Download Blood Gases

Respiratory Pathophysiology: Arterial Blood Gases (Huda)
INTRODUCTION:

Importance: diagnosis and management of many acute and chronic medical disorders

Interpretation: must always be interpreted in relation to clinical history and status of the patient

Components of Arterial Blood Gas:
Oxygen: efficiency of oxygenation of blood as it passes through the lungs
CO2: efficiency of the respiratory system to remove CO2 (measure of ventilation)
pH: with CO2 indicates the acid-base status of the patient
OXYGEN:

Transport in the Blood:
Dissolved (PaO2): measured by arterial O2 tension (PaO2)
o Indicator of efficiency of oxygenation of blood as it passes through lung capillaries
Hb Bound (SaO2): measured by arterial O2 saturation (SaO2)
o Indicates the amount of Hb that is saturated with O2
Oxygen Content Calculation (CaO2):
o Equation: CaO2= (1.39 x Hb x SaO2) + (0.003 x PaO2)

Dissolved O2:
Alveolar Gas Equation: predicts the partial pressure of O2 in the alveolus (PAO2)
o Equation: PAO2= PIO2 – (PaCO2/R)

R= 0.8 (under normal dietary conditions)
 Note: can also MULTIPLY PaCO2 by 1.25

PIO2= partial pressure of inspired O2
 Equation: PIO2= (FIO2) x (Pb-PH2O)
o FIO2= 0.21
o Pb= 760mmHg (at sea level)
o PH2O= 47 mmHg
 Normal: 150mmHg at sea level

PaCO2= normally 40 mHg
o **PAO2= normally 100 mmHg**
Alveolar-Arterial Gradient (A-a Gradient):
o PaO2 and PAO2 are not normally the same: due to normal V/Q relationships, presence of physiological
shunts, and shape of oxyHb desaturation curve

A-a gradient= PAO2-PaO2
o Normal Values: 10mmHg in a healthy 20 year old (ie. PaO2=90mmHg if PAO2=100mmHg)

Increases 2.5mmHg per decade due to normal physiological changes in the lung
 Therefore, PaO2 decreases by 2.5mmHg per decade
o Increased A-a Gradient: implies primary parenchymal lung disease

OxyHb Dissociation Curve:
General: describes the relationship between PaO2 and SaO2
o Sigmoidal Shape: due to configurational changes in Hb

Uptake of O2 enhances the uptake of any remaining O2 until Hb is saturated
o Physiological Consequences of Sigmoidal Shape:

Increases of PaO2 on plateau phase do not really increase SaO2 (already saturated) or total O2
content of the blood

Steep middle phase means large changes in saturation for small changes in PaO2 (condition in
peripheral tissues to increase release of O2 where needed the most)

Nonlinear relationship of PaO2 and SaO2 provides a reserve of O2 in the blood
Important PaO2 and SaO2 Combinations:
o PaO2 27mmHg= SaO2 50% (P50): indicator of the position of the dissociation curve
o PaO2 40mmHg= SaO2 75%: partial pressure/saturation of O2 in mixed venous blood
o PaO2 55mmHg= SaO2 88%: partial pressure/saturation of O2 that qualifies patients for home O2
o PaO2 60mmHg= SaO2 90%: value at the beginning of the plateau phase of the curve (above this, there
are smaller changes in CaO2- generally considered lower limits of normal)
o PaO2 90mmHg= SaO2 97%: Hb near fully saturated
Shifts of the Curve:
o Right Shift: affinity of Hb for O2 is DECREASED and ability to release O2 is ENHANCED

Physiological Importance: normal mechanism for delivering increased O2 during times of O2
deficit

Factors Shifting Curve to the Right:
 Increased PaCO2 (Bohr effect)
 Decreased pH (increased H+ concentration)
 Elevated body temperature
 Increased 2,3-DPG
 Hemoglobinopathies (may be secondary to increase in 2,3-DPG)
o Left Shift: affinity of Hb for O2 is INCREASED and the ability to release O2 is LOWERED

Factors Shifting Curve to the Left:
 Decreased PaCO2 (Bohr effect)
 Increased pH (decreased H+ concentration)
 Decreased body temperature
 Decreased 2,3-DPG
 Hemoglobinopathies:
o Fetal Hb
o CarboxyHb (binding of CO)
o MetHb (oxidation of Fe moiety from ferrous to ferric state)

Seen with congenital deficiencies or oxidant drugs
CO2-BICARBONATE SYSTEM:

Biologic Buffer System: plays critical role in maintaining relatively narrow range of pH necessary in the body
Major Buffer System: CO2-Bicarb system
Other Buffers:
o Intracellular proteins
o Hb
o Plasma proteins

Relationship of CO2 and Bicarbonate Anion:
Bicarbonate Anion: present in most body fluids and constitutes a large reservoir of buffer
o H+ + HCO3-  H2CO3 (Carbonic Anhydrase) H2O +CO2
Henderson Hasselbach Equation:
o Ka= [H+][HCO3-]/[H2CO3]
o pH=pKa + log [HCO3-]/[H2CO3]

[H2CO3]= 0.03 x PaCO2
Normal Conditions:
o pH= 7.4
o pKa= 6.1
o log[HCO3-]/(0.03 x PaCO2)= 1.3
Other Situations:
o Metabolic Alkalosis= increased bicarbonate AND pH
o Metabolic Acidosis= decreased bicarbonate AND pH
o Respiratory Acidosis= increased PaCO2 with decreased pH
o Respiratory Alkalosis= decreased PaCO2 with increased pH

Transport of CO2 in the Blood (3 Forms):
Dissolved CO2: 5% of CO2 in arterial blood (measured by PaCO2)
Bicarbonate Anion: 90% of CO2 in arterial blood
o CO2 + H2O occurs rapidly in RBCs (presence of CA enzyme)
o HCO3- accumulates in RBCs and diffuses into plasma in exchange for Cl- (chloride shift)

H+ impermeable and therefore this shift needs to occur to preserve electrical neutrality
o H+ buffered by combining to Hb

Haldane Effect: buffering enhanced in tissues with low O2 content (Hb deoxygenated)
Carbamino Compounds: 5% of CO2 in arterial blood; formed by reaction of CO2 with terminal amino groups of
blood proteins
o Hb: major CO2 binding protein in the blood

CO2 Hb Dissociation Curve:
Linear relationship: between CO2 and Hb at physiologic concentrations
Haldane Effect:
o Curve is shifted to the left if Hb is deoxygenated (enhances the affinity of Hb for CO2)
o Curve is shifted to the right if Hb is oxygenated (decreases affinity of Hb for CO2)
ACID BASE DISORDERS:

Four Primary Disorders:
Respiratory Acidosis: primary increase in PaCO2, leading to a decreased pH
Respiratory Alkalosis: primary decrease in PaCO2, leading to a increased pH
Metabolic Acidosis: primary increase in acid or decrease in base, leading to a decreased HCO3- and pH
Metabolic Alkalosis: primary increase in base or decrease in acid, leading to increased HCO3- and pH

Compensatory Responses:
Essential: physiologic processes are dependent on the pH being kept in a normal range
o Body compensates for changes in PaCO2 or HCO3- to adjust the changes in pH back to normal
o pH and PaCO2 do not completely go back to normal
Metabolic Disturbances:
o General: ventilatory system compensates for changes in the acid/base status via the chemoreceptors

Adjust ventilation in response to the slightest changes in PaCO2 (negative feedback)
o Metabolic Acidosis: if an acid is added to the system, CO2 is formed by HCO3- and H+ combine

Increased CO2  Increased ventilation  Decreased PaCO2  Increased pH
o Metabolic Alkalosis: if a base is added to the system, the formation H+ ions is favored

Decreased CO2  Decreased ventilation  Increased PaCO2  Decreased pH
Respiratory Disturbances:
o General: the kidneys will compensate for a chronic change in the PaCO2 by adjusting the renal
absorption of HCO3- (takes 7-10 days for compensation)
o Respiratory Acidosis:

Increased PaCO2  Increased HCO3- absorption (increased acid secretion)
o Respiratory Alkalosis:

Decreased PaCO2  Decreased HCO3- absorption (decreased acid secretion)
COMPENSATION IS NEVER PERFECT: pH never returns to normal
INTERPRETING ABGs:

PaO2:
Normal: 90-100mmHg (healthy 20 year old breathing room air)
o Decreases by 2.5mmHg per decade
o PaO2= 100 –(age/3)

Acid-Base Status:
Normal Values:
o pH: 7.4
o PaCO2: 40mmHg
o HCO3-: 24 meq/L
Prediction of Compensatory Response:
o Primary Respiratory Disturbance:

Changes in pH:
 Acute: pH will decrease or increase 0.08 units per 10mmHg increase or decrease in
PaCO2
 Chronic: pH will decrease or increase 0.03 units per 10mmHg increase or decrease
in PaCO2

Changes in HCO3- (Chronic Disturbance Only):
 Acidosis: HCO3- will increase 3meq/L per 10 mmHg increase in PaCO2
 Alkalosis: HCO3- will decrease 3meq/L per 10mmHg decrease in PaCO2
o Primary Metabolic Disturbance:

Acidosis: PaCO2 will decrease 1-1.5mmHg per 1 mmol/L decrease in HCO3
Alkalosis: PaCO2 will increase 0.5-1mmHg per 1 mmol/L increase in HCO3
Standard Abbreviation of Blood Gases:
pH/PaCO2/PaO2/HCO3-/SaO2:
o Normal: 7.40/40/90/24/100%

Anion Gap:
Definition: difference between unmeasured cations and unmeasured anions in the serum
o Unmeasured Cations: K+, Ca++, Mg++
o Unmeasured Anions: proteins (albumin), PO4, SO4, organic acids
Calculation: AG= [Na+]-[Cl-]-[HCO3-]
Normal Value: 10-12meq/L
Importance: important in the differential diagnosis of METABOLIC ACIDOSIS

o Increased Anion Gap: indicates an increase in unmeasured anions in the blood
o Normal AG: implies that there was a loss of base (or ingestion of a pure acid like HCl)
Reasons for Increased Anion Gap:
o Decreased Unmeasured Cations:

Hypokalemia

Hypomagnesia

Hypocalcemia
o Increased Unmeasured Anions:

Organic anions: lactate, ketones

Inorganic anions: PO4, SO4

Exogenous Anions: salicylates, methanol, polyethylene glycol
Differential Diagnosis of Major Acid-Base Disorders:
Respiratory Acidosis:
o Acute:

Drug overdose

Stroke

Asthma

COPD

NM syndromes like Guillan Barre
o Chronic:

Obesity-hypoventilation syndrome

COPD

Kyphoscoliosis

NM syndromes (ALS, MG)
Respiratory Alkalosis:
o Hypoxemia of any cause
o Cortical influences (anxiety, pain, fever)
o Disorders of the airway (asthma, COPD) or lung tissue (pulmonary edema, pneumonia)
o Drugs (salicylates)
o Pregnancy
Metabolic Acidosis:
o With Anion Gap:

Ketoacidosis (diabetic or alcoholic)

Lactic acidosis

Intoxicants (methanol, ethylene glycol, salicylates)

Renal failure
o Without Anion Gap:

GI bicarb loss (diarrhea)

Diuretics

Ingestion of HCl

Renal tubular acidoses

Early renal failure
Metabolic Alkalosis:
o Chloride Responsive: urine chloride <10mEq/L

Volume depletion

GI H+ loss (vomiting)

Diuretics

Ingestion of alkali
o Chloride Unresponsive: urine Cl- >20 mEq/L

Mineralcorticoid excess (primary aldosteronism)

Glucocorticoid excess (Cushing’s Syndrome)