acid base disorders

بسم الله الرحمن الرحيم

بسم الله الرحمن الرحيم

”رب اشرح لي صدري

ويسر لي أمريواحلل عقدة من

لسانييفقهوا قولي“

”رب اشرح لي صدري

ويسر لي أمريواحلل عقدة من

لسانييفقهوا قولي“

APPROACH TO ACID-BASE DISORDERS

APPROACH TO ACID-BASE DISORDERS

Definitions Definitions Acid: a substance that may donate protons

(hydrogen ions) Base: a substance that may receive protons pH: the negative logarithm of protons

concentration Strong acids vs. weak acids Volatile (Co2) vs. nonvolatile acids Buffers

Acid: a substance that may donate protons (hydrogen ions)

Base: a substance that may receive protons pH: the negative logarithm of protons

concentration Strong acids vs. weak acids Volatile (Co2) vs. nonvolatile acids Buffers

40 neq = 0.00000004 meq = pH 7.4

0.00000020= pH 6.7 0.00000010 = pH 7.00.00000008 = pH 7.10.00000006 = pH 7.20.00000005 = pH 7.30.00000004 = pH 7.40.00000003 = pH 7.50.00000002 = pH 7.70.00000001 = pH 8.0

Buffering SystemBuffering System

ACID-BASE DISORDERSACID-BASE DISORDERS

DEFINITIONS

ACIDEMIA VS ALKALEMIA

ACIDOSIS VS ALKALOSIS

RESPIRATORY VS METABOLIC

COMPENSATORY RESPONSES

SIMPLE (SINGLE) VS MIXED

DEFINITIONS

ACIDEMIA VS ALKALEMIA

ACIDOSIS VS ALKALOSIS

RESPIRATORY VS METABOLIC

COMPENSATORY RESPONSES

SIMPLE (SINGLE) VS MIXED


DIAGNOSIS BASED ON:

SUGGESTIVE HISTORY

SUGGESTIVE PHYSICAL EXAM

SUGGESTIVE CO2, K+, CL-

SUGGESTIVE pH, PCO2, HCO3-, AG

DIAGNOSIS BASED ON:

SUGGESTIVE HISTORY

SUGGESTIVE PHYSICAL EXAM

SUGGESTIVE CO2, K+, CL-

SUGGESTIVE pH, PCO2, HCO3-, AG

APPROACH TO THE DIAGNOSIS OF ACID-BASE DISORDERS

APPROACH TO THE DIAGNOSIS OF ACID-BASE DISORDERS

Suspicious clinical or lab findings Identify the major Acid-base disorder Determine if it is simple or mixed Establish the cause of the disorder Direct treatment to the underlying cause unless the

pH is in a dangerous range (7.10 < or > 7.60)

Suspicious clinical or lab findings Identify the major Acid-base disorder Determine if it is simple or mixed Establish the cause of the disorder Direct treatment to the underlying cause unless the

pH is in a dangerous range (7.10 < or > 7.60)

FORMULAS: HENDERSON-HASSELBALCH

pH = pK + log ([HCO3-]/[0.03* PCO2])

pH = 6.10 + log (24/0.03*40) = 7.40 MODIFIED HENDERSON

[H+] = 24* PCO2/[HCO3-]

[H+] = 24* (40/24) = 40 neq/L (pH=7.4)

FORMULAS: HENDERSON-HASSELBALCH

pH = pK + log ([HCO3-]/[0.03* PCO2])

pH = 6.10 + log (24/0.03*40) = 7.40 MODIFIED HENDERSON

[H+] = 24* PCO2/[HCO3-]

[H+] = 24* (40/24) = 40 neq/L (pH=7.4)


Simplified Henderson - Simplified Henderson - Hasselbach equationHasselbach equation

Simplified Henderson - Simplified Henderson - Hasselbach equationHasselbach equation

(H+) = (H+) = 24 x PaCO24 x PaCO22

HCOHCO33

Shows relationship between 3 major Shows relationship between 3 major factors:factors: H+H+ COCO22

HCOHCO33

(H+) = (H+) = 24 x PaCO24 x PaCO22

HCOHCO33

Shows relationship between 3 major Shows relationship between 3 major factors:factors: H+H+ COCO22

HCOHCO33

Primary Disorder pH HCO3- PCO2

Met. Acidosis Resp. Acidosis Met. Alkalosis Resp. Alkalosis

Primary Disorder pH HCO3- PCO2

Met. Acidosis Resp. Acidosis Met. Alkalosis Resp. Alkalosis

SIMPLE ACID-BASE DISORDERSSIMPLE ACID-BASE DISORDERS

FREQUENCY OF SIMPLE ACID-BASE DISORDERS

FREQUENCY OF SIMPLE ACID-BASE DISORDERS

Metabolic Acidosis 10%

Alkalosis 40%

Respiratory Acidosis 20%

Alkalosis 20%

Metabolic Acidosis 10%

Alkalosis 40%

Respiratory Acidosis 20%

Alkalosis 20%

CardiovascularCardiovascular

Impaired cardiac Impaired cardiac contractilitycontractilityArteriolar dilationArteriolar dilationVenoconstrictionVenoconstrictionCentralization of blood Centralization of blood volumevolumeIncreased pulmonary Increased pulmonary vascular resistancevascular resistanceDecreased cardiac outputDecreased cardiac outputDecreased systemic BPDecreased systemic BPDecreased hepatorenal Decreased hepatorenal blood flowblood flowDecreased threshold for Decreased threshold for cardiac arrhythmiascardiac arrhythmiasAttenuation of Attenuation of responsiveness to responsiveness to catecholaminescatecholamines

Arteriolar constrictionArteriolar constrictionReduced coronary blood flowReduced coronary blood flowReduced anginal thresholdReduced anginal thresholdDecreased threshold for Decreased threshold for cardiac arrhythmiascardiac arrhythmias

Consequences of acidosis vs. alkalosisConsequences of acidosis vs. alkalosis

Metabolic

Insulin resistanceInhibition of anaerobic glycolysisReduction in ATP synthesisHyperkalemiaProtein degradationBone demineralization (chronic)

Stimulation of anaerobic glycolysisFormation of organic acidsDecreased oxyhemoglobin dissociationDecreased ionized CaHypokalemiaHypomagnesemiaHypophosphatemia

Neurologic

Inhibition of metabolism and cell-volume regulationObtundation and coma

TetanySeizuresLethargyDeliriumStupor

Respiratory

Compensatory hyperventilation with possible respiratory muscle fatigue

Compensatory hypoventilation with hypercapnia and hypoxemia

RESPONSE TO SIMPLE ACID-BASE DISORDERSRESPONSE TO SIMPLE ACID-BASE DISORDERS

DisturbanceEquation Interval Level

Met. Ac. 1 = 1.2 12-24 hr 10

Met. Al. 1 = 0.7 24-36 hr 55

Ac. Resp. Ac. 1 = 0.1 5-10 min 43

Ch. Resp. Ac. 1 = 0.3 72-120 hr 45

Ac. Resp. Al. 1 = 0.2 5-10 min 18

Ch. Resp. Al. 1 = 0.4 48-72 hr 13

DisturbanceEquation Interval Level

Met. Ac. 1 = 1.2 12-24 hr 10

Met. Al. 1 = 0.7 24-36 hr 55

Ac. Resp. Ac. 1 = 0.1 5-10 min 43

Ch. Resp. Ac. 1 = 0.3 72-120 hr 45

Ac. Resp. Al. 1 = 0.2 5-10 min 18

Ch. Resp. Al. 1 = 0.4 48-72 hr 13

Calculation of appropriate compensationCalculation of appropriate compensation

OrOr In metabolic disorders add 15 to HCO3: Example: if HCO3=10 + 15 = 25 then the PCO2

should be 25, and the last two digits of pH 25 pH=7.25 HCO3=10 PCO2=25

In metabolic disorders add 15 to HCO3: Example: if HCO3=10 + 15 = 25 then the PCO2

should be 25, and the last two digits of pH 25 pH=7.25 HCO3=10 PCO2=25

Normal Anion GapNormal Anion Gap

A-10

HCO3-

25 pH 7.40

PaCO2 40

Na 140Na 140 CL

105CL 105

AG = Na – (HCO3+Cl) = 8-12AG = Na – (HCO3+Cl) = 8-12

METABOLIC ACIDOSISMETABOLIC ACIDOSIS

CL- =105

AG = 10

HCO3 =25

CL- =105

AG = 25

HCO3 =10

CL- =115

AG = 10

HCO3 =15

NORMALNORMAL

- HCO3

+ CL-

- HCO3

+ A-

HYPERCHLOREMICHYPERCHLOREMIC HIGH AGHIGH AG

THE SERUM ANION GAPTHE SERUM ANION GAP

AG = Na+ - (HCO3- + CL-), NL = 10

AG INDICATE ORGANIC MET. AC.

AG + HCO3 INDICATE MET. AL.

AG DECREASED WITH PARAPROTEIN

AG DECREASED WITH LOW ALBUMIN

AG = Na+ - (HCO3- + CL-), NL = 10

AG INDICATE ORGANIC MET. AC.

AG + HCO3 INDICATE MET. AL.

AG DECREASED WITH PARAPROTEIN

AG DECREASED WITH LOW ALBUMIN

Increased anion gap Increased anion gap

metabolic acidosis ketones, lactate, sulfates, or metabolites of methanol,

ethylene glycol, and salicylate hyperalbuminemia and uremia (increased

anions) hypocalcemia or hypomagnesemia (decreased

cations)

metabolic acidosis ketones, lactate, sulfates, or metabolites of methanol,

ethylene glycol, and salicylate hyperalbuminemia and uremia (increased

anions) hypocalcemia or hypomagnesemia (decreased

cations)

The effect of low albumin can be accounted for by adjusting the normal range for the anion gap 2.5 mEq/L for every 1 g/dL fall in albumin.

Decreased anion gap Decreased anion gap

hypoalbuminemia hypercalcemia hypermagnesemia Lithium intoxication hypergammaglobulinemia bromide or iodide intoxication

hypoalbuminemia hypercalcemia hypermagnesemia Lithium intoxication hypergammaglobulinemia bromide or iodide intoxication


EXAMPLE OF A SIMPLE DISORDER

pH (7.55) = C * [HCO3-] (18 mmol/L)

PCO2 (21 mm Hg)

Step 1: pH indicates alkalemia (Met. or Resp)

Step 2: HCO3- indicates Resp. Alkalosis

Step 3: PCO2 , confirms Resp. Alkalosis

EXAMPLE OF A SIMPLE DISORDER

pH (7.55) = C * [HCO3-] (18 mmol/L)

PCO2 (21 mm Hg)

Step 1: pH indicates alkalemia (Met. or Resp)

Step 2: HCO3- indicates Resp. Alkalosis

Step 3: PCO2 , confirms Resp. Alkalosis

The delta gap The delta gap The difference between the patient's anion gap

and the normal anion gap is termed the delta gap considered an HCO3 − equivalent, because for

every unit Rise in the anion gap, the HCO3 − should lower by 1

The delta gap is added to the measured HCO3 − , the result should be in the normal range for HCO3 −; elevation indicates the additional presence of a metabolic alkalosis

The difference between the patient's anion gap and the normal anion gap is termed the delta gap

considered an HCO3 − equivalent, because forevery unit Rise in the anion gap, the HCO3 − should lower by 1

The delta gap is added to the measured HCO3 − , the result should be in the normal range for HCO3 −; elevation indicates the additional presence of a metabolic alkalosis


EXAMPLE OF A MIXED DISORDER pH (7.55) = C * [HCO3

-] (30 mmol/L) PCO2 (35 mm Hg)

Step 1: Alkalemia Step 2: HCO3

- , indicates Met. alkalosis Step 3: PCO2 , indicates Resp. alkalosis Step 4: HCO3

- (25%) > PCO2 (12.5%) Step 5: The major disorder is metabolic alkalosis

EXAMPLE OF A MIXED DISORDER pH (7.55) = C * [HCO3

-] (30 mmol/L) PCO2 (35 mm Hg)

Step 1: Alkalemia Step 2: HCO3

- , indicates Met. alkalosis Step 3: PCO2 , indicates Resp. alkalosis Step 4: HCO3

- (25%) > PCO2 (12.5%) Step 5: The major disorder is metabolic alkalosis

MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERS

DOUBLE Metabolic and respiratory acidosis (serious) Metabolic and respiratory alkalosis (serious) Metabolic acidosis & respiratory alkalosis Metabolic alkalosis & respiratory acidosis

TRIPLE Metabolic acidosis & alkalosis + resp. disorder

DOUBLE Metabolic and respiratory acidosis (serious) Metabolic and respiratory alkalosis (serious) Metabolic acidosis & respiratory alkalosis Metabolic alkalosis & respiratory acidosis

TRIPLE Metabolic acidosis & alkalosis + resp. disorder


EXAMPLE OF DOUBLE DISORDER

Health Emphysema + Diarrhea

pH 7.40 7.32 7.10

PCO2 40 80 80

HCO3 24 40 24


Health Emphysema + Diarrhea

pH 7.40 7.32 7.10

PCO2 40 80 80

HCO3 24 40 24



Health Emphysema + Diuretic

pH 7.40 7.32 7.40

PCO2 40 80 80

HCO3 24 40 48


Health Emphysema + Diuretic

pH 7.40 7.32 7.40

PCO2 40 80 80

HCO3 24 40 48

MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERSEXAMPLE OF TRIPLE DISORDER

Health NG + Sepsis + Endotox.

pH 7.40 7.49 7.14 7.44

PCO2 40 44 24 12

HCO3 24 32 8 8

AG 9 11 33 35

AG 0 2 24 26

EXAMPLE OF TRIPLE DISORDER

Health NG + Sepsis + Endotox.

pH 7.40 7.49 7.14 7.44

PCO2 40 44 24 12

HCO3 24 32 8 8

AG 9 11 33 35

AG 0 2 24 26

Masked disorderMasked disorder

A vomiting, ill-appearing diabetic patient has laboratory results showing: Na, 137; K, 3.8; Cl, 90; HCO3 −, 22; pH, 7.40; Pco2, 41; Po2, 85

anion gap = 137 − (90 + 22) = 25 (normal :10) Respiratory compensation is evaluated by Winter's formula Predicted Pco2 = 1.5 (22) + 8 ± 2 = 41 ± 2 delta gap = 15 + 22 = 37

A vomiting, ill-appearing diabetic patient has laboratory results showing: Na, 137; K, 3.8; Cl, 90; HCO3 −, 22; pH, 7.40; Pco2, 41; Po2, 85

anion gap = 137 − (90 + 22) = 25 (normal :10) Respiratory compensation is evaluated by Winter's formula Predicted Pco2 = 1.5 (22) + 8 ± 2 = 41 ± 2 delta gap = 15 + 22 = 37

Normal ABG?Normal ABG? A diabetic patient presented with gastroentritis

found to have: pH: 7.4 HCO3: 24 PCO2: 40 Na: 144, K: 4, CL: 95, TCO2: 24, RBS: 520, Positive test for ketons

What is the acid-base status of this patient?

A diabetic patient presented with gastroentritis found to have: pH: 7.4 HCO3: 24 PCO2: 40 Na: 144, K: 4, CL: 95, TCO2: 24, RBS: 520, Positive test for ketons

What is the acid-base status of this patient?

Metabolic Acidosis


G I HC O 3 L O S SRE NA L HC O 3 L O S S

HYPO A L D O ST ERO NIS MT PN

NO RM A L A G10 m E q/L

K ET O A C ID O SIDL A C T IC A C ID O S ISRE NA L F A IL URE

INT O X IC A T IO N

HIG H A G> 15 m E q/L

C AU SES

PRIM A RY: D E C REA S D HC O 3RE SPO NSE : D E C RE S ED PC O 2


HIGH ANION GAP Ketoacidosis (DM1, ETOH, Starvation) Lactic acidosis (A, B, D) Intoxication

Ethylene glycol Methanol Salicylic acid

Advanced renal failure

HIGH ANION GAP Ketoacidosis (DM1, ETOH, Starvation) Lactic acidosis (A, B, D) Intoxication

Ethylene glycol Methanol Salicylic acid

Advanced renal failure


INTOXICATION: HIGH OSMOLAR GAP

ETHYLENE GLYCOL METHANOL

SALICYLATE RESPIRATORY ALKALOSIS METABOLIC ACIDOSIS MIXED

INTOXICATION: HIGH OSMOLAR GAP

ETHYLENE GLYCOL METHANOL

SALICYLATE RESPIRATORY ALKALOSIS METABOLIC ACIDOSIS MIXED


KETOACIDOSIS Diabetes 1 (Insulin lack) leads to fatty acids

oxidation and production of acetoacetate (2) and B-OH-butyrate (5), which is buffered by HCO3

-, causing high AG

ETOH (altered cell metabolism) Starvation (use of fatty acids), usually mild

KETOACIDOSIS Diabetes 1 (Insulin lack) leads to fatty acids

oxidation and production of acetoacetate (2) and B-OH-butyrate (5), which is buffered by HCO3

-, causing high AG

ETOH (altered cell metabolism) Starvation (use of fatty acids), usually mild


LACTIC ACIDOSIS (Dx by exclusion) Type A: O2 delivery to cells is inadequate

Shock, mesenteric vascular events, and pulmonary edema)

Type B: Cells cannot use O2

Hepatic failure, sepsis, acute pancreatitis Anaerobic glycolysis of glucose to pyruvate and then

lactate (buffered by HCO3-)

LACTIC ACIDOSIS (Dx by exclusion) Type A: O2 delivery to cells is inadequate

Shock, mesenteric vascular events, and pulmonary edema)

Type B: Cells cannot use O2

Hepatic failure, sepsis, acute pancreatitis Anaerobic glycolysis of glucose to pyruvate and then

lactate (buffered by HCO3-)


RENAL FAILURE:

Unable to excrete the daily acid load

Bone buffers keep HCO3-> 15 in CRF

In ARF HCO3- falls by 0.5 mmol/L/day

Retention of sulfate, phosphate, and organic anions

causes the increase in AG

RENAL FAILURE:

Unable to excrete the daily acid load

Bone buffers keep HCO3-> 15 in CRF

In ARF HCO3- falls by 0.5 mmol/L/day

Retention of sulfate, phosphate, and organic anions

causes the increase in AG


NORMAL ANION GAP GI HCO3

- LOSS (Diarrhea, fistula)

RENAL HCO3- LOSS

RTA (Proximal, Distal, Hyperkalemic) Acetazolamide, hypoaldostironism

Miscellaneous NH4Cl ingestion, Sulfur ingestion Pronounced dilution

NORMAL ANION GAP GI HCO3

- LOSS (Diarrhea, fistula)

RENAL HCO3- LOSS

RTA (Proximal, Distal, Hyperkalemic) Acetazolamide, hypoaldostironism

Miscellaneous NH4Cl ingestion, Sulfur ingestion Pronounced dilution


GI. BICARBONATE LOSS NORMAL AG, HYPERCHLOREMIC CAUSES

DIARRHEA EXTERNAL FISTULA URETEROSIGMOIDOSTOMY OR ILEAL LOOP

CONDUIT

GI. BICARBONATE LOSS NORMAL AG, HYPERCHLOREMIC CAUSES

DIARRHEA EXTERNAL FISTULA URETEROSIGMOIDOSTOMY OR ILEAL LOOP

CONDUIT


RENAL BICARBONATE LOSS TYPE I RTA (DISTAL, CLASSICAL)

PROTON SECRETION DEFECT

TYPE II RTA (PROXIMAL, FANCONOI) BICARBONATE REABSORPTION DEFECT

TYPE IV RTA (HYPERKALEMIC) HYPORENINEMIC HYPOALDOSTERONISM

RENAL BICARBONATE LOSS TYPE I RTA (DISTAL, CLASSICAL)

PROTON SECRETION DEFECT

TYPE II RTA (PROXIMAL, FANCONOI) BICARBONATE REABSORPTION DEFECT

TYPE IV RTA (HYPERKALEMIC) HYPORENINEMIC HYPOALDOSTERONISM


URINARY ANION GAP UAG = (Na+ + K+) - Cl-

UAG is an estimate of urinary ammonium Elevated in GI HCO3

- loss

Low in distal RTA

UAG: NEGATIVE -20 mEq/L IN GI LOSS UAG: POSITIVE + 23 mEq/L IN RTA

URINARY ANION GAP UAG = (Na+ + K+) - Cl-

UAG is an estimate of urinary ammonium Elevated in GI HCO3

- loss

Low in distal RTA

UAG: NEGATIVE -20 mEq/L IN GI LOSS UAG: POSITIVE + 23 mEq/L IN RTA

RENAL TUBULAR ACIDOSISRENAL TUBULAR ACIDOSIS

K+ Tubular Aldo Proximal

HCO3- + + + + +

K+ Urine pH >5.4 >5.4 <5.5 <5.5

FE HCO3- <5% <5% <5% >15%

Calculi + + + - + -

Bone + + - + + +

K+ Tubular Aldo Proximal

HCO3- + + + + +

K+ Urine pH >5.4 >5.4 <5.5 <5.5

FE HCO3- <5% <5% <5% >15%

Calculi + + + - + -

Bone + + - + + +

CAUSES OF DISTAL RTACAUSES OF DISTAL RTA

Primary Hypercalcemia and nephrocalcinosis Multiple myeloma Cirrhosis SLE Amphotericin B Lithium Transplant rejection Medullary sponge kidney

Primary Hypercalcemia and nephrocalcinosis Multiple myeloma Cirrhosis SLE Amphotericin B Lithium Transplant rejection Medullary sponge kidney

CAUSES OF HYPERKALEMIC RTA

CAUSES OF HYPERKALEMIC RTA

Hypoaldosteronism

Obstructive nephropathy

Sickle cell nephropathy

SLE

Cyclosporine A nephropathy

Hypoaldosteronism

Obstructive nephropathy

Sickle cell nephropathy

SLE

Cyclosporine A nephropathy

CAUSES OF PROXIMAL RTACAUSES OF PROXIMAL RTA Primary Cystinosis Wilson’s disease Lead toxicity Multiple myeloma Nephrotic syndrome Early transplant rejection Medullary cystic disease Outdated tetracycline

Primary Cystinosis Wilson’s disease Lead toxicity Multiple myeloma Nephrotic syndrome Early transplant rejection Medullary cystic disease Outdated tetracycline

METABOLIC ALKALOSISMETABOLIC ALKALOSIS

Norm al ECVAlkali load

Decreased ECVGI loss

Diuretics

<20 m Eq/L

Norm al ECVExcess

M ineralocorticoids

Decreased ECVBartter's

Hypokalem ia

>20 m Eq/L

URINARY CHLORIDE

Appropriate response?PCO2=0.7 HCO3

Prim ary: INCREASED HCO3RESPONSE: INCREASED PCO2

Metabolic Alkalosis

Effects of Metabolic AlkalosisEffects of Metabolic AlkalosisEffects of Metabolic AlkalosisEffects of Metabolic Alkalosis

Decreased serum potassiumDecreased serum potassium Decreased serum ionized calciumDecreased serum ionized calcium DysrhythmiasDysrhythmias Hypoventilation / hypoxemiaHypoventilation / hypoxemia Increased bronchial tone / atelectasisIncreased bronchial tone / atelectasis Left shift of the Oxygen curveLeft shift of the Oxygen curve

Decreased serum potassiumDecreased serum potassium Decreased serum ionized calciumDecreased serum ionized calcium DysrhythmiasDysrhythmias Hypoventilation / hypoxemiaHypoventilation / hypoxemia Increased bronchial tone / atelectasisIncreased bronchial tone / atelectasis Left shift of the Oxygen curveLeft shift of the Oxygen curve


Volume - depleted type: Gastric acid loss

Vomiting NGT suction

Renal chloride loss Diuretics Hypercapnia correction

Volume - depleted type: Gastric acid loss

Vomiting NGT suction

Renal chloride loss Diuretics Hypercapnia correction


Volume - repleted type:Mineralocorticoid excess

Hyperaldosteronism

Bartter’s syndrome

Cushing’s syndrome

Licorice excess

Profound potassium depletion

Volume - repleted type:Mineralocorticoid excess

Hyperaldosteronism

Bartter’s syndrome

Cushing’s syndrome

Licorice excess

Profound potassium depletion

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS

Pneum othoraxPneum onia

P u lm onary em bolusP u lm onary edem a

C O PDPulm onary fibros is

Pulm onary

C NS depressantBra in s tem les ionsS pina l cord les ions

Prim ary hypoventi la tionPoliom ye li tis

Neurom uscula r

C AU SES

A ppropria te response?A cute : HC O 3 (1 ) = PC O 2 (10 )

C hronic : HC O 3 (3 ) = PC O 2 (10 )

Prim ary: INC RE A S E D PC O 2RE S PO NS E : INC RE A S E D HC O 3

Respiratory Acidosis

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS

A C UT EPneum onia

Pulm onary em bolusS eps is

C HRO NICPulm onary fibros is

C HFC irrhos is

PE RIPHE RA L

A C UT ES a licyla te overdose

Pa inA nx ie ty

C HRO NICBra in tum orPregnancy

Pa in

C E NT RA L

C AU SES

A ppropria te response?A cute : HC O 3 (2 ) = PC O 2 (10 )

C hronic : HC O 3 (4 ) = PC O 2 (10 )

Prim ary: D E C RE A S E D PC O 2RE S PO NS E : D E C RE A S E D HC O 3

Respiratory Alkalosis

A-12 A-11 A-12

HCO3- HCO3- HCO3-

24 26 29

Cl- Cl- Cl-

104 104 99

Na+

140Na+

141Na+

140

Normal Ac. resp. acidosis Ch. resp. acidosis

pH 7.40 pH 7.26 pH 7.30

PaCO2 40 PaCO2 60 PaCO2 60

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS

A-12 A-14 A-14

HCO3-HCO3- HCO3-

24 20 15

Cl- Cl- Cl-

104 104 111

Na+

140Na+

138Na+

140

Normal Ac. resp. alkalosis Ch. resp. alkalosis

pH 7.40 pH 7.62 pH 7.49

PaCO2 40 PaCO2 20 PaCO2 20

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS

Acid - Base NomogramAcid - Base Nomogram

↑ CO2↑ 2,3 DPG↓ pH

↓ CO2↓ 2,3 DPG↑ pH

SaO2

pO2

Right shift—better tissue oxygenation

Left shift—worse tissue oxygenation

Acid - Base NomogramAcid - Base Nomogram

acid base disorders

Documents

hco3 hco3

pco2 ph

log hco3

na hco3

digits of ph

neql ph

hco3 elevation

hco3 equivalent