1. Practical Clinical Nephrology Using principles of renal physiology to analyze, diagnose and treat patients Professor Internal Medicine (nephrology) Molecular Physiology & Biophysics University of Iowa College of Medicine Iowa City, Iowa, USA Guest Professor in Renal Physiology Göteborgs Universitet Göteborg, Sweden Gerald F. DiBona (Jerry)

2. HYPONATREMIA

3. Prevalence of hyponatremia Patient GroupPrevalence (%) ICU11.0-29.6 Elderly outpatients7.2-11.0 Elderly inpatients18.0-53.0 Elderly with falls9.1-13.0 Heart Failure10.2-27.0 Cirrhosis20.8-49.4 Cancer3.7-47.0 Pneumonia8.1-27.9 CKD pre dialysis13.6 CKD on dialysis29.3 Marathon runners3.0-13.0

4. Relationship between SNa and mortality in patients admitted between 1996 and 2007 (N = 45,693) CJASN 6:960-965, 2011

5. Diagnostic + Therapeutic Approach to Patient with Hyponatremia

6. 24 yo male, chronic paranoid schizophrenia Sudden onset of seizures BP 108/83 mm Hg, HR 68/min lying and standing Na 116 K 4 Cl 88 HCO3 20 BUN (blood urea nitrogen)9 (3.2) SCreat1.0 (88) Glucose105 (5.8) HYPONATREMIA #1 What do you want next ? Posm = 231 (calculated = 241) Uosm = 79 Dx: Psychogenic Polydipsia Rx:IV 0.9% NaCl and water restriction

7. Clinical Evaluation of Volume Status Test of circulatory integrity BP and HR lying and standing > 20 mm Hg  in systolic > 10 mm Hg  diastolic > 10 bpm  HR HYPOVOLEMIA (  intravascular volume) WHY & HOW?

8.  P-Na   Posm   ADH   Uosm  P-Na   Posm   ADH   Uosm

9. Calculating Plasma Osmolality Posm = 2Na + glucose/18 + BUN/2.8 (mmol/L) (mg/100 ml) (mg/100 ml) Posm = 2 (116) + 105/18 + 9/2.8 Posm = 232 + 5.8 + 3.2 = 241 Posm = 2Na + glucose + BUN Posm = 232 + 5.8 + 3.2 = 241 (mmol/L) (mmol/L) (mmol/L)

10. Edema =  total body sodium Edema = increased interstitial fluid (pleural, peritoneal cavity, pulmonary alveoli, soft tissues, gravity). Interstitial fluid is protein-free ultrafiltrate of plasma, has same Na concentration as plasma.

11. 62 yo man admitted with chief complaint of hemoptysis of 2 wks duration. HX: gradually worse dyspnea over 10 years, productive cough and multiple lung infections in winter months. Recent worsening of generalized malaise, loss of appetite and fatigue. Smoking 1 pack/day x 20-30 years. MEDS: terbutaline inhaler. PE: BP 168/92 mm Hg and HR 84 bpm lying/standing. Mentally confused, disoriented as place and time. Scattered coarse breath sounds both lungs, decreased breath sounds and percussion dullness right base. No peripheral edema LAB: Na 100, K 3.5, Cl 72, HCO3 30 mEq/L; Screatinine 0.6 mg/dl (53 umol/L) Glucose 108 mg/dl (6 mmol/L) Blood Urea Nitrogen (BUN) 6 mg/dl (2 mmol/L) Posm = 2 x PNa + BUN + Glucose = 200 + 2 + 6 = 208 mOsm/kg No change in volume status: nl BP, no edema, UNa 45 What do you do next?

12. But Uosm=600 > Posm=208, (U/P)osm = 600/208 = 3.  PNa and Posm should  ADH   Uosm to < Posm with (U/P)osm < 1 Excretion of a dilute urine Thus, ADH present when it shouldn’t be = inappropriate Syndrome of Inappropriate ADH Secretion, SIADH Excess water retention + low Posm; what should happen? Treatment ? Hypoosmotic euvolemic hyponatremia (U/P)osm > 1 ALWAYS MEANS ADH IS PRESENT water restriction, 0.9%/3.0% NaCl

13. 40 yo female with chief complaint of nausea and vomiting for 4 days. HX: Unable to keep solid food down at all and minimally able to tolerate liquids. PE: BP and HR supine100/70 mm Hg and 90 bpm BP and HR standing 90/60 mm Hg and 116 bpm No edema LAB: Na 129, K 3.9, Cl 88, HCO3 28 mEq/L Screatinine 1.0 mg/dl (88 umol/L) Blood Urea Nitrogen (BUN) 20 mg/dl (7 mmol/L) Glucose 90 mg/dl (5 mmol/L) What do you want next? UNa=9 mEq/L; Posm=2 x 129 + 7 + 5=270 mOsm/kg; Uosm=600 mOsm/kg What is the diagnosis? Explain. ECV (intravascular) + Na depletion: orthostatic BP,  UNa Despite  Posm which should  ADH  dilute urine with  Uosm, there is  Uosm + (U/P)osm = 600/270 = 2.2  ADH present; hypoosmotic hypovolemic hyponatremia Volume depletion (> 15%) with  BP stimulates ADH release and overrides effect of  Posm to  ADH ? Treatment NaCl 0.9%/3.0% iv volume repletion, restrict free water, hypertonic intake

14. Decrease in mean arterial pressure or intravascular volume, % Plasma ADH, pmol/L ADH increase with 3% increase in Posm  CO +  BP stimulates baroreceptor mediated ADH release and overrides effect of  Posm to  ADH

15. Increase in ADH with 10% decrease in AP or blood volume Increase in ADH with 3% increase in Posm (285  290 mOsm/kg)

16. 50 yo man with chief complaint of  fatigue, dyspnea on exertion, leg swelling HX: Post MI dilated cardiomyopathy, chronic congestive heart failure. PE: BP 100/70 mm Hg, HR 96 bpm. Jugular vein distension, cardiomegaly, signs of pleural effusion and pitting edema to the thigh. LAB: Na 129, K 3.9, Cl 88, HCO3 28 mEq/L Screatinine 1.0 mg/dl (88 umol/L) Blood Urea Nitrogen (BUN) 20 mg/dl (7 mmol/L) Glucose 90 mg/dl (5 mmol/L) What do you want next? UNa=9 mEq/L; Posm=2 x 129 + 7 + 5=270 mOsm/kg; Uosm=600 mOsm/ kg What is the diagnosis? Explain Despite  Posm which should  ADH  dilute urine with  Uosm, there is  Uosm + (U/P)osm = 600/270 = 2.2  ADH present Congestive heart failure:  cardiac output,  BP; hypoosmotic hypervolemic hyponatremia (  TB Na,  TB H2O) Treatment? Diuretic, NaCl 0.9%.3.0%, free water restriction, vaptans

17. HYPERNATREMIA

18. En 30-årig man söker på sin vårdcentral p.g.a. ökad törst och stora urinmängder. Tester på plasma och urin ger följande data: Glukos i urin: negativ Uosm: 60 mOsm/kg U-[Na+]: 15 mM Analyser från blodprov gav följande resultat: S-Na 154 mM S-K 4,2 mM S-Cl 114 mM S-HCO3 28 mM S-[kreatinin] 110  M Posm: 312 mOsm/kg B-glukos: 4,5 mM a. Vad i lab-data stöder antagandet att det är primärt stora urinförluster, följt av ökad törst och inte tvärtom? High PNa and Posm should increase ADH and increase Uosm (but it is low) b. Vad finns det för tänkbara orsaker till ökade urinmängder (polyuri)? c. Vad är sannolikaste orsaken i detta fall? DM (but blood glucose normal and urine glucose negative). Diabetes insipidus ADH sc, im, iv, nasal inhalation d. Hur kan tillståndet behandlas?

19. A 40 yo male alcoholic was admitted to the hospital because of severe head injury sustained in falling down a flight of stairs. He remained comatose, and over a period of three days his S-Na increased from 145 mEq/L to 170 mEq/L. Urine output was not accurately measured, but specific gravity in a random specimen was 1.004 (Uosm = 100 mOsm/kg). What is the probable cause of the hypernatremia? A. Inappropriate normal saline administration B. Diabetes insipidus due to head trauma C. Insufficient water intake alone D. Acute renal failure The patient weighed 60 kg on admission but was not weighed thereafter. What was the magnitude of change in total body water (assuming negligible changes in total body sodium)? A. 5.3 liter reduction B. 2.5 liter reduction C. 11.7 liter reduction D. 8.1 liter reduction total body sodium before = total body sodium after total body water before x PNa before = total body water after x PNa after 60 kg x 0.6 x 145 = total body water after x 170 36 x 145 = total body water after x 170 total body water after = 30.7 liters; total body water deficit = 36-30.7 = 5.3 liters

20. En äldre person med diabetes typ 2 drabbas av en streptokock-infektion och blir sängliggande ensam i hemmet. Hög feber och bristande vätskeintag, samt det faktum att diabetes medicineringen glöms bort, leder till förvirring på grund av rubbad vätske- och elektrolyt-balans. Efter några dagar hittas personen medvetslös. Labdata vid inkomst till akuten: Posm 354 mOsm/kg B-glukos 44 mM S-Na 153 mM S-Ca2+ 2,7 mM S-Cl113 mM pH 7,4 S-K 5,0 mM pCO2 5,3 kPa (40 mm Hg) S- HCO324 mM BE -0.4 Anion gap21 mMS-kreatinin88  M Diagnosis? Why is Posm increased? Why are S-Na and S-Cl increased? What is total body water? Why are serum ketones not increased? non-ketotic hyperosmolar diabetic coma hyperglycemia, water loss from glucose osmotic diuresis water loss from glucose osmotic diuresis, fever decreased insulin resistance everywhere but fat Why no metabolic acidosis? no ketones Treatment? hypoglycemic medicines; water….10%  PNa due to water loss

21. HYPERKALEMIA

22. A patient has S-K = 6.5 mEq/L. What do you do? Calcium gluconate IV: fastest initial therapy is stabilization of excitable cardiac membranes with calcium gluconate IV; short-lived 30 mins. How? Real or artifact? hemolysis,  WBC,  plts Clinical effect? EKG Treatment? Reduction in serum K : IV insulin + glucose & nebulized beta-2 agonist lower serum K by shifting K into cells (also NaHCO3 if acidosis If due to mineral but not organic acids). How? Removal of excess K from body: through GI tract with sodium polystyrene sulfonate exchange resin (hours) or via dialysis (hemo>PD).

23. HYPOKALEMIA

24. 56 yo female secretary with history of essential hypertension for 12 years. Rx: low sodium diet, hydrochlorothiazide (HCTZ) 50 mg per day. She states that she has "occasionally felt puffy" and has increased HCTZ 50 mg 4 times per day. Lab: S-Na138 mEq/LBUN 21 mg% (7.5) S-K 2.2 mEq/LCreatinine 1.2 mg% (106) S-Cl 90 mEq/LArterial pCO 2 = 48 mmHg (6.4) S-HCO337 mEq/LArterial pH = 7.50 Acid-base Dx?Metabolic alkalosis Why S-Cl  ?HCTZ blocks DCT Na/Cl cotransport;  urine Na+Cl Why S-K  ? 1.  Na delivery to CD with  Na/K exchange;  urine K 2.  flow favors K gradient for K diffusion into lumen;  urine K 3. Volume loss  aldosterone, stimulates Na/K exchange;  urine K Why S-HCO3  ?  Na delivery to CD with  Na/H exchange;  urine H (low urine pH); loss of H = gain of HCO3 Why arterial pCO 2  ? Respiratory compensation (hypoventilation) for metabolic alkalosis Why arterial pCO 2 not higher? hypoventilation  hypoxia

25. NaKCLHCO3OtherDx 1452.810429UCl 50 1352.88535UCl 10 1402.911815UpH 6.5 1402.911815UpH 5.4, UK 8 1383.18436UK 50 Aldosteronism Vomiting Distal RTA Diarrhea HCTZ HYPOKALEMIA

26. ACID – BASE

27.  pCO2 means:  pCO2 means: alveolar hypoventilation alveolar hyperventilation Compensatory responses never completely normalize pH; if pH normalized, another acid base disturbance is present

28. Anion gap, AG = (Na + K) – (Cl + HCO3) Normal = 16  4 AG = unmeasured anions in plasma, mainly negatively charged proteins. Acid anions (e.g. lactate, acetoacetate, sulfate) produced during metabolic acidosis usually not measured = unmeasured anions. H + reacts with HCO3 - (buffering), CO 2 produced is excreted via lungs (respiratory compensation). Net effect:  measured anions (i.e. HCO 3 ) +  unmeasured anions (acid anions)   AG  Anion Gap Metabolic Acidosis M-methanol  formic acid (formate) U-uremia (chronic renal failure)  sulfuric acid (sulfate), phosphoric acid (phosphate) D-diabetic ketoacidosis  acetoacetic acid (aceoacetate),  -OH-butyric acid (  -OH-butyrate) P-propylene glycol  lactic acid (lactate), proprionic acid (proprionate) I-infection L-lactic acidosis  lactic acid (lactate) E-ethylene glycol  oxalic acid (oxalate) S-salicylic acid  salicylate

29. Major Clinical Uses of the Anion Gap (AG) Signal the presence of a metabolic acidosis (confirm other findings). Differentiate between causes of metabolic acidosis:  AG versus normal AG metabolic acidosis. Inorganic metabolic acidosis (e.g. HCl infusion): infused Cl - replaces HCO 3 and AG remains normal. Organic metabolic acidosis: lost HCO3 is replaced by the acid anion (e.g. acetoacetate) which is not measured and AG . Determine severity of metabolic acidosis and follow response to treatment

30. Step 1: Acidemic, alkalemic, or normal? Step 2: Is the primary disturbance respiratory or metabolic? Step 3: For a primary respiratory disturbance, is it acute or chronic? Step 4: For a metabolic disturbance, is the respiratory system compensating OK? Step 5: For a metabolic acidosis, is there an increased anion gap? Step 6: For an increased anion gap metabolic acidosis, are there other abnormalities? Stepwise approach to interpreting arterial blood gas

31. 1.Hx & PE 2. Look at blood pH: pH 7.45, alkalosis 3. Look at blood PCO2, HCO3- Both PCO2 and HCO3-  : respiratory acidosis or metabolic alkalosis Both PCO2 and HCO3-  : respiratory alkalosis or metabolic acidosis Acid Base DisorderpH Initial Chemical Change Compensatory Response Respiratory Acidosis< 7.35↑ PCO2 ↑HCO3- Respiratory Alkalosis>7.45↓ PCO2 ↓ HCO3- Metabolic Acidosis< 7.35 ↓ HCO3-↓ PCO2 Metabolic Alkalosis>7.45 ↑ HCO3-↑ PCO2

32. Acid-Base Algorithm

33. A 56 yo man, chronic smoker with COPD, comes to the emergency room together with his 15 yo son who has allergic bronchial asthma. The father has no acute symptoms but there is a long history of dyspnea and limited exercise capacity. The son has acute audible wheezing, air hunger and difficult expiration. pHpCO2HCO3 Father7.3360 (8)31 Son7.2260 (8)24 What is acid-base diagnosis for father + son? Father: chronic respiratory acidosis with compensation, chronic, time Son: acute respiratory acidosis without compensation, acute, time What is compensation?  Renal reabsorption and generation of HCO3 What is signal to kidney to  reabsorption and generation of HCO3?  pCO2 pHpCO2HCO3 Father7.5040 (5.3)31 Son7.4040 (5.3)24 Both father and son are treated with vigorous assisted mechanical ventilation What happened?

34. Day 1Day 3 no RxDay 3 p Rx Posm290317290 S-Na128133148 S-K6,08,13,0 S-Cl 9310694 S- HCO38.83.932.2 pH7,156,917,54 pCO23,5 kPa (26 mm Hg) 2,7 kPa (20 mm Hg) 5,2 kPa (39 mm Hg) Anion gap (AG)32.231.224.8 B-glukos35 mM44 mM4 mM A 55 yo man with diabetes mellitus is admitted What’s this? What’s changed? What’s happened?

35. 18-year-old male with confusion, nausea, headache, and decreased vision after a camping trip. The patient’s friends state that he became ill 12 to 24 hours ago. Blood urea nitrogen14 mg/dL (5 mmol/L) Serum creatinine1.0 mg/dL (88 umol/L) Serum Na140 meq/L Serum K4 meq/L Serum Cl100 meq/L Serum HCO312 meq/L AG 32 meq/L Serum glucose108 mg/dL (6 mmol/L) Measured Posm326 mOsm/kg Serum ketonesNegative Serum lactate0.7 meq/L (0.08 mmol/L) NL pH7.29 Pco 2 26 mm Hg (3.5 kPa) 1. Dx?metabolic acidosis with high anion gap (32)  Anion Gap Metabolic Acidosis M-methanol U-uremia (chronic renal failure) D-diabetic ketoacidosis P-propylene glycol I-infection L-lactic acidosis E-ethylene glycol S-salicylate 2. Posm?Calc Posm = 291 mOsm/kg Osmolar gap = Meas Posm - Calc Posm = 35  osmolar gap (> 15): methanol, ethanol propylene glycol, ethylene glycol Methanol: formic acid Ethanol: acetic acid Ethylene glycol: oxalic acid Propylene glycol:proprionic acid

36. En 50-årig kvinna ådrar sig multipla frakturer vid en trafikolycka. Vid ankomsten till sjukhus är hon i prechock men stabiliseras cirkulatoriskt efter 500 ml syntetisk kolloid samt 4 påsar blod. Under följande dygn behövs ytterligare 2 påsar blod. Under 2:a dygnet viss andningspåverkan och syrgas ges via näskateter. pH 7,51; pCO 2 3,9 (29 mm Hg); HCO3 22; pO 2 8,0 (60 mm Hg); Sa-O 2 91 % Patienten blir alltmer respiratoriskt och cirkulatoriskt påverkad och röntgen pulm visar nu diffusa förtätningar över bägge lungfälten. pH 7,21; pCO 2 6,0 (45 mm Hg); HCO3 17; pO 2 7,2 (54 mm Hg); Sa-O 2 84 % Hur bedömer du syra-bas status, inklusive pO 2 ? Acute respiratory alkalosis, hypoxia stimulates hyperventilation (  pCO2), acute as HCO3 not  Tolkning av syra – bas status? Åtgärder? Metabolic acidosis, hypoxia but no hyperventilation (pCO2  ) (? respiratory muscle fatigue) + no respiratory compensation Orsak till skillnaden mellan de två blodgasanalyserna? Oxygen diffusion block in lungs, ? pulmonary edema Intubation, mechanical ventilation (respirator)

37. 50 year old man with duodenal ulcer, several days of intermittent vomiting. PE: volume depletion-orthostatic changes in blood pressure, sunken eyes, flat neck veins, and poor skin turgor Lab: S-Na 140 mEq/L S-K 3.0 mEq/L S-Cl 98 mEq/L S-HCO3 33 Arterial pH 7.49 Arterial Pco2 45 mm Hg (6 kPa) Urine Na 5 mEq/L Urine Cl 5 mEq/L Urine K 40 mEq/L Urine pH 5.5 1. Acid-base disorder and its cause ? metabolic alkalosis, vomiting, HCl loss 2. Compensatory response? respiratory, limited by hypoxia 4.  Serum K? urine K loss (aldosterone  K secretion by CD principal cell, Na/K) 3. Volume status?  ; clinical findings,  aldosterone   urine Na,  urine K 5. Why urine pH 5.5? With volume depletion, proximal reabsorption maximal no HCO3 gets out of PCT.  aldosterone  H secretion by CD intercalated cell, Na/H 6. Treatment?normalize volume with isotonic NaCl, with KCl

38. En 65-årig man med kronisk obstruktiva lungsjukdom har även en ulcus sjukdom med ett flertal röntgen-verifierade sår. Sedan 1 vecka tilltagande andningsbesvär men även dagliga kräkningar under denna tid. pH7,35 pCO 2 10,4 kPa (78 mm Hg) HCO3 42 mEq/L O 2 6,5 kPa (49 mm Hg) Sa-O 2 68 % Vilken typ av syra – basrubbning föreligger? Mixed acid base disorder. COPD with hypoventilation (  pCO2) gives chronic respiratory acidosis but pH is near normal. Vomiting with loss of stomach HCl leads to metabolic alkalosis and higher HCO3 and pH than expected for this degree of hypercapnea (HCO3  3.5 for every 10 mm Hg  in pCO2 over 40 mm Hg).

39. What’s is the acid-base disturbance? pHHCO3pCO2 A7.231025 (3.3) B7.483244 (5.9) C7.343160 (6.7) D7.662220 (2.7) E7.262660 (6.7) F7.581820 (2.7) Metabolic acidosis Metabolic alkalosis Chronic respiratory acidosis Acute respiratory alkalosis Acute respiratory acidosis Chronic respiratory alkalosis

40. A 62 year-old male engineer with difficult-to-control hypertension. High blood pressure was first noted 10months ago and has not responded to increasing doses of amlodipine, losartan and hydrochlorothiazide/triamterene. He has no history of cardiovascular or renal disease. Renal function studies, urinalysis and renal scan obtained by his referring physician were normal. PE: BP 170/105 mmHg seated and standing. Funduscopic examination shows grade II hypertensive retinopathy. Cardiopulmonary examination is normal. Abdominal examination discloses no masses, bruits, or enlarged organs. Trace bilateral pedal edema is noted. Plasma glucose89 mg/dL (4.9) Blood urea nitrogen16 mg/dL (5.9) S-creatinine0.7 mg/dL (87) S-Na140 meq/L S-K3.0 meq/L S-Cl100 meq/L S-HCO327 meq/L What do you do? Discontinue losartan and hydrochlorothiazide/triamterene for 2 weeks; obtain a 24-hour urine specimen for sodium, potassium, and aldosterone excretion during oral/iv NaCl loading.

41. CALCIUM AND PHOSPHOROUS

42. 37 yo man was referred for evaluation of renal insufficiency + hypercalcemia. S-Na140 S-K 3.3 S-Cl110 S-HCO316 AG17.3 S-creat3.0 mg/dl (265 μmol/L) S-Ca 10.8 mg/dl (2.7 mmol/L) S-P 2.1 mg/dl (0.7 mmol/L) PTH 100 pg/ml What is the most likely diagnosis? Renal tubular acidosis Primary hypoparathyroidism Familial hypocalciuric hypercalcemia Salicylate overdose Paget’s disease An abdominal X-ray shows: Hyperchloremic hypokalemic metabolic acidosis with normal anion gap Diffuse nephrocalcinosis

43. 50 yo male presented with a large mass in the right iliac wing. History of membranous nephropathy and has been on hemodialysis for 10 years. Lab: S-Creatinine: 5.7 mg/dl Hematocrit: 23% S-Ca: 7.9 mg/dl, normal 8.5-11.0 mg/dl (1.8 mmol/L) S-P: 9.1 mg/dl, normal 2.4-4.7 mg/dl (2.6 mmol/L) CaxP product: 71 (normal < 55) S-PTH Intact: 1491 ng/L, normal 16-87 ng/L Lytic lesion Why is S-Ca low?  active vitamin D, kidney Why is S-P high?renal failure, GFR<30 ml/min Vascular calcification Cause of lytic lesion ?  PTH  osteoclast Cause of vascular calcification?  CaxP product

44. 3a. Distinguish initial change from compensatory response Initial change: abnormal value correlates with abnormal pH Acidosis, low pH: PCO2 high (respiratory) or HCO3- low (metabolic) Alkalosis, high pH: PCO2 low (respiratory) or HCO3- high (metabolic) Direction of other abnormal parameter: Compensatory: same direction as initial change Mixed disorder: opposite direction from initial change Acid Base DisorderpH Initial Chemical Change Compensatory Response Respiratory Acidosis< 7.35↑ PCO2 ↑HCO3- Respiratory Alkalosis>7.45↓ PCO2 ↓ HCO3- Metabolic Acidosis< 7.35 ↓ HCO3-↓ PCO2 Metabolic Alkalosis>7.45 ↑ HCO3-↑ PCO2 3b. Initial change + compensatory response distinguished, identify disorder - If PCO2 initial change, then respiratory. - if HCO3- initial change, then metabolic.

45. En 75-årig man som tidigare drabbats av skalltrauma med intracerebrala blödningar, men från detta hämtat sig väl, infördes medvetslös till akutmottagningen. Pat får krampanfall av grand mall typ (generaliserat anfall). Behandling inleds med benzodiazepin (Stesolid) men först efter intravenös tillförsel av fenantoin (Proepanutin) kan anfallet brytas. Patienten är cirkulatoriskt helt stabil. Strax efter att patienten blivit krampfri och under pågående syrgastillförsel tas en arteriell blodgas med följande svar: pH 7.01 PaCO 2 : 9,2 kPa (69 mm Hg) HCO3: 17 PaO 2 : 54,6 kPa (410 mm Hg) Vilken (vilka) syra-basrubbningar föreligger? Hur kan patientens blodgas status förklaras? Metabolic acidosis (lactic acidosis), respiratory acidosis Muscle contraction during seizures coupled with hypoventilation (  PaCO 2 ) + hypoxia (now absent due to oxygen treatment)

46. 18 year old man with insulin-dependent (Type I) diabetes mellitus in ER. He reports not taking his insulin during the previous 24 hours because he did not feel well and was not eating. Now has weakness, nausea, thirst, and frequent urination. PE: BP 100/60 mmHg supine and 80/50 standing; HR 100/min supine and 120/min standing. Deep rapid respiration (Kussmaul). Lab data at 0100 : P-Na130 mEq/L P-K 6.5 mEq/L P-Cl 95 mEq/L P-HCO37 mEq/L Arterial pH 6.99 Arterial Pco218 mmHg (2.4 kPa)) P- glucose 600 mg/dL (33.3 mmol)) Urine positive glucose + ketones DX: ? Metabolic acidosis with increased anion gap (AG). AG=Na+K-(Cl+HCO3)=130+6.5- (95+7)=136.5-102=34.5. Unmeasured anions: ketones, acetoacetate, b-hydroxybutyrate 1. Acid-base disorder ? 2. Respiratory pattern?blow off pCO2 3. K status? Hyperkalemia: K out of cells from  ECF osm and insulin lack. Effect of acidosis on K shift out of cells varies with mineral (HCl, +) vs organic (Hlactate, -) acid. Total body K depletion: K out of cells, osmotic diuresis  UK excretion. diabetic ketoacidosis; Rx - isotonic NaCl, insulin iv

47. Results of treatment over time: P- K P-HCO3 P-glucose Time(mEq/L) Arterial pH (mEq/L) (mg/dL)(mmol) 0100 6.5 6.99 7600 (33.3) 0300 4.5 7.10 12400 (22.2) 0400 4.0 7.16 14300 (16.7) 0500 3.5 7.20 16 250 (13.9) 0700 3.2 7.24 18200 (11.1) 4. Why  P-K in first 2 hrs Rx? (a) Insulin moves K into cells; (b) insulin  blood glucose and  ECFosm; (c) iv isotonic NaCl dilutes P-K. Need for K replacement (when urine volume , P-K < 5.5) to avoid hyperkalemia…..kl 0500-0700

48. 60 yo woman with essential hypertension admitted after 7 days of severe vomiting. Systolic BP 110 mm Hg seated, 70 mm Hg standing. Pulse rate seated 120/min. Abdominal exam reveals rebound tenderness and absent bowel sounds. Blood urea nitrogen90 mg/dL (32) S-creatinine3 mg/dL (264) S-Na140 meq/L S-K3.0 meq/L S-Cl80 meq/L S-HCO311 meq/L S-glucose90 mg/dL (5) pHpH 7.29 Pco 2 24 mm Hg (3.2) Acid-base analysis? pH AG pCO2 Acidemia 52  METABOLIC ACIDOSIS  AG Respiratory compensation renal insufficiency + ? ischemic bowel  lactic acidosis volume depletion  renal insufficiency Vomiting  hypoK, hypoCl; metabolic alkalosis masked by lactic acidosis Dx ?

49. 42 yo male, weakness, tiredness, loss of appetite, dizzy on standing, lost 21 lbs/3 mos Na 125 K 6.5 Cl98 HCO317 SCr 1.5 (133) BUN 30 (11) pH 7.31 pCO227 (3.6) Glucose76 (4.2) HYPONATREMIA #5 Diagnosis: Hormone levels: Acid-Base Dx: metabolic acidosis, AG nl (  aldo  Na-H exchange) Dark pigment of gums, oral mucosa BPHR Lying100/7095 Standing80/?110 HypoNa: Addison’s Dz ACTH , Cortisol + Aldo   Cortisol  free water formation  ACTH  ADH (Uosm>Posm) HypoK:  Aldo Orthostasis:Na loss, volume depletion What do you want next ? Calc Posm = 265 mOsm/kg Uosm = 350 mOsm/kg UNa=75, UK = 10 U(Na/K) = 7.5

50. Question 4: A patient with diabetic ketoacidosis has S-K = 4 mEq/l. Which of the following statements is TRUE? a. This patient has normal K stores. b. This patient has high K stores due to volume contraction and the concomitant oliguria. c. The patient has low K stores due to an osmotic diuresis, but S-K is normal because K losses are not large enough. d. The patient has low K stores due to an osmotic diuresis, but S-K is normal because K shifts out of cells in response to the metabolic acidosis. e. The patient has low K stores due to an osmotic diuresis, but S-K is normal because K shifts out of cells in response to insulin deficiency.

51. 47-årig ensamstående sjukpensionerad kronisk alkoholist som tidigare har vårdats på medicin kliniken under diagnos akut pericardit (hjärtsäcksinflammation). Patienten inkommer nu akut med hjärtinfarktambulansen p.gr.a. tryckkänsla över bröstet samt svår andfåddhet. EKG visar snabbt förmaksflimmer, frekvens ca 160, men inga säkra tecken på hjärtinfarkt. Vid inkomsten noteras tecken till uttorkning, stor djup andning av Kussmaul typ samt kraftig leverförstoring. Akut blodgasanalys visar: pH 6,83 pCO 2 2,0 kPa (15 mm Hg) HCO33 BE-26,3 Syra - bas rubbning? Tänkbara orsaker? Vilka kompletteringar i anamnes och provtagning vill du ha? Behandlingsförslag? Metabolic acidosis Alcoholic ketoacidosis, lactic acidosis Anamnes: methanol, ethylene glycol, drugs Tests: alcohol, methanol, ethylene glycol, lactate, Posm + osmolar gap, K

52. TidKl. 10.15Kl. 11.55Kl. 16.40Kl. 21.40 pH7,167,257,297,32 pCO 2 6,9 (52)6,8 (51)5,18 (39)4,52 (34) HCO318221817 pO 2 11,621,112,513,3 Behandling NaHCO 3 180 mmol60 mmol120 mmol 65-årig tidigare väsentligen frisk man inkommer med peritonit bild (bukhinne inflammation). Vid operation finner man en nekrotiserande kolit och resektion (bortoperation) av colon descendens görs. Post operativt respiratorbehandlas patienten. Patienten utvecklar chockbild som ej går att häva. Hur förklarar du utvecklingen av patientens syra-bas status? Vad visar den första blodgasanalysen? Metabolic acidosis (? lactic acidosis) + respiratory acidosis) 11.55: improvement in metabolic acidosis, still respiratory acidosis 16.40: improvement in respiratory acidosis with  pCO2, metabolic acidosis 21.40: respiratory acidosis gone with some hyperventilation (  pCO2 as compensatory response to metabolic acidosis)

53. 20-årig man som tidigare gjort suicidförsök med tabletter inkommer nu genom anhörigas försorg efter att enligt uppgift tagit tabletter. Patienten är medvetslös och andas forcerat. pHpCO 2 HCO3BEpO 2 Sa-O 2 Admit7.562.92 (22)19-314.1 (106)98% 1 st day7.354.0 (30)16-911.1 (83)95% ADMIT: Vilken typ av syra – basrubbning föreligger? Vilken(a) mekanismer kan ligga bakom? 1st DAY: Vilken typ av syra – basrubbning föreligger nu? Orsak(er) till utvecklingen? Respiratory alkalosis CNS stimulation of respiration Metabolic acidosis ASA poisoning, initially ASA acts in CNS to stimulate respiratory center with respiratory alkalosis, later metabolism of ASA to salicylic acid results in metabolic acidosis.

54. pHpO2pCO2HCO3 Sedative overdose7.22506726 COPD7.32506733 COPD with vomiting7.47506747 2. Same pO2 and pCO2 but different pH. Why? different HCO3 3. Why are HCO3 different?renal compensation, acute vs chronic 1. Diagnosis? both have  pCO2, respiratory acidosis 4. In COPD with vomiting, what is the acid-base status? Secondary acid-base disorder: metabolic alkalosis (loss of gastric HCl = gain of HCO3). Compensatory mechanisms never complete. If pH normalized or overshoot, then a secondary acid-base disorder Compensatory Response vs Mixed Acid-Base Disorder