بسم الله الرحمن الرحيمبسم الله الرحمن الرحيم

ABGDr.JarahzadehDr.JarahzadehIntensivistIntensivist

IntroductionIntroduction• Acids and Alkali are produced continuously in Acids and Alkali are produced continuously in

body.body.

• Daily Production of acid:Daily Production of acid:

1.Carbonic Acid 1.Carbonic Acid : 15000: 15000 meq/day meq/day

-From the metabolism of -From the metabolism of carbohydrates carbohydrates and and fatfat

-Excreted by -Excreted by lungslungs

2.Non-carbonic acids (Organic):2.Non-carbonic acids (Organic):50-10050-100 meq/day meq/day

-From the metabolism of -From the metabolism of proteinsproteins

-Excreted by -Excreted by kidneyskidneys

PhysiologyPhysiology Normal values for arterial blood:Normal values for arterial blood:

pH = 7.37-7.43 pH = 7.37-7.43 (7.4)(7.4)

[H ] = 37-43 nanoeq/l [H ] = 37-43 nanoeq/l (40)(40)

[HCO[HCO33 ] = 22-26 meq/l ] = 22-26 meq/l (24)(24)

pCOpCO22= 35-45 mmHg = 35-45 mmHg (40)(40)

minimal tolerable pH = minimal tolerable pH = 6.86.8

maximal tolerable pH = maximal tolerable pH = 7.87.8

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Cont’dCont’d

These values are kept in normal or near normal These values are kept in normal or near normal

range through 3 major mechanisms :range through 3 major mechanisms :

1.Chemical buffers:1.Chemical buffers: Intracellular & Extracellular Intracellular & Extracellular

2.Ventilation:2.Ventilation: Increase or decrease blood CO2 Increase or decrease blood CO2

3.Kidneys:3.Kidneys: Increase or decrease blood HCO3 Increase or decrease blood HCO3--

Protein

H + HCO3

CO2

Glutamine

NH4+TA +

CaCO3

PO4

HCO3HCO3

GUT

BONE

NH4+

Daily excertion 15,000 mEq/d

Daily excretion 60-80 mEq/d

Liver

KetoacidLactic acid

Review of acid-base homeostasis

Fat, CHO

Proximal tubule and acid-base homeostasis

Distal tubule and acid-base homeostasis

• Buffers: Buffers: Consist of weak acids.Consist of weak acids.• Extra cellular buffers:Extra cellular buffers:

1.Bicarbonate:1.Bicarbonate:

CO2 CO2+ H2O H2CO3 H + HCO3CO2 CO2+ H2O H2CO3 H + HCO3

[H ] = 24[H ] = 24

*Advantages :Large amount*Advantages :Large amount

Regulation of PCO2 by lungsRegulation of PCO2 by lungs

BuffersBuffers

++ -(gas)(gas) (dis)(dis)

PCO2PCO2HCO3HCO3

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BuffersBuffers NaHco3/H2co3+Hcl=H2co3+NacLNaHco3/H2co3+Hcl=H2co3+NacL

NaHco3/H2co3+NaoH=NaHco3+H20NaHco3/H2co3+NaoH=NaHco3+H20

V1=V2V1=V2 k1 [CO2] [H2O] = k2 [H+] [HO3-]k1 [CO2] [H2O] = k2 [H+] [HO3-]

K=[H+] [HCO3-] / [CO2] [H2O]K=[H+] [HCO3-] / [CO2] [H2O]

K=[H+] [HCO3-] / [CO2]disK=[H+] [HCO3-] / [CO2]dis

[H] =K [CO2] dis / [HCO3-][H] =K [CO2] dis / [HCO3-]

3737°°C: K=800C: K=800

[CO2]dis=0.03 PCO2[CO2]dis=0.03 PCO2

[H+] = 800 [H+] = 800 0.03 PCO2 / [HCO3-]0.03 PCO2 / [HCO3-]

[H ] = 24[H ] = 24

Law of mass action:Law of mass action:

PCO2PCO2HCO3HCO3

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2.Inorganic Phosphate:2.Inorganic Phosphate:

Less important due to low amount (1 mmol/lit)Less important due to low amount (1 mmol/lit)

3.Plasma proteins:3.Plasma proteins:

H + Pr HPr (pr/hpr)H + Pr HPr (pr/hpr)

• Intracellular Buffers & Bone :Intracellular Buffers & Bone :

1.Proteins:1.Proteins:HemoglobinHemoglobin

H + Hb HHb(Hb/HHb)H + Hb HHb(Hb/HHb)

2.Bone:2.Bone:

-Exchange of H with Na & K on the bone surface-Exchange of H with Na & K on the bone surface

-Dissolving bone minerals Release of buffers-Dissolving bone minerals Release of buffers

Cont’dCont’d

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-++

++ + + ++

PathophysiologyPathophysiology• Acidemia , AlkalemiaAcidemia , Alkalemia

• Acidosis , AlkalosisAcidosis , Alkalosis

• Metabolic , RespiratoryMetabolic , Respiratory

Primary DiseasePrimary Disease Compensatory ResponseCompensatory Response

HCO3 (M. acidosis) PCO2 HCO3 (M. acidosis) PCO2

HCO3 (M. alkalosis) PCO2HCO3 (M. alkalosis) PCO2

PCO2 (R. alkalosis) HCO3 PCO2 (R. alkalosis) HCO3

PCO2 (R. acidosis) HCO3 PCO2 (R. acidosis) HCO3

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Predicted CompensationPredicted Compensation Disease Disease Primary Primary CompensationCompensation abnormalityabnormality

Met. acidosis Met. acidosis 1 1meq/lit HCO3 meq/lit HCO3 1.21.2 mmHg PCO2 mmHg PCO2

Met. alkalosis Met. alkalosis 11meq/lit HCO3 meq/lit HCO3 0.70.7mmHg PCO2mmHg PCO2

Resp. alkalosis Resp. alkalosis 1010 mmHgmmHg PCO2 PCO2 2 2 meq/lit HCO3 meq/lit HCO3 (acute)(acute)

Resp. alkalosis Resp. alkalosis 1010 mmHg mmHg PCO2 PCO2 44 meq/lit HCO3 meq/lit HCO3 (chronic)(chronic)

Resp. acidosis Resp. acidosis 1010 mmHg PCO2 mmHg PCO2 11 meq/lit HCO3 meq/lit HCO3 (acute)(acute)

Resp. acidosis Resp. acidosis 1010 mmHg PCO2 mmHg PCO2 3.53.5 meq/lit HCO3 meq/lit HCO3 (chronic)(chronic)

• Metabolic acidosis (Winter’s Formula):Metabolic acidosis (Winter’s Formula): pCO2=1.5 [HCO3 ] + 8pCO2=1.5 [HCO3 ] + 8±± 2 2

• Metabolic alkalosis :Metabolic alkalosis : pCO2= 0.7[HCO3 ] + 21pCO2= 0.7[HCO3 ] + 21 ± ± 2 2

• Nomogram can also be used.Nomogram can also be used.

Other EquationsOther Equations

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Respiratory acidosis

Acute PH =7/40- 0.008(Paco2-40)

Chronic PH = 7/40- 0.003(Paco2-40)Respiratory Alkalosis

Acute PH =7/40+ 0.008(40-Paco2)

Chronic PH = 7/40+ 0.003(40-Paco2)

• Use the formula and these figures:Use the formula and these figures: pH [ H pH [ H ]] (nanomol/lit)(nanomol/lit)

7.8 167.8 16 7.7 207.7 20 7.6 267.6 26 7.5 327.5 32 7.4 407.4 40 7.3 507.3 50 7.2 637.2 63 7.1 807.1 80 7.0 1007.0 100 6.9 1256.9 125 6.8 1606.8 160

Are the measurements correct?Are the measurements correct?

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0.80.8

1.251.25

Blood pH [ H ] PCO2 [ HCO3 ]Blood pH [ H ] PCO2 [ HCO3 ] ((nanoeq/lit) (mmHg) (meq/lit)nanoeq/lit) (mmHg) (meq/lit)

Arterial Arterial 7.37-7.43 37-43 36-44 22-26 7.37-7.43 37-43 36-44 22-26 (7.4) (40) (40) (24)(7.4) (40) (40) (24)

Venous Venous 7.32-7.37 42-48 42-50 23-27 7.32-7.37 42-48 42-50 23-27 (7.35) (45) (46) (25)(7.35) (45) (46) (25)

Remember!Remember!

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Compensatory Response:Compensatory Response:

11 mmol/lit [HCO3 ] mmol/lit [HCO3 ] 1.21.2 mmHg pCO2 mmHg pCO2

pCO2=1.5 [HCO3 ] + 8 ± 2pCO2=1.5 [HCO3 ] + 8 ± 2

(Base excess)BE=-2,+2

(Buffer base)BB=42+BE

Anion Gap• Anion Gap = Na - (Cl + HCO3) = UA –

UC– Because Na + UC has to equal Cl + HCO3 +

UA– Remember algebra?

• UA = Unmeasured anions = albumin, phosphate, sulfate, lactate

• UC = Unmeasured cations = Ca, K, Mg

Low Anion Gap• Caused by decrease in UA

– albuminuria secondary to nephrotic syndrome

• Caused by increase in UC– Multiple myeloma (positively charged

Ab’s)

Concept of Anion GapConcept of Anion Gap

Na(140)

Na(140)

Na(140)

Cl(108)

Cl(108)

Cl(116)

HCO3(24)

HCO3(16)

HCO3(16)

AG=8AG=8 AG=8AG=8AG=16AG=16

Metabolic AcidosisMetabolic Acidosis• May be due to:May be due to: 1.Increased production of acid:1.Increased production of acid: Lactic acidosis , Ketoacidosis , some poisonings Lactic acidosis , Ketoacidosis , some poisonings e.g. salicylatese.g. salicylates 2.Decreased excretion of acid from kidneys: 2.Decreased excretion of acid from kidneys: Decreased ammonia production (CRF) , RTA Decreased ammonia production (CRF) , RTA (type I or IV)(type I or IV) 3.Alkali Loss: 3.Alkali Loss: From GI tract (diarrhea) or Kidneys (type II From GI tract (diarrhea) or Kidneys (type II RTA)RTA)

Classification & EtiologyClassification & Etiology• According to anion gap:According to anion gap:

A.G.=[Na ] – ( [Cl ] + [HCO3 ] )A.G.=[Na ] – ( [Cl ] + [HCO3 ] )

• High A.G. acidosis:High A.G. acidosis:

Ketoacidosis , Lactic acidosis , Most poisonings , Ketoacidosis , Lactic acidosis , Most poisonings ,

Renal failureRenal failure

• Normal A.G. acidosis:Normal A.G. acidosis:

GI HCO3 loss (diarrhea) , Other renal disordersGI HCO3 loss (diarrhea) , Other renal disorders

(RTA I , II and IV) , Ammonium chloride (RTA I , II and IV) , Ammonium chloride

poisoning poisoning

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• Clinical Manifestations:Clinical Manifestations: (MA) (MA)

Kussmaul respiration , Fatigability , confusion , Kussmaul respiration , Fatigability , confusion , stupor , coma , decreased heart contractility , stupor , coma , decreased heart contractility ,

osteomalacia and rickets (long term)osteomalacia and rickets (long term)

• Treatment:Treatment:

-Primary cause-Primary cause

-If severe &/or symptomatic treat with alkali -If severe &/or symptomatic treat with alkali

Needed NaHCO3=0.50 LBM(24- patient HCO3)Needed NaHCO3=0.50 LBM(24- patient HCO3)

-First give half of the needed NaHCO3 and -First give half of the needed NaHCO3 and

calculate again.calculate again.

Clinical Manifestations & RxClinical Manifestations & Rx

Quiz 1Quiz 1• A patient with diarrhea has the following ABG:A patient with diarrhea has the following ABG:

pH=7.25 , HCO3=10 , PCO2=23pH=7.25 , HCO3=10 , PCO2=231.Are the measurements correct?1.Are the measurements correct?2.What is the acid-base disorder?2.What is the acid-base disorder?

1.1.pH=7.25 [H ]=56.5 H = 24pH=7.25 [H ]=56.5 H = 24 pCO2/HCO3 pCO2/HCO3

H = 24H = 24 23.5/10 23.5/10

H = 55H = 55

So the measurement is correct.So the measurement is correct.

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2.2.pH=7.25 Acidosis ; Decreased HCO3 M.acidosispH=7.25 Acidosis ; Decreased HCO3 M.acidosis

pCO2 should be=(1.5pCO2 should be=(1.5HCO3)+8±2=1.5 HCO3)+8±2=1.5 10 +8 ±2=23±210 +8 ±2=23±2

So the disorder is simple M.acidosis.So the disorder is simple M.acidosis.

1010meq/lit HCO3 meq/lit HCO3 0.150.15meq PHmeq PH1010mmHg CO2 mmHg CO2 0.080.08meq PHmeq PH

Bicarbonate= BD( meq) . Kg 4

Quiz Quiz PH=7.06 Paco2=50BE= -11 Hco3=18

W=60Kg• 10 PCo2 0/08 PH• PH calculate=7.40-0.08=7.32

• PH-PHc=7.32- 7.06=0/26• 10 Hco3 0/15 PH• BD=17• 17 . 60 kg =255meq• 4

Metabolic AlkalosisMetabolic Alkalosis• May be due to:May be due to:

1.H Loss1.H Loss

2.HCO3 Retention2.HCO3 Retention

3.Volume Depletion (Contraction Alkalosis)3.Volume Depletion (Contraction Alkalosis)

• Compensatory response:Compensatory response:

11 meq/lit HCO3 meq/lit HCO3 0.70.7 mmHg PCO2mmHg PCO2

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Quiz 2Quiz 2• A patient with heart failure receiving A patient with heart failure receiving

diuretics has the following ABG:diuretics has the following ABG:

pH=7.46 , HCO3=30 , pCO2=45pH=7.46 , HCO3=30 , pCO2=45

What is the acid-base disorder?What is the acid-base disorder?

pH=7.46 pH=7.46 AlkalosisAlkalosis

Increased HCO3 M.AlkalosisIncreased HCO3 M.Alkalosis

pCO2 should be about =44.2pCO2 should be about =44.2

So the disorder is simple M.AlkalosisSo the disorder is simple M.Alkalosis

Why Metabolic Why Metabolic Alkalosis? Alkalosis?

• In every patient with metabolic In every patient with metabolic

alkalosis there is a:alkalosis there is a:

1.Precipitating cause1.Precipitating cause

2. Continuing factor2. Continuing factor

EtiologyEtiology• H Loss:H Loss: 1.GI Loss:Vomiting or NG tube1.GI Loss:Vomiting or NG tube 2.Renal Loss: Diuretics , MC excess , Post chronic 2.Renal Loss: Diuretics , MC excess , Post chronic Hypercapnia , Milk-Alkali syndrome , High doseHypercapnia , Milk-Alkali syndrome , High dose CarbenicilinCarbenicilin 3.H shift into cells: Hypokalemia (<2 meq/lit)3.H shift into cells: Hypokalemia (<2 meq/lit)• HCO3 RetentionHCO3 Retention:: 1.Massive Blood Transfusion (>8 units)1.Massive Blood Transfusion (>8 units) 2.Administration of NaHCO3 2.Administration of NaHCO3 3.Milk-alkali syndrome3.Milk-alkali syndrome• Contraction Alkalosis:Contraction Alkalosis: 1.Diuretics1.Diuretics 2.Cystic Fibrosis (sweat loss)2.Cystic Fibrosis (sweat loss) 3.Achlorhydria (Gastric Loss)3.Achlorhydria (Gastric Loss)

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Why does Metabolic Alkalosis Why does Metabolic Alkalosis Continue?Continue?

• Increased Bicarbonate Reabsorption due to:Increased Bicarbonate Reabsorption due to:

1.Decreased GFR: decreased effective 1.Decreased GFR: decreased effective circulating volume) circulating volume)

2.Chloride depletion2.Chloride depletion

3.Hypokalmia3.Hypokalmia

4.Hyperaldosteronism4.Hyperaldosteronism

• So you shall treat these factors in order to treat So you shall treat these factors in order to treat metabolic alkalosis. metabolic alkalosis.

Clinical ManifestationsClinical Manifestations

• Clinical Manifestations:Clinical Manifestations:

-Symptoms/Signs of Volume Depletion & -Symptoms/Signs of Volume Depletion &

hypokalemiahypokalemia

-Lethargy , confusion and coma in severe cases-Lethargy , confusion and coma in severe cases

-Tetany if hypocalcemia present-Tetany if hypocalcemia present

Differential DiagnosisDifferential Diagnosis

• Urine Cl <25 mmol/litUrine Cl <25 mmol/lit Urine Cl >40 mmol/litUrine Cl >40 mmol/lit

1.Vomiting 1 M.C. Excess1.Vomiting 1 M.C. Excess

2.Diuretics (late) 2.Diuretics (early)2.Diuretics (late) 2.Diuretics (early)

3.Post hypercapnia 3.Alkali Load3.Post hypercapnia 3.Alkali Load

4.Low Cl intake 4.Severe hypokalemia4.Low Cl intake 4.Severe hypokalemia

5.Cystic fibrosis 5.Barter’s or 5.Cystic fibrosis 5.Barter’s or

6.Fastidious diarrhea Giltleman’s syndrome6.Fastidious diarrhea Giltleman’s syndrome

TreatmentTreatment• Saline responsive alkalosis:Saline responsive alkalosis:-Cases with urine Chloride< 25 meq/lit-Cases with urine Chloride< 25 meq/lit-Treat hpovolemia and Cl deficit with N/S-Treat hpovolemia and Cl deficit with N/S-Also treat the primary cause such as vomiting -Also treat the primary cause such as vomiting • Saline resistant alkalosis:Saline resistant alkalosis:-Cases with urine Chloride >40 meq/lit and -Cases with urine Chloride >40 meq/lit and

edematous statesedematous states-Cases with edema:Use acetazolamide, HCl-Cases with edema:Use acetazolamide, HCl-If not effective and severe IV HCl can be used-If not effective and severe IV HCl can be used Needed HCl=50% Weight (Plasma HCO3 -24)Needed HCl=50% Weight (Plasma HCO3 -24)-Treat the primary cause such as diuretic use-Treat the primary cause such as diuretic use

Respiratory acidosis

Acute H+/Paco2=0/7Chronic H+/Paco2=0/3

Respiratory Alkalosis

Acute H+/Paco2=0/7

Chronic H+/Paco2=0/17

Respiratory AcidosisRespiratory Acidosis• Due to decrease in effective ventilation.Due to decrease in effective ventilation.• Etiology:Etiology:1.Suppression of respiratory center:1.Suppression of respiratory center: Drugs ,central apnea , Drugs ,central apnea ,

cardiac arrest ,CNS disease (rare), Morbid obesitycardiac arrest ,CNS disease (rare), Morbid obesity

2.Disorders of respiratory muscles and chest wall :2.Disorders of respiratory muscles and chest wall :

Myasthenia Gravis, Hypokalemia , hypophosphatemia, Myasthenia Gravis, Hypokalemia , hypophosphatemia,

Kyphoscoliosis, Spinal cord lesions, Morbid obesityKyphoscoliosis, Spinal cord lesions, Morbid obesity

3.Disorders of upper respiratory tract:3.Disorders of upper respiratory tract: Layrgospasm, Layrgospasm, Foreign body, Obstructive sleep apneaForeign body, Obstructive sleep apnea

4.Defects in alveolar-capillary exchange:4.Defects in alveolar-capillary exchange:ARDS, Acute ARDS, Acute pulmonary edema, severe pneumonia, Pneumothorax, pulmonary edema, severe pneumonia, Pneumothorax,

COPD, Morbid obesity,...COPD, Morbid obesity,...

Clinical Manifestations & DxClinical Manifestations & Dx• Clinical manifestations:Clinical manifestations:-Confusion to Coma in severe (pCO2>70) &/or acute cases-Confusion to Coma in severe (pCO2>70) &/or acute cases

-Vasodialation :Red eye and face-Vasodialation :Red eye and face

-Increased ICP:Papilledema-Increased ICP:Papilledema

• Diagnosis:Diagnosis:1.Clinical manifestations1.Clinical manifestations

2.History (to differentiate 2.History (to differentiate acute acute from from chronic chronic ))

3.Degree of compensation:3.Degree of compensation:

Resp. acidosisResp. acidosis : : 10 10 mmHg PCO2 mmHg PCO2 11meq/lit HCO3meq/lit HCO3 (acute)(acute)

Resp. acidosisResp. acidosis : : 10 10 mmHg PCO2 mmHg PCO2 33 meq/lit HCO3 meq/lit HCO3 (chronic)(chronic)

Quiz 3Quiz 3• A 20 yr old girl has attempted suicide A 20 yr old girl has attempted suicide with 200 mg of with 200 mg of

diazepam.She is in deep coma and has shallow respiration.ABG diazepam.She is in deep coma and has shallow respiration.ABG is as the following:is as the following:

pH=7.2 , pCO2=70 , HCO3=27pH=7.2 , pCO2=70 , HCO3=271.What is the acid-base disorder?1.What is the acid-base disorder?2.What would you expect HCO3 to be if it was a case of COPD?2.What would you expect HCO3 to be if it was a case of COPD?

1.The 1.The HxHx is consistent with is consistent with acute R. acidosisacute R. acidosis. So you expect . So you expect 11 meq/lit rise of HCO3 for every meq/lit rise of HCO3 for every 1010 mmHg rise in pCO2 & mmHg rise in pCO2 & 33 meq/l for meq/l for 3030 mmHg. mmHg.

The patient has pure R. acidosis.The patient has pure R. acidosis.

2.In COPD we have chronic R. acidosis.So we expect about 2.In COPD we have chronic R. acidosis.So we expect about 3.53.5 meq/l rise in HCO3 for every meq/l rise in HCO3 for every 1010 mmHg rise in pCO2 . mmHg rise in pCO2 .

HCO3 would be about 34. pH would be about 7.3 HCO3 would be about 34. pH would be about 7.3

TreatmentTreatment

1.Correction of primary disease1.Correction of primary disease

2.Mechanical Ventilation in severe cases2.Mechanical Ventilation in severe cases

3.Rapid infusion of bicarbonate in very 3.Rapid infusion of bicarbonate in very

severe cases such as cardio-pulmonary severe cases such as cardio-pulmonary

arrestarrest

Respiratory AlkalosisRespiratory Alkalosis• Due to Increased ventilationDue to Increased ventilation

• Etiology:Etiology:

I.Hypoxemia:I.Hypoxemia: Pneumonia, Acute asthma,Acute Pneumonia, Acute asthma,Acute

Pulmonary edema, Pulmonary fibrosis, AnemiaPulmonary edema, Pulmonary fibrosis, Anemia

2.Stimulation of respiratory center:2.Stimulation of respiratory center: Anxiety, Fever, G Anxiety, Fever, G

sepsis, Salicylate poisoning, CNS disease (Tumor, sepsis, Salicylate poisoning, CNS disease (Tumor,

Encephalitis), Cirrhosis, Pregnancy, After correction of Encephalitis), Cirrhosis, Pregnancy, After correction of

metabolic acidosismetabolic acidosis

3.Mechanical ventilation3.Mechanical ventilation (too much) (too much)

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Clinical Manifestations & DxClinical Manifestations & Dx• Hypoxemia stimulates respiratory center when Hypoxemia stimulates respiratory center when

pO2 is less than 50-60 mmHg.pO2 is less than 50-60 mmHg.

• In hypotention and anemia reduced O2 delivery In hypotention and anemia reduced O2 delivery

to chemoreceptors of the great vessels stimulates to chemoreceptors of the great vessels stimulates

respiratory center.respiratory center.

• Clinical Manifestations:Clinical Manifestations:

1.Paresthesia to tetany1.Paresthesia to tetany

2.Stupor to coma2.Stupor to coma

33..Asymptomatic in chronic casesAsymptomatic in chronic cases

Cont’dCont’d• Degree of compensation:Degree of compensation:R. alkalosis:R. alkalosis: 1010 mmHgmmHg PCO2 PCO2 22meq/lit HCO3 meq/lit HCO3 (acute)(acute)R. alkalosis:R. alkalosis: 10 10 mmHg mmHg PCO2 PCO2 44 meq/lit HCO3 meq/lit HCO3 (chronic)(chronic)

• Diagnosis:Diagnosis:Clinical manifestations, Clinical manifestations, HistoryHistory (acute vs chronic) & ABG(acute vs chronic) & ABG• Treatment:Treatment:1.Primary Disorder1.Primary Disorder2.If symptomatic , breathing in a nylon bag2.If symptomatic , breathing in a nylon bag

Quiz 4Quiz 4A 40 y/o cirrhotic man is brought to hospital with stuporA 40 y/o cirrhotic man is brought to hospital with stupor

ABG is as following:ABG is as following:

pH=7.46 , HCO3=20 , pCO2=30pH=7.46 , HCO3=20 , pCO2=30What is the acid-base disorder?What is the acid-base disorder?

According to According to Hx, Hx, the patient has an underlying chronic the patient has an underlying chronic

disease precipitating to disease precipitating to chronic R.alkalosis.chronic R.alkalosis.

4-54-5 meq/L decrease in HCO3 is expected for every meq/L decrease in HCO3 is expected for every 10 10

mmHg decrease in pCO2.mmHg decrease in pCO2.

So the patient has pure R. alkalosisSo the patient has pure R. alkalosis

Cont’dCont’dThe patient develops oliguria & hypotension on the The patient develops oliguria & hypotension on the

next day.ABG changes as follows:next day.ABG changes as follows:

pH=7.38 , HCO3=13, pCO2=25pH=7.38 , HCO3=13, pCO2=25What is the acid-base disorder now?What is the acid-base disorder now?

The patient has normal pH with decreased pCO2 & The patient has normal pH with decreased pCO2 &

HCO3.So there should be a mixed acid-base disorder. HCO3.So there should be a mixed acid-base disorder.

According to Hx According to Hx chronic R. alkalosischronic R. alkalosis is expected. But is expected. But

the decrease in HCO3 is more than expected (18).So the decrease in HCO3 is more than expected (18).So

there is there is also M.acidosisalso M.acidosis which is explained by which is explained by

hypotension & oliguria.hypotension & oliguria.

Mixed acid-base disordersMixed acid-base disordersI.M. acidosis & R. acidosis:I.M. acidosis & R. acidosis:

1.Cardio-pulmonary arrest1.Cardio-pulmonary arrest

2.Severe pulmonary edema2.Severe pulmonary edema

3.Poisoning with both salicylate & a sedative drug3.Poisoning with both salicylate & a sedative drug

4.Renal Failure with COPD4.Renal Failure with COPD

II.M. acidosis & R. alkalosis:II.M. acidosis & R. alkalosis:

1.Salicylate poisoning1.Salicylate poisoning

2.Severe sepsis2.Severe sepsis

3.Combined renal & hepatic failure3.Combined renal & hepatic failure

4.Ethanol Toxicity 4.Ethanol Toxicity

Cont’dCont’dIII.M. alkalosis & R. alkalosis:III.M. alkalosis & R. alkalosis: 1.Pregnancy with vomiting1.Pregnancy with vomiting 2.Chronic liver disease on diuretic therapy2.Chronic liver disease on diuretic therapyIV.M. alkalosis & R. acidosis: IV.M. alkalosis & R. acidosis: Seen in COPD with :Seen in COPD with : 1.Diuretics 2.Steroids 1.Diuretics 2.Steroids 3.Vomiting 4.To much ventilatory support3.Vomiting 4.To much ventilatory supportV.M. acidosis & M. alkalosis:V.M. acidosis & M. alkalosis:Seen in vomiting with:Seen in vomiting with: 1.Renal failure 1.Renal failure 2.Alcoholic or diabetic ketoacidosis2.Alcoholic or diabetic ketoacidosis**Only R. alkalosis & R. acidosis can not happen Only R. alkalosis & R. acidosis can not happen together. together.

Dx Of Mixed DisordersDx Of Mixed Disorders• For mixed metabolic & respiratory disorders ,For mixed metabolic & respiratory disorders ,

see if pCO2 & HCO3 changes correspond to see if pCO2 & HCO3 changes correspond to

compensatory changes or not. compensatory changes or not. • For mixed metabolic acidosis & alkalosis or triple For mixed metabolic acidosis & alkalosis or triple

disorders use :disorders use :

Anion GapAnion Gap

BicarbonateBicarbonate

1-2:1-2: High anion gap metabolic acidosis High anion gap metabolic acidosis

>2:>2: Mixed metabolic acidosis & alkalosis Mixed metabolic acidosis & alkalosis

<1:<1: Mixed normal- & high anion gap m. acidosis Mixed normal- & high anion gap m. acidosis

Respiratory acidosis

Acute H+/Paco2=0/8Chronic H+/Paco2=0/3

Respiratory Alkalosis

Acute H+/Paco2=0/8

Chronic H+/Paco2=0/17

A patient with salicylate overdose is found to have the following ABG:

pH:7.45 pCO2:20

[HCO3-]:13

• pH slightly high indicates alkalemia• This is due to low pCO2

• [HCO3-] should fall from 24 to 20

• [HCO3-] drop to 13

• The patient has combined RES. ALK & MET. ACI

A previously well 55 year old woman is admitted with a compliant of sever vomiting for 5 days.

Physical examination reveals postural hypotension tachycardia and diminished skin turgor. The laboratory finding include the following:

[Na+]=140 [K+]=3.4 [Cl-]=77 [HCO3]=9 pH=7.23 Pco2=22

• pH is low

• Pco2 & [HCO3] was decreased

pH=7.25 , HCO3=22 , PCO2=50pH=7.25 , HCO3=22 , PCO2=50Pao2=60mmhgPao2=60mmhg

pH=7.25 , HCO3=17 , PCO2=40pH=7.25 , HCO3=17 , PCO2=40

Pao2=90mmhgPao2=90mmhg

pH=7.20 , HCO3=20 , PCO2=55pH=7.20 , HCO3=20 , PCO2=55

pH=7.32 , HCO3=18 , PCO2=40pH=7.32 , HCO3=18 , PCO2=40

pH=7.37 , HCO3=11, PCO2=20pH=7.37 , HCO3=11, PCO2=20

pH=7.29 , HCO3=12, PCO2=25pH=7.29 , HCO3=12, PCO2=25

pH=7.49 , HCO3=44, PCO2=60pH=7.49 , HCO3=44, PCO2=60

pH=7.25 , HCO3=17, PCO2=40pH=7.25 , HCO3=17, PCO2=40

pH=7.50 , HCO3=30, PCO2=40pH=7.50 , HCO3=30, PCO2=40

pH=7.43 , HCO3=19, PCO2=30pH=7.43 , HCO3=19, PCO2=30

pH=7.20 , HCO3=34, PCO2=90pH=7.20 , HCO3=34, PCO2=90

pH=7.60 , HCO3=14, PCO2=15pH=7.60 , HCO3=14, PCO2=15

pH=7.10 , HCO3=20 , PCO2=28pH=7.10 , HCO3=20 , PCO2=28

pH=7.70 , HCO3=20 , PCO2=17pH=7.70 , HCO3=20 , PCO2=17

pH=7.06 , HCO3=18 , PCO2=50pH=7.06 , HCO3=18 , PCO2=50

BE=-11BE=-11

pH=7.26 , HCO3=18 , PCO2=50pH=7.26 , HCO3=18 , PCO2=50

pH=7.30 , HCO3=18 , PCO2=52pH=7.30 , HCO3=18 , PCO2=52