METABOLIC ACIDOSIS D8. HISTORY 45 year old Diabetic woman 4 th day Fever (39.5 C) Chills Myalgia Diarrhea Denies taking any medications, drugs or alcohol

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 Reference range

Remarks

Hemoglobin 15.5 g/dL 12-16 Normal

Hematocrit 48% 38-48% Normal

WBC count 22,800 5,000-10,000

Normal

Segmenters 66% 50-70% Normal

Band forms 23% 0-5% Increased

LABORATORY CHEMISTRY


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



Remark

pH 7.39 7.35-7.45 Normal

pCO2 17.0 mmHg 35-45 Decreased

HCO3 10.0 meq/L 21-28 Decreased



Remark

BUN 28.0 mg/dL 7-20 Increased

Creatinine 2.4 mg/dL 0-8-1.4 Increased



Remark

Glucose 342.0 mg/dL

<100 Increased

Lactate 3.0 meq/L 0.5-1.0 Increased

Ketones None Negative Normal

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

Extracellular & intracellular buffers Acts within a fraction of second

Respiratory regulation 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?

Metabolic Acidosis

Metabolic Alkalosis

Respiratory Acidosis

Respiratory Alkalosis

pH

H+

PCO2

HCO3-

Arterial blood sample

pH < 7.40 pH > 7.40

HCO3 < 24 pCO2 > 40

Metabolic acidosis

pCO2 < 40

Respiratory acidosis

HCO3 > 24

HCO3 >24

Metabolic alkalosis

pCO2 > 40

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 buffersIncreased renal acid excretion

Respiratory alkalosis

blood pCO2 Intracellular buffers renal acid excretion

Metabolic acidosis

in plasma [HCO3]

Intracellular & extracellular bufferHyperventilation to pCO2

Urinary excretion of H+

Metabolic Acidosis

Metabolic Alkalosis



Hx: hypercapnia, dyspnea, anxiety, delirium, obtundation

Hx: dizziness, mental confusion, seizures, tetany

Hx: palpitations, chest pain, visual changes, mental confusion, dyspnea, n/v, diarrhea, tachypnea, hyperpnea

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

INCREASED ALVEOLARVENTILATION

FALL OF pCO2

RAISE pH TOWARDNORMAL

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 DIAGNOSIS1. Obtain arterial blood gases (ABGs)

and electrolytes (lytes) simultaneously.2. 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).

5. Know two causes of high hyperchloremic or nongap acidosis (bicarbonate loss from GI tract, renal tubular acidosis).

6. Estimate compensatory response.

7. Compare ΔAG and Δ HCO3

8. Compare change in [Cl] with changes in [Na].

STEPS IN ACID-BASE DIAGNOSIS1. Obtain arterial blood gases (ABGs) and electrolytes (lytes)

simultaneously.

2. Compare [HCO3] on ABG and lytes to verify accuracy. * ± 2mmol/L








simultaneously.

2. 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).






simultaneously.



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).





simultaneously.




5. Know two causes of high hyperchloremic or nongap acidosis(bicarbonate loss from GI tract, renal tubular acidosis).





simultaneously.





6. Estimate compensatory response.7. Compare ΔAG and Δ HCO3


Prediction of Compensatory Responses on Simple Acid Base DisturbancesMetabolic Acidosis

PaCO2 = (1.5 x HCO) + 8 or

PaCO2 will 1.25 mmHg per mmol/L in HCO3

Metabolic Alkalosis

PaCO2 will 0.75 mmHg per mmol/L in HCO3 or

PaCO2 = HCO3 + 15


HCO3 will 2-4 most per 10 mmHg in PaCO2


HCO3 will 1-4 mmol/L per 10 mmHg in PaCO2

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


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


Acid-Base Nomogram pH 7.39 HCO3 10 mEq/L PCO2 17 mmHg


simultaneously.






7. Compare ΔAG and Δ HCO38. Compare change in [Cl] with changes in [Na].


simultaneously.








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 reabsorptionOR

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..

Documents

METABOLIC ACIDOSIS D8. HISTORY 45 year old Diabetic woman 4 th day Fever (39.5 C) Chills Myalgia Diarrhea Denies taking any medications, drugs or alcohol