Respiratory acidosis

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Respiratory acidosis
Classification and external resources

ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH

Davenport diagram E87.2 276.2 95 92 med!2 8 D "#2

Respiratory acidosis i$ a medical condition in %hich decrea$ed ventilation &hypoventilation' ca($e$ increa$ed )lood car)on dio*ide concentration and decrea$ed p+ &a condition generally called acido$i$'. ,ar)on dio*ide i$ prod(ced contin(o($ly a$ the )ody-$ cell$ re$pire, and thi$ ,.2 %ill acc(m(late rapidly if the l(ng$ do not ade/(ately e*pel it thro(gh alveolar ventilation. 0lveolar hypoventilation th($ lead$ to an increa$ed Pa,.2 &called hypercapnia'. 1he increa$e in Pa,.2 in t(rn decrea$e$ the +,.23!Pa,.2 ratio and decrea$e$ p+.

Contents

" 1erminology 2 1ype$ of re$piratory acido$i$ 2 ,a($e$

o o

2." 0c(te 2.2 ,hronic

# 4hy$iological re$pon$e
o

#." 5echani$m

#.2 E$timated change$

5 6ee al$o 6 7eference$ 7 E*ternal link$

Terminology

cidosis refer$ to di$order$ that lo%er cell!ti$(e p+ to 8 7.25. cidemia refer$ to a arterial p+ 8 7.25.

Types o! respiratory acidosis

7e$piratory acido$i$ can )e ac(te or chronic.

9n acute respiratory acidosis, the Pa,.2 i$ elevated a)ove the (pper limit of the reference range &over 6.2 k4a or #7 mm +g' %ith an accompanying acidemia &p+ 87.25'. 9n chronic respiratory acidosis, the Pa,.2 i$ elevated a)ove the (pper limit of the reference range, %ith a normal )lood p+ &7.25 to 7.#5' or near:normal p+ $econdary to renal compen$ation and an elevated $er(m )icar)onate &+,.23 ;2 mm +g'.

Causes
cute
0c(te re$piratory acido$i$ occ(r$ %hen an a)r(pt fail(re of ventilation occ(r$. 1hi$ fail(re in ventilation may )e ca($ed )y depre$$ion of the central re$piratory center )y cere)ral di$ea$e or dr(g$, ina)ility to ventilate ade/(ately d(e to ne(rom($c(lar di$ea$e &e.g., mya$thenia gravi$, amyotrophic lateral $clero$i$, <(illain:=arr> $yndrome, m($c(lar dy$trophy', or air%ay o)$tr(ction related to a$thma or chronic o)$tr(ctive p(lmonary di$ea$e &,.4D' e*acer)ation.

C"ronic
,hronic re$piratory acido$i$ may )e $econdary to many di$order$, incl(ding ,.4D. +ypoventilation in ,.4D involve$ m(ltiple mechani$m$, incl(ding decrea$ed re$pon$ivene$$ to hypo*ia and hypercapnia, increa$ed ventilation:perf($ion mi$match leading to increa$ed dead $pace ventilation, and decrea$ed diaphragm f(nction $econdary to fatig(e and hyperinflation. ,hronic re$piratory acido$i$ al$o may )e $econdary to o)e$ity hypoventilation $yndrome &i.e., 4ick%ickian $yndrome', ne(rom($c(lar di$order$ $(ch a$ amyotrophic lateral $clero$i$, and $evere re$trictive ventilatory defect$ a$ o)$erved in inter$titial fi)ro$i$ and thoracic deformitie$.

?(ng di$ea$e$ that primarily ca($e a)normality in alveolar ga$ e*change ($(ally do not ca($e hypoventilation )(t tend to ca($e $tim(lation of ventilation and hypocapnia $econdary to hypo*ia. +ypercapnia only occ(r$ if $evere di$ea$e or re$piratory m($cle fatig(e occ(r$.

P"ysiological response
Mec"anism
5eta)oli$m rapidly generate$ a large /(antity of volatile acid &+2,.2' and nonvolatile acid. 1he meta)oli$m of fat$ and car)ohydrate$ lead$ to the formation of a large amo(nt of ,.2. 1he ,.2 com)ine$ %ith +2. to form car)onic acid &+2,.2'. 1he l(ng$ normally e*crete the volatile fraction thro(gh ventilation, and acid acc(m(lation doe$ not occ(r. 0 $ignificant alteration in ventilation that affect$ elimination of ,.2 can ca($e a re$piratory acid:)a$e di$order. 1he Pa,.2 i$ maintained %ithin a range of 29@#" mm +g in normal $tate$. 0lveolar ventilation i$ (nder the control of the central re$piratory center$, %hich are located in the pon$ and the med(lla. Aentilation i$ infl(enced and reg(lated )y chemoreceptor$ for Pa,.2, 4a.2, and p+ located in the )rain$tem,and in the aortic and carotid )odie$ a$ %ell a$ )y ne(ral imp(l$e$ from l(ng $tretch receptor$ and imp(l$e$ from the cere)ral corte*. Fail(re of ventilation /(ickly increa$e$ the Pa,.2. 9n ac(te re$piratory acido$i$, compen$ation occ(r$ in 2 $tep$.

1he initial re$pon$e i$ cell(lar )(ffering that occ(r$ over min(te$ to ho(r$. ,ell(lar )(ffering elevate$ pla$ma )icar)onate &+,.23' only $lightly, appro*imately " mE/!? for each " :mm +g increa$e in Pa,.2. 1he $econd $tep i$ renal compen$ation that occ(r$ over 2@5 day$. With renal compen$ation, renal e*cretion of car)onic acid i$ increa$ed and )icar)onate rea)$orption i$ increa$ed. For in$tance, 4E4,B i$ (preg(lated in renal pro*imal t()(le )r($h )order cell$, in order to $ecrete more C+2 and th($ to prod(ce more +,.23.D"E

#stimated c"anges
9n renal compen$ation, pla$ma )icar)onate ri$e$ 2.5 mE/!? for each increa$e of " mm +g in Pa,.2. 1he e*pected change in $er(m )icar)onate concentration in re$piratory acido$i$ can )e e$timated a$ follo%$F

0c(te re$piratory acido$i$F +,.23 increa$e$ " mE/!? for each " mm +g ri$e in Pa,.2. ,hronic re$piratory acido$i$F +,.23 ri$e$ 2.5 mE/!? for each " mm +g ri$e in Pa,.2.

1he e*pected change in p+ %ith re$piratory acido$i$ can )e e$timated %ith the follo%ing e/(ation$F

0c(te re$piratory acido$i$F ,hange in p+ G .

8 H &# 3 Pa,.2'

,hronic re$piratory acido$i$F ,hange in p+ G .

2 H &# 3 Pa,.2'

7e$piratory acido$i$ doe$ not have a great effect on electrolyte level$. 6ome $mall effect$ occ(r on calci(m and pota$$i(m level$. 0cido$i$ decrea$e$ )inding of calci(m to al)(min and tend$ to increa$e $er(m ioniIed calci(m level$. 9n addition, acidemia ca($e$ an e*tracell(lar $hift of pota$$i(m, )(t re$piratory acido$i$ rarely ca($e$ clinically $ignificant hyperkalemia.