ASSESMENT OF BLOOD GAS ANALYSIS

ASSOCIATED WITH HYPOXIA AND

OXYGEN TREATMENT

Dr. H. Kutluk Pampal

Dr. Ercan Yıldırım

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 RESPIRATORY FAILURE

• Definition
• Physiopathology
• Clinical and PE findings
• Approach to the patient
• Treatment

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• Respiratory Failure →

• PaO2 < 50-60 mmHg

• PaCO2 > 45 mmHg

• Inability of the lung to meet the metabolic demands of

the body
• Characterized by the inability of O2 delivery and/or CO2
elimination

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 HYPOXIA

Normal: PaO2 100-80mmHg

Mild: PaO2 60-80mmHg
Moderate: PaO2 40-60mmHg
Severe: PaO2 < 40mmHg
O2: Changes with age and position
CO2 and pH: Does not change. Usually 40 mmHg and 7.40

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 TISSUE OXYGENATION

1) Cardiovascular system

2) Hematological system

3) Respiratory system

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Causes of acute respiratory failure. (October 11, 2011. Patrick J. Neligan, MD. Galway, Ireland)
 CLASSIFICATION

• Clinical
Acute
Chronic
• Physiopathological
Hypoxemic (Type I)
Hypercapnic (Type II)
Perioperative (Type III)
Shock (Type IV)

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 MECHANISMS of HYPOXEMIA AND HYPERCARBIA

1. Low FiO2; High altitude (O2 disorder)

2. Diffusion disorder. Alveolar-capillary block syndrome (O2 and
CO2 both effected)
3. V/Q mismatch
4. Shunt
5. Alveolar hypoventilation (CO2 and O2 both effected)

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P50
p50 is the oxygen tension
when hemoglobin is 50 %
saturated with oxygen

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 1. LOW FiO2

• Rare
• High altitude
• Indoor environment
• Toxic gas inhalation

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 2. DIFFUSION DISORDERS
• Most important mechanismsm for hypoxemia
• Also known as Alveolar capillary block syndrome
• Diffusion of O2 and CO2 are impaired
• The mechanism of hypoxemia is V/Q mismatch rather than
block
• Alveoloarterial membrane thickens
• Pulmonary vascular and interstitial lung diseases may cause
diffusion disorders
• Impairment of gas exchange occurs
• Quick response to O2 treatment

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 3. V/Q MISMATCH

• Primary pathophysiological mechanism of impairment of gas

exchange. Mild and moderate disease effects only O2 and
severe disease effects both O2 and CO2
• P(A-a)O2 increases

– V=4-6 L/min
– Q=4-6 L/min
– V/Q≈0.8-1.2

• Hypoxemia quickly responds to O2 treatment

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 4. SHUNT

• Mixed venous blood bypasses the functional parts (where gas

exchange occurs) of the lung and directly joins to the arterial
circulation

V/Q=0

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• Anatomical shunt
• Bronchial, pleural and thebesian veins directly joins to the
arterial circulation. Its nearly 2-3% of CO

• Physiological shunt
• Non ventilated but perfused parts of the lungs
• Shunt<30% à May respond to O2 therapy
• Shunt>50% à No response to O2 therapy. Moreover,
hypercapnia may be observed

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 SHUNT

• Intracardiac shunts
– ASD, VSD
• Pulmonary vascular shunts
– AVM
• Pulmonary parenchymal shunts
– Pneumonia
– Pulmonary edema
– ARDS
– Diffuse alveolar hemorrhage
– Atelectasis

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 5. HYPOVENTILATION

• Best marker for adequate ventilation is PaCO2

• PaCO2>45 mm Hg (6.0 kPa)
• pH≥7.35 à Chronic
• pH<7.35 à Acute
• Hypoxemia
• Mechanisms for hypercapneic respiratory failure
• 1. Hypoventilation
• 2. Elevated physiological dead ventilation respiration
• 3. V/Q mismatch
• 4. Higher rate of production of CO2 than elimination

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 HYPOVENTILATION
• Decrease in minute ventilation
• Inhibition of respiratory center
• Spinal chord trauma
• Neuromuscular disease (MG)
• Thoracic wall abnormalities (Kyphoscoliosis)
• Heart failure, ARDS, Pneumonia, Atelectasis, bronchospasm
and pulmonary embolism
• Cystic fibrosis (Chronic respiratory failure)

• Rarely isolated
• P(A-a)O2 is Normal
• Hypercapnia

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 PERIOPERATIVE (Type III) RESPIRATORY FAILURE

• Primary Mechanism
• First 24 hours after upper abdominal surgery
• VC decrease 50% and reaches to normal value at postoperative
day 7
• First 24 hours after lower abdominal surgery
• VC decreases 25% and reaches to normal value at
postoperative day 3
• Also VC decreases up to 30% after cardiac surgery and
thoracotomy

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 PERIOPERATIVE (Type III) RESPIRATORY FAILURE

• Pulmonary Reasons
• Atelectasis
• Pneumonia
• Aspiration
• ARDS
• Fluid overload, Heart failure
• Pulmonary embolism
• Bronchospasm, COPD

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 PERIOPERATIVE (Type III) RESPIRATORY FAILURE

• Extrapulmonary Reasons
• Inhibition of respiratory center
• Sedative drugs
• Anesthesia
• Opioid drugs
• Diaphragm paralysis
• Phrenic nerve injury
• Obstructive sleep apnea syndrome

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 SHOCK (Type IV) RESPIRATORY FAILURE

• Respiratory failure due to hypoperfusion in a patient without

previous respiratory failure
• Factors impairing tissue oxygenation and normal respiratory
muscle function should be treated
• Anemia, Acidosis, Electrolyte imbalance, Fever, Hypotension, Malnutrition,
Sepsis

• Target for the treatment is providing adequate

perfusion of the vital organs

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 DIAGNOSTIC TOOLS FOR RESPIRATORY FAILURE

• History and physical examination

• Pulmonary X-ray (Pneumonia, PE, PTE)
• ABG sampling (Type I/II?, Acute/Chronic?)
• P(A-a)O2 Arterioalveolar O2 gradient
• Pulmonary function tests
• ECG, Echocardiography
• Doppler USG
• CT
• V/Q scintigraphy
• Pulmonary angiography

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 CLINICAL FINDINGS
• Hypoxemia
• Anxiety, agitation
• Dyspnea, bradipnea
• Tachypnea, tachycardia
• Hypotension, hypertension
• Sweating
• Arrhythmias
• Confusion
• Cyanosis
• Lactic acidosis
• Hypercapnia
• Tachypnea
• Tachycardia, hypertension
• Sweating, flushing
• Flapping tremor
• Pupillary edema
• Headache, lethargy
• Hallucinations,
• Convulsion
• Coma
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 APPROACH TO THE PATIENT WITH RESPIRATORY
FAILURE

• Is the patient hypoxemic?

• Is the patient hypercapneic?
• P(A-a)O2 value?
• Response to O2 treatment?

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 TREATMENT

• Primary Target
• Immediate correction of hypoxemia and preventing tissue
hypoxia

• Secondary Target
• Controlling CO2 and respiratory acidosis

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 TREATMENT

• ABC
• Maintaining adequate ventilation
• O2 treatment
• Mechanical ventilation
• Improving hemodynamic parameters
• Treatment of anemia
• Treatment of underlying disease
• Symptomatic treatment

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 O2 TREATMENT

• Close follow-up
• PO2≥60mm Hg and SaO2≥90%

• Nasal cannula 1-5 L/min

• Face mask 5-8 L/min
• Face mask with reservoir
• Noninvasive/invasive positive pressure ventilation

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• If hypoxemia persists decrease patient’s O2 consumption
(sedation or paralysis)
• Optimize hemoglobin levels
• Optimize CO
• Prone position
• Pulmonary vasodilators (impairs V/Q match)
• In case of hypercapnia in a hypoxic patient O2 should be
kept under 2-4 L/min

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• All metabolic reactions maintained in a narrow range of pH
• pH alterations lead to changes in enzyme activity, electrolyte
balance which effects organ functions (cardiorespiratory, CNS)
and pharmacological properties of the drugs

• Acidemia: pH < 7.35 in arterial blood

• Alkalemia: pH > 7.45 in arterial blood

• Acidosis and alkalosis refers to changes in acid-base balance

at tissue level

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 SYSTEMS REGULATING
ACİD-BASE BALANCE

1. Chemical Buffering Systems

• Bicarbonate/carbonic acid buffer
• Phosphate buffer protein
• Hemoglobin buffer
2. Respiratory Compensation
3. Renal Compensation

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 RESPIRATORY ACIDOSIS

• Elevation of carbonic acid levels leading to increase in PaCO2

over 45 mm Hg
• Muscle weakness, fatigue, lethargy, disorientation
• Inhibition of cardiac contractility
• Tremor, convulsion
• Flushing
• Rapid respiratory rate followed by depression and coma

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RESPIRATOY ACIDOSIS

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 RESPIRATOY ACIDOSIS

• Impair ventilation and allow extraction of CO2

• Do not administer HCO3 unless pH<7.10 and HCO3<15 mEq/L
• Treatment of the underlying disease
• Kidneys eliminate H+ and conserve bicarbonate
• 1 mEq/L of bicarbonate elevation for every 10 mm Hg
increase in PaCO2 in acute respiratory acidosis
• 4 mEq/L of bicarbonate elevation for every 10 mm Hg
increase in PaCO2 in chronic respiratory acidosis

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 RESPIRATOY ALKALOSİS

• PaCO2<35 mm Hg
• Most frequent form of acid-base disorders
• Inappropriate increase in alveolar ventilation relative to VCO2
• Anxiety, irritability, vertigo, syncope
• Tetanus can be observed in severe cases
• Primary pathology is hyperventilation

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RESPIRATORY ALKALOSİS

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 RESPIRATORY ALKALOSİS

• Treatment of the underlying pathology

• Rebreathing
• Hydrochloric acid IV in severe alkalemi (pH>7.60)
• Kidneys conserve H+ and eliminate bicarbonate

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 METABOLIC ACIDOSIS

• [HCO3-]<22 mEq/L
• Fatigue, weakness
• Headache, lethargy
• Nausea, vomiting and diarrhea
• Stupor and coma

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 ANION GAP

• The anion gap in plasma is most commonly defined as the

difference between the major measured cations and the
major measured anions

• Anion Gap=[Na+]-([Cl-]+[HCO3-]

• Anion gap=140-(104-24)=12 mEq/L

• Normal range of AG is 7-14 mEq/L

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METABOLIC ACIDOSIS

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 METABOLIC ALKALOSIS

• [HCO3-]>26 mEq/L
• Shallow breathing with decreased frequency
• Hyperactive reflexes
• Electrolyte imbalance
• Atrial tachycardia
• Dysrhythmia

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 METABOLIC ALKALOSIS

• Vomiting leading to loss of gastric acid

• Extensive use of alkaline drugs
• Diuretics
• Endocrine pathologies
• Massive absorption of antacids
• Severe dehydration

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 METABOLIC ALKALOSIS

• Correct electrolyte imbalance

• Treat underlying disease
• Hydrochloric acid is indicated in severe alkalosis (pH>7.60)
• Related to renal dysfunction in most of the patients
• Respiratory compensation is difficult as hypoxia does not
allow the clinician to hypoventilate the patients

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 PARAMETERS IN ARTERIAL BLOOD GAS

• pH=7.35-7.45
• PaO2=104-(0.27xage)=80-100mmHg
• PaCO2=35-45mmHg
• Total CO2=25-29 mmol/L
• HCO3act=24(22-26)mmol/L
• HCO3std=24(22-26)mmol/L
• Base excess= (-3)-(+3)

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 pH PaCO2 HCO3

Respiratory acidosis ↓ ↑ N

Respiratory alkalosis ↑ ↓ N

Metabolic acidosis ↓ N ↓

Metabolik acidosis ↑ N ↑

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• PaO2 for oxygenation
• PaCO2 for ventilation

• P(A-a)O2 for gas exchange

• P(A-a)O2=2.2+0.21xage
• P(A-a)O2=145-(PaO2+PaCO2)
• 5-10 mm Hg (room air) is normal
• P(A-a)O2>20 mm Hg indicates pulmonary insufficiency
• 25-65 mm Hg is normal under 100% FiO2

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1. Evaluate pH àAcidemia or alkalemia
2. Evaluate PaCO2 and HCO3 à Respiratory or metabolic
3. Differential diagnosis of the primary acid-base imbalance
4. Evaluate for the compensation à Acute, chronic/simple or
mixed

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• If the expected compensation does not occur, especially at
the late stage of the diseases, combined acid-base imbalance
should be kept in mind

pH PaCO2 HCO3
Combined metabolic/respiratory
acidosis ↓ ↑ ↓
Combined metabolic/respiratory
alkalosis ↑ ↓ ↑

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THANK YOU…

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