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Tratamento da hipertensão na asma e DPOC

AUTOR: Steven E Weinberger, MD, MACP, FRCP
EDITORES DE SEÇÃO: George L. Bakris, MD, Umur Hatipoglu, MD, MBA
EDITORES ADJUNTOS: Lei Karen, MD, John P Forman, MD, MSc

Todos os tópicos são atualizados à medida que novas evidências são disponibilizadas e nosso processo de revisão por
pares é concluído.

Revisão da literatura atualizada até:  julho de 2023.

Última atualização deste tópico:  17 de maio de 2022.

INTRODUÇÃO

O manejo da hipertensão em paciente com asma ou doença pulmonar obstrutiva crônica

(DPOC) é um problema comum devido à alta prevalência de cada condição na população
adulta. As indicações para o tratamento da hipertensão e o uso de abordagens não
farmacológicas são semelhantes em pacientes com ou sem qualquer uma dessas condições.
(Consulte "Visão geral da hipertensão em adultos" .)

VISÃO GERAL

O tratamento farmacológico da hipertensão em pacientes com asma ou DPOC pode ser

complicado pelo efeito exacerbador da asma de alguns anti-hipertensivos. Por exemplo, os
betabloqueadores devem ser usados ​com muita cautela ou não devem ser usados ​em
pacientes com asma crônica (mas não com DPOC), broncoespasmo alérgico agudo ou
induzido por exercício, ou síndrome de sobreposição asma-DPOC. Os inibidores da enzima
conversora de angiotensina (ECA), entre os medicamentos anti-hipertensivos mais utilizados,
não são contraindicados na asma ou na DPOC, mas podem induzir uma tosse incômoda que,
embora não seja prejudicial aos pulmões, pode ser confundida com tosse devido à tosse
subjacente. doenças pulmonares como asma e DPOC.

Betabloqueadores  –  Os betabloqueadores podem aumentar a reatividade das vias aéreas

e interferir na atividade dos beta-agonistas. No entanto, os betabloqueadores são seguros
para uso na maioria dos pacientes com DPOC, mas menos em pacientes com asma.

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DPOC  —  Os betabloqueadores, particularmente os betabloqueadores seletivos para beta-1

( tabela 1 ), parecem ser seguros na maioria dos pacientes com DPOC.

Em alguns estudos observacionais de pacientes com DPOC, o uso de betabloqueadores

(incluindo beta-1 seletivo e não seletivo) foi associado a uma redução na mortalidade e
exacerbações de sintomas respiratórios [1,2 ] . Além disso, em uma meta-análise incluindo
10 ensaios de pacientes com DPOC, a terapia com betabloqueadores seletivos de curto prazo
não alterou o volume expiratório forçado basal no primeiro segundo (VEF1) nem aumentou
os sintomas respiratórios [3 ] .

No entanto, num ensaio subsequente que incluiu doentes com DPOC moderada a grave e
sem indicação cardiovascular primária para betabloqueadores, o metoprolol aumentou o
risco de hospitalização por exacerbações da DPOC (HR 1,91, IC 95% 1,29-2,83), embora a taxa
global de exacerbações da DPOC não foi aumentado [ 4 ]. No entanto, no Estudo de
Rotterdam, um estudo observacional que incluiu mais de 1.300 participantes com DPOC, os
betabloqueadores cardiosseletivos foram associados a um risco reduzido de exacerbações
da DPOC apenas entre aqueles que tinham indicação cardiovascular para o uso de um
betabloqueador, mas não naqueles sem indicação cardiovascular [ 5 ]. (Ver "Manejo do
paciente com DPOC e doença cardiovascular", seção 'Efeito dos betabloqueadores
cardiosseletivos na função pulmonar' .)

Asma  —  Em pacientes com asma, os betabloqueadores podem causar aumento da

obstrução brônquica e da reatividade das vias aéreas, bem como resistência aos efeitos de
agonistas dos receptores beta inalados ou orais (como albuterol ou terbutalina ) [ 6–8 ].
Mesmo a administração oftálmica tópica de betabloqueadores não seletivos para o
tratamento do glaucoma levou a exacerbações asmáticas [ 9 ]. Embora o mecanismo preciso
da broncoconstrição induzida por betabloqueadores seja desconhecido, as vias
parassimpáticas de controle das vias aéreas podem estar envolvidas, uma vez que o
medicamento anticolinérgico brometo de oxitrópio pode inibir o efeito do propranolol
inalado [ 10 ].

Embora os bloqueadores beta-1 seletivos sejam mais seguros que os betabloqueadores não
seletivos ( tabela 1 ), eles ainda devem ser usados ​com cautela em pacientes com asma,
particularmente naqueles com obstrução grave ou função pulmonar acentuadamente
reduzida no início do estudo [11 ] . Por exemplo, em uma meta-análise de 32 ensaios
randomizados incluindo mais de 1.300 pacientes com asma, os betabloqueadores não
seletivos causaram uma redução maior no VEF1 em comparação com os betabloqueadores
beta-1 seletivos (em 10 versus 7%) e também atenuaram a resposta. aos agonistas beta
inalados em comparação com bloqueadores seletivos beta-1 (em 20 versus 10 por cento) [ 6
]. No entanto, um em cada oito pacientes em uso de bloqueadores seletivos beta-1 teve uma
diminuição de 20% ou mais no VEF1.

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ACE inhibitors — ACE inhibitors are not first-line therapy in patients with COPD or asthma.
They increase the likelihood of cough (which may be confused with an exacerbation of COPD
or asthma) and, in patients with asthma, they may worsen airflow obstruction (although this
is uncommon). However, their use is not contraindicated in such patients.

The most common side effect of therapy with angiotensin-converting enzyme (ACE)
inhibitors is cough (typically described as dry, irritative, and persistent, but rarely productive),
which develops in 3 to 20 percent of patients [12]. When this cough develops in a patient with
either asthma or COPD, it can be confused with an increase in symptoms related to
underlying airway disease. There are conflicting data on whether patients with underlying
asthma are more likely than non-asthmatics to develop cough after ACE inhibition [12,13].

There is no evidence of adverse effects of ACE inhibitors on the course of COPD [14].
However, in asthmatic patients, some cases of worsening asthma with ACE inhibitors have
been described. In one study examining adverse respiratory effects to ACE inhibitors,
reactions diagnosed as asthma, bronchospasm, or dyspnea were reported at one-tenth the
frequency of cough, with several cases of bronchospasm occurring in patients with known
asthma [15]. In addition, the possibility that ACE inhibitor cough may represent an asthma
equivalent has been suggested by the demonstration of bronchial hyperresponsiveness in
some, but not all, affected patients [16,17]. (See "Major side effects of angiotensin-converting
enzyme inhibitors and angiotensin II receptor blockers", section on 'Cough'.)

An alternative, when it is desirable to block the renin-angiotensin system, is administration of

an angiotensin II receptor blocker. (See "Renin-angiotensin system inhibition in the
treatment of hypertension" and 'Angiotensin receptor blockers' below.)

Angiotensin receptor blockers — Angiotensin II receptor blockers (ARBs) do not appear to

induce cough, and may be used safely in patients with asthma or chronic obstructive
pulmonary disease (COPD). In one small trial including hypertensive patients with asthma,
there was no increase in cough or bronchial hyperreactivity with an ARB, and it was as well
tolerated as calcium channel blockers [18].

Diuretics — Thiazide diuretics are generally safe to use among patients with chronic
obstructive pulmonary disease (COPD) [19].

However, there may be potential issues related to metabolic alkalosis and, among those also
using beta agonists or glucocorticoids, hypokalemia:

● Among patients with COPD and chronic hypercapnia, diuretics can also induce a
metabolic alkalosis, which can suppress the ventilatory drive and potentially exacerbate
hypoxemia [20,21].

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● Inhaled beta agonists can drive potassium into the cells, acutely lowering the plasma
potassium concentration by as much as 0.5 to 1 mEq/L [22]. Glucocorticoids may lower
serum potassium by mildly enhancing urinary potassium excretion [22,23]. Thiazide
diuretics also reduce the serum potassium, and therefore concomitant use of these
agents with beta agonists or glucocorticoids can exacerbate hypokalemia [21]. (See
"Causes of hypokalemia in adults".)

Thus, it is safest to administer only low thiazide doses (eg, 12.5 to 25 mg of

hydrochlorothiazide once daily) to nonedematous hypertensive patients with asthma or
COPD. Low-dose therapy may be effective and less likely to produce unwanted side effects
such as metabolic alkalosis and hypokalemia. (See "Use of thiazide diuretics in patients with
primary (essential) hypertension".)

Calcium channel blockers — The calcium channel blockers (especially those of the

dihydropyridine group, such as nifedipine and nicardipine) are excellent agents for the
treatment of hypertension in asthma [21,24]. (See "Major side effects and safety of calcium
channel blockers".)

In addition to effectively lowering the blood pressure, calcium channel blockers also have the
theoretical advantages of opposing muscle contraction in tracheobronchial smooth muscle,
inhibiting mast cell degranulation, and possibly reinforcing the bronchodilator effect of beta
agonists. Nifedipine, for example, can antagonize the bronchoconstricting effects of antigen,
histamine, or cold air challenge [25]. Although some studies have shown a mild improvement
in airway function [25], most studies have demonstrated no effect of calcium antagonists on
asthma [26,27] .

Sympathetic blockers — Clonidine and other alpha-2 receptor agonists (methyldopa,

guanabenz) should be used with caution in asthmatics. Oral doses of these agents do not
change baseline air flow in asthmatics, but they do increase bronchial reactivity to inhaled
histamine [28].

Other — Little specific information is available for the remaining antihypertensive agents,

such as hydralazine. However, if asthma occurs with these or other drugs, one should always
consider the possibility that the tartrazine dye within the drug preparation may be the
culprit.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Hypertension in
adults".)

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SUMMARY

● Overview – Indications for treatment of hypertension and use of nonpharmacologic

approaches are similar in patients with or without asthma or chronic obstructive
pulmonary disease (COPD). The management of hypertension in a patient with either of
these conditions may be made difficult by the asthma-exacerbating effect of some
antihypertensive drugs. (See 'Introduction' above and 'Overview' above.)

● Beta blockers – Beta blockers can cause increased bronchial obstruction and airway
reactivity, as well as resistance to the effects of inhaled or oral beta receptor agonists
(such as albuterol or terbutaline) in patients with asthma but not COPD. Although the
clinical effects of more beta-1-selective beta blockers on pulmonary function appear to
be less severe, even beta-1-selective agents should be used with caution in asthmatic
patients with severe obstruction or markedly reduced baseline pulmonary function
( table 1). (See 'Beta blockers' above.)

● ACE inhibitors and angiotensin receptor blockers – Angiotensin-converting enzyme

(ACE) inhibitors are not first-line therapy in patients with COPD or asthma. They increase
the likelihood of cough (which may be confused with an exacerbation of COPD or
asthma) and, in patients with asthma, they may worsen airflow obstruction (although
this is uncommon). However, their use is not contraindicated in such patients. An
alternative, when it is desirable to block the renin-angiotensin system, is administration
of an angiotensin II receptor blocker. (See 'ACE inhibitors' above and 'Angiotensin
receptor blockers' above.)

● Diuretics – Diuretics can be effectively used in asthmatics but may cause serious
hypokalemia if used concurrently with inhaled beta-2 receptor agonists, which drive
potassium into the cells, and oral corticosteroids, which enhance urinary potassium
excretion. In addition, diuretic-induced metabolic alkalosis can suppress ventilatory
drive, potentially exacerbating the degree of hypoxemia. It is safest to administer only
low thiazide doses (12.5 to 25 mg of hydrochlorothiazide once daily) to nonedematous
hypertensive patients with asthma or COPD. (See 'Diuretics' above.)

● Calcium channel blockers – The calcium channel blockers (especially those of the
dihydropyridine group, such as nifedipine and nicardipine) are excellent agents for the
treatment of hypertension in asthma. In addition to effectively lowering the blood
pressure, they also have the theoretical advantages of opposing muscle contraction in
tracheobronchial smooth muscle, inhibiting mast cell degranulation, and possibly
reinforcing the bronchodilator effect of beta agonists. (See 'Calcium channel blockers'
above.)

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ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Norman Kaplan, MD, who contributed to an
earlier version of this topic review.

Use of UpToDate is subject to the Terms of Use.

REFERENCES

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2. Bhatt SP, Wells JM, Kinney GL, et al. β-Blockers are associated with a reduction in COPD
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3. Salpeter SR, Ormiston TM, Salpeter EE. Cardioselective beta-blockers in patients with
reactive airway disease: a meta-analysis. Ann Intern Med 2002; 137:715.
4. Dransfield MT, Voelker H, Bhatt SP, et al. Metoprolol for the Prevention of Acute
Exacerbations of COPD. N Engl J Med 2019; 381:2304.
5. Karimi L, Lahousse L, De Nocker P, et al. Effect of β-blockers on the risk of COPD
exacerbations according to indication of use: the Rotterdam Study. ERJ Open Res 2021;
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6. Morales DR, Jackson C, Lipworth BJ, et al. Adverse respiratory effect of acute β-blocker
exposure in asthma: a systematic review and meta-analysis of randomized controlled
trials. Chest 2014; 145:779.

7. Benson MK, Berrill WT, Cruickshank JM, Sterling GS. A comparison of four beta-
adrenoceptor antagonists in patients with asthma. Br J Clin Pharmacol 1978; 5:415.
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Med 2019; 381:1046.
9. Fraunfelder FT, Barker AF. Respiratory effects of timolol. N Engl J Med 1984; 311:1441.
10. Ind PW, Dixon CM, Fuller RW, Barnes PJ. Anticholinergic blockade of beta-blocker-
induced bronchoconstriction. Am Rev Respir Dis 1989; 139:1390.

11. Finks SW, Rumbak MJ, Self TH. Treating Hypertension in Chronic Obstructive Pulmonary
Disease. N Engl J Med 2020; 382:353.

12. Israili ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-
converting enzyme inhibitor therapy. A review of the literature and pathophysiology.
Ann Intern Med 1992; 117:234.

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13. Kaufman J, Casanova JE, Riendl P, Schlueter DP. Bronchial hyperreactivity and cough due
to angiotensin-converting enzyme inhibitors. Chest 1989; 95:544.
14. Mancini GB, Etminan M, Zhang B, et al. Reduction of morbidity and mortality by statins,
angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers in patients
with chronic obstructive pulmonary disease. J Am Coll Cardiol 2006; 47:2554.
15. Lunde H, Hedner T, Samuelsson O, et al. Dyspnoea, asthma, and bronchospasm in
relation to treatment with angiotensin converting enzyme inhibitors. BMJ 1994; 308:18.

16. Bucknall CE, Neilly JB, Carter R, et al. Bronchial hyperreactivity in patients who cough
after receiving angiotensin converting enzyme inhibitors. Br Med J (Clin Res Ed) 1988;
296:86.
17. Boulet LP, Milot J, Lampron N, Lacourcière Y. Pulmonary function and airway
responsiveness during long-term therapy with captopril. JAMA 1989; 261:413.

18. Tanaka H, Teramoto S, Oashi K, et al. Effects of candesartan on cough and bronchial
hyperresponsiveness in mildly to moderately hypertensive patients with symptomatic
asthma. Circulation 2001; 104:281.

19. Herrin MA, Feemster LC, Crothers K, et al. Combination antihypertensive therapy among
patients with COPD. Chest 2013; 143:1312.

20. Bear R, Goldstein M, Phillipson E, et al. Effect of metabolic alkalosis on respiratory

function in patients with chronic obstructive lung disease. Can Med Assoc J 1977;
117:900.

21. Cazzola M, Noschese P, D'Amato G, Matera MG. The pharmacologic treatment of

uncomplicated arterial hypertension in patients with airway dysfunction. Chest 2002;
121:230.
22. Lipworth BJ, McDevitt DG, Struthers AD. Prior treatment with diuretic augments the
hypokalemic and electrocardiographic effects of inhaled albuterol. Am J Med 1989;
86:653.
23. Wong CS, Pavord ID, Williams J, et al. Bronchodilator, cardiovascular, and hypokalaemic
effects of fenoterol, salbutamol, and terbutaline in asthma. Lancet 1990; 336:1396.
24. Barnes PJ. Clinical studies with calcium antagonists in asthma. Br J Clin Pharmacol 1985;
20 Suppl 2:289S.
25. Schwartzstein RS, Fanta CH. Orally administered nifedipine in chronic stable asthma.
Comparison with an orally administered sympathomimetic. Am Rev Respir Dis 1986;
134:262.

26. Ann Twiss M, Harman E, Chesrown S, Hendeles L. Efficacy of calcium channel blockers as
maintenance therapy for asthma. Br J Clin Pharmacol 2002; 53:243.

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27. Patakas D, Maniki E, Tsara V, Dascalopoulou E. Nifedipine treatment of patients with

bronchial asthma. J Allergy Clin Immunol 1987; 79:959.

28. Dinh Xuan AT, Matran R, Regnard J, et al. Comparative effects of rilmenidine and
clonidine on bronchial responses to histamine in asthmatic subjects. Br J Clin Pharmacol
1988; 26:703.
Topic 3831 Version 33.0

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GRAPHICS

Propriedades do bloqueador beta

Bloqueio Seletividade Dose

Medicamento É UM MSA Lipofilicidade
alfa beta-1 habitual*

Acebutolol No Yes Yes Yes Low 100 to 400 mg

twice per day

Atenolol No Yes No No Low 50 to 200 mg

once daily

Betaxolol No Yes No Yes Low 10 to 20 mg

once daily

Bisoprolol No Yes No No Moderate 2.5 to 20 mg

once daily

Carteolol No No Yes No Low 2.5 to 5 mg

once daily

Carvedilol Yes No No Yes High 3.125 to 25 mg

twice per day

Esmolol No Yes No No Low IV only 250 to

500
micrograms/k
over one
minute then
25 to 50
micrograms/k
per minute as
IV infusion;
titrate
incrementally
up to
maximum of
300
microgram/kg
per minute Δ

Labetalol Yes No Yes Low Moderate IV 20 mg Δ

(Beta2)

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Orally 100-400
mg two or
three times
per day

Metoprolol No Yes No Low Moderate IV 1.25 to 5

tartrate mg Δ

Orally 25 to
100 mg two
times per day

Metoprolol No Yes No Low Moderate Orally 50 to

succinate 400 mg once
(extended daily
release)

Nadolol No No No No Low 40 to 160 mg

once daily

Nebivolol No Yes No No High 5 to 40 mg

once daily

Oxprenolol ◊ No No Yes Yes Moderate 40 to 80 mg

three times
per day

Penbutolol No No Yes No High 10 to 40 mg

once daily

Pindolol No No Yes Low Moderate 5 to 30 mg

twice per day

Propranolol No No No Yes High IV 1 to 5 mg Δ

Orally 10 to 80
mg two to fou
times daily

Sotalol § No No No No Low 80 to 160 mg

twice per day

Timolol No No No No Moderate 10 to 30 mg
twice per day

ISA: intrinsic sympathomimetic activity; MSA: membrane stabilizing activity; IV: intravenous.

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* Range of usual, oral, anti-hypertensive dose, unless "IV" noted.

¶ Duration of hypotensive effect, in general, is longer than may be predicted by serum half-life.

Δ Usual initial IV dose. Subsequent dosing generally needed. See drug monograph for detail.

◊ Not available in US.

§ Sotalol has independent class III antiarrhythmic activity.

Prepared with data from:

1. Frishman WH, Alwarshetty M. β-Adrenergic blockers in systemic hypertension pharmacokinetic considerations
related to current guidelines. Clin Pharmacokinet 2002; 41:505.
2. Brubacher JR. β-Adrenergic Antagonists. In: Goldfrank's Toxicologic Emergencies, 9th ed, Nelson LS (Ed), McGraw-
Hill, New York 2010.

Gráfico 82571 Versão 11.0

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Contributor Disclosures
Steven E Weinberger, MD, MACP, FRCP No relevant financial relationship(s) with ineligible companies
to disclose. George L Bakris, MD Grant/Research/Clinical Trial Support: Bayer [Diabetic nephropathy];
KBP Biosciences [Resistant hypertension]; Novo Nordisk [Diabetic kidney disease]. Consultant/Advisory
Boards: Alnylam [Resistant hypertension]; AstraZeneca [Diabetic nephropathy]; Bayer [Nephropathy];
Ionis [Resistant hypertension]; KBP BioSciences [Resistant hypertension]; Vifor [Hyperkalemia]. All of
the relevant financial relationships listed have been mitigated. Umur Hatipoglu, MD, MBA No relevant
financial relationship(s) with ineligible companies to disclose. Karen Law, MD No relevant financial
relationship(s) with ineligible companies to disclose. John P Forman, MD, MSc Nenhuma relação
financeira relevante com empresas inelegíveis para divulgar.

As divulgações dos colaboradores são revisadas quanto a conflitos de interesse pelo grupo editorial.
Quando encontrados, estes são abordados através de um processo de revisão multinível e através de
requisitos para referências a serem fornecidas para apoiar o conteúdo. O conteúdo referenciado
adequadamente é exigido de todos os autores e deve estar em conformidade com os padrões de
evidência do UpToDate.

Política de conflito de interesses

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