i.s. md 5/18/01abg interpretation1 abg interpretation

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5/18/01 ABG Interpretation 1 I.S.

MD

ABG INTERPRETATION

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ABG (Astrup)

o pH - measured

o pCO2 - measured

o HCO3- - calculated

o pO2 - measured

o BE (BD) - calculated

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ABG Interpretation

o First, does the patient have an acidosis or an alkalosis

o Second, what is the primary problem – metabolic or respiratory

o Third, is there any compensation by the patient – respiratory compensation is immediate while renal compensation takes time

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ABG Interpretation

o It would be extremely unusual for either the respiratory or renal system to overcompensate

o The pH determines the primary problem

o After determining the primary and compensatory acid/base balance, evaluate the effectiveness of oxygenation

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Normal Values

o pH 7.35 to 7.45

o paCO2 36 to 44 mm Hg

o HCO3 22 to 26 meq/L

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Abnormal Values

pH < 7.35o Acidosis (metabolic

and/or respiratory)

paCO2 > 44 mm Hg

o Respiratory acidosis (alveolar hypoventilation)

HCO3 < 22 meq/L

o Metabolic acidosis

pH > 7.45o Alkalosis (metabolic

and/or respiratory)

paCO2 < 36 mm Hg

o Respiratory alkalosis (alveolar hyperventilation)

HCO3 > 26 meq/L

o Metabolic alkalosis

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Putting It Together - Respiratory

SopaCO2 > 44 with a pH < 7.35 represents a respiratory

acidosispaCO2 < 36 with a pH > 7.45 represents a respiratory

alkalosis

For a primary respiratory problem, pH and paCO2 move in the opposite directiono For each deviation in paCO2 of 10 mm Hg in

either direction, 0.08 pH units change in the opposite direction

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Putting It Together - Metabolic

And HCO3 < 22 with a pH < 7.35 represents a

metabolic acidosis HCO3 > 26 with a pH > 7.45 represents a

metabolic alkalosis

For a primary metabolic problem, pH and HCO3 are in the same direction

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Metabolic Acidosis

Increase in H+ involves:

Extracellular bufferingIntracellular bufferingRespiratory compensationRenal excretion of the H+ load

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Compensation

Compensationo metabolic alkalosiso respiratory alkalosiso metabolic acidosiso respiratory acidosis

The body’s attempt to return the acid/base status to normal (i.e. pH closer to 7.4)

Primary Problemo respiratory acidosiso metabolic acidosiso respiratory alkalosiso metabolic alkalosis

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Expected Compensation

Respiratory acidosis

o Acute – the pH decreases 0.08 units for every 10 mm Hg increase in paCO2;

(HCO3 0.1-1 mEq/liter per 10 mm Hg paCO2)

o Chronic – the pH decreases 0.03 units for every 10 mm Hg increase in paCO2;

(HCO3 1.1-3.5 mEq/liter per 10 mm Hg paCO2)

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Expected Compensation

Respiratory alkalosis

o Acute – the pH increases 0.08 units for every 10 mm Hg decrease in paCO2;

HCO3 0-2 mEq/liter per 10 mm Hg paCO2

o Chronic - the pH increases 0. 17 units for every 10 mm Hg decrease in paCO2;

HCO3 2.1-5 mEq/liter per 10 mm Hg paCO2

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Expected Compensation

Metabolic acidosis

o paCO2 10-15 per 10 mEq/liter HCO3

Metabolic alkalosis

o paCO2 5-10 per 10 mEq/liter HCO3

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Classification of primary acid-base disturbances and

compensation

o Respiratory acidosis (alveolar hypoventilation) - acute, chronic

o Respiratory alkalosis (alveolar hyperventilation) - acute, chronic

o Metabolic acidosis – uncompensated, compensated

o Metabolic alkalosis – uncompensated, partially compensated

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Acute Respiratory Acidosis

o paCO2 is elevated and pH is acidotic

o The decrease in pH is accounted for entirely by the increase in paCO2

o Bicarbonate and base excess will be in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms

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Acute Respiratory Acidosis

o Causeso Respiratory pathophysiology - airway

obstruction, severe pneumonia, chest trauma/pneumothorax

o Acute drug intoxication (narcotics, sedatives)

o Residual neuromuscular blockadeo CNS disease (head trauma)

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ChronicRespiratory Acidosis

o paCO2 is elevated with a pH in the acceptable range

o Renal mechanisms increase the excretion of H+ within 24 hours and may correct the resulting acidosis caused by chronic retention of CO2 to a certain extent

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ChronicRespiratory Acidosis

o Causeso Chronic lung disease (BPD, COPD)o Neuromuscular diseaseo Extreme obesityo Chest wall deformity

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Acute Respiratory Alkalosis

o paCO2 is low and the pH is alkalotic

o The increase in pH is accounted for entirely by the decrease in paCO2

o Bicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanisms

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Respiratory AlkalosisCauses

o Paino Anxietyo Hypoxemiao Restrictive lung

diseaseo Severe congestive

heart failureo Pulmonary emboli

o Drugso Sepsiso Fevero Thyrotoxicosiso Pregnancyo Overaggressive

mechanical ventilation

o Hepatic failure

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Uncompensated Metabolic Acidosis

o Normal paCO2, low HCO3, and a pH less than 7.30

o Occurs as a result of increased production of acids and/or failure to eliminate these acids

o Respiratory system is not compensating by increasing alveolar ventilation (hyperventilation)

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Compensated Metabolic Acidosis

o paCO2 less than 30, low HCO3, with a pH of 7.3-7.4

o Patients with chronic metabolic acidosis are unable to hyperventilate sufficiently to lower paCO2 for complete compensation to 7.4

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Anion Gap and Acidosis

(AG) represents the concentration of all the unmeasured anions in the plasma

Anion gap = )[Na+] +[K+])- ([Cl-] - [HCO3-])

Normal = 8-14

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Anion Gap and Acidosis

(AG) represents the concentration of all the unmeasured anions in the plasma

0 = )[Na+] +[K+] + [?+]) -

- ([Cl-] + [HCO3-] + [?-])

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Anion Gap and Acidosis

[?+] – Ca+, Mg+

[?-] – plasma proteins, phosphate, sulfate, organ. anions

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Anion Gap and Acidosis

[?+] – Ca+, Mg+

and

[?-] – phosphate, sulfate, organ. anions

Tend to balance out

So plasma proteins [Pro-] – account for most of the missing anions

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Anion Gap and Acidosis

[?-] > [?+]i.e.

AG = [?-] - [?+]

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Anion Gap and Acidosis

AG = [?-] - [?+]i.e.

AG if ?+ - very small, 1-3 meq/l

or

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Anion Gap and Acidosis

or

AG if ?- may be significant

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Anion Gap and Acidosis

[?-] may be induced by high Albumin

concentration (i.e. hypovolemia)

or

[?-] accumulation of different anions

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Elevated AGMetabolic Acidosis

Causes

o Ketoacidosis - diabetic, alcoholic, starvation

o Lactic acidosis - hypoxia, shock, sepsis, seizures

o Toxic ingestion - methanol, ethylene glycol, ethanol, isopropyl alcohol, paraldehyde, toluene

o Renal failure - uremia

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Normal AG Metabolic Acidosis - Causes

o Renal tubular acidosis

o Hypoaldosteronism

o Diarrheao Potassium

sparing diuretics

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Effectiveness of Oxygenation

o Further evaluation of the arterial blood gas requires assessment of the effectiveness of oxygenation of the blood

o Hypoxemia – decreased oxygen content of blood - paO2 less than 60 mm Hg and the saturation is less than 90%

o Hypoxia – inadequate amount of oxygen available to or used by tissues for metabolic needs

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Mechanisms of Hypoxemia

o Inadequate inspiratory partial pressure of oxygen

o Hypoventilationo Right to left shunto Ventilation-perfusion mismatcho Incomplete diffusion equilibrium

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Summary

o First, does the patient have an acidosis or an alkalosis o Look at the pH

o Second, what is the primary problem – metabolic or respiratory

o Look at the pCO2

o If the pCO2 change is in the opposite direction of the pH change, the primary problem is respiratory

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Summary

o Third, is there any compensation by the patient - do the calculationso For a primary respiratory problem, is

the pH change completely accounted for by the change in pCO2

o if yes, then there is no metabolic compensation

o if not, then there is either partial compensation or concomitant metabolic problem

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Summary

o For a metabolic problem, calculate the expected pCO2

o if equal to calculated, then there is appropriate respiratory compensation

o if higher than calculated, there is concomitant respiratory acidosis

o if lower than calculated, there is concomitant respiratory alkalosis

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Summary

o Next, don’t forget to look at the effectiveness of oxygenation, (and look at the patient)o your patient may have a significantly

increased work of breathing in order to maintain a “normal” blood gas

o metabolic acidosis with a concomitant respiratory acidosis is concerning

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Case 1

Little Billy got into some of dad’s barbiturates. He suffers a significant depression of mental status and respiration. You see him in the ER 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained (after doing the

ABC’s, of course).

It shows pH = 7.16, pCO2 = 70, HCO3 = 22

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Case 1

What is the acid/base abnormality?

1. Uncompensated metabolic acidosis2. Compensated respiratory acidosis3. Uncompensated respiratory acidosis4. Compensated metabolic alkalosis

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Case 1

Uncompensated respiratory acidosis

o There has not been time for metabolic compensation to occur. As the barbiturate toxicity took hold, this child slowed his respirations significantly, pCO2 built up in the blood, and an acidosis ensued.

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Case 2

Little Suzie has had vomiting and diarrhea for 3 days. In her mom’s words, “She can’t keep anything down and she’s

running out.” She has had 1 wet diaper in the last 24 hours. She appears lethargic

and cool to touch with a prolonged capillary refill time. After addressing her

ABC’s, her blood gas reveals:

pH=7.34, pCO2=26, HCO3=12

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Case 2

What is the acid/base abnormality?

1. Uncompensated metabolic acidosis2. Compensated respiratory alkalosis3. Uncompensated respiratory acidosis4. Compensated metabolic acidosis

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Case 2

Compensated metabolic acidosis

o The prolong history of fluid loss through diarrhea has caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool. The body has compensated by “blowing off” the CO2 with increased respirations.

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Case 3

You are evaluating a 15 year old female in the ER who was brought in by EMS from school because of abdominal pain and vomiting. Review of system is negative except for a 3.5 kg weight loss over the past 2 months and polyuria for the past 2 weeks. She denies any sexual activity or drug use. On exam, she is alert and oriented, HR 115, RR 26, BP 114/75, pulse ox 95% on RA, mild abdominal tenderness on palpation in the midepigastric region and capillary refill time of 3 seconds. The result of the blood gas:

pH = 7.21 pCO2= 24 pO2 = 45 HCO3 = 10 BE = -10

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Case 3

What is the blood gas interpretation?

o Uncompensated respiratory acidosis with severe hypoxia

o Uncompensated metabolic alkalosiso Combined metabolic acidosis and

respiratory acidosis with severe hypoxiao Metabolic acidosis with respiratory

compensation

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Case 3

Metabolic acidosis with respiratory compensation

o This is a patient with new onset diabetes mellitus in ketoacidosis. Her pulse oximetry saturation and clinical examination do not reveal any respiratory problems except for tachypnea which is her compensatory mechanism for the metabolic acidosis. The nurse obtained the blood gas sample from the venous stick when she sent off the other labs.

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