BLOOD GAS ANALYS : VENOUS AND ARTERIAL
- Importance of O2 evaluation: adequate tissue oxygenation necessary for correct organ function
 When delivery ↓ consumption will also ↓ → switch to anaerobic metabolism w/ lactate production → late sign
- O2 delivery (ml/min) = CO x arterial blood content (CaO2=1.34 x SaO2 x Hb) → insight on lung, heart, Hb
 ↓ O2 delivery will comes about only if compensatory mechanisms are not enough (delivery at baseline is x4 of
actual need)
- Arterial blood gas analysis = what is going on inside the cells
- Venous blood gas analysis = O2 delivery vs consumption
ARTERIAL BLOOD GAS
BLOOD GAS ANALYSIS → info about: acid/base balance, gas exchange (oxygenation=PaO2, ventilation=PaCO2)
- Used to: assess presence and severity of respiratory failure, monitor pts on ventilator, assess metabolic dysfunction
- Normal values:
pH : 7,35-7,45 → the value does not directly correlate with the severity of the situation: it depends on how
fast the change occur and how much the pts is able to sustain it
PaO2 : 80-100 mmHg (109-0.4xage) → hypoxemia < 80 mmHg, hypoxic respiratory failure < 60 mmHg
PaCO2: 35-45 mmHg → hypercapnia > 50 mmHg
HCO3: 24-26 mEq/L
BE : +/- 2 mmol/L = amount of acid that would be need to buffer blood to a normal pH
Lattato: < 1,5 mmol/L
Na : 135-150 mEq/L
K: 3,5-5 mEq/L
Ca: 8,5-10,5 mEq/L
Cl: 95-105 mEq/L
- Step by step evaluation:
1) Is the BGA actually arterial?
- Is SaO2 and PaO2 too low is probably venous
- Consider parameters that can alter values: temperature, cell count (O2 consumption, analyze w/in 10 min) , air
bubbles (↑PaO2)
2) Oxygenation → PaO2, PaO2/FiO2 ⇒ respiratory failure? Compare with PaCO2 to define type
- Type 1 (lung failure): hypoxia + normo/hypocapnia
- Type 2 (pump failure): hypoxia + hypercapnia
3) pH analysis ⇒ normal, alkalosis, acidosis ?
4) PaCO2 analysis + HCO3 ⇒ respiratory vs metabolic ?
- PaCO2 is altered in the opposite direction of pH = respiratory → Mnemonic ROME = Respiratory Opposite, Metabolic
Equal
- HCO3 is altered in the same direction of pH = metabolic
5) Acute vs chronic + simple vs mixed condition (estimated compensation not satified)
Respiratory acidosis
For every 10 CO2 ↑
Respiratory alkalosis
For every 10 CO2 ↓
Metabolic acidosis
Metabolic alkalosis
For every 1 HCO3 ↓
For every 1 HCO3 ↑
Acute
Chronic
Acute
Chronic
6) If metabolic acidosis calculate AG to define etiology
- ↑ AG : Acidosis due to ↑ metabolic acids w/ ↓ HCO3 in attempt to buffer
- Normal AG: Acidosis due to loss of HCO3 (renal or extrarenal) w/ ↑ Cl
Expected compensation
1 HCO3 ↑
3 HCO3 ↑
2 HCO3 ↓
4 HCO3 ↓
1 CO2 ↓
0.5 CO2 ↑
Parameters and their meaning
GAS EXCHANGE PARAMETERS
- PaCO2: ventilation = volume of air transported btw alveoli and external air in 1 min
 Depends on : respiratory CNS centers, muscles, diaphragm
 Is the main trigger for ventilation: low PaCO2 → ↓RR by inhibit muscle function. In chronic hypercapnic pts
PaCO2 is no longer used as stimulus bc loose sensitivity , PaO2 is instead used (hypoxic drive) → oxygen
supplementation might suppress respiratory drive !
- Arterial blood O2 content = (0.0031 x PaO2) + (1,34 x [Hb] x SaO2)
 Distribution of O2 inside blood: 1% free (represented by PaO2) + 99% bound to Hb (carrying capacity)
 PaO2 = driving force for O2-Hb binding → affinity expressed by oxygen-Hb dissociation curve
 Factors ↓ affinity (O2 released in tissues) : acidosis (effetto Bohr) , ↑ T°, ↑ DPG, ↑ PaCO2
 Factors ↑ affinity (O2 remains in the blood) : alkalsosi, ↓ T°, ↓ DPG, ↓ PaCO2
 steep for values of PaO2 < 60 mmHg (SaO2 < 90%) → PaO2 unable to sustain Hb saturation for correct
tissue oxygenation
 [Hb] = carrying capacity: how much O2 can be carried
 SaO2 = used carrying capacity =% of O2 binding sites on Hb carrying O2 (Hb saturation)
- Oxygen delivery formula = cardiac output x arterial O2 content
- SaO2 : O2 arterial transport
- PaO2 : lung gas exchange
 Depends on: pts age, alveolar ventilation, V/Q, FiO2 (FiO2-PaO2≥10mmHg; FiO2 room air=21 %)
- Horowitz index = PaO2 / FiO2 (n.v ≥ 300) → if < 300: gas exchange alteration
 Considered alone is more informative than PaO2
ACID BASE BALANCE PARAMETERS
- Acids (H+)
 Come from metabolic activity in the form of CO2 and metabolic acids
 Excretion by : respiration (CO2, regulated by RR), renal metabolism (H+ excretion, HCO3 reabsorption)
 Detrimental effect of acidosis on protein structure
- Maintenance of electrolyte neutrality :
 Expressed by Anion Gap = difference btw positive charged electrolytes and negatively charged electrolytes that
can be measured in lab = unmeasured anions
 AG = (Na+K) – (Cl + HCO3) = 12±4 (or 10±2 if K not counted)
 + charged: Na+ exchanged with H or K → H and K increase and decrease together
 - charged: Cl- and HCO3- balance each other by exchanging → one rise while the other fall
 Must be corrected with albumin: AG ↑ by 2.5 mEq/L for every 1 g/dL ↓ in serum albumin
 ↓ AG = wasting of ions (diarrhea, vomiting, renal tubule acidosis)
 ↑ AG = metabolic alterations (sepsis, liver disease, intoxication)
Main alterations and causes:
- Simple / Primary acid-base disorder = single process of alkalosis / acidosis due to change in PCO2 or HCO3
- Compensation = normal respiratory or kidney response to pH change
- Mixed acid-base disorder = ≥1 acid-base disorder together
• Acidosis
- CP : ↑ RR (Kausmall respiration as compensation mechanism), fatique, lethargy, coma
- Respiratory acidosis: alveolar hypoventilation due to : pulmonary edema, BPCO, airways obstruction, thoracic
trauma, neuromuscular disease, opioid overdose, coma, compensation of metabolic alkalosis
- Metabolic acidosis
 ↑ AG : Acidosis due to ↑ metabolic acids w/ ↓ HCO3 in attempt to buffer : lactic acid (shock, sepsis),
diabetic ketoacidosis, alcholic acidosis, renal insufficiency, salycilate, uremia
 Confirm lactic acidosis: lactate ≥ 50% of BE
 Low or Normal AG: Acidosis due to loss of HCO3 (renal or extrarenal) w/ ↑ Cl : tubular renal acidosis,
diarrhea, physiological solution infusion (high Cl), post hypocapnia, spironolactone, aacetazolamide
• Alkalosis
- CP: ↓ RR (compensatory bradypnea), shallow breathing, vertigo, confusion, irritable state
 Respiratory alkalosis: hyperventilation due to initial phase of pulmonary embolism (n.b unresponsive to O2
delivery, check right ventricle dilation at eco cardio),panic attack, fever, pregnancy, hypoxia, high altitude
 Metabolic alkalosis: loss of acid gastric secretion (vomit, NG tube), dehydration, loss of H+ (loop diuretics loosing
K+), antacid intoxication, Cushing, primary aldosteronism, diarrhea with loss of Cl-, hypocalcemia, cirrhosis, HCO3
reabsorption, HCO3 exogenous
VENOUS BGA
- Represent scvO2 = central venous oxygen saturation
 Measured by central venous catheter = tip lies in superior vena cava close to the right atrium (access is
variable: subclavian, internal jugular, femoral)
 Other indications beside VBGA: drug infusion, unavailable peripheral venous access, dialysis, need for a
long-term venous access
 Represent how much of the delivered arterial blood O2 has been unutilized by cells → ScvO2 = O2 delivery / O2
consumption ⇒ you don’t know the absolute values but only if O2 delivery is enough
 Is a flow-weighted representation (higher flow=more represented) of blood with different O2 saturations from
different vascular beds all mixing inside the inferior vena cava → is a marker of general oxygenation state, not
informative for the single organ → an ischemia of a low flow organ can be completely masked if high flow
organs are not affected → check for specific organ signs of hypoperfusion
- Difference btw venous and arterial blood: lower pH, higher PCO2, lower pO2, lower SaO2, comparable amount: Hb,
glucose, lactate, electrolytes
- When a venous BGA is enough (easier to perform, so if you can avoid an arterial one is better):
 Define levels of : Hb, glucose, lactate, electrolytes
 Rule out respiratory acidosis
 Rule out hypercapnia
 Rule out respiratory failure
- When a venous BGA is NOT enough
 Evaluation of arterial oxygenation (PaO2, SaO2) → pulse oximetry might be enough, arterial BGA is not always
required (oxy-Hb dissociation curve=relation btw PaO2 and SaO2 → if SaO2 is 100% you can rule out hypoxemia)
cvSaO2 values :
- Lactate is a late sign as it comes about only in the emergency range, so look out for intermediate values of
abnormalities
- < 50% : easier interpretation, check for:
 ↓ Delivery (DO2)
 Lung (hypoxemia) : pulse oximetry (SaO2) → if 100% you
can rule out a respiratory problem
 Hb (anemia) measure it via venous BGA
 Heart (low tissue perfusion) : if lung and Hb is normal,
conclude is an heart problem by exclusion
 ↑ Consumption (VO2) : fever, pain, shivering, respiratory effort, muscle activity, agitation
- Normal / > 85% (no cellular extraction) → cannot rule out localized tissue hypoxia, check for hypoperfusion signs
(altered mental status, hyperlactatemia, mottled skin, oliguria, hypotension, tachycardia)
Summary for bedside assessement