ASIT-BAZ DENGESI
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ASIT-BAZ DENGESI

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1. ASIT-BAZ DENGESI Prof.Dr.Tayfun G?ler ?ukurova ?niversitesi Tip Fak?ltesi Anesteziyoloji A.D. Adana

2. OLGU SUNUMU 1 aylik erkek ?ocugu Tani: Anorektal malformasyon Tedavi: Anoplasti

3. OLGU SUNUMU Postoperatif d?nem: Konjestif kalp yetersizligi Aorta koarktasyonuna bagli Fizik muayene bulgulari: Tasipne Idrar ?ikisinda azalma Periferik perf?zyonda bozulma Hepatomegali Kardiyomegali

4. OLGU SUNUMU Endotrakeal int?basyon Mekanik ventilasyon Solunum hizi: 20/dk FiO2 = 1.0

5. AVL OMNI MEASUREMENT REPORT PaO2 209 mmHg PaCO2 11 mmHg pH 7.47 Calculated values: B.E. - 14.6 mmol/L Total CO2 8 mEq/L HCO3- 7.7 mmol/L Hb 9.5 g/dl Na+ 135 mEq/L Cl- 95 mEq/L K+ 5.5 mEq/L Hastada a?ik bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 10 mmHg d?sm?s oldugundan (40-10) / 10 x 2 mmol/L = 6 beklenen HCO3 d?zeyi = 24-6= 18 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu da var. Tani: Primer respiratuar alkaloz ve primer metabolik asidoz. Hastada a?ik bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 10 mmHg d?sm?s oldugundan (40-10) / 10 x 2 mmol/L = 6 beklenen HCO3 d?zeyi = 24-6= 18 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu da var. Tani: Primer respiratuar alkaloz ve primer metabolik asidoz.

6. KAPSAM Kan gazi analizi parametreleri Tanimlar Asidoz Alkaloz Fizyolojik etkileri Anestezide dikkat edilecek noktalar Kompansasyon Tedavi ilkeleri

7. KAN GAZI PARAMETRELERI Total CO2 eksikTotal CO2 eksik

8. pH = 40 x 10-9 mol/L pH = - log [H+] = 7.40

9. pH ve [H+] [H+] mmol/L pH 140- 120- 100- 80- 60- 40- 20- 0- 6.9 7.1 7.3 7.5 7.7 7.0 7.2 7.4 7.6 Normal Alkalemi Asidemi

10. ASIDEMI-ALKALEMI pH 6.8 7.4 8.0 Asistoli Kardiyovask?ler kollaps ?l?m Tetani Aritmiler ?l?m H+ 160 40 10 ASIDEMI ALKALEMI

11. HCO3- Akt?el HCO3-: ?l??len HCO3- Standart HCO3-: Hesaplanan HCO3- CO2 = 40 mmHg Serum HCO3- konsantrasyonu: pH = 6.10 + log (HCO3- ? 0.03 X PaCO2) HCO3- = 24 X PaCO2 ? [H+] HCO3-= Total CO2 ? ??z?nm?s CO2 Bicarbonate (HCO3-) HCO3- is quantitatively the second most important anionic fraction in serum. CO2 produced by cellular metabolism diffuses into the plasma and combines with H2O inside red cells to form H2CO3 (carbonic acid). Carbonic acid dissociates to form H+ and HCO3-. The H+ is buffered by reduced hemoglobin and as the bicarbonate concentration builds up in the red cells, it diffuses down its concentration gradient into the plasma, being replaced by Cl-. This movement of Cl- into the red cell to conserve electrical balance is called the "chloride shift". A small amount of CO2 is also carried in the blood bound to amino groups of hemoglobin. Clinically, bicarbonate and other forms of carbon dioxide are measured together as total CO2. Reference values are 24-30 mEq/L for venous blood. Two ways to determine the serum bicarbonate concentration exist. The first method is calculating serum bicarbonate concentration from a blood gas sample using the Henderson-Hasselbalch equation, as follows: pH = 6.10 + log (HCO3- ? .03 X PaCO2) Alternatively, HCO3- = 24 X PaCO2 ? [H+] Because pH and PaCO2 are directly measured, bicarbonate can be calculated. The second method is measuring the total carbon dioxide content in serum, which is routinely measured with serum electrolytes obtained from venous blood. In this method, a strong acid is added to serum, which interacts with bicarbonate in the serum sample, forming carbonic acid. Carbonic acid dissociates to carbon dioxide and water; then, carbon dioxide is measured. Note that the carbon dioxide measured includes bicarbonate and dissolved carbon dioxide. The contribution of dissolved carbon dioxide is quite small (0.03 X PaCO2) and is usually ignored, although it accounts for a difference of 1-3 mEq/L between the measured total carbon dioxide content in venous blood and the calculated bicarbonate in arterial blood. Thus, at a PaCO2 of 40, a total carbon dioxide content of 25 means a true bicarbonate concentration of 23.8 (ie, 25 - 0.03 X 40).Two ways to determine the serum bicarbonate concentration exist. The first method is calculating serum bicarbonate concentration from a blood gas sample using the Henderson-Hasselbalch equation, as follows: pH = 6.10 + log (HCO3- ? .03 X PaCO2)Alternatively, HCO3- = 24 X PaCO2 ? [H+] Because pH and PaCO2 are directly measured, bicarbonate can be calculated. The second method is measuring the total carbon dioxide content in serum, which is routinely measured with serum electrolytes obtained from venous blood. In this method, a strong acid is added to serum, which interacts with bicarbonate in the serum sample, forming carbonic acid. Carbonic acid dissociates to carbon dioxide and water; then, carbon dioxide is measured. Note that the carbon dioxide measured includes bicarbonate and dissolved carbon dioxide. The contribution of dissolved carbon dioxide is quite small (0.03 X PaCO2) and is usually ignored, although it accounts for a difference of 1-3 mEq/L between the measured total carbon dioxide content in venous blood and the calculated bicarbonate in arterial blood. Thus, at a PaCO2 of 40, a total carbon dioxide content of 25 means a true bicarbonate concentration of 23.8 (ie, 25 - 0.03 X 40).

12. B.D.E. Bir litre kani pH=7.4 ve PaCO2=40 mmHg kosullarina getirmek i?in gereken asit miktari SBE = 0.9287 x [HCO3- - 24.4 + (pH-7.4)] Siggard-Andersen nomogrami Baz defisiti veya fazlaligi; PCO2 40 mmHg, sicakligi 38 C olarak kabul ettigimizde kan ?rneginin pH?sini 7.40 yapmak i?in eklenmesi gereken kuvvetli asit ya da baz miktari. Kan gazi analiz?rleri, standart BE degerini asagidaki form?l? kullanarak hesaplamaktadir: SBE = 0.9287 x [HCO3- - 24.4 + (pH-7.4)] Siggard-Anderson 1958Baz defisiti veya fazlaligi; PCO2 40 mmHg, sicakligi 38 C olarak kabul ettigimizde kan ?rneginin pH?sini 7.40 yapmak i?in eklenmesi gereken kuvvetli asit ya da baz miktari. Kan gazi analiz?rleri, standart BE degerini asagidaki form?l? kullanarak hesaplamaktadir: SBE = 0.9287 x [HCO3- - 24.4 + (pH-7.4)] Siggard-Anderson 1958

13. TOTAL CO2 Total CO2 [HCO3-]+ [??z?nm?s CO2] + [Karbamino CO2] + [H2CO3] Normal deger: 21.0-31.0 mEq/L % 95 % 5

14. G??L? IYONLAR (Stewart Yaklasimi) Na+, Cl- K+, SO4++, Mg++, Ca++ SID = G??l? iyon farki (strong ion difference) SID =([Na+]+[K+]+[Ca++]+[Mg++]) ? ([Cl-]+[A-]) SID = 40-44 mEq/L Asit-baz dengesine Stewart yaklasimi: Ekstrasell?ler sivi (ECF), suyun disosiasyonunu dogrudan etkileyen pek ?ok sayida farkli molek?l i?eren bir sol?syondur. N?tral suyun pH dege7.0?ri 7.0 (1.0 x 10-7 mmol/L) iken ECF?nin fizyolojik pH degeri 7.4 olup, alkalendir. Bu rakama g?re sivinin asidik ya da alkalik oldugu kabul edilir. Intrasell?ler pH ise 6.8- G??l? iyonlar: Ekstrasell?ler alandaki en g??l? iyonlar Na ve Cl?dur. Diger iyonlar ise K, SO4, Mg ve Ca?dur. G??l? iyonlar i?eren bir sol?syonda g??l? katyonlar ile g??l? anyonlar arasindaki fark, SID degerini verir. Bu deger H iyonunundan etkilenmeyen bir degerdir. Insanda ECF?da SID degeri pozitiftir. SID =([Na+]+[K+]+[Ca++]+[Mg++]) ? ([Cl-]+[A-]) SID = 40-44 mEq/L Asit-baz dengesine Stewart yaklasimi: Ekstrasell?ler sivi (ECF), suyun disosiasyonunu dogrudan etkileyen pek ?ok sayida farkli molek?l i?eren bir sol?syondur. N?tral suyun pH dege7.0?ri 7.0 (1.0 x 10-7 mmol/L) iken ECF?nin fizyolojik pH degeri 7.4 olup, alkalendir. Bu rakama g?re sivinin asidik ya da alkalik oldugu kabul edilir. Intrasell?ler pH ise 6.8- G??l? iyonlar: Ekstrasell?ler alandaki en g??l? iyonlar Na ve Cl?dur. Diger iyonlar ise K, SO4, Mg ve Ca?dur. G??l? iyonlar i?eren bir sol?syonda g??l? katyonlar ile g??l? anyonlar arasindaki fark, SID degerini verir. Bu deger H iyonunundan etkilenmeyen bir degerdir. Insanda ECF?da SID degeri pozitiftir. SID =([Na+]+[K+]+[Ca++]+[Mg++]) ? ([Cl-]+[A-]) SID = 40-44 mEq/L

15. ASIT-BAZ DENGESINI ETKILEYEN ASIT VE BAZLAR Bazlar: NaHCO3 KHCO3 Respiratuar (volatil) asitler 12.000-24.000 mmol/g?n Metabolik (fiks) asitler 1-1.5 mmol/kg/g?n Each day there is always a production of acid by the body?s metabolic processes and to maintain balance, these acids need to be excreted or metabolised. The various acids produced by the body are classified as respiratory (or volatile) acids and as metabolic (or fixed) acids. The body normally can respond very effectively to perturbations in acid or base production. 2.1.1 Respiratory Acid The acid is more correctly carbonic acid (H2CO3) but the term 'respiratory acid' is usually used to mean carbon dioxide. But CO2 itself is not an acid in the Bronsted-Lowry system as it does not contain a hydrogen so cannot be a proton donor. However CO2 can instead be thought of as representing a potential to create an equivalent amount of carbonic acid. Carbon dioxide is the end-product of complete oxidation of carbohydrates and fatty acids. It is called a volatile acid meaning in this context it can be excreted via the lungs. Of necessity, considering the amounts involved there must be an efficient system to rapidly excrete CO2. The amount of CO2 produced each day is huge compared to the amount of production of fixed acids. Basal CO2 production is typically quoted at 12,000 to 13,000 mmols/day. Basal Carbon Dioxide Production Consider a resting adult with an oxygen consumption of 250 mls/min and a CO2 production of 200 mls/min (Respiratory quotient Increased levels of activity will increase oxygen consumption and carbon dioxide production so that actual daily CO2 production is usually significantly more than the oft-quoted basal level. [Different texts quote different figures usually in the range of 12,000 to 24,000 mmoles/day but the actual figure simply depends on the level of metabolic activity and whether you quote basal or typical figures.] Daily CO2 production can also be calculated from the daily metabolic water production. The complete oxidation of glucose produces equal amounts of CO2 and H20. The complete oxidation of fat produces approximately equal amounts of CO2 and H2O also. These two processes account for all the body?s CO2 production. Typically, this metabolic water is about 400 mls per day which is 22.2 moles (ie 400/18) of water. The daily typical CO2 production must also be about 22,200 mmoles.

16. ASITLER

17. ASIT ELIMINASYONU Respiratuar asitler: Ventilasyon Metabolik asitler: B?brekler Karaciger

18. ASIT-BAZ DENGESI BOZUKLUKLARI Basit bozukluklar: Asidoz Respiratuar asidoz Metabolik asidoz Alkaloz Respiratuar alkaloz Metabolik alkaloz

19. ASIDOZ RESPIRATUAR ASIDOZ METABOLIK ASIDOZ

20. RESPIRATUAR ASIDOZ PaCO2?de artma H2O + CO2 ? ? H2CO3 ? H+ ? + HCO3- ?

21.

22. ETYOLOJI Yetersiz alveolar ventilasyon Santral respiratuar depresyon & SSS sorunlari Sinir-kas hastaliklari Akciger & g?g?s duvari defektleri Havayolu hastaliklari Yetersiz mekanik ventilasyon CO2 ?retiminde artis Hiperkatabolik hastaliklar CO2 aliminda artis Yeniden soluma RESPIRATUAR ASIDOZ Causes of Respiratory Acidosis (classified by Mechanism) A: Inadequate Alveolar Ventilation Central Respiratory Depression & Other CNS Problems Drug depression of resp. center (eg by opiates, sedatives, anaesthetics) CNS trauma, infarct, haemorrhage or tumour Hypoventilation of obesity (eg Pickwickian syndrome) Cervical cord trauma or lesions (at or above C4 level) High central neural blockade Poliomyelitis Tetanus Cardiac arrest with cerebral hypoxia Nerve or Muscle Disorders Guillain-Barre syndrome Myasthenia gravis Muscle relaxant drugs Toxins eg organophosphates, snake venom Various myopathies Lung or Chest Wall Defects Acute on COAD Chest trauma -flail chest, contusion, haemothorax Pneumothorax Diaphragmatic paralysis or splinting Pulmonary oedema Adult respiratory distress syndrome Restrictive lung disease Aspiration Airway Disorders Upper Airway obstruction Laryngospasm Bronchospasm/Asthma External Factors Inadequate mechanical ventilation B: Over-production of Carbon Dioxide Hypercatabolic Disorders Malignant Hyperthermia C: Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery)Causes of Respiratory Acidosis (classified by Mechanism) A: Inadequate Alveolar Ventilation Central Respiratory Depression & Other CNS Problems Drug depression of resp. center (eg by opiates, sedatives, anaesthetics) CNS trauma, infarct, haemorrhage or tumour Hypoventilation of obesity (eg Pickwickian syndrome) Cervical cord trauma or lesions (at or above C4 level) High central neural blockade Poliomyelitis Tetanus Cardiac arrest with cerebral hypoxia Nerve or Muscle Disorders Guillain-Barre syndrome Myasthenia gravis Muscle relaxant drugs Toxins eg organophosphates, snake venom Various myopathies Lung or Chest Wall Defects Acute on COAD Chest trauma -flail chest, contusion, haemothorax Pneumothorax Diaphragmatic paralysis or splinting Pulmonary oedema Adult respiratory distress syndrome Restrictive lung disease Aspiration Airway Disorders Upper Airway obstruction Laryngospasm Bronchospasm/Asthma External Factors Inadequate mechanical ventilation B: Over-production of Carbon Dioxide Hypercatabolic Disorders Malignant Hyperthermia C: Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery)

23. METABOLIK ASIDOZ HCO3- konsantrasyonunda azalma Plazma bikarbonat d?zeyindeki bir d?s?s, eslik eden bir PaCO2 azalmasi olmadigi s?rece arteryel pH?da azalmaya neden olur. Pulmoner kompansatuar yanit, PaCO2 d?zeyini pH?yi normale getirecek kadar azaltamaz.Plazma bikarbonat d?zeyindeki bir d?s?s, eslik eden bir PaCO2 azalmasi olmadigi s?rece arteryel pH?da azalmaya neden olur. Pulmoner kompansatuar yanit, PaCO2 d?zeyini pH?yi normale getirecek kadar azaltamaz.

24. MEKANIZMA HCO3-?in g??l? bir nonvolatil asit tarafindan t?ketilmesi Bikarbonat kaybi Renal Gastrointestinal Ekstrasell?ler sivi kompartmaninin hizli dil?syonu (bikarbonatsiz mayi) METABOLIK ASIDOZ Ekstrasell?ler sivi kompartmaninin hizli dil?syonu (bikarbonatsiz mayi NEDEN???

25. ETYOLOJI-1 Artmis anyon gap: Endojen nonvolatil asitlerin artmasi Renal yetersizlik, ketoasidoz, laktik asidoz Toksinler Salisilat, metanol, etilen glikol, paraldehid Rabdomiyoliz METABOLIK ASIDOZ Artmis anyon gap: Endojen nonvolatil asitlerin artmasi: Renal yetersizlik: Akut, kronik Ketoasidoz: Diabetik, a?lik Laktik asidoz Miks: Nonketotik hiperosmolar koma, Alkol Yenidogan metabolizma hatalari Toksinler: salisilat, metanol, etilen glikol, paraldehid, toluen, s?lf?r Rabdomiyoliz Artmis anyon gap: Endojen nonvolatil asitlerin artmasi: Renal yetersizlik: Akut, kronik Ketoasidoz: Diabetik, a?lik Laktik asidoz Miks: Nonketotik hiperosmolar koma, Alkol Yenidogan metabolizma hatalari Toksinler: salisilat, metanol, etilen glikol, paraldehid, toluen, s?lf?r Rabdomiyoliz

26. ETYOLOJI-2 Normal anyon gap: HCO3- kaybi: Gastrointestinal sistem Renal sistem Dil?syon Total parenteral n?trisyon Klorid i?eren asit alimi METABOLIK ASIDOZ Normal anyon gap: Gastrointestinal sistemden HCO3- kaybi: Diyare Anyon degistirici resinler Fist?ller (pankreatik, bilier, ince barsak) Renal HCO3- kaybi: Renal t?b?ler asidoz Karbonik anhidraz inhibit?rleri Hipoaldosteronizm Dil?syon: ?ok miktarda bikarbonatsiz mayi alimi Total parenteral n?trisyon Klorid i?eren asit alimi: Amonyum klorid, lizin hidroklorid, arginin hidroklorid Normal anyon gap: Gastrointestinal sistemden HCO3- kaybi: Diyare Anyon degistirici resinler Fist?ller (pankreatik, bilier, ince barsak) Renal HCO3- kaybi: Renal t?b?ler asidoz Karbonik anhidraz inhibit?rleri Hipoaldosteronizm Dil?syon: ?ok miktarda bikarbonatsiz mayi alimi Total parenteral n?trisyon Klorid i?eren asit alimi: Amonyum klorid, lizin hidroklorid, arginin hidroklorid

27. ANYON GAP = [Na+] ? ([Cl-] + [HCO3-]) = 140 ? (104 + 24) = 12 meq/L (8-16 meq/L) ANYON GAP Maj?r plazma katyonlari Maj?r plazma anyonlari ? = Anion Gap Since serum is electrically neutral, total anions and total cations must be equal. Na+ and K+ are the major reported cations. Cl- and HCO3- are the major reported anions. The totals of these two sets of laboratory data are not equal. The sum of unreported cations, such as, Ca++ and Mg++ average 7 mEq/L, and the sum of unmeasured anions (proteins, phosphate, sulfates, organic acids), average 24 mEq/L. Therefore, normally, there is a net excess of about 17 mEq/L of unmeasured anions in serum. The total Cl- and total CO2 concentrations are added together and subtracted from the Na+ and K+ concentrations; the difference should be equal to, or less than, 17 mEq/L. If the anion gap exceeds 17 mEq/L, it indicates an increase in one or more of unmeasured anions present. Etiologies for increased anion gap are: metabolic acidosis (e.g., lactic acidosis) uremia with retention of fixed acids ketotic states toxin ingestion, such as methanol and salicylates Anyon gap: Plazmada ?l??len maj?r katyonlar ile anyonlar arasindaki farktir. Anyon gap= [Na+] ? ([Cl-] ? [HCO3-] Normal degerler kullanildiginda Anyon gap= 140 ? (104 + 24) = 12 meq/L (Normal sinirlari = 9-15 meq/L) 1?atmos?=?760?mmHg? =?1000?cmH2O?=?100?kPa? The term anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. The negatively charged proteins account for about 10% of plasma anions and make up the majority of the unmeasured anion represented by the anion gap under normal circumstances. The acid anions (eg lactate, acetoacetate, sulphate) produced during a metabolic acidosis are not measured as part of the usual laboratory biochemical profile. The H+ produced reacts with bicarbonate anions (buffering) and the CO2 produced is excreted via the lungs (respiratory compensation). The net effect is a decrease in the concentration of measured anions (ie HCO3) and an increase in the concentration of unmeasured anions (the acid anions) so the anion gap increases. AG is calculated from the following formula: Anion gap = [Na+] - [Cl-] - [HCO3-] Reference range is 8 to 16 mmol/l. An alternative formula which includes K+ is sometimes used particularly by Nephrologists. In Renal Units, K+ can vary over a wider range and have more effect on the measured Anion Gap. This alternative formula is: AG = [Na+] + [K+] - [Cl-] - [HCO3-] The reference range is slightly higher with this alternative formula. The [K+] is low relative to the other three ions and it typically does not change much so omitting it from the equation doesn?t have much clinical significance. Major Clinical Uses of the Anion Gap To signal the presence of a metabolic acidosis and confirm other findings Help differentiate between causes of a metabolic acidosis: high anion gap versus normal anion gap metabolic acidosis. In an inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3 and the anion gap remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased. To assist in assessing the biochemical severity of the acidosis and follow the response to treatment Anyon gap: Plazmada ?l??len maj?r katyonlar ile anyonlar arasindaki farktir. Anyon gap= [Na+] ? ([Cl-] ? [HCO3-] Normal degerler kullanildiginda Anyon gap= 140 ? (104 + 24) = 12 meq/L (Normal sinirlari = 9-15 meq/L) 1?atmos?=?760?mmHg? =?1000?cmH2O?=?100?kPa? The term anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. The negatively charged proteins account for about 10% of plasma anions and make up the majority of the unmeasured anion represented by the anion gap under normal circumstances. The acid anions (eg lactate, acetoacetate, sulphate) produced during a metabolic acidosis are not measured as part of the usual laboratory biochemical profile. The H+ produced reacts with bicarbonate anions (buffering) and the CO2 produced is excreted via the lungs (respiratory compensation). The net effect is a decrease in the concentration of measured anions (ie HCO3) and an increase in the concentration of unmeasured anions (the acid anions) so the anion gap increases. AG is calculated from the following formula: Anion gap = [Na+] - [Cl-] - [HCO3-] Reference range is 8 to 16 mmol/l. An alternative formula which includes K+ is sometimes used particularly by Nephrologists. In Renal Units, K+ can vary over a wider range and have more effect on the measured Anion Gap. This alternative formula is: AG = [Na+] + [K+] - [Cl-] - [HCO3-] The reference range is slightly higher with this alternative formula. The [K+] is low relative to the other three ions and it typically does not change much so omitting it from the equation doesn?t have much clinical significance. Major Clinical Uses of the Anion Gap To signal the presence of a metabolic acidosis and confirm other findings Help differentiate between causes of a metabolic acidosis: high anion gap versus normal anion gap metabolic acidosis. In an inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3 and the anion gap remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased. To assist in assessing the biochemical severity of the acidosis and follow the response to treatment

28. ANYON GAP Fosfatlar S?lfatlar T?m organik anyonlar (plazma proteinleri) ANYON GAP ?l??lmeyen anyonlar ?l??lmeyen katyonlar ? = K+ Ca++ Mg++ Ger?ekte, anyon gap olmasi m?mk?n degildir, elektron?tralite s?rd?r?lmek zorunda oldugu i?in, t?m anyonlarin miktari, katyonlarin miktarina esit olmak durumundadir. Bu nedenle anyon gap=?l??lmeyen anyonlar ? ?l??lmeyen katyonlar olarak d?s?n?lmelidir. ?l??lmeyen katyonlar K+, Ca++ ve Mg++?dan olusurken ?l??lmeyen anyonlar da fosfatlar, s?lfatlar ve plazma proteinleri de dahil olmak ?zere t?m organik anyonlardan olusur. Plazma alb?mini normalde anyon gapin ?nemli bir b?l?m?n? ifade eder (11 mEq/L) Bu durumda ?l??lmeyen anyonlarin artmasi veya katyonlarin azalmasi durumunda anyon gap da artacaktir. Anion Gap. Gap = Na+ + K+ - Cl- - HCO3- Some causes of metabolic acidosis, e.g., lactic acidosis, release anions into the extracellular fluid which are not normally measured. When this occurs there will be an unexpected discrepancy between the sums of the principal cations and anions. The usual sum is: Gap ? = ? Na+ ? + ? K+ ? - ? Cl- ? - ? HCO3- ? ? ? ? ? ? ? ? 15 ? = ? 140 ? + ? 5 ? ? - ?105? - ? ? 25 ? ? mMol/L In addition to Cl- + HCO3- there are extra unmeasured anions which increase the "gap". A gap greater than 30 indicates a significant concentration of unmeasured anions. Unfortunately, this calculation relies upon the accuracy of the other measurements. Small errors in the larger numbers cause a disproportionately great error in the "gap". If information is required about the anions, it is probably more appropriate to measure their concentration. In practice it suffices to analyze lactate in tissue hypoxia, 3-hydroxybutyrate in diabetic ketosis, and phosphate or sulfate in renal failure. Ger?ekte, anyon gap olmasi m?mk?n degildir, elektron?tralite s?rd?r?lmek zorunda oldugu i?in, t?m anyonlarin miktari, katyonlarin miktarina esit olmak durumundadir. Bu nedenle anyon gap=?l??lmeyen anyonlar ? ?l??lmeyen katyonlar olarak d?s?n?lmelidir. ?l??lmeyen katyonlar K+, Ca++ ve Mg++?dan olusurken ?l??lmeyen anyonlar da fosfatlar, s?lfatlar ve plazma proteinleri de dahil olmak ?zere t?m organik anyonlardan olusur. Plazma alb?mini normalde anyon gapin ?nemli bir b?l?m?n? ifade eder (11 mEq/L) Bu durumda ?l??lmeyen anyonlarin artmasi veya katyonlarin azalmasi durumunda anyon gap da artacaktir. Anion Gap. Gap = Na+ + K+ - Cl- - HCO3- Some causes of metabolic acidosis, e.g., lactic acidosis, release anions into the extracellular fluid which are not normally measured. When this occurs there will be an unexpected discrepancy between the sums of the principal cations and anions. The usual sum is: Gap ? = ? Na+ ? + ? K+ ? - ? Cl- ? - ? HCO3- ? ? ? ? ? ? ? ? 15 ? = ? 140 ? + ? 5 ? ? - ?105? - ? ? 25 ? ? mMol/L In addition to Cl- + HCO3- there are extra unmeasured anions which increase the "gap". A gap greater than 30 indicates a significant concentration of unmeasured anions. Unfortunately, this calculation relies upon the accuracy of the other measurements. Small errors in the larger numbers cause a disproportionately great error in the "gap". If information is required about the anions, it is probably more appropriate to measure their concentration. In practice it suffices to analyze lactate in tissue hypoxia, 3-hydroxybutyrate in diabetic ketosis, and phosphate or sulfate in renal failure.

29. LAKTIK ASIDOZ Ven?z: 4.5 - 19.8 mg/dL - Arteryel: 4.5 - 14.4 mg/dL (0.4-1.4 mmol/L) Venous: 4.5 - 19.8 mg/dL Arterial: 4.5 - 14.4 mg/dL 0.3-1.3 mmol/LVenous: 4.5 - 19.8 mg/dLArterial: 4.5 - 14.4 mg/dL 0.3-1.3 mmol/L

30. METABOLIK ASIDOZLU HASTANIN DEGERLENDIRILMESI Asidozun nedeni: ?l??len anyonlar mi? ?l??lmeyen anyonlar mi? Anyon gapi hesaplayin Na+ + K+ - Cl- - HCO3- Metabolik asidozlu bir hastada ?ncelikle asidozun ?l??len anyonlardan mi yoksa ?l??lmeyen anyonlardan mi kaynaklandigi ayirt edilmelidir. Bunun i?in ?nce anyon gap hesaplanir: Na+ + K+ - Cl- Metabolik asidozlu bir hastada ?ncelikle asidozun ?l??len anyonlardan mi yoksa ?l??lmeyen anyonlardan mi kaynaklandigi ayirt edilmelidir. Bunun i?in ?nce anyon gap hesaplanir: Na+ + K+ - Cl-

31. ANYON GAPIN DEGERLENDIRILMESI Normal anyon gap: 10-12 mEq/L ECF?da ?ok fazla klor?r: Asiri alim Asiri Na kaybi (diyare, ileostomi vb.) Renal tubuler asidoz Y?ksek anyon gap > 16 mEq/L ?l??lmeyen anyonlar Anyon gap normal ?ikarsa ekstrasell?ler sivida ?ok falz klor?r oldugu d?s?n?lmelidir. Bu durum da ya asiri Cl alimi, ya asiri sodyum kaybi (diyare, ileostomi vb) ya da renal tub?ler asidozdan kaynaklanir. Anyon gap y?ksek ?ikarsa bu durumda asidoz ?l??lmeyen iyonlardan kaynaklanmaktadir.Anyon gap normal ?ikarsa ekstrasell?ler sivida ?ok falz klor?r oldugu d?s?n?lmelidir. Bu durum da ya asiri Cl alimi, ya asiri sodyum kaybi (diyare, ileostomi vb) ya da renal tub?ler asidozdan kaynaklanir. Anyon gap y?ksek ?ikarsa bu durumda asidoz ?l??lmeyen iyonlardan kaynaklanmaktadir.

32. ?L??LMEYEN IYONLARIN DEGERLENDIRILMESI Laktik asit d?zeyi: > 2 mEq/L: Dolasim yetersizligi var: Tip A laktik asidoz Dolasim yetersizligi yok Tip B laktik asidoz ? Y?ksek anyon gapli asidozda ?nce laktat d?zeyine bakilir. Eger laktat d?zeyi y?ksek ise ve hastada dolasim yetersizligi (sok, hipovolemi, olig?ri, yetersiz res?sitasyon, anemi, CO entoksikasyonu, n?bet) bu y?ksekligi izah ediyorsa Tip A laktik asidozdan bahsedilir. Eger asidozu dolasim yetersizligi izah etmiyorsa Tip B laktik asidoz nedenlerini (nadir) arastirin: biguanidler, fruktoz, sorbitol, nitroprussid, etilen glikol, kanser, karaciger hastlaiklari vb.Y?ksek anyon gapli asidozda ?nce laktat d?zeyine bakilir. Eger laktat d?zeyi y?ksek ise ve hastada dolasim yetersizligi (sok, hipovolemi, olig?ri, yetersiz res?sitasyon, anemi, CO entoksikasyonu, n?bet) bu y?ksekligi izah ediyorsa Tip A laktik asidozdan bahsedilir. Eger asidozu dolasim yetersizligi izah etmiyorsa Tip B laktik asidoz nedenlerini (nadir) arastirin: biguanidler, fruktoz, sorbitol, nitroprussid, etilen glikol, kanser, karaciger hastlaiklari vb.

33. ?L??LMEYEN IYONLARIN DEGERLENDIRILMESI Kreatinin ve idrar miktari: Akut renal yetersizlik Neden: Renal asitler Glisemi ve idrar keton d?zeyi Hiperglisemi + ketoz Neden: Diyabetik ketoasidoz Normoglisemi + ketoz Neden: Alkol, a?lik Eger laktik asidoz tabloyu izah etmiyorsa Kreatinin ve idrar miktarina bakin. Akut renal yetersizlik tanisi koyarsaniz asidozun nedeni Renal asitlerdir. Kan sekeri ve idrar keton d?zeyine bakin. Eger hasta Hiperglisemik ve ketotik ise Neden: Diyabetik ketoasidoz Normoglisemi + ketoz Neden: Alkol (kan alkol d?zeyine bakin), a?lik ketozudur. Eger laktik asidoz tabloyu izah etmiyorsa Kreatinin ve idrar miktarina bakin. Akut renal yetersizlik tanisi koyarsaniz asidozun nedeni Renal asitlerdir. Kan sekeri ve idrar keton d?zeyine bakin. Eger hasta Hiperglisemik ve ketotik ise Neden: Diyabetik ketoasidoz Normoglisemi + ketoz Neden: Alkol (kan alkol d?zeyine bakin), a?lik ketozudur.

34. ASIDOZUN FIZYOLOJIK ETKILERI Kardiyak kontraktilitede azalma Periferik vask?ler diren?te azalma Progressif hipotansiyon Katekolaminlere yanitta azalma Ventrik?ler fibrilasyon esiginde azalma Progressif hiperkalemi pH: ? 0.10 / K+: ? 0.6 mEq/L

35. ASIDOZ?DA ANESTEZI Sedatifler ve anestezik ajanlar: Depresan etki Santral sinir sistemi Kardiyovask?ler sistem Havayolu refleksleri Halotan: Aritmojenik etkide artis S?ksinilkolin: Hiperpotasemide artis

36. ALKALOZ RESPIRATUAR ALKALOZ METABOLIK ALKALOZ

37. RESPIRATUAR ALKALOZ PaCO2?de azalma Mekanizma: Alveolar ventilasyonda artis

38. NEDENLER Santral stim?lasyon Agri, anksiyete, iskemi, inme T?m?r, enfeksiyon, ates, ila?lar Periferik stim?lasyon Hipoksemi, y?kseklik, pulmoner hastaliklar Bilinmeyen Sepsis, metabolik ansefalopati Iatrojenik Ventilat?r tedavisi RESPIRATUAR ALKALOZ Santral stim?lasyon Agri, anksiyete, iskemi, inme T?m?r, enfeksiyon, ates, ila?lar(salisilat, progesteron (gebelik), analeptikler (doksapram)) Periferik stim?lasyon Hipoksemi, y?kseklik, pulmoner hastaliklar (KKY, nonkardiyojenik pulmoner ?dem, astma, pulmoner emboli) Bilinmeyen Sepsis, metabolik ansefalopati Iatrojenik Ventilat?r tedavisi Santral stim?lasyon Agri, anksiyete, iskemi, inme T?m?r, enfeksiyon, ates, ila?lar(salisilat, progesteron (gebelik), analeptikler (doksapram)) Periferik stim?lasyon Hipoksemi, y?kseklik, pulmoner hastaliklar (KKY, nonkardiyojenik pulmoner ?dem, astma, pulmoner emboli) Bilinmeyen Sepsis, metabolik ansefalopati Iatrojenik Ventilat?r tedavisi

39. METABOLIK ALKALOZ Plazma HCO3- d?zeyinde artis

40. METABOLIK ALKALOZ Mekanizma Hidrojen iyon kaybi Hidrojen iyonlarinin intrasell?ler alana kaymasi Alkali uygulamasi Kontraksiyon alkalozu Generation of metabolic alkalosis Metabolic alkalosis may be generated by 1 of the following mechanisms: Loss of hydrogen ions: Whenever a hydrogen ion is excreted, a bicarbonate ion is gained into the extracellular space. Hydrogen ions may be lost through the kidneys or the GI tract. Vomiting or nasogastric (NG) suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Renal losses of hydrogen ions occur whenever the distal delivery of sodium increases in the presence of excess aldosterone, which stimulates the electrogenic epithelial sodium channel (ENaC) in the collecting duct. As this channel reabsorbs sodium ions, the tubular lumen becomes more negative, leading to the secretion of hydrogen ions and potassium ions into the lumen. Shift of hydrogen ions into the intracellular space: This mainly develops with hypokalemia. As the extracellular potassium concentration decreases, potassium ions move out of the cells. To maintain neutrality, hydrogen ions move into the intracellular space. Alkali administration: Administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate may cause metabolic alkalosis. This capacity is reduced when a reduction in filtered bicarbonate occurs, as observed in renal failure, or when enhanced tubular reabsorption of bicarbonate occurs, as observed in volume depletion (see Maintenance of metabolic alkalosis). Contraction alkalosis: Loss of bicarbonate-poor, chloride-rich extracellular fluid, as observed with thiazide diuretic or loop diuretic therapy or chloride diarrhea, leads to contraction of extracellular fluid volume. Because the original bicarbonate mass is now dissolved in a smaller volume of fluid, an increase in bicarbonate concentration occurs. This increase in bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration. Generation of metabolic alkalosis Metabolic alkalosis may be generated by 1 of the following mechanisms: Loss of hydrogen ions: Whenever a hydrogen ion is excreted, a bicarbonate ion is gained into the extracellular space. Hydrogen ions may be lost through the kidneys or the GI tract. Vomiting or nasogastric (NG) suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Renal losses of hydrogen ions occur whenever the distal delivery of sodium increases in the presence of excess aldosterone, which stimulates the electrogenic epithelial sodium channel (ENaC) in the collecting duct. As this channel reabsorbs sodium ions, the tubular lumen becomes more negative, leading to the secretion of hydrogen ions and potassium ions into the lumen. Shift of hydrogen ions into the intracellular space: This mainly develops with hypokalemia. As the extracellular potassium concentration decreases, potassium ions move out of the cells. To maintain neutrality, hydrogen ions move into the intracellular space. Alkali administration: Administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate may cause metabolic alkalosis. This capacity is reduced when a reduction in filtered bicarbonate occurs, as observed in renal failure, or when enhanced tubular reabsorption of bicarbonate occurs, as observed in volume depletion (see Maintenance of metabolic alkalosis). Contraction alkalosis: Loss of bicarbonate-poor, chloride-rich extracellular fluid, as observed with thiazide diuretic or loop diuretic therapy or chloride diarrhea, leads to contraction of extracellular fluid volume. Because the original bicarbonate mass is now dissolved in a smaller volume of fluid, an increase in bicarbonate concentration occurs. This increase in bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate concentration.

41. METABOLIK ALKALOZ KLOR?RE DUYARLI KLOR?RE DIREN?LI

42. KLOR?RE DUYARLI METABOLIK ALKALOZ-2 (Idrar Cl < 20 mEq/L) Ekstrasell?ler sivi kaybi: Di?retikler: Furosemid, etakrinik asit, tiazidler Gastrik sivi kaybi Kusma, gastrik drenaj PaCO2?nin hizla d?s?r?lmesi

43. KLOR?RE DIREN?LI METABOLIK ALKALOZ (Idrar Cl > 20 mEq/L) Mineralokortikoid aktivitesinde artis Sodyum retansiyonu Ekstrasell?ler sivi artisi Y?ksek doz NaHCO3 Kan ?r?nleri Y?ksek doz sodyum penisilin meg'yi d?zeltmeg'yi d?zelt

44. ALKALOZ Sistemik Etkileri: Hemoglobinin oksijene ilgisinde artis Oksijen disosiasyon egrisinde sola kayma Hipokalemi Plazma iyonize Ca++ miktarinda azalma Serebral kan akiminda azalma Sistemik vask?ler rezistansta artma Koroner vazospazm

45. ALKALOZDA ANESTEZI Opioidler: Respiratuar depresyonda uzama Alkaloz + hipotansiyon: Serebral kan akiminda azalma Serebral iskemi Alkaloz + hipokalemi: Ciddi atriyal ve ventrik?ler aritmiler Nondepolarizan kas gevseticileirn etkisinde uzama

46. ASIT-BAZ DENGESI BOZUKLUKLARI Miks bozukluklar: Asidoz Miks respiratuar & metabolik asidoz Alkaloz Miks respiratuar & metabolik alkaloz

47. ASIT-BAZ DENGESI BOZUKLUKLARI Miks bozukluklar: Alkaloz & Asidoz Miks respiratuar alkaloz & metabolik asidoz Miks respiratuar asidoz & metabolik alkaloz

48. pH 1 2 3 ASIT-BAZ DENGESI ANALIZINDE BASAMAKLAR

49. KOMPANSATUAR MEKANIZMALAR Hizli, kimyasal tamponlama Respiratuar kompansasyon: PaCO2?de degisiklik (dakikalar-saatler) Yavas, renal kompansasyon HCO3- atiliminda degisiklik (g?nler) [H+] konsantrasyonundaki degisikliklere fizyolojik yanitlar ?? asamada ger?eklesir: (1) Hizli, kimyasal tamponlama, (2) respiratuar kompansasyon (m?mk?n oldugunda), (3) daha yavas fakat daha etkili olarak renal kompansasyon. 2.1.3 Response to an Acid-Base Perturbation The body?s response to a change in acid-base status has three components: First defence: Buffering Second defence: Respiratory : alteration in arterial pCO2 Third defence: Renal : alteration in HCO3- excretion The word 'defence' is used because these are the three ways that the body 'defends' itself against acid-base disturbances. This is not the complete picture as it neglects some metabolic responses (eg changes in metabolic pathways) that occur. This response can be considered by looking at how the components affect the ( [HCO3] / pCO2 ) ratio in the Henderson-Hasselbalch equation. The 3 components of the response are summarised below. [H+] konsantrasyonundaki degisikliklere fizyolojik yanitlar ?? asamada ger?eklesir: (1) Hizli, kimyasal tamponlama, (2) respiratuar kompansasyon (m?mk?n oldugunda), (3) daha yavas fakat daha etkili olarak renal kompansasyon. 2.1.3 Response to an Acid-Base Perturbation The body?s response to a change in acid-base status has three components: First defence: Buffering Second defence: Respiratory : alteration in arterial pCO2 Third defence: Renal : alteration in HCO3- excretion The word 'defence' is used because these are the three ways that the body 'defends' itself against acid-base disturbances. This is not the complete picture as it neglects some metabolic responses (eg changes in metabolic pathways) that occur. This response can be considered by looking at how the components affect the ( [HCO3] / pCO2 ) ratio in the Henderson-Hasselbalch equation. The 3 components of the response are summarised below.

50. V?CUTTAKI MAJ?R TAMPON SISTEMLERI In review Titratable acidity is an important part of excretion of fixed acids under normal circumstances but the amount of phosphate available cannot increase very much. Also as urine pH falls, the phosphate will be all in the dihyrogen form and buffering by phosphate will be at its maximum. A further fall in urine pH cannot increase titratable acidity (unless there are other anions such as keto-anions present in significant quantities) The above points mean that titratable acidity cannot increase very much (so cannot be important in acid-base regulation when the ability to increase or decrease renal H+ excretion is required) In acidosis, ammonium excretion fills the regulatory role because its excretion can increase very markedly as urine pH falls. In review Titratable acidity is an important part of excretion of fixed acids under normal circumstances but the amount of phosphate available cannot increase very much. Also as urine pH falls, the phosphate will be all in the dihyrogen form and buffering by phosphate will be at its maximum. A further fall in urine pH cannot increase titratable acidity (unless there are other anions such as keto-anions present in significant quantities) The above points mean that titratable acidity cannot increase very much (so cannot be important in acid-base regulation when the ability to increase or decrease renal H+ excretion is required) In acidosis, ammonium excretion fills the regulatory role because its excretion can increase very markedly as urine pH falls.

51. KOMPANSASYON

52. KOMPANSATUAR YANITLAR Morgan GE, Clinical Anesthesiology

53. TEDAVI RESPIRATUAR ASIDOZ Alveolar ventilasyonun arttirilmasi Ge?ici ?nlemler: Bronkodilatasyon Hipnozun geri d?nd?r?lmesi Respiratuar stim?lan (doksapram) Akciger kompliansinin d?zeltilmesi (di?rez)

54. TEDAVI RESPIRATUAR ASIDOZ CO2 ?retiminin azaltilmasi: Dantrolen Kas paralizisi Antitiroid medikasyon Karbonhidrat aliminin azaltilmasi Orta-ciddi asidoz (pH<7.20), CO2 narkozu ve respiratuar kas yorgunlugu mekanik ventilasyon i?in endikasyondur. Hiipokesmi siklikla eslik ettigi i?in oksijen uygulamasi da gerekli olur. Ciddi asidoz (ph<7.1) ve eslik eden kardiyovask?ler kollaps bulunmadik?a NaHCO3 nadiren gerekli olur. Sodyum bikarbonat tedavisi, ge?ici olarak PaCO2?yi arttiri.Orta-ciddi asidoz (pH<7.20), CO2 narkozu ve respiratuar kas yorgunlugu mekanik ventilasyon i?in endikasyondur. Hiipokesmi siklikla eslik ettigi i?in oksijen uygulamasi da gerekli olur. Ciddi asidoz (ph<7.1) ve eslik eden kardiyovask?ler kollaps bulunmadik?a NaHCO3 nadiren gerekli olur. Sodyum bikarbonat tedavisi, ge?ici olarak PaCO2?yi arttiri.

55. TEDAVI METABOLIK ASIDOZ Respirasyonun kontrol? NaHCO3 Spesifik tedavi: Diyabetik ketoasidoz Laktik asidoz Salisilat entoksikasyonu Metanol, etilen glikol entoksikasyonu Spesifik tedavi: Diyabetik ketoasidoz: Sivi replasmani, ins?lin, potasyum, fosfat Laktik asidoz: Oksijnasyonun d?zeltilmesi, doku perf?zyonunun d?zeltilmesi Salisilat entoksikasyonu:Idrar alkalinizasyonu Metanol, etilen glikol entosikasyonu: Etanol inf?zyonuSpesifik tedavi: Diyabetik ketoasidoz: Sivi replasmani, ins?lin, potasyum, fosfat Laktik asidoz: Oksijnasyonun d?zeltilmesi, doku perf?zyonunun d?zeltilmesi Salisilat entoksikasyonu:Idrar alkalinizasyonu Metanol, etilen glikol entosikasyonu: Etanol inf?zyonu

56. HCO3 DOZUNUN HESAPLANMASI-1 Doz (mEq) = 0.3 x kg x BE (mEq/L) ?rnek: 70 kg , BE=18 mEq/L Doz = 0.3 x 70 x 18 = 378 mEq The diagram shows an example of a patient with a (pure) metabolic acidosis, SBE = -18 mEq/L. To achieve complete correction for someone weighing 70 kg: Dose (mEq)?=?0.3? x?Wt (kg)?x?SBE (mEq/L) 378 ? ? ? =?0.3 ?x ? ? 70 ? ? x ? ? ? 18 ? ? The diagram shows an example of a patient with a (pure) metabolic acidosis, SBE = -18 mEq/L. To achieve complete correction for someone weighing 70 kg: Dose (mEq)?=?0.3? x?Wt (kg)?x?SBE (mEq/L)378 ? ? ? =?0.3 ?x ? ? 70 ? ? x ? ? ? 18 ? ?

57. HCO3 DOZUNUN HESAPLANMASI-2 Calculating the Dose. (Move mouse over the Diagram) The diagram shows an example of a patient with a (pure) metabolic acidosis, SBE = -18 mEq/L. To achieve complete correction for someone weighing 70 kg: Dose (mEq)?=?0.3? x?Wt (kg)?x?SBE (mEq/L) 378 ? ? ? =?0.3 ?x ? ? 70 ? ? x ? ? ? 18 ? ? This assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters. Our intention , of course, is to normalize the "Bath Water", ? i.e., the extracellular fluid, which is 20% of the body (about 14 liters). But, because the injected bicarbonate also equilibrates to some extent with the intracellular fluid, the "treatable volume" is larger. Calculating the Dose. (Move mouse over the Diagram) The diagram shows an example of a patient with a (pure) metabolic acidosis, SBE = -18 mEq/L. To achieve complete correction for someone weighing 70 kg: Dose (mEq)?=?0.3? x?Wt (kg)?x?SBE (mEq/L)378 ? ? ? =?0.3 ?x ? ? 70 ? ? x ? ? ? 18 ? ? This assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters. Our intention , of course, is to normalize the "Bath Water", ? i.e., the extracellular fluid, which is 20% of the body (about 14 liters). But, because the injected bicarbonate also equilibrates to some extent with the intracellular fluid, the "treatable volume" is larger.

58. HCO3 DOZUNUN HESAPLANMASI-2

59. YARI DOZ TERCIHININ NEDENLERI Reasons to Limit Bicarbonate Dose. 1. Injected into Plasma Volume. (Move mouse over the Diagram) The bicarbonate is injected initially into the three liter plasma volume instead of the calculated 21 liters of treatable volume (it does not cross the cell membrane to enter the two liters of red cells.) At first, therefore, the dose hugely "over-treats" this small compartment. 2. "Fizzes with Acid". (Move mouse over the Diagram) When bicarbonate is added to acid it "fizzes". Literal "fizzing", fortunately, does not occur in the blood stream. This vivid picture, nevertheless, reinforces our understanding: the majority of the injected bicarbonate is converted to carbon dioxide and it then has to be eliminated by an increase in ventilation. Reasons to Limit Bicarbonate Dose. 1. Injected into Plasma Volume. (Move mouse over the Diagram) The bicarbonate is injected initially into the three liter plasma volume instead of the calculated 21 liters of treatable volume (it does not cross the cell membrane to enter the two liters of red cells.) At first, therefore, the dose hugely "over-treats" this small compartment. 2. "Fizzes with Acid". (Move mouse over the Diagram) When bicarbonate is added to acid it "fizzes". Literal "fizzing", fortunately, does not occur in the blood stream. This vivid picture, nevertheless, reinforces our understanding: the majority of the injected bicarbonate is converted to carbon dioxide and it then has to be eliminated by an increase in ventilation.

60. YARI DOZ TERCIHININ NEDENLERI

61. YARI DOZ TERCIHININ NEDENLERI 3. Causes Respiratory Acidosis. (Move mouse over the Diagram - TWICE!) This initial production of CO2 raises the PCO2 in the plasma and tends to causing relative respiratory acidosis. For each 100 mEq of bicarbonate which is converted, about 2.24 liters of carbon dioxide has to be exhaled, equivalent to ten minutes normal production. The marked metabolic acidosis here is treated with half the calculated dose. This corrects the metabolic disturbance half way but produces a transient respiratory acidosis. Then, continuing ventilation eliminates the excess CO2 to reach a more modest level of partially compensated metabolic acidosis. 3. Causes Respiratory Acidosis. (Move mouse over the Diagram - TWICE!) This initial production of CO2 raises the PCO2 in the plasma and tends to causing relative respiratory acidosis. For each 100 mEq of bicarbonate which is converted, about 2.24 liters of carbon dioxide has to be exhaled, equivalent to ten minutes normal production. The marked metabolic acidosis here is treated with half the calculated dose. This corrects the metabolic disturbance half way but produces a transient respiratory acidosis. Then, continuing ventilation eliminates the excess CO2 to reach a more modest level of partially compensated metabolic acidosis.

62. YARI DOZ TERCIHININ NEDENLERI

63. YARI DOZ TERCIHININ NEDENLERI

64. INTRASELL?LER ASIDOZ 4. Raises Intracellular PCO2. (Move mouse over the Diagram) The carbon dioxide which is produced enters the cells freely, unlike the bicarbonate ions which have been administered. Therefore, the added PCO2 inside tends to cause the intracellular fluid to become more acid. However, direct studies employing nuclear magnetic resonance indicate that this change may be insignificant (Severinghaus, Personal Communication 1986). 4. Raises Intracellular PCO2. (Move mouse over the Diagram) The carbon dioxide which is produced enters the cells freely, unlike the bicarbonate ions which have been administered. Therefore, the added PCO2 inside tends to cause the intracellular fluid to become more acid. However, direct studies employing nuclear magnetic resonance indicate that this change may be insignificant (Severinghaus, Personal Communication 1986).

65. INTRASELL?LER ASIDOZ

66. TEDAVI RESPIRATUAR ALKALOZ Hiperventilasyonun d?zeltilmesi Ciddi alkalemi (pH > 7.55): Hidroklorik asit, iv. Amonyum klor?r, iv.

67. TEDAVI METABOLIK ALKALOZ Altta yatan durumun d?zeltilmesi Dakika ventilasyon hacminin azaltilmasi

68. TEDAVI METABOLIK ALKALOZ Klor?re duyarli metabolik alkaloz: Intraven?z salin Potasyum replasmani Simetidin, ranitidin Asetazolamid Klor?re duyarli metabolik alkalozun tedavisinde: Intraven?z salin ve Potasyum replasmani yeterli. Asiri gastrik sivi kaybi olan hastalarda Simetidin, ranitidin yarar saglar. ?demat?z hastalarda Asetazolamid yararli olabilir. Klor?re duyarli metabolik alkalozun tedavisinde: Intraven?z salin ve Potasyum replasmani yeterli. Asiri gastrik sivi kaybi olan hastalarda Simetidin, ranitidin yarar saglar. ?demat?z hastalarda Asetazolamid yararli olabilir.

69. TEDAVI METABOLIK ALKALOZ Klor?re diren?li metabolik alkaloz: Aldosteron antagonistleri pH > 7.60 : Hidroklorik asit (0,1 mol/L), iv Amonyum klor?r (0,1 mmol/L), iv. Arginin hidroklor?r Hemodializ Klor?re diren?li hastalarda ise artmis mineralokortikoid aktivitesi aldosteron antagonsitlerine hizla cevap verir.Klor?re diren?li hastalarda ise artmis mineralokortikoid aktivitesi aldosteron antagonsitlerine hizla cevap verir.

70. PaO2 209 mmHg PaCO2 11 mmHg pH 7.47 Calculated values: B.E. - 14.6 mmol/L Total CO2 8 mEq/L HCO3 7.7 mmol/L Hb 9.5 g/dl Na+ 135 mEq/L Cl- 95 mEq/L K+ 5.5 mEq/L AVL OMNI MEASUREMENT REPORT Bu slaydi hatirliyoruz. Hastada a?ik bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 10 mmHg d?sm?s oldugundan (40-10) / 10 x 2 mmol/L = 6 beklenen HCO3 d?zeyi = 24-6= 18 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu da var. Tani: Primer respiratuar alkaloz ve primer metabolik asidoz. Bu slaydi hatirliyoruz. Hastada a?ik bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 10 mmHg d?sm?s oldugundan (40-10) / 10 x 2 mmol/L = 6 beklenen HCO3 d?zeyi = 24-6= 18 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu da var. Tani: Primer respiratuar alkaloz ve primer metabolik asidoz.

71. OLGU SUNUMU Respiratuar alkaloz: KKY ? Hava a?ligi ? Hiperventilasyon Metabolik asidoz: Perf?zyon bozuklugu ? Laktik asidoz Bu hastada asit-baz dengesizliginin nedenleri neler olabilir ? Respiratuar alkaloz, olasilikla KKY?ne (hava a?ligi-hiperventilasyon) baglidir. Metabolik asidoz, perf?zyon bozukluguna bagli laktik asidozun sonucudur. Bunu dogrulamak i?in anyon gapi hesaplayalim. Bu hastada asit-baz dengesizliginin nedenleri neler olabilir ? Respiratuar alkaloz, olasilikla KKY?ne (hava a?ligi-hiperventilasyon) baglidir. Metabolik asidoz, perf?zyon bozukluguna bagli laktik asidozun sonucudur. Bunu dogrulamak i?in anyon gapi hesaplayalim.

72. OLGU SUNUMU Anyon Gap: = Na+ ? Cl- ? tCO2 = 135 ? 95 ? 8 = 32 mEq/L Laktat = 14.4 mmol/L

73. OLGU SUNUMU TEDAVI Konjestif kalp yetersizligi tedavisi Digoksin Furosemid Transf?zyon FiO2 = 0.5 Tasikardide d?zelme Perf?zyon hala k?t?

74. PaO2 136 mmHg PaCO2 23 mmHg pH 7.52 Calculated values: B.E. - 3.0 mmol/L Total CO2 18.5 mEq/L HCO3 18.0 mmol/L Hb 10.3 g/dl Na+ 137 mEq/L Cl- 92 mEq/L K+ 3.9 mEq/L Laktat 2.7 mmol/L AVL OMNI MEASUREMENT REPORT TEDAVI SONRASI Hastada hala bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 20 mmHg d?sm?s oldugundan (40-20) / 10 x 2 mmol/L = 4 beklenen HCO3 d?zeyi = 24-4= 20 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu hala var. Anyon gap= 137-92-18= 27 mEq/L. Laktat d?zeyi = 2,7 mmol/L Tedavi, primer soruna KKY?a y?nelik olmali. Digoksin ve furosemid tedavisi baslaniyor. Hb d?s?k oldugu i?in di?rez sonrasinda transf?zyon yapiliyor. Di?rez sonrasinda tasipne d?zeliyor, ancak perf?zyon hala k?t?. Yineleyen ?l??mlerde sonu?lar yukaridaki gibi.Hastada hala bir alkaloz vardir (pH>7.45), respiratuar orijinli olma olasiligi d?s?k (PaCO2 < 40 mmHg) PaCO2, yaklasik 20 mmHg d?sm?s oldugundan (40-20) / 10 x 2 mmol/L = 4 beklenen HCO3 d?zeyi = 24-4= 20 mmol/L. Hastanin HCO3 degeri, 10 mmol/L, beklenenden daha az. Asidozu hala var. Anyon gap= 137-92-18= 27 mEq/L. Laktat d?zeyi = 2,7 mmol/L Tedavi, primer soruna KKY?a y?nelik olmali. Digoksin ve furosemid tedavisi baslaniyor. Hb d?s?k oldugu i?in di?rez sonrasinda transf?zyon yapiliyor. Di?rez sonrasinda tasipne d?zeliyor, ancak perf?zyon hala k?t?. Yineleyen ?l??mlerde sonu?lar yukaridaki gibi.

75. PaO2 124 mmHg PaCO2 35 mmHg pH 7.51 Calculated values: B.E. + 5.0 mmol/L Total CO2 27 mEq/L HCO3 26.8 mmol/L Hb 15 g/dl Na+ 136 mEq/L Cl- 91 mEq/L K+ 3.2 mEq/L Laktat 2.7 mmol/L AVL OMNI MEASUREMENT REPORT 24 SAAT SONRA Respiratuar alkaloz ve metabolik asidoz d?zelmis, metabolik alkaloz ?n plana ?ikmis. iv, KCL replasmani ve bir miktar salin inf?zyonundan sonra metabolik alkaloz da d?zelmistir. Hasta daha sonra koarktasyon onarimi operasyonuna alinmistir. Respiratuar alkaloz ve metabolik asidoz d?zelmis, metabolik alkaloz ?n plana ?ikmis. iv, KCL replasmani ve bir miktar salin inf?zyonundan sonra metabolik alkaloz da d?zelmistir. Hasta daha sonra koarktasyon onarimi operasyonuna alinmistir.

76. OLGU SUNUMU TEDAVI Metabolik alkaloz tedavisi: KCl, iv NaCL, iv Aorta koarktasyonu cerrahisi

77. ?ZET

78. pH = PaCO2 = HCO3 = 7.42 43.9 26.8 SORU 1 Normal kan gazi

79. SORU 2 pH = PaCO2 = HCO3 = 7.38 52.6 32.5 Respiratuar asidoz, kompanse

80. SORU 3 pH = PaCO2 = HCO3 = 7.52 30.9 24.8 Respiratuar alkaloz, kompanse degil

81. SORU 4 pH = PaCO2 = HCO3 = 7.21 33.3 17.6 Metabolik asidoz, kismen kompanse

82. SORU 5 pH = PaCO2 = HCO3 = 7.42 58.0 38.0 Respiratuar asidoz, kompanse

83. SORU 6 pH = PaCO2 = HCO3 = 7.14 24.6 8.0 Metabolik asidoz

84. SON SORU pH = PaCO2 = HCO3 = 7.49 48.9 39.0 Metabolik alkaloz, kompanse degil


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