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  • Acute Metabolic Alkalosis PDF

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    Edil M Jama
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    10 visualizações4 páginas

    Acute Metabolic Alkalosis PDF

    Enviado por

    Edil M Jama

    Direitos autorais:

    © All Rights Reserved
    Baixe no formato PDF ou leia online no Scribd
    Sinalizar o conteúdo como inadequado
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    bopen|consuuT cet ae ee Seconp EpItion ecole CTaMmely 0 eee SAUNDERS. x Fa Fe a 4 i ne e 5 fe “4 5 5 4 5 5 5 5 a = = = = = = = A. Kellum ‘Opsecrives Bases San Poors: syndromes ond complications associated with rele aloe, a ea eae aan drones of scute table alkalosis rest rom a fogs of chloride (Ci) lading t increased stung pn next fl Acitareae Cocopt isa pata a mx ald be daar. [sa the presence of alain (ose! p= on bose exenea (SBE) highest 2 ill pallets, mtabolicallaosis account, fall ucd-base disorder and ts esociated tuoraliy rato tn patints with an areal pit 2.58 wth ar 3 mortality rate patients DE higher than 785° Given the cliaial oy of cay Ie ipratn pe Crs cinclans correctly recognize tnd oat on. This chaptr dicusees the pathophysiol- eas, end management of ccute metbolle ‘OF ACUTE ALKALOSIS lons Bion concentration ar, less commonl eA te eee pesca mera ane rite St issuing tn acute loss of anions, such as si vowing, nasogastic suction), teed to its ion dineronee (SID) which tn tum ssociation of wate. thereby lowering Ht mui th olavating pH. Thor are thive coma int © acute ineease in SID. formal physiological conditions, serum Na? ha lt Svar than serum Cl-concentretion, ran ation i ee wale concettion ete both Nev and CI concentrations. O ‘sting value of serum Na in comparsoi te Metabolic Alkalosis ‘Modden, Raghavan Murugan, Mathew A. Butkus, Chapter 128/ Acute Metabolic Alkalosts 667 with Cr foo wator depletion causes incrses in Nat rele- veto thereby leading toa net erase ‘in SID, Critically il patients oftan scrub ta five water depletion because of depressed level of consciousness and ttiminished response ta thst stimull ‘Second, chloride loss ffom the gastrointestinal tract, (eg. from vomiting or gastric drainage) or trom urine {ea in diurtic use} Is greator than the corresponding Na loss, For instance, if gastric secrtions are removed! from he patent hgh dtr conus tin att or vomiting, Gris lost progressively and the SID increases sadly. The Cl los, not the H lost a the determinaat ‘of plasma pH, Although H's lost ae HCL, it also is lost with every molecule of water removed ffom the body When CI (a strong anion) is lost without the loss of a strong cation, the ‘SID 1s Increased, and therefor, the plasme Hf concentration Is decreased. When His lost as Water, rather than a HCl, there 1s no change in the SID) and, hence, no change in the plastna Ht" concentration, Similarly; the loss of ehloride-tich uid in the stool in lores leads to contraction of extrscellalar Muld volume 5 well as metabolic alkalosis, Altematively, Cl. depletion ‘can have a renal origin, a8 whem loop diuretics ae boing ‘administered, Tho mechanism involves increased stile lon of the reninangiotensin-aldosterone pathway. The fend result ofthe pathway, aldosterono, ie atsoclated with fn increase in Nav roabsorption and a loss of K" and Gl ‘The excretion of K-and Cr results nat only fou increased aldosterone concentrations but also fram the diuretic Itself, The mavemeat of those ions du to the dirotic leads toa more rapid onset of metabolic alkalosis, ‘Third, elthough loss common, an increate i SID du to cation administration rather than anion depletion ca also genorate metabolic alkalosis (Tabla 128-0, Acuto mete. ‘bolic alkalosis rsults when Na°is administered in excoss of CE for instance wits blood wansfusions (sodium citrate), parenteral ‘nutrition (sodum acetate), plasma volume ‘expanders (acetate or citrate), oF lactated Ringer's sation (odium Iactato), when an antibiotic (o, penicillins) to ‘administered asa sodium salt, or with use of excessive Sodium bicarbonate, During blood tansfusions, Ne" is given with citrate ratherthan Cl: Ascittate is metabolized, ‘SID rise, Role of Total Weak Acid Concentration ‘The second mechanism for the ganeration of acute mtr bolic alkalosis is a change in weak acid concentration, ‘Weak acid, unlike strong fons, can exist ina ontzed [2¢) fr protonated [AHI state In normal physiological condi- tons, such thet: Ag “TAHA ‘Ay represents te total concentration of nonvolatile weak ‘acids {most commonly albumin and phosphate). All else os Ftiologies of Acute Metabolic Alkalosis ‘Raion depletion Gate lore (og, vomiting neces dstoge alii) Uncut core dures Thaneteide chiootaide, tno) ‘isa! sates (villous adenoma, congenital elites) oriypmcapnie ste Guatossetopisty Sate lela eypdzome Solan sat amines (cette, ‘ints ‘loo transfsions loa volume expanders Sodium lactate Pareto auton Hypealeatnomla Hypophosphaterla Disorder of tu ‘hoevolael oak telds (d. etic uote aes being constant, 3 decrease in A vet ‘ibe fos agniicant, fo yield acute metabolic alkalosis tt eoalbuminemia ald bypopbosphatemla)- Hy pole exnahia ie eamony found t entaly il pact ‘Aiowgh albumin syatids ie rogalatd largely By oxo: itl Sh the extavascular hepatic space and cool Te gets Tow concentrations of allumin not only seul rom hopati iovgulasies but also can be induced Seti asp and tnd, he cree the surface of albumin, pearly the function SPARE ne mseton, Mucustes with changes in Ui, haute ws op ¢ lasna weak. aid, and. tho albu atpantaton must be considered in deerminaton ofthe cating caus a lbalosa, Likewise, posphate serves wre'nonplatle weak ack Ke reprntation In Subagh em propoueed than tha f abun, ca hs ign eda implications in taes of hypophospha- eee cll hs dsordar anions an ttrcalalae Shit un emnn iy tn dhofeencls ‘COMPLICATIONS {eon tat, In metaolle alas, is typically higher tan mip sees alan tn ner ean levels of oxygen delivery throughout te system ee vaio gifs 780) Soveremeteboc aalost cat fest in appreciable pester. metabolic ardlovas- Sue She notologteal complications. Las sovers cares Sony use fw symptoms that ar unique tothe lkalons Fesplratory complications generally include a decent in aereen delivery incre Pon). Tho Bohr effet, which eEhanced by elevations of HCO, Ip the asociated daoanarpee: Ar incrose in moot ally fr oye "mately onl. In sovere motabolie alkalosis, hypoxia aati teypokalemia, ypophosphatomiay decraned GE TGnzation, and hypomagnesemia ay lao be present ‘The cardiovascular responses are primar tle ends pubsoquent decrease In coe Hoe neoed fnotopy and digoxin toc dn eaters ces of mere pronounced mat Tas cardiac arrhythmias may be detectable. Nee Symptoms of metabolic acidons include dling’ SRE oela excabilty and in more sean MANAGEMENT ‘The primary goal of management of a pany Tied ieubolleeuatons is suspected should th anerying elope bitin he arose inal dass og Sie op cori sstt) a as En Spe Obtaining a thorough istry ind Crain wll mom ly Sones stead Stotogy. In cases of acute metaboltealelois og seer tetaninal eat volute contain” al (eube'otmonchlorid sodium sll are the mato ‘hows, Serum electrolyte loves and ater Cats should be reviewed. Adaitionally, {rine Cl concentration 1 useful in difeenttigt "Elondesspousive and chloride resistant Ghapter 118, Additional constdaralon must ba fo owsblityof «concomitant respiratory ca the BelSbase dloorden The expected areal Shiotieed with motabolc slkaloss shoul beg thupugh the uso of the HOO,” concentration or wale, as follows Poo, (mm Hy) e 7

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