Transcript Acid-Base Disorders - Harvard University

Arterial blood gas interpretation
Larissa Bornikova, MD
July, 2006
Objectives
• Review the basic pathophysiology of acid-base
disturbances.
• Develop a practical systematic approach to
interpretation of acid-base disturbances.
• Understand the clinical application of the A-a
gradient in interpreting causes of hypoxemia.
Questions to ask when evaluating ABG’s.
1. What is acid/base status?
2. What is the oxygenation status?
Overview
Only one equation you must know to understand acid-base
problems:
HCO3 + H ↔ H2CO3 ↔ H20 + CO2
You must understand what effect ventilation has on pH and
HCO3 and what effect metabolic disturbances have on
ventilation.
Overview (cont’d)
The body has three general mechanisms to defend against changes in body
fluid pH produced by acid-base disturbances:
1.
2.
Extracellular and intracellular buffering. Instantaneous to
minutes. Main physiological buffer systems are CO2/HCO3,
phosphate and protein buffer system.
Respiratory defense (adjustments in blood pCO2). Minutes to
hours to complete. Chemoreceptors located in the brain and in the
periphery (carotid and aortic bodies) sense changes in pCO2 and H+
and alter the ventilatory rate. In metabolic acidosis, pCO2 can be
reduced to approximately 10mmHg. In metabolic alkalosis,
hypoventilation cannot rise pCO2 above ~ 55 mm Hg (limited by
hypoxemia -> stimulator of respiratory drive)
* Kussmaul respiration
3.
Renal defense. Takes several days to complete because enzymes
need to be synthesized and upregulated.
* Acidic urine in contraction metabolic alkalosis
A systematic approach to acid-base
1.
Is the patient acidemic or alkalemic?
Action: Determine blood pH (pH <7.38 acidemia; pH >7.42 alkalemia)
2.
Is the primary disturbance metabolic or respiratory?
Action: Use CO2 and bicarbonate level to figure out the primary disturbance
3.
If a primary respiratory disturbance is present, is it acute or chronic?
Action: Compare measured pH with expected pH
4.
Is compensation appropriate?
Action: Compare measured pCO2/bicarb and expected pCO2/bicarb
5.
Is there an increased anion gap?
Action: Calculate anion gap (AG = Na – (Cl + HCO3))
6.
Are other metabolic disturbances present in the patient with an
anion gap metabolic acidosis?
Action: Calculate delta/delta
A systematic approach to acid-base (cont’d)
1.
Is the patient acidemic or alkalemic?
Action: Determine blood pH (pH <7.38 acidemia; pH >7.42 alkalemia)
2.
Is the primary disturbance metabolic or respiratory?
Action: Use CO2 and bicarbonate level to figure out the primary disturbance
3.
If a primary respiratory disturbance is present, is it acute or chronic?
Action: Compare measured pH with expected pH
4.
Is compensation appropriate?
Action: Compare measured pCO2/bicarb and expected pCO2/bicarb
5.
Is there an increased anion gap?
Action: Calculate anion gap (AG = Na – (Cl + HCO3))
6.
Are other metabolic disturbances present in the patient with an
anion gap metabolic acidosis?
Action: Calculate delta/delta
A systematic approach to acid-base (cont’d)
3.
If a primary respiratory disturbance is present, is it acute or chronic?
Action: Compare measured pH with expected pH
Acute Resp Acidosis: for every 10 increase pCO2, pH decreases by 0.08
Chronic Resp Acidosis: for every 10 increase pCO2, pH decreases by 0.03
Acute Resp Alkalosis: for every 10 decrease pCO2, pH increases by 0.08
Chronic Resp Alkal: for every 10 decrease pCO2, pH increases by 0.05
A systematic approach to acid-base (cont’d)
4. Is compensation appropriate?
Action: Compare measured pCO2/bicarb and expected pCO2/bicarb
Metabolic Acidosis
Expected pCO2= 1.5[HCO3] + 8 ± 2
Metabolic Alkalosis
10 increase HCO3 : 7 increase pCO2
Resp Acidosis Acute
10 increase pCO2 : 1 increase HCO3
Resp Acidosis Chronic
10 increase pCO2 : 4 increase HCO3
Resp Alkalosis Acute
10 decrease pCO2 : 2 decrease HCO3
Resp Alkalosis Chronic10 decrease oCO2 : 4 decrease HCO3
A systematic approach to acid-base (cont’d)
1.
Is the patient acidemic or alkalemic?
Action: Determine blood pH (pH <7.38 acidemia; pH >7.42 alkalemia)
2.
Is the primary disturbance metabolic or respiratory?
Action: Use CO2 and bicarbonate level to figure out the primary disturbance
3.
If a primary respiratory disturbance is present, is it acute or chronic?
Action: Compare measured pH with expected pH
4.
Is compensation appropriate?
Action: Compare measured pCO2/bicarb and expected pCO2/bicarb
5.
Is there an increased anion gap?
Action: Calculate anion gap (AG = Na – (Cl + HCO3))
Normal anion gap 12 mEq/L.
6.
Are other metabolic disturbances present in the patient with an
anion gap metabolic acidosis?
Action: Calculate delta/delta
A systematic approach to acid-base (cont’d)
6. Are other metabolic disturbances present in the patient with an anion
gap metabolic acidosis?
Action: Calculate delta/delta
Delta AG / Delta Bicarb = (12 – AG) / (24 – HCO3)
If ratio is ~ 1, pure AG metabolic acidosis
If ratio is < 1, suggests concurrent non-AG metabolic acidosis is present
If ratio is ≥ 2, suggests that metabolic alkalosis is present
Evaluation of oxygenation.
Calculating the alveolar-arterial gradient can help determine whether there
is a primary defect in gas exchange or whether hypoxemia is due to
extrinsic factors.
A-a gradient = PA O2 – Pa O2.
A-a gradient = FiO2 (Barometric P – Water P) – (PaCO2)/0.8 – PaO2.
A-a gradient = 150 – (PaCO2)/0.8 – PaO2 (under standard conditions)
A-a gradient increases with age.
Normal ≤ 0.21 x age + 2.5 or
age/4 + 2.5
or
0.29 x age
There are 5 causes of hypoxemia:
Increased A-a gradient
Normal A-a gradient
1.
1.
2.
3.
V/Q mismatch (asthma,
COPD, alveolar disease,
pulmonary vascular disease,
PE, pulmonary HTN).
R->L shunting (does NOT
respond to 100% O2)
Decreased diffusion (does
NOT respond well to suppl
O2)
** Low mixed venous O2 will
contribute to hypoxemia in all
of the above causes
2.
Low inspired FiO2 (high
altitude)
Hypoventilation. Will always
have high PCO2 associated
with hypoxemia.
Case I
A 38-year-old man with a 2-day history of nausea,
vomiting and diarrhea presents to the emergency
department because of weakness and dizziness.
ABG 7.20/25/
Na = 130 mEq/L; K = 3.2 mEq/L; Cl 80 mEq/L; HCO3 = 10 mEq/L
1.
2.
3.
What acid/base disturbance is present?
What additional laboratory studies you may order for work up of
this acid-base disorder?
What conditions may affect the anion gap?
Case II
A 22-year-old heroin addict is brought to you comatose.
ABG 7.00/80/44
Na = 140; K = 3.2; Cl 80; HCO3 = 20; BUN = 28; Glu = 180
1.
2.
3.
4.
What acid/base disturbance is present?
What additional laboratory studies you may order for work up of
this acid-base disorder?
What is the differential diagnosis for respiratory acidosis in this
patient?
What is her A – a gradient?
Case III
A 24-year-old man with AIDS presents to the ED with a 5day history of progressive shortness of breath, cough and
fevers. Except for fever, tachycardia and tachypnea his
physical exam is normal. CXR is taken. The film is
overpenetrated, but appears normal. His oxygen
saturation by oximetry is 93% but you ask for an ABG
anyway.
ABG 7.46/20/60
1.
2.
3.
Na = 129 mEq/L; Cl = 102 mEq/L; HCO3 = 15 mEq/L.
What acid/base disturbance is present?
What is the oxygenation status (A – a gradient)?
What do you suspect is the cause of his symptoms? What additional
studies you may consider to order?
Case IV
ABG 7.43/46/86
Na = 134 mEq/L; Cl 86 mEq/L; HCO3 = 36 mEq/L.
1.
2.
3.
What is the primary acid-base disturbance?
What is the differential?
What additional tests you may consider ordering to
narrow down the potential causes?
References
1. Morganroth, ML. Six steps to acid-base analysis: Clinical applications.
The Journal of Crit Ill. 1990; 5; 460 – 469.
2. Up To Date