Practical Clinical Nephrology

Using principles of renal physiology to analyze, diagnose and treat patients

ProfessorInternal Medicine (nephrology)

Molecular Physiology & BiophysicsUniversity of Iowa College of Medicine

Iowa City, Iowa, USA

Guest Professor in Renal PhysiologyGöteborgs Universitet

Göteborg, Sweden

Gerald F. DiBona (Jerry)

HYPONATREMIA

Prevalence of hyponatremia

Patient Group Prevalence (%)ICU 11.0-29.6

Elderly outpatients 7.2-11.0

Elderly inpatients 18.0-53.0

Elderly with falls 9.1-13.0

Heart Failure 10.2-27.0

Cirrhosis 20.8-49.4

Cancer 3.7-47.0

Pneumonia 8.1-27.9

CKD pre dialysis 13.6

CKD on dialysis 29.3

Marathon runners 3.0-13.0

Relationship between SNa and mortality in patients admitted between 1996 and 2007 (N = 45,693)

CJASN 6:960-965, 2011

Diagnostic + Therapeutic Approach to Patient with Hyponatremia

24 yo male, chronic paranoid schizophreniaSudden onset of seizures

BP 108/83 mm Hg, HR 68/min lying and standing

Na 116K 4Cl 88HCO3 20BUN (blood urea nitrogen) 9 (3.2)SCreat 1.0 (88)Glucose 105 (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

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?

P-Na Posm ADH Uosm

P-Na Posm ADH Uosm

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)

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.

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?

But Uosm=600 > Posm=208, (U/P)osm = 600/208 = 3.

PNa and Posm should ADH Uosm to < Posm with (U/P)osm < 1Excretion 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

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 supine 100/70 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/LScreatinine 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 isUosm + (U/P)osm = 600/270 = 2.2 ADH present; hypoosmotic hypovolemic hyponatremia

Volume depletion (> 15%) with BP stimulates ADH release and overrideseffect of Posm to ADH

? Treatment NaCl 0.9%/3.0% iv volume repletion, restrict free water, hypertonicintake

Decrease in mean arterial pressure orintravascular volume, %

Pla

sma

AD

H,

pm

ol/

L

ADH increase with 3% increase in Posm

CO + BP stimulates baroreceptor mediated ADH release and overrides effect of Posm to ADH

Increase in ADH with 10% decrease in AP or blood volume

Increase in ADH with3% increase in Posm(285290 mOsm/kg)

50 yo man with chief complaint of fatigue, dyspnea on exertion, leg swellingHX: Post MI dilated cardiomyopathy, chronic congestive heart failure.PE: BP 100/70 mm Hg, HR 96 bpm. Jugular vein distension, cardiomegaly, signsof pleural effusion and pitting edema to the thigh.

LAB: Na 129, K 3.9, Cl 88, HCO3 28 mEq/LScreatinine 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 hypervolemichyponatremia ( TB Na, TB H2O)

Treatment? Diuretic, NaCl 0.9%.3.0%, free water restriction, vaptans

HYPERNATREMIA

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: negativUosm: 60 mOsm/kgU-[Na+]: 15 mMAnalyser från blodprov gav följande resultat:S-Na 154 mMS-K 4,2 mMS-Cl 114 mMS-HCO3 28 mMS-[kreatinin] 110 MPosm: 312 mOsm/kgB-glukos: 4,5 mM

a. Vad i lab-data stöder antagandet att det är primärt stora urinförluster, följt avökad 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 inhalationd. Hur kan tillståndet behandlas?

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 administrationB. Diabetes insipidus due to head trauma C. Insufficient water intake aloneD. 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 reductionB. 2.5 liter reductionC. 11.7 liter reductionD. 8.1 liter reduction

total body sodium before = total body sodium aftertotal body water before x PNa before = total body water after x PNa after60 kg x 0.6 x 145 = total body water after x 17036 x 145 = total body water after x 170total body water after = 30.7 liters; total body water deficit = 36-30.7 = 5.3 liters

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-Cl 113 mM pH 7,4 S-K 5,0 mM pCO2 5,3 kPa (40 mm Hg) S- HCO3 24 mM BE -0.4 Anion gap 21 mM S-kreatinin 88 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

HYPERKALEMIA

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 acidosisIf 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).

HYPOKALEMIA

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-Na

138 mEq/L

BUN 21 mg% (7.5)

S-K

2.2 mEq/L

Creatinine 1.2 mg% (106)

S-Cl

90 mEq/L

Arterial pCO2 = 48 mmHg (6.4)

S-HCO3

37 mEq/L

Arterial 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 K2. flow favors K gradient for K diffusion into lumen; urine K3. 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 pCO2 ? Respiratory compensation (hypoventilation) for metabolic alkalosis

Why arterial pCO2 not higher? hypoventilationhypoxia

Na K CL HCO3 Other Dx145 2.8 104 29 UCl 50

135 2.8 85 35 UCl 10

140 2.9 118 15 UpH 6.5

140 2.9 118 15 UpH 5.4, UK 8

138 3.1 84 36 UK 50

Aldosteronism

Vomiting

Distal RTA

Diarrhea

HCTZ

HYPOKALEMIA

ACID – BASE

pCO2 means:

pCO2 means:

alveolar hypoventilation

alveolar hyperventilation

Compensatory responses never completelynormalize pH; if pH normalized, another

acid base disturbance is present

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), CO2 produced is excreted via lungs (respiratory compensation).

Net effect: measured anions (i.e. HCO3) + unmeasured anions (acid anions) AG

Anion Gap Metabolic AcidosisM-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

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 HCO3 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

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

Stepwise approach to interpreting arterial blood gas

1.Hx & PE

2. Look at blood pH: pH < 7.35, acidosis; 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 Disorder pHInitial Chemical

ChangeCompensatory

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

Acid-Base Algorithm

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.

pH pCO2 HCO3

Father 7.33 60 (8) 31

Son 7.22 60 (8) 24

What is acid-base diagnosis for father + son?

Father: chronic respiratory acidosis with compensation, chronic, timeSon: 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

pH pCO2 HCO3

Father 7.50 40 (5.3) 31

Son 7.40 40 (5.3) 24

Both father and son are treated with vigorous assisted mechanical ventilation

What happened?

Day 1 Day 3 no Rx Day 3 p Rx

Posm 290 317 290

S-Na 128 133 148

S-K 6,0 8,1 3,0

S-Cl 93 106 94

S- HCO3 8.8 3.9 32.2

pH 7,15 6,91 7,54

pCO2 3,5 kPa (26 mm Hg)

2,7 kPa (20 mm Hg)

5,2 kPa (39 mm Hg)

Anion gap (AG) 32.2 31.2 24.8

B-glukos 35 mM 44 mM 4 mM

A 55 yo man with diabetes mellitus is admitted

What’s this?

What’s changed?

What’s happened?

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 nitrogen 14 mg/dL (5 mmol/L)Serum creatinine 1.0 mg/dL (88 umol/L)Serum Na 140 meq/LSerum K 4 meq/LSerum Cl 100 meq/L Serum HCO3 12 meq/LAG 32 meq/LSerum glucose 108 mg/dL (6 mmol/L)Measured Posm 326 mOsm/kgSerum ketones NegativeSerum lactate 0.7 meq/L (0.08 mmol/L) NLpH 7.29Pco2 26 mm Hg (3.5 kPa)

1. Dx? metabolic acidosis with high anion gap (32) Anion Gap Metabolic AcidosisM-methanolU-uremia (chronic renal failure)D-diabetic ketoacidosis P-propylene glycol I-infection L-lactic acidosisE-ethylene glycol S-salicylate

2. Posm? Calc Posm = 291 mOsm/kg

Osmolar gap = Meas Posm - Calc Posm = 35

osmolar gap (> 15): methanol, ethanolpropylene glycol, ethylene glycol

Methanol: formic acidEthanol: acetic acidEthylene glycol: oxalic acidPropylene glycol:proprionic acid

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; pCO2 3,9 (29 mm Hg); HCO3 22; pO2 8,0 (60 mm Hg); Sa-O2 91 %

Patienten blir alltmer respiratoriskt och cirkulatoriskt påverkad och röntgen pulm visar nu diffusa förtätningar över bägge lungfälten. pH 7,21; pCO2 6,0 (45 mm Hg); HCO3 17; pO2 7,2 (54 mm Hg); Sa-O2 84 %

Hur bedömer du syra-bas status, inklusive pO2?Acute respiratory alkalosis, hypoxia stimulates hyperventilation ( pCO2), acuteas HCO3 not

Tolkning av syra – bas status?

Åtgärder?

Metabolic acidosis, hypoxia but no hyperventilation (pCO2 ) (? respiratorymuscle fatigue) + no respiratory compensation

Orsak till skillnaden mellan de två blodgasanalyserna?Oxygen diffusion block in lungs, ? pulmonary edema

Intubation, mechanical ventilation (respirator)

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 33Arterial pH 7.49Arterial 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

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. pH 7,35pCO2 10,4 kPa (78 mm Hg)

HCO3 42 mEq/LO2 6,5 kPa (49 mm Hg)

Sa-O2 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).

What’s is the acid-base disturbance?

pH HCO3 pCO2

A 7.23 10 25 (3.3)

B 7.48 32 44 (5.9)

C 7.34 31 60 (6.7)

D 7.66 22 20 (2.7)

E 7.26 26 60 (6.7)

F 7.58 18 20 (2.7)

Metabolic acidosis

Metabolic alkalosis

Chronic respiratory acidosis

Acute respiratory alkalosis

Acute respiratory acidosis

Chronic respiratory alkalosis

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 glucose 89 mg/dL (4.9)Blood urea nitrogen 16 mg/dL (5.9)S-creatinine 0.7 mg/dL (87)S-Na 140 meq/LS-K 3.0 meq/LS-Cl 100 meq/LS-HCO3 27 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.

CALCIUM AND PHOSPHOROUS

37 yo man was referred for evaluation of renal insufficiency + hypercalcemia. S-Na 140S-K 3.3 S-Cl 110S-HCO3 16AG 17.3S-creat 3.0 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 acidosisPrimary hypoparathyroidismFamilial hypocalciuric hypercalcemiaSalicylate overdosePaget’s disease

An abdominal X-ray shows:

Hyperchloremic hypokalemic metabolic acidosis with normal anion gapDiffuse nephrocalcinosis

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

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 changeMixed disorder: opposite direction from initial change

Acid Base Disorder pHInitial Chemical

ChangeCompensatory

ResponseRespiratory 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.

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 7.01PaCO2: 9,2 kPa (69 mm Hg)

HCO3: 17PaO2: 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 ( PaCO2 )

+ hypoxia (now absent due to oxygen treatment)

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-Na 130 mEq/L P-K 6.5 mEq/LP-Cl 95 mEq/L P-HCO3 7 mEq/L Arterial pH 6.99 Arterial Pco2 18 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. Effectof 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

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 7 600 (33.3)0300 4.5 7.10 12 400 (22.2)0400 4.0 7.16 14 300 (16.7)0500 3.5 7.20 16 250 (13.9)0700 3.2 7.24 18 200 (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

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 nitrogen 90 mg/dL (32)S-creatinine 3 mg/dL (264)S-Na 140 meq/LS-K 3.0 meq/LS-Cl 80 meq/LS-HCO3 11 meq/LS-glucose 90 mg/dL (5)pH pH 7.29Pco2 24 mm Hg (3.2)

Acid-base analysis?pHAGpCO2

Acidemia52 METABOLIC ACIDOSIS AGRespiratory compensation

renal insufficiency + ? ischemic bowel lactic acidosisvolume depletion renal insufficiencyVomitinghypoK, hypoCl; metabolic alkalosis masked by lactic acidosis

Dx ?

42 yo male, weakness, tiredness, loss of appetite, dizzy on standing, lost 21 lbs/3 mos

Na 125K 6.5Cl 98HCO3 17SCr 1.5 (133)BUN 30 (11)pH 7.31pCO2 27 (3.6)Glucose 76 (4.2)

HYPONATREMIA #5

Diagnosis: Hormone levels:

Acid-Base Dx: metabolic acidosis, AG nl( aldo Na-H exchange)

Dark pigment of gums, oral mucosa BP HR

Lying 100/70 95

Standing 80/? 110

HypoNa:

Addison’s DzACTH , Cortisol + Aldo

Cortisol free water formation ACTH ADH (Uosm>Posm)

HypoK: Aldo

Orthostasis: Na loss, volume depletionWhat do you want next ?Calc Posm = 265 mOsm/kgUosm = 350 mOsm/kgUNa=75, UK = 10U(Na/K) = 7.5

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.

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 6,83pCO2 2,0 kPa (15 mm Hg)

HCO3 3BE -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

Tid Kl. 10.15 Kl. 11.55 Kl. 16.40 Kl. 21.40pH 7,16 7,25 7,29 7,32pCO2 6,9 (52) 6,8 (51) 5,18 (39) 4,52 (34)HCO3 18 22 18 17pO2 11,6 21,1 12,5 13,3BehandlingNaHCO3

180 mmol 60 mmol 120 mmol 120 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 acidosis16.40: improvement in respiratory acidosis with pCO2, metabolic acidosis21.40: respiratory acidosis gone with some hyperventilation ( pCO2 as

compensatory response to metabolic acidosis)

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.

pH pCO2 HCO3 BE pO2 Sa-O2

Admit 7.56 2.92 (22) 19 -3 14.1 (106) 98%

1st day 7.35 4.0 (30) 16 -9 11.1 (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.

pH pO2 pCO2 HCO3

Sedative overdose 7.22 50 67 26

COPD 7.32 50 67 33

COPD with vomiting 7.47 50 67 47

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 normalizedor overshoot, then a secondary acid-base disorder

Compensatory Response vs Mixed Acid-Base Disorder