May 26, 2015
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
ACID-BASE DISORDERSACID-BASE DISORDERS
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)
ACID-BASE DISORDERSACID-BASE DISORDERS
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
ACID-BASE DISORDERSACID-BASE DISORDERS
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
ACID-BASE DISORDERSACID-BASE DISORDERS
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
MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERS
EXAMPLE OF DOUBLE DISORDER
Health Emphysema + Diarrhea
pH 7.40 7.32 7.10
PCO2 40 80 80
HCO3 24 40 24
EXAMPLE OF DOUBLE DISORDER
Health Emphysema + Diarrhea
pH 7.40 7.32 7.10
PCO2 40 80 80
HCO3 24 40 24
MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERS
EXAMPLE OF DOUBLE DISORDER
Health Emphysema + Diuretic
pH 7.40 7.32 7.40
PCO2 40 80 80
HCO3 24 40 48
EXAMPLE OF DOUBLE DISORDER
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
METABOLIC ACIDOSISMETABOLIC 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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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-)
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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
METABOLIC ALKALOSISMETABOLIC ALKALOSIS
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
METABOLIC ALKALOSISMETABOLIC ALKALOSIS
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