Acid-Base Disorder. Objectives: Develop an approach to acid base problems Identify the primary acid base disturbance Solve simple acid base cases

Transcription

1 Acid-Base Disrder Objectives: Develp an apprach t acid base prblems Identify the primary acid base disturbance Slve simple acid base cases Team Members: Yazeed Al--suhaibani, Salem Basamad, Qaiss Al-muhaideb, Rana Barasain Team Leader: Nawaf Alkhudhayri Revised By: Basel almeflh Resurces: 436 slides team + Davidsn + kumar + Recall questins step up t medicine. Editing file Feedback Clr index: IMPORTANT - NOTES - EXTRA - Bks

2 Intrductin Nrmal value Helpful vide: 3: 21 minutes Arterial bld ph = while nrmal ph f venus bld is PaCO2 = Serum HCO3-= Anin gap = 8-12 Nrmal values are different due t different references. Check the given reference in the test. maintaining nrmal ph is imprtant t maintain the integrity f prtein functin (Enzyme functin and membrane prteins). Basic RECALL Acid-base balance is cncerned with maintaining a nrmal hydrgen in cncentratin in the bdy fluids. This balance is achieved by buffers utilizatin f in extracellular fluid and intracellular fluid, by respiratry mechanisms that excrete carbn dixide, and by renal mechanisms that reabsrb bicarbnate and secrete hydrgen ins. Bld ph refers t the level f H + ins and maintained by several buffering systems. A decrease in bld ph is called acidemia and is caused by acidsis. An increase in bld ph is called alkalemia and is caused by alkalsis. Disturbances f acid-base balance are described as either metablic r respiratry, depending n whether the primary disturbance is in HCO 3 r CO 2. The assessment f acid base abnrmalities is typically dne using arterial bld gases (ABG) Given the ease f btaining venus bld gases (VBG) and capillary bld gases (CBG) these are ften used in clinical practice Always check the reference range in yur lcal labratry Buffering A buffered slutin resists a change in ph. Mst imprtantly the bicarbnate-carbnic acid buffer pair that depends n the balance between bicarbnate ins and carbnic acid. In cmpensatin, Ph gets clse t the nrmal value but des nt reach nrmal. ur bdies cmpensate by 3 mechanisms: Breathing in r ut (if it is metablic ), Excreting / retaining hydrgen (respiratry) and Buffers in bld. In cases f nrmal Ph levels, lk at the patient s health. if the patient has a disease with a nrmal ph level think f mixed acidsis and alkalsis. If the patient appears healthy with a nrmal ph they re mst prbably nrmal 2

3 Respiratry Acidsis Definitin Increased PaCO2 and decreased ph. Mechanism Prcess that primarily causes elevatin in PaCO2 : Reduce effective ventilatin e.g. many chrnic respiratry diseases r drugs depressing the respiratry center. Alvelar Hypventilatin Accumulatin f CO2 Increases in PaCO2 Respiratry acidsis ph decreases. HCO3 will increase (Cmpensatin) but it needs time (12-24 h) as the kidney need time t cmpensate. Etilgy Hypventilatin f any cause: CNS Peripheral nervus system Neurmuscular junctin Muscular disease Chest wall Brnchial tree Other Damage f the respiratry center in the brainstem Caused by: Strke, Hemrrhage, Trauma, Tumr, Medicatin (Cmmnly sleeping pills, ther: mrphine, anesthetics and narctics) Demyelinating disease Of PNS ex. Guillain-Barre syndrme 1 Myasthenia gravis Intercstal muscle atrphy, such as: Duchenne dystrphy Cngenital muscle atrphy Severe sclisis COPD 2 retain CO2 exchange gases lung defect leading t acute/chrnic Respiratry acidsis) Drwning, Sleep apnea and Mrbid besity. 1 usually fllw diarrhea r flu like illness fllwed by ascending paralysis frm legs ging up (reach respiratry muscles). 2 Any disrder that reduces CO2 clearance (i.e., inhibits adequate ventilatin) can lead t respiratry acidsis. 3

4 Clinical Features: Symptms: Smnlence 3, cnfusin, myclnus with asterixis (Flapping tremrs) Signs f acute CO2 retentin: headaches, cnfusin, and papilledema 4. Classificatin: Each f the simple respiratry disrders has tw ranges f expected values, ne fr the acute disrder and ne fr the chrnic disrder. The acute disrder is present befre renal cmpensatin has ccurred, and, therefre, values fr bld ph tend t be mre abnrmal. The chrnic disrder is present nce renal cmpensatin has ccurred, which takes several days (starts within 24 hurs). Renal mechanisms increase the excretin f H+ within 24 hurs and may crrect the resulting acidsis caused by chrnic retentin f CO2 t a certain extent. Because f the cmpensatry prcess, values fr bld ph tend t be mre nrmal in the chrnic phase. Causes Acute Respiratry Acidsis 1. Respiratry: airway bstructin, severe pneumnia, chest trauma/pneumthrax 2. Acute drug intxicatin: narctics, sedatives. 3. Residual neurmuscular blckade. 4. CNS disease (head trauma) Chrnic Respiratry Acidsis 1. Chrnic lung disease (COPD) 2. Neurmuscular disease 3. Extreme besity 4. Chest wall defrmity 5. Muscular e.g. Duchenne dystrphy ph LOW Almst NORMAL due cmpensatry mechanism. Cmpensatin Immediate cmpensatry f HCO3. HCO3 by 1 meq/l fr every 10 mmhg in PaCO2. HCO3 by meq/l fr every 10 mmhg in PaCO2 (Due t renal adaptatin) 3 Drwsiness r sleepiness 4 Papilledema is ptic disc swelling that is secndary t elevated intracranial pressure. Pathphysilgy: Increased PaCO2 causes increased cerebral bld flw which increases CSF pressure Resulting in generalized CNS depressin. 4

5 Treatment: Verify patency f airways. Give supplemental xygen: If PaO2 is lw (<60 mmhg), Oxygen is cntraindicated in COPD patients (CO2 retentin) as it can exacerbate symptms. The explanatin is that hypxia drives breathing, s when the patient is n lnger hypxic, hypventilatin can result and hypercapnia wrsens, causing a respiratry acidsis. Treat underlying cause. Intubatin and mechanical ventilatin might be required fr: Severe acidsis (PH <7). PaCO2 > 60 r inability t increase PaO2. Mental deteriratin. Impending respiratry fatigue. Respiratry Alkalsis Definitin: Decreased PaCO2 and increased ph. Mechanism: Prcess that primarily causes reductin in PaCO2 : Increase ventilatin e.g.in respnse t hypxia r secndary t metablic acidsis. Alvelar hyperventilatin increased wash ut CO2 decrease in PaCO2 increased ph. Cmpensatin: HCO3- will decrease after (12-24 h). Etilgy Hyperventilatin 5 f any Cause: Overaggressive mechanical ventilatin. Anxiety (mst cmmn), Fever (nt severe) 2nd mst cmmn. Pain, Sepsis, Pregnancy 6, Hepatic failure (cirrhsis) Hypxemia, Restrictive lung disease Medicatin (salicylate txicity e.g. aspirin verdse 7 ) Severe cngestive heart failure, Thyrtxicsis. Pulmnary emblism, asthma, pneumnia. Respiratry alkalsis can be caused by anything that causes hyperventilatin (anxiety causing panic attack) 5 Any disrder that increases the respiratry rate inapprpriately can lead t respiratry alkalsis 6 increase serum prstaglandin Hyperventilatin. 7 verstimulatin f respiratry center Hyperventilatin. Aspirin can cause bth respiratry alkalsis and metablic acidsis. 5

6 Clinical Features: (lightheadedness, dizziness, anxiety, paresthesia, and periral numbness) 8 Tetany 9, Arrhythmias, Trusseau s sign and Chvstek s sign may be psitive Classificatin: Acute Respiratry Alkalsis HCO3 by 2 meq/l fr every 10 mmhg in PaCO2. Chrnic Respiratry Alkalsis HCO3 by 4-5 meq/l fr every 10 mmhg in PaCO2. Treatment: Treat the underlying cause. Smetimes this des nt need t be treated (e.g., in the case f pregnancy). Breathe int paper bag t recycle the exhaled CO2 (especially wh have anxiety). Metablic Acidsis Definitin: Lss f [HCO3] r additin f [H + ] and decreased ph. Mechanism: Prcess that primarily reduce bicarbnate: Excessive H + frmatin e.g. lactic acidsis, ketacidsis. Reduce H + excretin e.g. renal failure. Excessive HCO3 - lss e.g. diarrhea. Increase acid gaining either Exgenus Intake r Endgenus prductin. Or Decrease acid excretin. Or Lss r decrease prductin f bicarbnate. Cmpensatin 10 : Hyperventilatin decrease PCO2 immediately. If the kidneys are intact and the primary cause f acidsis is nt renal in rigin, the kidney can gradually increase acid secretin ver days t weeks and restre a new steady state 8 Symptms are mstly related t decreased cerebral bld flw (vascnstrictin). 9 Indistinguishable frm hypcalcemia 10 Metablic prblems always shw cmpensatin. 6

7 here s a helpful vide t explain the Anin gap! The Anin gap: The difference between primary measured catins (Na+ and K+) and the primary measured anins (Cl - and HCO 3 - ) in serum: Anin gap = catins - anins AG= ([Na+] + [K+]) - ([Cl-] + [HCO 3]) Or Anin gap = Sdium - (Chlride + Bicarbnate) AG = [Na+] - ([Cl-] + [HCO 3-]). It is helpful in determining the cause f a metablic acidsis Classificatin & Etilgy: It s mainly divided int nrmal Anin gap acidsis and High Anin gap acidsis Causes f High Anin Gap Metablic Acidsis (MUD PILES): Methanl Uremia DKA (check glucse) Prpylene glycl (nt paraldehyde) INH (impaired hepatic clearance f lactate) Lactic acidsis Ethanl/Ethylene Glycl Salicylates Prblem Causes Increased Endgenus prductin Increased Exgenus Intake Lactic acidsis Diabetic Ketacidsis Uremia Oxalic acid Frmic acid Lw tissue perfusin (decreased xygen delivery t tissues) Shck states (septic, cardigenic, hypvlemic) DM, Prlnged starvatin and prlnged alchl abuse Renal failure decreased NH4 + excretin (thus decreasing net acid) Decreased excretin f rganic anins, sulfate, and phsphate increases AG. Ethylene glycl verdse/intxicatin (manifestatins include cardipulmnary failure, calcium xalate crystals and renal failure) Methanl verdse (manifestatins include blurred visin) Other Salicylates 11 (Aspirin verdse), aldehyde, Acetaminphen, alchl 11 Salicylate verdse causes bth primary respiratry alkalsis and primary metablic acidsis. 7

8 Nrmal AG Acidsis The lw HCO3 is assciated with high Cl, s that the AG remains nrmal. GI lss f HCO3 Diarrhea, fistula in intestine r pancreas, Uretersigmidstmy: (cln secretes HCO3 in urine in exchange fr Cl) RENAL 12 HCO3 reabsrptin. prductin f HCO3 Carbnic anhydrase inhibitin Prximal Tubular Acidsis (RTA Type 2) Distal Tubular Acidsis (RTA Type 1) Due t diuretics as acetazlamide. Other Pst- hypcapnia Respiratry alkalsis renal wasting f HCO 3 rapid crrectin f respiratry alkalsis transient Acidsis until HCO 3 regenerated Dilutinal Due t rapid infusin f bicarbnate - free IV fluids. One f the causes f metablic acidsis with nrmal anin gap is Urinary diversin prcedure. In this prcedure the ureter is taken frm kidney and attached t gut, urine is excreted with stl. With that, there is retentin f chlride frm urine leading t hyperchlremic acidsis In summary: 1) Gain acid frm A) Outside: alchl ethanl, methanl r B) Inside: renal failure, lactic acidsis, ketacidsis 2) Lss HCO 3 frm diarrhea r RTA REMEMBER! 1- High Anin Gap a. Endgenus: +ve Ketnes: ketacidsis because f starvatin r diabetic ketacidsis -ve ketnes: lactic acidsis because f ischemia r hypxia, r uremia in renal failure. b. Exgenus: (e.g. alchl, ethanl, methanl, paraldehyde and aspirin verdse) 2- Nrmal Anin Gap Diarrhea and Renal tubular acidsis. 12 T distinguish between RTA & Diarrhea we perfrm Urine Anin Gap (UAG= Sdium - Chlride): In RTA there is a defect in acid secretin s less Cl int urine result f UAG psitive number. In Diarrhea Excretin acid is intact H+ is excreted with Cl- in urine UAG negative number. 8

9 Clinical Features: Hyperventilatin (deep rhythmic breathing) als called Kussmaul respiratin. Decreased in Cardiac utput and tissue perfusin. a. Occurs with severe metablic acidsis (bld ph < 7.2) b. Acidsis diminishes tissue respnsiveness t catechlamines. This can lead t an undesirable chain f events: pr tissue perfusin lactic acidsis decreased cardiac utput hyptensin further decrease in tissue perfusin. Treatment: 1. Treat the underlying cause. 2. Sdium bicarbnate is smetimes used in severe acidsis (esp. in nrmal AG acidsis). 3. Mechanical ventilatin might be needed if the patient is fatigued (esp. in DKA) Metablic Alkalsis Definitin: Additin f [HCO3] r lss f [H + ] and increase ph Mechanism: Prcess that primarily raises bicarbnate: Extracellular fluid vlume lss e.g. due t vmiting r diuretics Excessive ptassium lss with subsequent hyperaldsternism Initiating metablic alkalsis by either: Gaining f HCO 3- Or Lss f acid (H+) ex: frm vmiting. 13 Maintaining Metablic alkalsis due t the kidney inability t excrete the excess HCO 3 Cmpensatin: Hypventilatin increased PCO 2 (respiratry Acidsis) immediately (PaCO 2 by 0.6 mmhg fr every 1 meq/l in HCO 3). 13 Uncmplicated metablic alkalsis is typically transient, because kidney can nrmally excrete the excess HCO3-9

10 Classificatin & causes: Saline Respnsive Urine (cl-) <20 Saline resistant Urine (cl-) >20 Definitin Causes Metablic alkalsis with ECF cntractin (due t fluid lss). Gastric lss f H+ and generatin f HCO3 such as vmiting (HCl lss), NGT drainage Diuretic use These decrease the ECF vlume, bdy HCO3 cntent is nrmal, but plasma HCO3 increases due t ECF cntractin. Vlume depletin: Lss f sdium and fluid leads t hypvlemia and secndary hyperaldsternism, triggering prximal sdium bicarbnate reabsrptin and additinal acid secretin by the distal tubule Hypkalemia ccurs due t ptassium lss in the vmitus and by the kidney as the result f secndary hyperaldsternism, and itself is a stimulus t acid secretin. Pst-hypercapnia Villus adenma f cln, diarrhea with high chlride cntent Metablic alkalsis with ECF vlume expansin (n fluid lss) Hypertensive: Primary Hyperaldsternism either Nn-mineralcrticid, Cushing Syndrme Hyp/nrm tensive: Exgenus alkali lad either IV r ral sdium bicarbnate Bartter's syndrme & Gitelman's syndrme, Severe hypkalemia Treatment Treat by saline due t vlume depletin Accrding t Etilgy Clinical Features: There are n characteristic signs and symptms (mst imp. Hx) Treatment: Treat the underlying cause. Give nrmal saline plus ptassium in saline respnsive. Spirnlactne (K+ sparing diuretic) might be cnsidered in saline resistant. Steps in Acid-Base Analysis Helpful Vide: 8: 38 min Nrmal value Arterial bld ph = PaCO 2 = Serum HCO 3-= Anin gap =

11 Step 1: Take a thrugh histry and physical examinatin, lk fr clues that may lead t the abnrmalities in ph Fr example: Vmiting (metablic alkalsis), Diarrhea (metablic acidsis), COPD CO2 Hypventilatin (respiratry acidsis), hyperventilatin Respiratry alkalsis, Medicatins: laxatives, diuretics, etc (metablic alkalsis), Diabetes (DKA) metablic acidsis Vmiting Diarrhea Hypventilatin Respiratry disease Medicatins (laxatives, diuretics, etc) Diabetes etc Step 2: Lk at the ph: Determine if this is Nrmal (N abnrmality r mixed acidsis and alkalsis) Lw <7.35 (acidemic) High >7.45 (alkalemic) Step 3-a: ph Nrmal r mixed acidsis and alkalsis Determine the primary abnrmality that is causing the abnrmal ph If the ph is acidemic (<7.35), then lk fr Lw HCO3 (Metablic) r High PCO2 (Respiratry) If the ph is alkalemic (>7.45), then lk fr High HCO3 (Metablic) r Lw PCO2 (Respiratry) T determine whether the disturbance affects primarily the arterial PaCO2 r the serum HCO3. Primary disturbance is in CO2 Respiratry (nrmal value 35-45) Primary disturbance is in HCO3 Metablic (nrmal value 22-26) As mentined earlier, Cmpensatin will nt return the ph t the nrmal range, it s just a mechanism which the bdy trying t reduce the impact. 11

12 Step 3-b: If ph is nrmal, that desn t rule ut mixed acidsis and alkalsis (Determine what is being mixed) Lk fr high r lw PCO2 Lk fr high r lw HCO3 Lw PCO2 suggests respiratry alkalsis High PCO2 suggests respiratry acidsis Lw HCO3 suggests metablic acidsis High HCO3 suggests metablic alkalsis Is the respiratry disturbance acute r chrnic? Acute respiratry acidsis: HCO3 increase by 1 meq/l fr every 10 mmhg increase in PaCO2. Chrnic respiratry acidsis: HCO3 increase by meq/l fr every 10 mmhg increase in PaCO2. Acute respiratry alkalsis: HCO3 decrease by 2 meq/l fr every 10 mmhg decrease in PaCO2. Chrnic respiratry alkalsis: HCO3 decrease by 4-5 meq/l fr every 10 mmhg decrease in PaCO2. Step 4: After determining the primary abnrmality, check fr cmpensatin: Cmpensatin is the mechanism by which the bdy adapts t either acidsis r alkalsis, it will nt fully crrect the abnrmality, Fr example: A patient has diabetic ketacidsis, ph is 7.29, HCO3 is 15 Expected PCO2 by using Winter s frmula PCO2 = 1.5 x HCO3 + 8 ( ±2 ) = 1.5 x = 30.5 S yu expect the PCO2 in this patient t be in the range f If the PCO2 in this patient is higher than 32.5 cnsider additinal respiratry acidsis If the PCO2 in the patient is lwer than 28.5 cnsider additinal respiratry alkalsis 12

13 Cmpensatin calculatins: Memrize ne cmpensatin equatin fr each acid base abnrmality. Example: If patient has metablic acidsis, calculate PCO2, Higher r lwer than expected means it is Mixed. If the PCO2 in this patient is high ( mixed metablic and respiratry acidsis) If the PCO2 in the patient is lw mixed metablic acidsis respiratry alkalsis Step 5: Calculate the anin gap (AG): AG = Na (Cl + HCO3) Albumin is the main unmeasured anin. T vercme the effects f the hypalbuminemia n the AG, the crrected AG can be used which is AG + (0.25 X (40-albumin) expressed in g/l. when we see increase in anin gap that s mean there s additinal acids like lactic acid and ket acid. Metablic acidsis with nrmal anin gap suggests: 13

14 Fr a metablic acidsis, is there an increased anin gap? Anin gap = [Sdium] - ([Chlride] + [Bicarbnate]) (nrmal AG 8-12) Serum Osmlality = (2 x (Na + K)) + (BUN) + (glucse) Are there ther metablic prcesses present in a patient with an increased anin gap metablic acidsis? t simplfy things: 14

15 Imprtant Cases frm the Dctr s Slides Nrmal reference range ph ( ), PCO2 (35-45 mmhg), PO2 ( mmhg), HCO3 (22-26 mml/l), AG (8-12) Creatinine ( uml/l), Urea ( mml/l), Na ( mml/l), K (3.5-5 mml/l) Case 1 A 75-year-ld man is admitted with septic shck. Shrtly after admissin, bld tests reveal the fllwing: ph 7.18, PO 2= 150 mmhg, PaCO 2= 16 mmhg, HCO 3 7 mml/l Na 138 mml/l, K 3.9 mml/l, Cl 95 mml/l, Urea 8.2 mml/l, Creatinine 102 μml/l Please identify the acid base disturbance : 1.The disturbance is metablic acidsis. Why? Because the ph is less than the nrmal range ( ) and the bicarbnate is less than 22 mml/l. 2. Is the bdy prperly cmpensating? 1.5 x 7 + 8= 18.5 ± 2. The patient s value is 16 Which almst falls within the range, that means that the metablic acidsis is being cmpensated prperly with respiratry alkalsis. 3. Anin gap: Na (Cl+HCO3) = 138 (95+7) = 36 The anin gap is higher than nrmal. which indicates metablic acidsis. Please indicate what is causing the acid base disturbance The cause is Lactic acidsis because which assciated with shck. Case 2 A 68-year-ld wman is being treated fr cngestive heart failure in the crnary care unit. After several days f treatment, the fllwing results are returned: ph 7.49, PO2= 86 mmhg, PaCO2= 48.5 mmhg, HCO3 39 mml/l Na 142 mml/l, K 3.0 mml/l, Cl 85 mml/l, Urea 9.3 mml/l, Creatinine 84 μml/l Please identify the acid base disturbance 1. The disturbance is metablic alkalsis. Why? Because the ph is higher than the nrmal range ( ) and the bicarbnate is als higher than 26 mml/l. 2. Is the bdy prperly cmpensating? Here the calculatin is different: 0.7 x (39-24) = 10.5 ( ) = 50.5 ±2 (this is the estimated increase in PaCO2). S it shuld be between mmhg which means that the metablic alkalsis is cmpensating prperly with respiratry acidsis. 3. Anin gap: Na (Cl+HCO3) = 142 (85+39) = 18 The anin gap is higher than nrmal here s the patient might have metablic acidsis aswell. but the dctr said t neglect it in this case fr simplicity* Please indicate what is causing the acid base disturbance. The cause f alkalsis here is the use f Diuretics (diuretics decrease bld vlume s as a respnse t that, the kidneys increase reabsrptin f sdium bicarbnate) 15

16 Case 3 A 70-year-ld man with chrnic bstructive pulmnary disease (COPD) is admitted with increasing cnfusin. Shrtly after admissin, bld tests reveal the fllwing: ph 7.21, PO 61.5 mmhg, PaCO2 83 mmhg, HCO3 34 mml/l Na 140 mml/l, K 4.7 mml/l, Cl 94 mml/l Urea 8.2 mml/l, Creatinine 66 μml/l Please identify the acid base disturbance 1.The disturbance is respiratry acidsis. Why? Because the ph is less than the nrmal range ( ) and the PaCO2 is als significantly higher than 40 mmhg. 2. Is the bdy prperly cmpensating? First we have t determine whether the cause is Acute r Chrnic, this mainly depends n the clinical scenari. Which means that if a patient presents with a strke 2 r 3 hurs ag and he cannt breathe s he develped Respiratry acidsis, this is Acute. A chrnic scenari (like the case mentined here) where the patient has COPD and he chrnically retains CO2 which eventually lead t respiratry acidsis x (83-40) = 15 (15+24=39 ±2) which means that 37-41mml/L is the expected HCO3. The dctr said this was a tugh call because it s clse t the expected range but if yu want t g by the bk it means that the patient s bdy isn t cmpensating prperly. S, the patient has respiratry acidsis with metablic acidsis. 3. Anin gap: Na (Cl+HCO3) =140 (94+34) = 12 (nrmal anin gap) Please indicate what is causing the acid base disturbance. The cause here is CO2 retentin caused by COPD (CO2 accumulatin may itself lead t drwsiness That further depresses respiratry drive.) Case 4 A 40-year-ld man develped prfuse diarrhea fllwing antibitic treatment f a chest infectin. He is thirsty, and light headed. Shrtly after admissin, bld tests reveal the fllwing: ph 7.25, PO 101 mmhg, PaCO mmhg, HCO3 17 mml/l Na 134 mml/l, K 3.4 mml/l, Cl 104 mml/l, Urea 9.3 mml/l, Creatinine 102 μml/l Please identify the acid base disturbance 1.The disturbance is metablic acidsis. Why? Because the ph is less than the nrmal range ( ) and the bicarbnate is less than 22 mml/l. 2. Is the bdy prperly cmpensating? The calculatin in this case is similar t the first case 1.5 x = 33.5 ± 2 mmhg ( s, expected PaCO2 shuld be between ) s the bdy here is cmpensating prperly with respiratry alkalsis. 3.Anin gap: Na (Cl+HCO3) =134 (104+17) = 13 (nrmal anin gap metablic acidsis) Please indicate what is causing the acid base disturbance. The cause here is diarrhea, which is ne f the causes f metablic acidsis with a nrmal anin gap. Because the bdy retains chlride in respnse t the lss f bicarbnate thrugh the GIT. 16

17 Summary Underlying cause Signs and symptms Treatment Underlying cause Signs and symptms Treatment Metablic Acidsis Hw t determine the underlying cause? By the anin gap. Nrmal AG Acidsis: Diarrhea, Renal tubular acidsis. High AG Acidsis MUD PILES: Methanl, Uremia, DKA, Prpylene glycl, INH, Lactic acidsis (r diabetic ketacidsis), Ethanl/Ethylene Glycl, Salicylates Hyperventilatin Decreased in Cardiac utput and tissue perfusin. Treat the underlying cause. Sdium bicarbnate fr severe acidsis (esp. in nrmal AG acidsis). Mechanical ventilatin if the patient is fatigued (esp. in DKA) Respiratry Acidsis Acute Respiratry Acidsis: airway bstructin, pneumnia, pneumthrax, chest trauma, head trauma, strke, drug txicity Chrnic Respiratry Acidsis: COPD, mrbid besity, muscular and neurmuscular diseases Drwsiness, cnfusin, headaches, flapping tremrs. Treat the underlying cause. Give supplemental xygen except in patients with COPD. Sme cases require intubatin and mechanical ventilatin. Metablic Alkalsis Hw t determine the underlying cause? By saline respnsiveness. Saline Respnsive Urine (cl-) <20 with ECF cntractin (due t fluid lss). Vmiting & diarrhea f high Cl (HCl lss), Diuretic (decreased ECF vlume) Saline resistant Urine (cl-) >20 with ECF vlume expansin (n fluid lss) Hypertensive: Hyperaldsternism (ptassium lss) Cushing Syndrme Hyp/nrm tensive: Exgenus alkali lad There are n characteristic signs and symptms (mst imp. Hx) Treat the underlying cause. Give nrmal saline + ptassium in saline respnsive. Spirnlactne (K+ sparing diuretic) in saline resistant. Hyperventilatin Respiratry Alkalsis mst cmmn Causes f hyperventilatin: Anxiety, Fever Dizziness, anxiety, paresthesia, and periral numbness. Tetany, Arrhythmias, Trusseau s sign & Chvstek s sign Treat the underlying cause. Breathing int a paper bag can help patients with anxiety. 17

18 Questins 1- In a man underging surgery, it was necessary t aspirate the cntents f the upper gastrintestinal tract. After surgery, the fllwing values were btained frm an arterial bld sample: ph 7.55, PCO2 52 mm Hg and HCO3-40 mml/l. What is the underlying disrder? A. Metablic Acidsis B. Metablic Alkalsis C. Respiratry Acidsis D. Respiratry Alkalsis 2- A student is nervus fr a big exam and is breathing rapidly, what d yu expect ut f the fllwings A. Metablic Acidsis B. Metablic Alkalsis C. Respiratry Acidsis D. Respiratry Alkalsis 3- Which f the fllwing labratry results belw indicates cmpensated metablic alkalsis? A. Lw pco2 nrmal bicarbnate and, high ph B. Lw pco2, lw bicarbnate, lw ph C. High pco2, nrmal bicarbnate and, lw ph D. High pco2, high bicarbnate and High ph 4- A yung wman is fund cmatse, having taken an unknwn number f sleeping pills an unknwn time befre. An arterial bld sample yields the fllwing values: ph 6.90, HCO3-13 meq/liter, PaCO2 68 mmhg. This patient s acid-base status is mst accurately described as which f the fllwing? A. Uncmpensated metablic acidsis B. Uncmpensated respiratry acidsis C. simultaneus respiratry and metablic acidsis D. Respiratry acidsis with partial renal cmpensatin 1.B 2.D 3.D 4.C 18