What is the acid-base disturbance present in this case?
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Transcript What is the acid-base disturbance present in this case?
METABOLIC
ACIDOSIS
D8
HISTORY
45 year old
Diabetic woman
4th day
Fever (39.5C)
Chills
Myalgia
Diarrhea
Denies taking any medications, drugs or
alcohol
PHYSICAL EXAMINATION
BP: 84/52 (Supine)
PR: 118 bpm
RR: 42 breaths/ minute
Dry mucous membrane
Flat neck veins
No edema
Abdomen distended, firm & mildly tender
Hyperactive bowel sounds
LABORATORY CBC
Result
Remarks
Hemoglobin 15.5 g/dL
Reference
range
12-16
Hematocrit
48%
38-48%
Normal
WBC count
22,800
Normal
Segmenters 66%
5,00010,000
50-70%
Band forms
0-5%
Increased
23%
Normal
Normal
LABORATORY CHEMISTRY
Result
Reference
range
Remark
Serum Na
138.0
meq/L
135-145
Normal
Serum Cl
108.0
meq/L
99-110
Normal
Serum K
4.2 meq/L
4-4.5
Normal
LABORATORY CHEMISTRY
Result
Reference
range
Remark
pH
7.39
7.35-7.45
Normal
pCO2
17.0 mmHg 35-45
Decreased
HCO3
10.0 meq/L
Decreased
21-28
LABORATORY CHEMISTRY
Result
Reference
range
Remark
BUN
28.0 mg/dL
7-20
Increased
Creatinine
2.4 mg/dL
0-8-1.4
Increased
LABORATORY CHEMISTRY
Result
Glucose
Lactate
342.0
mg/dL
3.0 meq/L
Ketones
None
Reference
range
<100
Remark
0.5-1.0
Increased
Negative
Normal
Increased
INTRODUCTION
Blood pH
7.35 – 7.45
Extracellular & intracellular buffering process
Respiratory & renal regulatory mechanisms
Dispose the body’s normal physiologic load of
carbonic acid (as carbon dioxide), non-volatile
acids & defend against occasional addition of
abnormal quantities of acids & alkalis
BODY SOURCES
Volatile acid
Carbon dioxide
Aerobic metabolism
Non-volatile acid
From breakdown of protein & phospholipid
metabolism
Ketoacids, lactic acid, from disease & anaerobic
metabolism
HYDROGEN REGULATION
Chemical buffering
Respiratory regulation
Extracellular & intracellular buffers
Acts within a fraction of second
Altering rate of breathing affecting rate of CO2 removal
Acts with minutes to days
Renal regulation
Excreting either acid or alkaline urine
Acts within hours to several days
QUESTION 1
What is the acid base disturbance present
in this case?
What is the acid-base disturbance
present in this case?
Respiratory
Acidosis
pH
H+
PCO2
HCO3-
Respiratory
Alkalosis
Metabolic
Acidosis
Metabolic
Alkalosis
Arterial blood sample
pH < 7.40
HCO3 < 24
pH > 7.40
pCO2 > 40
Metabolic acidosis
pCO2 < 40
HCO3 >24
Respiratory acidosis
HCO3 > 24
pCO2 < 40
Metabolic alkalosis
pCO2 > 40
Respiratory alkalosis
HCO3 < 24
Disturbance
Primary alteration
Defense mechanism
Metabolic
alkalosis
plasma [HCO3-]
Intracellular buffers
Hypoventilation to increase PCO2
Urinary excretion of HCO3-
Respiratory
acidosis
blood pCO2
Intracellular buffers
Increased renal acid excretion
Respiratory
alkalosis
blood pCO2
Intracellular buffers
renal acid excretion
Metabolic
acidosis
in plasma [HCO3] Intracellular & extracellular buffer
Hyperventilation to pCO2
Urinary excretion of H+
Respiratory
Acidosis
Hx: hypercapnia,
dyspnea, anxiety,
delirium,
obtundation
Respiratory
Alkalosis
Hx: dizziness,
mental confusion,
seizures, tetany
Metabolic
Acidosis
Hx: palpitations,
chest pain, visual
changes, mental
confusion,
dyspnea, n/v,
diarrhea,
tachypnea,
hyperpnea
Metabolic
Alkalosis
Hx: weakness,
myalgia, polyuria,
vomitting, diarrhea,
hypoventilation
METABOLIC ACIDOSIS
Addition of non-volatile acids
Loss of non-volatile alkali (Diarrhea)
Failure to excrete sufficient net acid load
COMPENSATION
ICF & ECF Buffers
Respiratory
Renal
RESPIRATORY COMPENSATION
METABOLIC ACIDOSIS
STIMULATE CENTRAL
& PERIPHERAL
CHEMORECEPTORS
RAISE pH TOWARD
NORMAL
FALL OF pCO2
INCREASED ALVEOLAR
VENTILATION
QUESTION 2
Present an algorithm for the diagnosis of
the acid base disorder. Present the table:
rule of thumb in bedside interpretation of
acid base disorder
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
3.
4.
5.
6.
7.
8.
Obtain arterial blood gases (ABGs) and
electrolytes (lytes) simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
STEPS IN ACID-BASE DIAGNOSIS
1.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
2.
Compare [HCO3] on ABG and lytes to
verify accuracy. * ± 2mmol/L
3.
4.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
5.
6.
7.
8.
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
3.
Calculate anion gap (AG).
4.
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
5.
6.
7.
8.
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
3.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
4.
Know four causes of high AG acidosis
(ketoacidosis, lactic acid acidosis, renal
failure and toxins).
5.
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
6.
7.
8.
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
3.
4.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid acidosis,
renal failure and toxins).
5.
Know two causes of high hyperchloremic
or nongap acidosis(bicarbonate loss
from GI tract, renal tubular acidosis).
6.
7.
8.
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
3.
4.
5.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
6.
Estimate compensatory response.
7.
8.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in [Na].
Prediction of Compensatory Responses on
Simple Acid Base Disturbances
Metabolic
Acidosis
Respiratory
Alkalosis
PaCO2 = (1.5 x HCO) + 8 or
PaCO2 will 1.25 mmHg per mmol/L
in HCO3
PaCO2 will 0.75 mmHg per mmol/L
in HCO3 or
PaCO2 = HCO3 + 15
HCO3 will 2-4 most per 10 mmHg
in PaCO2
Respiratory
Acidosis
HCO3 will 1-4 mmol/L per 10 mmHg
in PaCO2
Metabolic
Alkalosis
Prediction of Compensatory Responses on
Simple Acid Base Disturbances
Metabolic acidosis
pH, HCO3
Stimulate medullary chemoreceptors to
ventilation
Predict the degree of respiratory compensation:
PaCO2 = (1.5 x HCO3) + 8 = 23 *21-25 mmHg
Values <21 & >25 mixed disturbance
PaCO2 < 23 = met acidosis & respi alkalosis
PaCO2 > 23 = met alkalosis & respi acidosis
Prediction of Compensatory Responses on
Simple Acid Base Disturbances
Acid-Base Nomogram
Shaded areas show 95% confidence limits for
normal compensation
Finding acid-base values within the shaded
areas does not rule out a mixed disturbance
Not a substitute for computation
Prediction of Compensatory Responses on
Simple Acid Base Disturbances
Acid-Base Nomogram
pH 7.39
HCO3 10 mEq/L
PCO2 17 mmHg
STEPS IN ACID-BASE DIAGNOSIS
1.
6.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
7.
Compare ΔAG and Δ HCO3
8.
Compare change in [Cl] with changes in [Na].
2.
3.
4.
5.
STEPS IN ACID-BASE DIAGNOSIS
1.
2.
3.
4.
5.
6.
7.
8.
Obtain arterial blood gases (ABGs) and electrolytes (lytes)
simultaneously.
Compare [HCO3] on ABG and lytes to verify accuracy.
Calculate anion gap (AG).
Know four causes of high AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure and toxins).
Know two causes of high hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response.
Compare ΔAG and Δ HCO3
Compare change in [Cl] with changes in
[Na].
QUESTION 3
How do you compute for the anion gap?
What is its significance? Compute for the
anion gap.
ANION GAP
Represents the difference in concentration
between the major plasma cations & the
major plasma anions
Cations: Na+
Anions: Cl- & HCO3-
COMPUTING THE ANION GAP
Anion Gap = [Na+] – ([Cl-] + [HCO3-])
Normal range: 8-16 mEq/L
SIGNIFICANCE OF ANION GAP
It is a useful way to determine the cause of
metabolic acidosis because changes in the
concentration of anions are a result of
addition of nonvolatile acids.
Because the condition is diagnosed as
metabolic acidosis, nonvolatile acids are
added into the body fluids.
ANION GAP
If the nonvolatile acid contains Cl- the anion
gap will remain normal (because the
decrease in HCO3- is matched by the
increase in Cl-)
If the nonvolatile acid contains another
substance, the anion gap will increase
(because the Cl- concentration remains
unchanged)
COMPUTATION OF ANION GAP
Anion Gap = [Na+] – ([Cl-] + [HCO3-])
Anion Gap = [138.0] – ([108.0] + [10.0])
Anion Gap = (138.0) – (118.0)
Anion Gap = 20.0 mEq/L
NR: 8-16 mEq/L
** The anion gap is increased
QUESTION 4
What are the causes of high anion gap and
normal anion gap acidosis?
NOMAL VS HIGH
NORMAL ANION GAP
Acid gain or bicarbonate
loss is accompanied by
chloride gain
Anion gap remains
unchanged
HIGH ANION GAP
Accumulation of acid
anions in ECF
Exogenous acid
ingestion
Increased endogenous
acid production
DIARRHEA
↑ loss of HCO3 along w/ vol. depletion
Matabolic acidosis and hypokalemia
↑renal synthesis and excretion of NH4
NORMAL ANION GAP
RENAL TUBULAR ACIDOSIS
(GFR bet. 20 and 50 mL/min)
↓ # of functioning nephrons
Proximal RTA: ↓ HCO3 tubular reabsorption
OR
Distal RTA: ↓ acid excreation
↑renal synthesis and excretion of NH4
OTHER CAUSES OF NORMAL ANION GAP
Carbonic anhydrase inhibition
Drug-induced hyperkalemia (With renal insufficiency)
HIGH ANION GAP
Lactic Acidosis
Increase in plasma lactate
Secondary to poor tissue perfusion (Type A)
Aerobic disorders (Type B)
Ketoacidosis
Increase fatty acid metabolism
Accumulation of ketoacids (Acetoacetate & hydroxybutyrate)
Diabetic ketoacidosis, alcoholic ketoacidosis
↑ ANION GAP
Drug and toxin induced
Salicylates: ketones, lactate, salicylate
ethylene glycol: glycolate, oxalate
Methanol or formaldehyde: Formate
Advanced Renal failure: Sulfate, phosphate,
urate
↑ ANION GAP
Advanced RF
↓ # of functioning nephrons
Dec. NH4+ prod. and excretion
Failure to balance w/ net acid production
Inc. anion gap
QUESTION 5
How would you treat this patient?
Normal AG acidosis (hyperchloremic acidosis), a slightly
elevated AG (mixed hyperchloremic and AG acidosis), or
an AG attributable to a nonmetabolizable anion in the
face of renal failure: --> Alkali theraphy
orally (NaHCO3) or Shohl's solution)
IV (NaHCO3), in an amount necesarry to slowly increase the
plasma [HCO3-] into the 20 to 22 mmol/L range.
The condition that precipitated the metabolic acidosis in
the patient should also be managed. (Fever and diarrhea
~ Gastroenteritis??)
THANK YOU..