Interpretation of Arterial Blood Gases and Acid-Base Disorders

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Interpretation of Arterial Blood Gases and
Acid-Base Disorders

• Niki Paphitou, MD, FRCPC, FCCP
• Critical Care-Infectious Diseases,
• NGH ICU

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Normal Arterial Blood Gas Values

• pH 7.35-7.45
• PaCO2 35-45 mm Hg
• PaO2 70-100 mm Hg
• SaO2 95-100
• HCO3- 22-26 mEq/L
  
• MetHb lt2.0
• COHb lt3.0
• CaO2 16-22 ml O2/dl
• At sea level, breathing ambient air
  Age-dependent

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Gas Exchange 3 Key Equations For Evaluation Of

• 1) PaCO2 equation Evaluating alveolar
  ventilation
• 2)Alveolar gas equation Evaluating oxygen
  transfer at the alveolar level
• 3)Oxygen content equation Evaluating oxygen
  transfer at the tissue level

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PaCO2 equation PaCO2 reflects ratio of
metabolic CO2 production to alveolar ventilation

• VCO2 x 0.863 VCO2 CO2
  production
• PaCO2 ----------------- VA VE VD
• VA VE minute (total) ventilation
• VD dead space ventilation
  0.863 converts units to mm Hg
• Condition State of
• PaCO2 in blood alveolar ventilation
• gt45 mm Hg Hypercapnia Hypoventilation
• 35 - 45 mm Hg Eucapnia Normal
  ventilation
• lt35 mm Hg Hypocapnia Hyperventilation

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Hypercapnia

• VCO2 x 0.863
• PaCO2 ------------------
• VA
• The only physiologic reason for elevated
  PaCO2 is inadequate alveolar ventilation (VA) for
  the amount of the bodys CO2 production (VCO2).
  Since alveolar ventilation (VA) equals minute
  ventilation (VE) minus dead space ventilation
  (VD), hypercapnia can arise from insufficient VE,
  increased VD, or a combination.

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Hypercapnia

• VCO2 x 0.863
• PaCO2 ------------------
• VA VA VE VD
• Examples of inadequate VE leading to decreased VA
  and increased PaCO2 sedative drug overdose
  respiratory muscle paralysis central
  hypoventilation
• Examples of increased VD leading to decreased VA
  and increased PaCO2 chronic obstructive
  pulmonary disease severe pulmonary embolism,
  pulmonary edema.

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Physiologic effects of hypercapnia

• 1) An elevated PaCO2 will lower the PAO2 (see
  Alveolar gas equation), and as a result lower the
  PaO2.
• 2) An elevated PaCO2 will lower the pH (see
  Henderson-Hasselbalch equation).
• 3) The higher the baseline PaCO2, the greater it
  will rise for a given fall in alveolar
  ventilation, e.g., a 1 L/min decrease in VA will
  raise PaCO2 a greater amount when baseline PaCO2
  is 50 mm Hg than when it is 40 mm Hg.

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PCO2 vs. Alveolar Ventilation

• The relationship is shown for metabolic carbon
  dioxide production rates of 200 ml/min and 300
  ml/min (curved lines). A fixed decrease in
  alveolar ventilation (x-axis) in the hypercapnic
  patient will result in a greater rise in PaCO2
  (y-axis) than the same VA change when PaCO2 is
  low or normal.
• This graph also shows that, if alveolar
  ventilation is fixed, an increase in carbon
  dioxide production will result in an increase in
  PaCO2.

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Alveolar Gas Equation
PAO2 PIO2 - 1.2 (PaCO2) where PAO2 is the
average alveolar PO2, and PIO2 is the partial
pressure of inspired oxygen in the trachea
PIO2 FIO2 (PB 47 mm Hg) FIO2 is fraction of
inspired oxygen and PB is the barometric
pressure. 47 mm Hg is the water vapor pressure
at normal body temperature.
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Alveolar Gas Equation

• If FIO2 and PB are constant, then as PaCO2
  increases both PAO2 and PaO2 will decrease
  (hypercapnia causes hypoxemia).
• If FIO2 decreases and PB and PaCO2 are constant,
  both PAO2 and PaO2 will decrease.
• If PB decreases (e.g., with altitude), and PaCO2
  and FIO2 are constant, both PAO2 and PaO2 will
  decrease (mountain climbing causes hypoxemia).

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P(A-a)O2

• P(A-a)O2 is the alveolar-arterial difference in
  partial pressure of oxygen. It is commonly
  called the A-a gradient. It results from
  gravity-related blood flow changes within the
  lungs (normal ventilation-perfusion imbalance).
• Normal P(A-a)O2 ranges from 5 to 25 mm Hg
  breathing room air (it increases with age). A
  higher than normal P(A-a)O2 means the lungs are
  not transferring oxygen properly from alveoli
  into the pulmonary capillaries. Except for right
  to left cardiac shunts, an elevated P(A-a)O2
  signifies some sort of problem within the lungs.

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Physiologic causes of low PaO2

• NON-RESPIRATORY P(A-a)O2Cardiac right to left
  shunt Increased
• Decreased PIO2 Normal
• RESPIRATORYPulmonary right to left
  shunt IncreasedVentilation-perfusion
  imbalance IncreasedDiffusion barrier Increase
  dHypoventilation (increased PaCO2) Normal

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Ventilation-Perfusion imbalance

• A normal amount of ventilation-perfusion (V-Q)
  imbalance accounts for the normal P(A-a)O2.
• By far the most common cause of low PaO2 is an
  abnormal degree of ventilation-perfusion
  imbalance within the hundreds of millions of
  alveolar-capillary units. Virtually all lung
  disease lowers PaO2 via V-Q imbalance, e.g.,
  asthma, pneumonia, atelectasis, pulmonary edema,
  COPD.
• Diffusion barrier is seldom a major cause of low
  PaO2 (it can lead to a low PaO2 during exercise).

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SaO2 and oxygen content

• How much oxygen is in the blood? Oxygen content
  CaO2 (mlO2/dl).
• CaO2 quantity O2 bound quantity
  O2 dissolved to hemoglobin
  in plasmaCaO2 (Hb x 1.34 x SaO2)
  (.003 x PaO2)
• Hb hemoglobin in gm 1.34 ml O2 that can be
  bound to each gm of Hb SaO2 is percent
  saturation of hemoglobin with oxygen .003 is
  solubility coefficient of oxygen in plasma .003
  ml dissolved O2/mm Hg PO2.

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Oxygen dissociation curve SaO2 vs. PaO2 Also
shown are CaO2 vs. PaO2 for two different
hemoglobin contents 15 gm and 10 gm. CaO2
units are ml O2/dl. P50 is the PaO2 at which
SaO2 is 50.
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SaO2 is it calculated or measured?

• SaO2 is measured in a co-oximeter. The
  traditional blood gas machine measures only pH,
  PaCO2 and PaO2,, whereas the co-oximeter measures
  SaO2, carboxyhemoglobin, methemoglobin and
  hemoglobin content. Newer blood gas consoles
  incorporate a co-oximeter, and so offer the
  latter group of measurements as well as pH, PaCO2
  and PaO2.
• Always make sure the SaO2 is measured, not
  calculated. If it is calculated from the PaO2
  and the O2-dissociation curve, it provides no new
  information, and could be inaccurate --
  especially in states of CO intoxication or excess
  methemoglobin. CO and metHb do not affect PaO2,
  but do lower the SaO2.

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Carbon monoxide an important cause of hypoxemia

• Normal COHb in the blood is 1-2, from
  metabolism and small amount of ambient CO (higher
  in traffic-congested areas)
• All smokers have excess CO in their blood.
• CO binds _at_ 200x more avidly to hemoglobin than
  O2, displacing O2 from the heme binding sites.
• CO 1) decreases SaO2 by the amount of COHb
  present, and 2) shifts the O2-dissociation curve
  to the left, retarding unloading of oxygen to the
  tissues.
• CO does not affect PaO2, only SaO2. To detect CO
  poisoning, SaO2 and/or COHb must be measured
  (requires co-oximeter). In the presence of
  excess CO, SaO2 (when measured) will be lower
  than expected from the PaO2.

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CO does not affect PaO2!

• A patient presented to the ER with headache and
  dyspnea.
• His first blood gases showed PaO2 80 mm Hg, PaCO2
  38 mm Hg, pH 7.43. SaO2 on this first set was
  calculated from the O2-dissociation curve at 97,
  and oxygenation was judged normal.
• He was sent out from the ER and returned a few
  hours later with mental confusion this time both
  SaO2 and COHb were measured (SaO2 shown by X)
  PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2 53,
  carboxyhemoglobin 46.
• CO poisoning was missed on the first set of blood
  gases because SaO2 was not measured!

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Causes of Hypoxia

• 1. Hypoxemia (low PaO2 and/or low CaO2)
• a. reduced PaO2 usually from lung disease
  (most common physiologic mechanism V-Q
  imbalance)
• b. reduced SaO2 -- most commonly from reduced
  PaO2 other causes include carbon monoxide
  poisoning, methemoglobinemia, or rightward shift
  of the O2-dissociation curve
• c. reduced hemoglobin content -- anemia
• 2. Reduced oxygen delivery to the tissues
• a. reduced cardiac output -- shock, congestive
  heart failure
• b. left to right systemic shunt (as may be seen
  in septic shock)
• 3. Decreased tissue oxygen uptake
• a. mitochondrial poisoning (e.g., cyanide
  poisoning)
• b. left-shifted hemoglobin dissociation curve
  (e.g., from acute alkalosis, excess CO, or
  abnormal hemoglobin structure)

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Acid-Base Disorders A Systematic (step by
step) Approach
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Terminology

• Acidemia blood pH lt 7.35
• Alkalemia blood pH gt 7.45
• Acidosis a physiologic process that tends to
  cause acidemia
• Alkalosis a physiologic process that tends to
  cause alkalemia

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Step 1 Do the numbers make sense?

• Check for Internal consistency by using the
  Henderson-Hasselbach equation
• H 24 X PaCO2 / HCO3-

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Step 1 Internal consistency of ABGs

• PH is inversely related to H a pH change
  of 1.00 represents a 10-fold change in H
• pH H in nanomoles/L
• 7.00 100
• 7.10 80
• 7.30 50
• 7.40 40
• 7.52 30
• 7.70 20
• 8.00 10

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Step 1 Internal consistency of ABGs

• Examples Do these numbers have internal
  consistency?
• A man with sepsis has the following values
• PH 7.5, PaCO2 40, HCO3- 20.
• A woman with renal failure has the following
  PH 7.3, PaCO2 40, HCO3- 10.
• A diabetic child has the following
• PH 7.3, PaCO2 21 HCO3- 10.

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Step 2 Alkalemia or Acidemia?

• Determine whether an acidemia (PH lt 7.35) or an
  alkalemia (PH gt 7.45) is present.
• This usually signifies the primary disorder.
• Keep in mind The PH may be in normal range but a
  mixed disorder is present (look at the
  bicarbonate, PaCO2, anion gap).

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Step 3 Is the primary disturbance metabolic or
respiratory?

• Does any change in the PaCO2 account for the
  direction of the change in PH?

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Step 4 Is there appropriate compensation for the
primary disturbance?

• The bodys homeostatic mechanisms serve to return
  the ratio of bicarbonate to PaCO2 toward normal
  and thus normalize the PH.
• In most cases the compensatory mechanisms fail to
  fully return the PH to normal.

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Step 4 Appropriate compensation in simple
Acid-Base disorders

• Metabolic acidosis
• PCO2 (1.5 X HCO3-) 82
• Metabolic alkalosis
• PCO2 40 0.6 X ?HCO3-
• Respiratory acidosis
• Acute HCO3- 24 0.1 X ? PCO2
• Chronic HCO3- 24 0.3 X ? PCO2
• Respiratory alkalosis
• AcuteHCO3- 24 0.2X ? PCO2
• ChronicHCO3- 24 0.4X ? PCO2

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Step 5 Calculate the anion gap

• The total body concentration of anions cations.
• AG Na (Cl- HCO3-).
• The AG accounts for unmeasured anions such as
  endogenous acids (Phosphates, sulfates, etc) and
  cations such as albumin.
• Normally the unmeasured anions exceed the
  unmeasured kations.
• Normal value is 122.
• Low anion gap can be caused by low serum albumin.

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Step 5 Calculate the anion gap

• Calculation of the AG is crucial in metabolic
  acidosis.
• When the AG is high this signifies a rise in an
  unmeasured anion such as an endogenous acid
  (lactate, ketoacids) OR presence of an exogenous
  acid (methanol, ethylene glucol, salicylates
  etc).
• An exogenous compound with osmolar molecules
  (methanol, ethylene glygol etc) will create an
  osmolar gap Measured serum osmolality
  calculated serum osmolality. Normally lt 10
  mOsm/l.
• Calc. Osmol 2 x Na glucose/18 BUN/2.8

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Step 6 Calculate the Delta AG

• Compare the change in AG with the change in serum
  bicarbonate.
• Useful to identify additional or hidden metabolic
  disorders.
• In a simple metabolic acidosis, the change in
  AGthe decrease in bicarbonate i.e
• DAGD HCO3 or
• measured AG-12 24- measured HCO3

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Step 6 Calculate the Delta AG

• If the decrease in bicarbonate is more than the
  rise in the AG, concurrent with the AG metabolic
  acidosis there is also a second type of metabolic
  acidosis present, a non-AG metabolic acidosis.
• If the decrease in bicarbonate is less than the
  rise in AG, a metabolic alkalosis is
  concurrently present with the AG metabolic
  acidosis.

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Respiratory acidosis-Etiology

• Upper airway obstruction
• Lower airway obstruction
• Cardiogenic or non-cardiogenic pulmonary edema
• Pneumonia
• Pulmonary emboli
• Fat emboli
• Central nervous system depression
• Neuromascular impairment
• Ventilatory restriction

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Respiratory alkalosis-Etiology

• Central nervous system stimulation Fever, pain,
  fear, cerebrovascular accident, CNS infection,
  trauma, tumor.
• Hypoxia High altitude, profound anemia,
  pulmonary disease.
• Stimulation of chest receptors Pulmonary edema,
  pulmonary emboli, pneumonia, pneumothorax,
  pleural effusion.
• Drugs or hormones Salicylates,
  medroxyprogesterone, catecholamines.
• Miscellaneous Sepsis, pregnancy, liver disease,
  hyperthyroidism.

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Metabolic Acidosis

• Elevated AG acidosis
• Ketoacidosis Diabetic, starvation, alcoholic.
• Lactic acidosis.
• Uremia (phosphates, sulfates, organic anions).
• Toxins Ethylene glycol, methanol, salicylate.

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Metabolic Acidosis

• Normal AG acidosis
• The fall in bicarbonate is matched by a
  proportional rise in serum chloride
  (hyperchloremic metabolic acidosis).
• Most common causes are gastrointestinal and renal
  loses of bicarbonate.
• More rarely, it is caused by rapid dilution of
  the plasma bicarbonate by saline.

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• Normal AG metabolic acidosis- etiology
• GI losses
• Diarrhea
• Ileostomy, pancreatic or bile drainage
• Renal losses
• Renal insufficiency
• Proximal RTA
• Distal RTA
• Type 4 RTA
• Acetazolamide
• Rapid saline administration

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Normal AG metabolic acidosis GI or Renal loss of
bicarbonate?

• Calculate the urine anion gap (UAG)
• It provides information on whether the kidney is
  able to produce ammonium (NH4)
• UAG UK UNa - UCl-
• A negative UAG suggests that there is NH4
  present in the urine , ie the kidney is able to
  excrete hydrogen kations and regenerate
  bicarbonate. Therefore the bicarbonate losses are
  from the GI tract. The opposite is true with a
  positive UAG.

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Metabolic alkalosis

• Most common cause is volume depletion, urine Cl-
  is low and the alkalosis resolves after volume
  replacement (vompiting, NG suction).
• Can also occur with bicarbonate administration,
  mineralcorticoid excess, acetates in TPN,
  diuretics. Urine Cl- is 40 mEq/l.

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• Thank you..

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Case study 1

• A 25 y old asthmatic presents acutely short of
  breath to the ER with a PH of 7.56, pa CO2 20,
  HCO3 24 and
• 02 Sat. 96.

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Case study 2

• A 30 y old woman with a history of eating
  disorder comes to the ER with a change in mental
  status and vomiting. An empty bottle of aspirin
  is found in her bedroom.
• Na 134, K 4.3, Cl 90, HCO3 10, BUN 20,
  creatinine 0.7, PH 7.52, PaCO2 28,
• Pa O2 73, Sat. 93.

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Case study 3

• A 19 y old girl with type I DM and depression
  with alcoholism, has severe nausea and vomiting
  for several days. Lethargic, RR 34/min, HR
  120/min, BP orthostatic.
• Na 135, Cl 70, K 3.6, HCO3 19, BUN 21, Glucose
  580, sOsm. 315, PH 7.58, PaCO2 21, PaO2 104.

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Case study 4

• A 50 y old man with a history of renal transplant
  and baseline creatinine 2.0, is brought to the
  ICU with tachypnea and lethargic after surgery
  for VP shunt placement for NPH. His RR is 35, he
  moans to paiful stimuli BP 120/70, HR 120. He
  underwent cataracts surgery 10 days ago.
• Creatinine is 3.O, urea 40, HCO3 8,
• PH 7.10, Paco2 25, PaO2 9o on room air, Na
  134, CL96.