Arterial Blood Gas Analysis

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Arterial Blood Gas Analysis

• October 27, 2009
• Prepared by Dr. Trey Woods D.O.
• Presented by Dr. Nick Cardinal D.O.

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What is an ABG?

• The Components
• pH / PaCO2 / PaO2 / HCO3 / O2sat / BE
• Desired Ranges
• pH - 7.35 - 7.45
• PaCO2 - 35-45 mmHg
• PaO2 - 80-100 mmHg
• HCO3 - 21-27
• O2sat - 95-100
• Base Excess - /-2 mEq/L

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ABG analysis

• Why do we care ?
• Critical care requires a good understanding
• Helps in the differential and final diagnosis
• Helps in determining treatment plan
• Treating acid/base disorders helps medications
  work better (i.e. antibiotics, vasopressors,
  etc.)
• Helps in ventilator management
• Severe acid/base disorders may need dialysis
• Changes in electrolyte levels in acidosis
  (increased K and Na, and decreases in HCO3)

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Logistics

• When to order an arterial line --
• Need for continuous BP monitoring
• Need for multiple ABGs
• Where to place -- the options
• Radial
• Femoral
• Brachial
• Dorsalis Pedis
• Axillary

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Acid Base Balance

• The body produces acids daily
• 15,000 mmol CO2
• 50-100 mEq Nonvolatile acids
• The lungs and kidneys attempt to maintain balance

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Acid Base Balance

• Assessment of status via bicarbonate-carbon
  dioxide buffer system
• CO2 H2O lt--gt H2CO3 lt--gt HCO3- H
• ph 6.10 log (HCO3 / 0.03 x PCO2)

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The Terms

• ACIDS
• Acidemia
• Acidosis
• Respiratory
• ?CO2
• Metabolic
• ?HCO3

BASES Alkalemia Alkalosis Respiratory
?CO2 Metabolic ?HCO3
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Transport of CO2 In the Blood

• At rest 100ml of blood transports 4 ml CO2 from
  tissue to lungs. CO2 in blood affects acid-base
  balance.
• CO2 is transported in blood in three forms
• Dissolved CO2, bicarb, comb with proteins as
  carbamino cmpds.
• Dissolved 0.36ml of CO2 /100ml blood (9 of
  all)
• Bicarbonate reacts wit water in blood to form
  carbonic acid and then bicarb (accounting for
  60-70 of CO2 transport to tissues).
• Carbonic acid formed in RBC dissoc into H and
  bicarb ions.
• H bind to Hb making it reduced, a better proton
  acceptor, this helps in peripheral blood with
  loading of CO2.
• Deoxygenation of blood increases its ability to
  carry CO2 Haldance Effect

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Transport of CO2 In the Blood

• Carbaminohemoglobin and carbaminoproteins Are
  formed from CO2 with terminal amine groups in
  blood proteins. Ie globin of hemoglobin HbCO2
• This occurs with a very loose bond allowing easy
  release in the alveoli, where the PCO2 lower than
  tissue capillaries. Unloading of O2 in
  peirpheral capillaries facilitates the loading of
  CO2 .
• CO2 can be carried to the lungs in combo with Hb
  about 20-30 of total, about 1.5ml of CO2 in each
  100 ml of blood.

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Change in Acidity during CO2 Transport

• CO2 transport has profound effect on acid-base
  status of blood.
• Partial pressure of arterial oxygen
• PaO2 normal 90-100mm Hg
• PaO2 reflects the functional capabilities of the
  lungs and determines the rate at which O2 enters
  the tissues.
• Factors that affect PaO2
• Va, FIO2, Altitude, age, and oxyhb dissoc. curve

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Partial pressure of arterial oxygen

• Alveolar Ventilation (Va)
• If the pt hyperventilates PaCO2 tends to fall and
  PaO2 rise
• If PaCO2 Falls by 1mm Hg then PaO2 rises by
  1.-1.2mmHg
• This is how lungs make up for some pulm
  dysfuntion, by hyperventilating.
• FIO2 is often not considered well in evaluating
  PaO2
• O2 by nasal cannula actual delivered FIO2 is
  25-30.
• Mask inhaled FIO2 is usually half that delivered
  to the mask
• EXPECTED PaO2 multiply percentage by 6.
• ie 60 O2 x 6360mm HG

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Partial pressure of arterial oxygen

• Altitude
• Greater altitude, the lower the PO2
• PaO2 drops about 3-4mm Hg for each 1000 foot rise
  above sea level.
• Ie 30,000 feet inspired air air at barometric
  pressure of 226 mm Hg PaO2 is only 21mm Hg
• Age
• PaO2 drops 3-4mm Hg per decade after the patient
  reaches 20-30 yrs of age.

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Alveolar-Arterial Oxygen difference

• Determine degree to which lung function is
  impaired use P(A-a)O2
• Usually P(A-a)O2 should be 10 plus 1/10th pts
  age.
• P(A-a)O2 of 20-30 mm Hg mild pulm dysfuntion
• P(A-a)O2 of greater than 50 mm Hg on room air
  usually indicates severe pulmonary dysfunction.
  The cause of Increase A-a gradient include
• Intrapulmonary shunt (less ventilation than
  perfusion, or a V/Q ratio) intracardiac shunt,
  and diffusion abnormalities.

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Shunting in the lung

• Four types of alveolar capillary units
• 1st vent and perfuse are normal then unit is
  normal
• 2nd is if there is vent without perfuse, the unit
  is considered to be dead space (of high V/Q)
• 3rd if there is perfuse without vent, unit is R?L
  shunt or (low V/Q
• 4th if there is neither vent nor perfuse, unit is
  silent
• Shunt is the fraction of blood passing the lung
  without being oxygenated.

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Oxygen Content

• O2 is carried in blood either dissolved or on hb.
• Fully saturated hb can carry 1.34ml of O2 , thus
  a pt with hb 15 can carry 20.1 ml of O2 per
  100ml
• PaO2

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Oxyhemoglobin Saturation

• PaO2 of 60mm Hg correlates to and SaO2 of 90
• Hb is 15 and tissue removes 5.0ml of oxygen from
  each 100ml of blood.
• Factors that affect curve
• Left shift
• Alkalosis, hypothermia, abnormal and fetal
  hemoglobin, carboxyhemoglobin, methemoglobin, CO,
  Decreased 2,3 DPG
• Right Shift
• Acidosis, Increased Pco2
• Hyperthermia
• Increased 2,3 DPG

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Acid Base Disturbances
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The Anion Gap

• Na (Cl HCO3)
• NaHCO3 HCL ? NaCL H2CO3
• NaHCO3 HX? NaX H2CO3
• Unmeasured cations calcium, magnesium, gamma
  globulins, potassium.
• Unmeasured anions albumin, phosphate, sulfate,
  lactate.

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Gap Acidosis

• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde
• INH
• Lactic acidosis
• Ethylene Glycol
• Salicylate

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Non Gap Acidosis

• H hyperalimentation
• A acetazolamide
• R RTA
• D diarrhea
• U rectosigmoidostomy
• P pancreatic fistula

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Metabolic Acidosis

• Respiratory compensation process takes 12-24
  hours to become fully active. Protons are slow to
  diffuse across the blood brain barrier. In the
  case of LA this will be faster because LA is
  produced in the brain.
• The degree of compensation can be assessed by
  using Winters Formula. It is INAPPROPRIATE to
  use this formula before the acidosis has existed
  for 12-24 hours.
• PCO2 1.5 (HCO3) 8 /-2.
• ?pH, ?HCO3

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Decreased anion gap

• Decrease in unmeasured anions
• Hypoalbuminemia
• Increase in unmeasured cations
• Hypercalcemia
• Hypermagnesemia
• Hyperkalemia
• Multiple myeloma
• Lithium toxicity

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Metabolic Alkalosis

• Generation by gain of HCO3 and maintained by
  abnormal renal HCO3 absorption.
• This is almost always secondary to volume
  contraction (low Cl in urine, responsive to NaCl,
  maintained at proximal tubule)
• Vomiting net loss of H and gain of HCO3.
• Diuretics ECFV depletion
• Chronic diarrhea ECFV depletion
• Profound hypokalemia
• Renal failure if we cannot filter HCO3 we cannot
  excrete it.
• Mineralocorticoid excess increased H secretion,
  hypokalemia (Na/K exchanger), saline resistant).

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Metabolic Alkalosis

• ?pH, ?HCO3
• ?PCO2 by 0.7 for every 1mEq/L ? in HCO3

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Respiratory Acidosis

• Acute or Chronic has the kidney had enough time
  to partially compensate?
• The source of the BUFFER (we need to produce
  bicarb) is different in these states and thus we
  need to make this distinction.
• ?ph, ?CO2, ?Ventilation

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Respiratory Acidosis

• Acute H is titrated by non HCO3 organic tissue
  buffers. Hb is an example. The kidney has little
  involvement in this phase.
• 10 mm Hg increase in CO2 / pH should decrease by
  .08
• Chronic The mechanism here is the renal
  synthesis and retention of bicarbonate. As HCO3
  is added to the blood we see that Cl will
  decrease to balance charges.
• This is the hypochloremia of chronic metabolic
  acidosis.
• 10 mm H increase in CO2 / pH should decrease by
  .03

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Respiratory Acidosis

• Elevation of CO2 above normal with a drop in
  extracellular pH.
• This is a disorder of ventilation.
• Rate of CO2 elimination is lower than the
  production
• 5 main categories
• CNS depression
• Pleural disease
• Lung diseases such as COPD and ARDS
• Musculoskeletal disorders
• Compensatory mechanism for metabolic alkalosis

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Respiratory Alkalosis

• Initiated by a fall in the CO2 ? activate
  processes which lower HCO3.
• Associated with mild hypokalemia. Cl is retained
  to offset the loss of HCO3 negative charge.
• Acute response is independent of renal HCO3
  wasting. The chronic compensation is governed by
  renal HCO3 wasting.
• Causes
• Intracerebral hemorrhage
• Drug use salicylates and progesterone
• Decreased lung compliance Anxiety
• Liver cirrhosis
• Sepsis

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Mixed Acid-Base Disorders

• Patients may have two or more acid-base disorders
  at one time
• Delta Gap
• Delta HCO3 HCO3 Change in anion gap
• gt24 metabolic alkalosis

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Arterial Blood Gas (ABG) Analysis

• ABG interpretation
• Follow rules and you will always be right !!
• 1) determine PH
• acidemia or alkalemia
• 2) calculate the anion gap
• 3) determine Co2 compensation (winters
  formula)
• 4) calculate the delta gap (delta HCO3)

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ABG analysis

• Arterial Blood Gas (ABG) interpretation
• Always evaluate PH first
• Alkalosis PH gt 7.45
• Acidosis PH lt 7.35
• Determine anion gap (AG) AG NA (HCO3 CL)
• AG metabolic acidosis
• Non AG acidosis determined by delta gap
• Winters formula
• Calculates expected PaCO2 for metabolic acidosis
• PaCO2 1.5 x HCO3 8

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ABG analysis

• Delta gap
• Delta HCO3 HCO3 (electrolytes) change in AG
• Delta gap lt 24 non AG acidosis
• Delta gap gt 24 metabolic alkalosis
• Note The key to ABG interpretation is following
  the above steps in order.

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• Look at the pH.
• pH lt 7.35, acidosis
• pH gt 7.45, alkalosis
• Look at PCO2, HCO3-
• Main pathology will be the change correlates with
  the pH.
• If alkalosis pCO2 will be low or Bicarb high
• If acidosis pCO2 will be high or Bicard low
• The other abnormal parameter is the compensator
  response
• Respiratory or Metabolic
• pCO2 - respiratory
• Bicarb - metabolic

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• Metabolic Acidosis? Anion Gap?
• gt12 - ketoacidosis, uremia, lactic acidosis, or
  toxins
• Delta ratio to check for gap and non gap
  disorders , or metabolic alkalosis happening
  simultaneously
• Normal anion gap - diarrhea OR unknown. If
  unknown calculate urine anion gap, if positive
  likely RTA, if neg liekly diarrhea
• Metabolic Alkalosis
• If urin Cl is gt 20 it is chloride-resistant
  alkalosis (increased mineralcorticoid activity
• If lt20 chloride responsive alkalosis (vomitting
  or gastric loss)

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Sample Problem 1

• An ill-appearing alcoholic male presents with
  nausea and vomiting.
• ABG - 7.4 / 41 / 85 / 22
• Na- 137 / K- 3.8 / Cl- 90 / HCO3- 22

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Sample Problem 1

• Anion Gap 137 - (90 22) 25
• ? anion gap metabolic acidosis
• Winters Formula 1.5(22) 8 2
• 39 2
• ? compensated
• Delta Gap 25 - 10 15
• 15 22 37
• ? metabolic alkalosis

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Sample Problem 2

• 22 year old female presents for attempted
  overdose. She has taken an unknown amount of
  Midol containing aspirin, cinnamedrine, and
  caffeine. On exam she is experiencing
  respiratory distress.

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Sample Problem 2

• ABG - 7.47 / 19 / 123 / 14
• Na- 145 / K- 3.6 / Cl- 109 / HCO3- 17
• ASA level - 38.2 mg/dL

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Sample Problem 2

• Anion Gap 145 - (109 17) 19
• ? anion gap metabolic acidosis
• Winters Formula 1.5 (17) 8 2
• 34 2
• ? uncompensated
• Delta Gap 19 - 10 9
• 9 17 26
• ? no metabolic alkalosis

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Sample Problem 3

• 47 year old male experienced crush injury at
  construction site.
• ABG - 7.3 / 32 / 96 / 15
• Na- 135 / K-5 / Cl- 98 / HCO3- 15 / BUN- 38 / Cr-
  1.7
• CK- 42, 346

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Sample Problem 3

• Anion Gap 135 - (98 15) 22
• ? anion gap metabolic acidosis
• Winters Formula 1.5 (15) 8 2
• 30 2
• ? compensated
• Delta Gap 22 - 10 12
• 12 15 27
• ? mild metabolic alkalosis

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Sample Problem 4

• 1 month old male presents with projectile emesis
  x 2 days.
• ABG - 7.49 / 40 / 98 / 30
• Na- 140 / K- 2.9 / Cl- 92 / HCO3- 32

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Sample Problem 4

• Metabolic Alkalosis, hypochloremic
• Winters Formula 1.5 (30) 8 2
• 53 2
• ? uncompensated

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ABG analysis

• 33 y/o with DKA presents with the following
• Na 128, Cl 90, HCO3 4, Glucose 800
• 7.0/14/90/4/95
• PH acidemia
• AG 128 (90 4) 34
• Winters formula 1.5(4) 8 14
• Delta gap 4 (34 12) 26

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ABG analysis

• Answer
• AG acidosis with appropriate respiratory
  compensation
• History c/w ketoacidosis secondary to DKA with
  appropriate respiratory compensation

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ABG analysis

• 56 y/o with COPD exacerbation and hypotension and
  associated diarrhea x 7 days presents with the
  following ABG
• 7.22/30/65/10/90
• PH(7.22) acidemia
• AG 139 (10 110) 19 (nl AG 8-12)
• Winters formula
• PaCO2 1.5 (HCO3) 8 1.5 (10) 8 23
• Delta gap
• Delta gap HC03 change in the AG 24
• Delta gap 10 (19 12) 10 7 17
• Delta gap 17

139
110
20
120
4.0
10
1.5
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ABG - example

• Triple disorder
• AG acidosis -
• Incomplete respiratory compensation
• Non AG acidosis
• History would suggest AG acidosis is secondary to
  hypotension with lactic acid build up and the
  patient is not able to compensate with his COPD
  therefore there is no respiratory compensation
  and the non AG acidosis is secondary to diarrhea
  with associated HCO3 loss.

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Extra Problems
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Example 1

• 44 yo M 2 weeks post-op from total
  proctocolectomy for ulcerative colitis.
• Na 134, K 2.9, Cl- 108, HCO3- 16, BUN 31, Cr
  1.5
• BG 7.31/ 33 /93 / 16

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Example 2

• 9 yo M presents with N/V.
• Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 650
• BG 7.27/23/96/11/-8

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Example 3

• 70 yo M s/p lap chole, on the morning of POD 1.
  Pt received 2L bolus of crystalloid throughout pm
  for tachycardia. Now with SOB.
• 7.24 / 60 / 52 / 27 /3

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Example 4

• 54 yo F s/p mult debridements for necrotizing
  fasciitis, now on vassopressin to maintain blood
  pressure
• BG - 7.29/40/83/17/-6

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Example 5

• 35 yo M involved in crush injury, boulder vs
  body.
• Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38, Cr 1.7,
  CK 42,346
• BG 7.30/32/96/15/-4

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Example 6

• 4 wks M with projectile emesis
• Na 140, K2.9, Cl 92
• 7.49/40/98/30/6