FJ</given-names>
            </name>
            <name>
              <surname>Allolio</surname>
              <given-names>B</given-names>
            </name>
            <name>
              <surname>Schonecke</surname>
              <given-names>OW</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B39">
        <mixed-citation>39. Jayasinghe SR. Yoga in cardiac health (a review). Eur J Cardiovasc Prev    Rehabil. 2004; 11 (5): 369-75. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Yoga in cardiac health</article-title>
          <source>Eur J Cardiovasc Prev Rehabil</source>
          <date>
            <year>2004</year>
          </date>
          <fpage>369</fpage>
          <lpage>75</lpage>
          <issue>5</issue>
          <volume>11</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Jayasinghe</surname>
              <given-names>SR</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B40">
        <mixed-citation>40. Stancak A Jr, Kuna M, Novak P, Srinivasan MA, Dostalek C, Vishnudevananda    S. Observations on respiratory and cardiovascular rhythmicities during yogic    high-frequency respiration. Physiol Res. 1991; 40 (3): 345-54. </mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Observations on respiratory and cardiovascular rhythmicities during yogic high-frequency respiration</article-title>
          <source>Physiol Res</source>
          <date>
            <year>1991</year>
          </date>
          <fpage>345</fpage>
          <lpage>54</lpage>
          <issue>3</issue>
          <volume>40</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Stancak</surname>
              <given-names>A Jr</given-names>
            </name>
            <name>
              <surname>Kuna</surname>
              <given-names>M</given-names>
            </name>
            <name>
              <surname>Novak</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Srinivasan</surname>
              <given-names>MA</given-names>
            </name>
            <name>
              <surname>Dostalek</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Vishnudevananda</surname>
              <given-names>S</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
    </ref-list>
  </back>
  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Original Articles</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Spontaneous respiratory modulation improves cardiovascular control in essential hypertension</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Recent studies show that controlled breathing improves baroreflex and heart rate variability and lowers blood pressure in hypertensive patients. OBJECTIVE: To evaluate the effects of slow breathing training on cardiorespiratory system modulation of patients (n=10, men and women, ages ranging from 45 to 60) with essential hypertension seen in an outpatient setting. METHODS: According to the study design, each patient was used as his/her own control, and data were collected before and after the intervention. The following parameters were assessed: heart rate variability (HRV), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), respirometry, chest expansion measurement, and statistical data analysis. Respiratory training was performed in 30-minute sessions held twice a week over one month using slow breathing exercises. RESULTS: Our results were as follows: a reduction in SBP, DPB, and MAP (p &lt; 0.05 vs control); an increase in heart rate variability, as evidenced by greater RR interval variation and SDNN index; a decline in respiratory rate (p &lt; 0.01 vs control); and an increase in tidal volume (p &lt; 0.01 vs control) and thoracic expansibility (p &lt; 0.01 vs control). CONCLUSION: Respiratory retraining using the slow breathing technique appears to be a useful adjunctive for cardiorespiratory control in hypertensive patients.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Respiration</kwd>
        <kwd>blood pressure</kwd>
        <kwd>hypertension</kwd>
        <kwd>breathing exercises</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ORIGINAL ARTICLE</bold>
      </p>
      <p>Spontaneous respiratory modulation improves cardiovascular control in essential hypertension </p>
      <p>
        <bold>Carlos Hermano da Justa Pinheiro; Renato Ant&#244;nio Ribeiro Medeiros; Denise Gon&#231;alves Moura Pinheiro; Maria de Jesus Ferreira Marinho</bold>
      </p>
      <p>Laborat&#243;rio de Cardiopneumologia e Fisiologia do Exerc&#237;cio da Universidade de Fortaleza, Escola de Sa&#250;de P&#250;blica do Estado do Cear&#225;, Imperial College of Science Technology and Medicine - IC - Fortaleza, CE - Brazil - London - England </p>
      <p>
        <xref ref-type="corresp" rid="corr1-body2">Mailing address</xref>
      </p>
      <p>
        <bold>SUMMARY</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Recent studies show that controlled breathing improves baroreflex and heart rate variability and lowers blood pressure in hypertensive patients. </p>
      <p><bold>OBJECTIVE:</bold> To evaluate the effects of slow breathing training on cardiorespiratory system modulation of patients (n=10, men and women, ages ranging from 45 to 60) with essential hypertension seen in an outpatient setting.</p>
      <p><bold>METHODS:</bold> According to the study design, each patient was used as his/her own control, and data were collected before and after the intervention. The following parameters were assessed: heart rate variability (HRV), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), respirometry, chest expansion measurement, and statistical data analysis. Respiratory training was performed in 30-minute sessions held twice a week over one month using slow breathing exercises. </p>
      <p><bold>RESULTS:</bold> Our results were as follows: a reduction in SBP, DPB, and MAP (p &lt; 0.05 <italic>vs </italic>control); an increase in heart rate variability, as evidenced by greater RR interval variation and SDNN index; a decline in respiratory rate (p &lt; 0.01 <italic>vs </italic>control); and an increase in tidal volume (p &lt; 0.01 <italic>vs</italic> control) and thoracic expansibility (p &lt; 0.01 <italic>vs</italic> control). </p>
      <p><bold>CONCLUSION:</bold> Respiratory retraining using the slow breathing technique appears to be a useful adjunctive for cardiorespiratory control in hypertensive patients. </p>
      <p><bold>Key words:</bold> Respiration; blood pressure; hypertension; breathing exercises.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Systemic hypertension is one of the major risk factors for cardiovascular disease (CVD), and represents a public health problem in Brazil, where it affects 22% of the population of both genders<sup>1</sup>. Worldwide, according to the <italic>Seven Countries Study</italic><sup>2 </sup><italic>, </italic>each 10 mm Hg increase in blood pressure doubles the risk of death in hypertensive patients. As hypertension is an independent risk factor for the two leading causes of death in Brazil, namely myocardial in farction and stroke<sup>3</sup>, its primary prevention by pharmacological and non-pharmacological interventions reduces the morbidity and mortality associated with the disease<sup>4,5</sup>. Among non-pharmacological therapies, changes in life style, such as weight loss, alcohol and dietary salt restriction, and moderate-intensity exercise are recommended for the clinical control of the disease<sup>6</sup>. In this respect, recent evidence has emerged that a decrease in respiratory rate thanks tone wel ectronic devices that interact with the patients, guiding them towards slow breathing, lowers blood pressure in patients with mild and moderate hypertension and those with resistant hypertension, with out changes in medication<sup>7,8</sup>. In a recent study carried out by our group, slow breathing stimulation through greater chest expansion successfully lowered blood pressure and heart rate of a hypertensive patient in the postoperative period after myocardial resvascularization surgery<sup>9</sup>. Scientific evidence suggests that slow breathing improves baroreflex sensitivity in healthy<sup>10 </sup>and hypertensive subjects<sup>11</sup>. Therefore, respiratory modulation may be of therapeutic value in controlling hypertension. According to Scheinetal<sup>7</sup>, such improvement is associated with a change in patient's breathing pattern, which would breathe at lower frequency and higher amplitude. However, the few studies described in the international literature report only acute changes, or those that take place in a single session, in the respiratory system, with repercussions on the cardiovascular system. In view of this problem, our study sought to evaluate the effects of slow breathing in respiratory retraining and modulation of cardiovascular and respiratory control of patients with essential hypertension.</p>
      <p>
        <bold>Methods </bold>
      </p>
      <p>After being approved by the Institutional Research Ethics Committee, this research was conducted at the Cardiopulmonary and Exercise Physiology laboratory of the University of Fortaleza (<italic>Laborat&#243;rio de Cardiopneumologia e Fisiologia do Exerc&#237;cio da Universidade de Fortaleza</italic>). Informed consent was obtained from each subject, and all the principles postulated in the Declaration of Helsinki in 1974<sup>12 </sup> and revised in 1983<sup>13 </sup>were followed. </p>
      <p>Ten patients (five men and five women, ages ranging from 45 to 60) diagnosed with essential hypertension and under clinical and pharmacological treatment (<xref ref-type="table" rid="tab1-body2">Table 1</xref> and <xref ref-type="fig" rid="en_a05fig01-body2">Figure 1</xref>) were included in the study. All of them were seen at the Integrated Medical Assistance Nucleus (<italic>N&#250;cleo de Assist&#234;ncia M&#233;dica Integrada</italic> - NAMI) of the University of Fortaleza. </p>
      <p content-type="asset">
        <fig id="en_a05fig01-body2">
          <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf01-en.jpg"/></fig>
      </p>
      <table-wrap id="tab1-body2">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gt01-en.jpg"/></table-wrap>
      <p>No patient was obese (mean BMI was 26 &#177; 1.4) or had other comorbidities associated with hypertension, except for dyslipidemia (<xref ref-type="table" rid="tab1-body2">Table 1</xref>). Subjects with essential hypertension and under clinical treatment were considered eligible. Study patients were selected based on their clinical follow-up forms. After the inclusion and exclusion criteria described below were applied, interviews were conducted to collect data on subjects' clinical and pharmacological treatment and their epidemiological profile. </p>
      <p>Exclusion criteria were the following: patients with secondary hypertension; renal, heart or liver failure; recent cardiovascular event; pulmonary disease, diabetes mellitus, neuropathies, autoimmune diseases, Chagas disease, cardiac arrhythmias, and other diseases that impair autonomicnervous system control. Alcohol consumption and cigarette smoking, as well as the use of oral contraceptives, antidepressants, neuroleptics, anti-arrhythmics, and lithium, were also exclusion criteria. </p>
      <p><italic>Study design</italic> - At the beginning of the study, data were collect to assess systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate variability (HRV). The following respiratory variables were monitored: tidal volume (TV), respiratory rate (RR), minute volume (MV), plus thoracic expansibility and diaphragmatic expansibility. Upon conclusion of the study, and after one month of slow breathing training, all these measurements were repeated for the final collection of data and statistical analysis. </p>
      <p><italic>Measurement of blood pressure and analysis of cardiac autonomic balance</italic> - Blood pressure was measured in three different time points, on an outpatient basis, using a properly calibrated aneroid sphygmomanometer and according to the IV Guide lines for Hypertension issued by the Brazilian Society of Cardiology<sup>14 </sup>and those of the Joint National Committee<sup>15</sup>. Autonomic balance, or cardiac sympathetic-parasympathetic balance, was assessed by analyzing heart rate variability, which was calculated based on mean RR intervals, RR interval variation, and the time-domain method (SDNN and PNN50 indices) in all 12 ECG leads. Data were tabulated using Microsoft Excel 2003, and statistical analyses were performed using the SPSS software version 10.0. </p>
      <p><italic>Respiratory mechanics analysis</italic> - Minute volume (MV) and respiratory rate (RR) were measured using a Wright's respirometer, and tidal volume was calculated by the RR/ MV ratio. Chest wall expansion was assessed by thoracic expansibility (at the axillary level) and diaphragmatic expansibility (at the xiphoid process level) measurements.</p>
      <p><italic>Respiratory retraining protocol</italic> - A training protocol for breathing control was applied using, first, diaphragmatic, intercostal, and upper chest breathing pattern to make the patient aware of his respiratory movements. Patients were asked to lie supine, with knees flexed and feet flat on the floor, and raise their hands to the are a of the chest (<xref ref-type="fig" rid="en_a05fig02-body2">Figure 2</xref>) related to each breathing pattern: diaphragm, intercostal muscles, and clavicular region. At each breathing pattern, patients were instructed to feel and identify the rib cage motion and it samplitude. Subsequently, they were instructed to decrease their respiratory rate gradually while increasing respiratory amplitude. This procedure was performed ten times for each breathing pattern. </p>
      <p content-type="asset">
        <fig id="en_a05fig02-body2">
          <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf02-en.jpg"/></fig>
      </p>
      <p>The patients then sat down and performed the slow breathing technique, intended to promote quieter breathing by increasing respiratory amplitude and reducing respiratory rate while the three breathing patterns described above are simultaneously performed. This technique was done in 30minute sessions held twice a week during one month. </p>
      <p><italic>Statistical analysis</italic> - All data were analyzed using descriptive statistics. Baseline and final means were compared using Student's t test and underwent p-value analysis. Ventilatory variables and blood pressure measurements were assessed using Pearson's correlation coefficient and linear regression analysis (R-square). P values &lt; 0.05 were considered statistically significant. </p>
      <p>
        <bold>Results</bold>
      </p>
      <p>No changes were made in the medication used and life style reported by the patients at baseline (Data are not shown). The study results were the following: </p>
      <p><italic>Respiratory retraining and blood pressure</italic> - In our sample of hypertensive patients, there was a decrease in blood pressure (<xref ref-type="fig" rid="gr1-body2">Graphic 1</xref>). Systolic, mean, and diastolic BP all dropped (135 &#177; 14.32 mm Hg to 123 &#177; 14.29 mm Hg, p &lt; 0.05; 99 &#177; 7.8 mm Hg to 91 &#177; 7.5 mm Hg, p &lt; 0.05; and 81 &#177; 8.75 mm Hg to 74 &#177; 6.1 mm Hg, p &lt; 0. 05, respectively). </p>
      <fig id="gr1-body2">
        <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf03-en.jpg"/></fig>
      <p><italic>Respiratory retraining and cardiovascular autonomic modulation</italic> - Heart rate variability improved (<xref ref-type="fig" rid="en_a05gr02-body2">Graphic 2</xref>). However, no significant change was found in resting heart rate (74 &#177; 8 bpm to 72 &#177; 9.1 bpm, p &gt; 0.05) and mean RR intervals (1002 &#177; 3.4 ms to 1004 &#177; 3.2 ms, p &gt; 0.05). This improvement in heart rate variability was evidenced by an increase in RR interval variation and SDNN index, while the PNN50 index remained unchanged. </p>
      <p content-type="asset">
        <fig id="en_a05gr02-body2">
          <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf04-en.jpg"/></fig>
      </p>
      <p><italic>Respiratory retraining and thoracic mechanics</italic> - After the training period, changes in breathing pattern were noted (<xref ref-type="fig" rid="en_a05gr03-body2">Graphic 3</xref>). There was a decrease in resting respiratory rate (14.60 &#177; 1.6 breaths per minute to 10.10 &#177; 1.1 breaths per minute,p&lt;0.01). No significant changes were found in minute volume, which was attributed to the compensatory increase in tidal volume (419.75 &#177; 60,93 mL to 560.30 &#177; 60.76 mL, p &lt;0.01). This tidal volume increase, in turn, was at tributed the greater thoracic expansibility (1.9 &#177; 0.56 cm to 2.33 &#177; 0.49 cm, p &lt; 0.01), while diaphragmatic expansibility remained unaltered (<xref ref-type="fig" rid="en_a05gr03-body2">Graphic 3</xref>). In the study sample, a moderate negative correlation (Pearson's coefficient = 0.5 with p &lt; 0.05) was found between tidal volume and systolic and mean blood pressure (not shown), as shown by the linear regression analysis (<xref ref-type="fig" rid="en_a05gr04-body2">Graphic 4</xref>). </p>
      <p content-type="asset">
        <fig id="en_a05gr03-body2">
          <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf05-en.jpg"/></fig>
      </p>
      <p content-type="asset">
        <fig id="en_a05gr04-body2">
          <graphic xlink:href="1678-4170-abc-88-06-0651-00005-gf06-en.jpg"/></fig>
      </p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>This study sought to evaluate the effectiveness of a training program using the slow breathing technique in cardiovascular and blood pressure control in a sample of patients with essential hypertension. We have demonstrated that respiratory retraining may improve cardiorespiratory control and decrease blood pressure in hypertensive patients. </p>
      <p>Our data are consistent with the studies by Joseph et al<sup>11</sup>, Kaushik e tal<sup>16</sup>, Bernardi et al<sup>17</sup>, and Goso et al<sup>18</sup>. These studies evaluated the effects of a single exercise session using thes low breathing technique in healthy, hypertensive and heart failure patients and showed the benefits of spontaneous respiratory modulation in cardiovascular control and blood pressure reduction. We decided to assess the impact of a respiratory retraining program using the slow breathing technique over one month in hypertensive patients. We believed that, performed on a regular basis, these breathing exercises could exert some psychophysiological effects to change breathing pattern at rest. Despite the small sample size owing to the numerous exclusion criteria adopted in the study, data statistics were determinant. Further studies involving larger numbers of patients are needed and, if possible, with probability sampling to assess the effectiveness of this type of intervention and its impact on the population. </p>
      <p>Controlling blood pressure is considered the best strategy to reduce the impact of cardiovascular diseases in hypertensive patients; this may be accomplished by prevention campaigns, risk factor management, early diagnosis, and effective treatment for the disease<sup>19</sup>. Some scientific evidence suggests that changes in breathing control may also be regarded as a risk factor associated with lifestyle in hypertensive patients<sup>20</sup>. </p>
      <p><italic>Respiratory disorders as risk factor for hypertension</italic> - The relationship between breathing abnormalities and hypertension has come to the fore in the scientific community owing to reports about the greater prevalence of cardiovascular disease in subjects with sleep breathing disorders<sup>21 </sup>. The mechanism by which sleep breathing disorders affect blood pressure and hypertension remains unclear<sup>22</sup>. Nonetheless, Ehlenz et al<sup>23 </sup>have shown changes in blood pressure regulation in hypertensive patients, as compared with healthy subjects. Experimental animal studies have also demonstrated that obstructive sleep apnea (OSA), one of the major sleep-related breathing disorders, is strongly associated with changes in systemic and pulmonary blood pressure<sup>24</sup>. According to Brooks et al<sup>25</sup>, these changes in blood pressure control occur both during sleep and daytime, thereby suggesting a causal role of sleep breathing disorders in the development and main tenance of hypertension. Other than that, epidemiological studies show that sleep-disordered breathing is highly prevalent among hypertensive patients<sup>26,27</sup>, and also that 50 to 80% of the patients who experience such changes are hypertensive<sup>20 </sup>. In this regard, the causal relationship of respiratory disorders might become confusing or disappear when age, obesity prevalence, smoking status, and alcohol consumption are taken into account in hypertensive patients. However, Grote et al<sup>20</sup>, in a cross-sectional, controlled study involving 1,190 patients, have shown that sleep breathing disorders are risk factors for hypertension and do not depend on body mass index, age, smoking status, alcohol consumption, cholesterol levels, and oxygen and carbon dioxide partial pressures. Therefore, scientific data point to the existence of a cause and main tenance relationship of hypertension associated with changes in respiratory control. </p>
      <p><italic>Spontaneous respiratory modulation and blood pressure reduction</italic> - In patients with essential hypertension, these changes in blood pressure are correlated with changes in breathing patterns, as evidenced in this study by statistical correlation and linear regression. According to Joseph et al<sup>11</sup>, the decrease in blood pressure during slow breathing, more precisely less than ten breaths per minute (BPM), is associated with improved baroreflex sensitivity, which suggests a change in autonomic balance resulting from an absolute or relative reduction in sympathetic activity or increase in parasympathetic tone. One of the difficulties faced by our study was the lack of baroreflex measurement, because this is an expensive method that requires a laboratory specially equipped for this purpose. However, the significant clinical value of heart rate variability (HRV) analysis s is well characterized in the literature. It has the advantage to allow a selective and non-invasive assessment of the autonomic function<sup>28 </sup>. In our sample, blood pressure decrease was accompanied by improvement in heart rate variability, suggesting that this is an effect of the autonomic nervous system's respiratory modulation. Bernardi et al<sup>17 </sup>studied the effect of a single session of slow breathing in healthy subjects and hypertensive patients and found increased baroreflex sensitivity with a consequent reduction in blood pressure and heart rate. In our study, there were no changes in heart rate, a finding that contradicts the acute chronotropic effects reported in the literature<sup>17 </sup>and previously detected by us in one patient with acute myocardial infarction and hypertension<sup>9</sup>. We believe that this may be due to the lack of a more accurate methodology capable of detecting chronotropic changes. In future studies, it would be recommendable that Holter electrocardiographic recordings be used to better assess these heart rate changes, as well as ABPM (Ambulatory blood pressure monitoring), to analyze the degree of the anti-hypertensive effect afforded by this breathing technique.</p>
      <p><italic>Autonomic imbalance in hypertension and breathing</italic> - The autonomic nervous system plays a key role in controlling blood pressure and heart rate, and is an important pathophysiological factor in the development of hypertension<sup>29</sup>. Sympathetic hyperactivity has been frequently associated with hypertension, in which the sensitivity of baroreceptor control is impaired, thereby compromising the autonomic function<sup>30</sup>. This state of hyperexcitation with increased sympathetic discharges is well characterized in the literature, which also reports the benefits of mental relaxation associated or not with breathing exercises in hypertensive patients<sup>16</sup>. In essential hypertension, the sympathetic hyperactivity results not only in arteriolar vasoconstriction, but also in chemoreflex activation, an important mechanism that regulates breathing, since the excitatory state is distributed to all organs and systems<sup>31 </sup>. Hypertensive patients usually show signs of hyperventilation at rest, suggesting that the cardiovascular and respiratory abnormalities may be related to a common excitatory pattern of the autonomic nervous system that could be modulated by the adoption of a slower breathing pattern<sup>11</sup>. In this context, the generalized hyperexcitatory pattern could explain the signs of hyperventilation found in patients with essential hypertension<sup>11</sup>; and as breathing can be voluntarily controlled, the long-term practice of a breathing pattern may also induce changes in cardiovascular control. </p>
      <p>Heart rate variability is reduced in hypertensive patients, as compared with normotensive subjects, and PNN50 and SDNN indices are lower in the time-domain method, reflecting decreased vagal tone (parasympathetic) and increased sympathetic tone, respectively<sup>32</sup>. In the present study, there was an improvement in heart rate variability, based on an increase in RR interval variation and the SDNN index, while the PNN50 index did not change significantly (p &gt; 0.05). This suggests that respiratory retraining using the slow breathing technique enhanced autonomic function not by increasing the parasympathetic tone, but rather by decreasing sympathetic activity. Our data corroborate the studies by Joseph et al<sup>11 </sup>and Bernardi et al<sup>17</sup>, who also noted an improvement in heart rate variability. </p>
      <p>According to Kaushik et al<sup>16</sup>, the hyperexcitation caused by increased sympathetic discharges may be modulated by sessions of relaxation and breathing exercises, together or alone. However, in this author's opinion, breathing exercises and relaxation are likely to modulate the autonomic nervous system through different mechanisms that need to be further elucidated. In this study, the hypothesis that breathing exercises may have provided some degree of relaxation to the patients cannot be discarded. Nevertheless, given the negative and significant statistical correlation (p &lt; 0.05) between tidal volume and blood pressure, the modulation of respiratory mechanics is thought to play a key role in this anti-hypertensive effect. </p>
      <p><italic>Integration of cardiovascular control and benefits of respiratory retraining</italic> - Cardiovascular and respiratory systems have a close relationship regarding their mechanisms of neural control, the physiology of which is not discussed in this paper. It is noteworthy, however, that in this mechanism of cardiovascular and respiratory control, the solitary tract nucleus plays a major role, since it receives afferent inputs from baroreceptors located in the heart and blood vessels, chemoreceptors, and lung stretch receptors<sup>33</sup>. Accordingly, baroreflex, chemoreflex, and Hering-Breur reflex seem to have common neuroanatomical pathways, which may provide a biological basis for the effects of breathing modulation on cardiovascular control and blood pressure reduction. </p>
      <p>In view of this body of evidence, our findings might be explained in many ways. During slow breathing, tidal volume increases to compensate for the reduced respiratory rate and to maintain minute ventilation<sup>34,35</sup>, which may be responsible for the autonomic changes by reducing sympathetic activity or activating the Hering-Breuer reflex<sup>18</sup>. According to Bernardi et al<sup>17</sup>, this increase in baroreflex depends solely on a lower respiratory rate, rather than on controlled breathing and, thereby, a frequency of six breaths per minute increases baroreflex, while a frequency similar to that of spontaneous breathing, such as 15 breaths per minute, fails to do it. Joseph et al<sup>11 </sup>believe that changes in respiratory amplitude, that is, in chest expansion, may increase the fluctuations in RR intervals, render baroreflex more effective, and decrease blood pressure. On the other hand, the increase intidal volume and activation of the Hering-Breuer reflex, which reduces chemoreflex sensitivity and consequently may highlight baroreflex efficacy, decrease blood pressure and sympathetic activity. </p>
      <p>These results may be explained also by chemoreflex reduction, the increase of which is known to elevate sympathetic activity and blood pressure<sup>37</sup>. In the opinion of Bernardi et al<sup>17 </sup>, slow breathing training enhanced oxygen saturation and the regulation of thypoxic chemoreflex, improving exercise capacity in patients with cardiovascular disease. Although respiratory gas exchanges were not measured in our sample, we believe that the increase in tidal volume attributed to greater chest expansion enhanced oxygenation in these patients. Wesuggest that other studies be made to evaluate this metabolic parameter by analyzing maximal oxygen up take(VO<sub>2</sub>) and carbon dioxide production (VCO2). However, our data have shown that respiratory rate reduction does not induce hyperventilation in these patients following the technique, since minute volume remained unchanged and tidal volume underwent a compensatory increase. These data were confirmed by Joseph et al<sup>11</sup>, because in their study slow breathing did not change minute volume and end-tidal carbon dioxide (ETCO2). As CO<sub>2 </sub>is maintained within resting ranges, slow breathing is well tolerated by patients.</p>
      <p>Breathing pattern management seems to be a fairly reasonable tool since voluntary stimulation is used to induce reflex changes in the cardiovascular system. The existence of common neuroanatomical bases in the modulation of cardiovascular and respiratory control is regarded as the biological foundation for this intervention. However, the exact mechanism of such integration is yet to be established. Slow breathing is not a new method, but rather an ancient Eastern tradition of Yoga<sup>38</sup>. Thanks to the benefits that yoga provides patients with cardiovascular diseases, its components (stretching, relaxation, and breathing techniques) sparked interest within the scientific community<sup>39</sup>. Some studies have shown improvement in cardiorespiratory control in hypertensive patients who practice Bhramari Pranayama, a yogic technique that involves slow breathing patterns, while techniques that use high-frequency breathing show antagonistic effects<sup>40</sup>.</p>
      <p><italic>Study limitations and final remarks</italic> - Study sample consisted of patients with well-controlled hypertension. The next step would be to analyze how reproducible these findings are in patients with more severe degrees of hypertension with or without the presence of other comorbidities.</p>
      <p> Based on our findings, we came to the conclusion that the correction of abnormalities in respiratory control of hypertensive patients improves cardiovascular and respiratory control, acting as an adjunctive for clinical and pharmacological treatment of hypertension. Slow breathing is a straightforward method with no contraindications that offers a rather valid cost-benefit, improving autonomic balance and respiratory control and lowering blood pressure in patients with essential hypertension. However, further studies with larger series of patients and probability sampling are needed to assess the impact of this intervention on a greater cohort of hypertensive patients.</p>
      <p>
        <bold>Potential Conflict of Interest </bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported. </p>
      <p>
        <bold>References</bold>
      </p>
      <p>
        <fn id="corr1-body2" fn-type="corresp">
          <label>
            <bold>Mailing address:</bold>
          </label>
          <p> Carlos Hermano da Justa Pinheiro</p>
          <p> Avenida Jaguar&#233;, 249/124</p>
          <p> 05346-000 - S&#227;o Paulo, SP - Brazil</p>
          <p> E-mail: </p>
          <p>
            <email xlink:href="fisiologia_carlos@yahoo.com.br">fisiologia_carlos@yahoo.com.br</email>
          </p>
        </fn>
      </p>
      <p> Manuscript received September 3, 2006; revised received November 8, 2006; accepted December 14, 2006.</p>
    </body>
  </sub-article>
</article>
