1. Hypoxemia, defined as low oxygen levels in arterial blood, can be caused by hypoventilation, low inspired oxygen, right-to-left shunts, ventilation-perfusion mismatching, or diffusion impairment in the lungs. 2. Physical exam and arterial blood gas analysis are used to diagnose hypoxemia and its underlying causes. Treatment focuses on oxygen supplementation, treating the underlying condition, correcting acid-base imbalances, and mechanical ventilation if needed. 3. The causes, mechanisms, diagnosis and management of hypoxemia are complex but critical for treatment of respiratory failure.

1. APPROACH TO HYPOXEMIA
DR KALIPRASANNA CHATTERJEE
2ND YEAR PGT
DEPARTMENT OF PULMONARY MEDICINE
BURDWAN MEDICAL COLLEGE

2. DEFINATION
• Arterial hypoxemia is defined as a partial pressure of
oxygen in arterial blood (PaO2) less than 80 mmHg
while breathing in room air.
• Hypoxia is defined as a deficiency in either the
delivery or the utilization of oxygen at the tissue level,
which can lead to changes in function, metabolism
and even structure of the body.

3. CLASSIFICATION OF HYPOXEMIA
This classification is based on predicted normal values for a patient who is less
than 60 years old and breathing room air. For older patients, subtract 1 mm
Hg for every year over 60 years of age from the limits of mild and moderate
hypoxemia.
A PaO2 of less than 40 mm Hg represents severe hypoxemia at any age.

5. CAUSES OF HYPOXEMIA
The mechanisms that cause hypoxemia can be divided into
those that increase P(A-a)O2 and those where P(A-a)O2 is
preserved .
1. HYPOVENTILATION.
2. LOW INSPIRED OXYGEN.
3. RIGHT TO LEFT SHUNT.
4. VENTILATION PERFUSION INEQUALITY.
5. DIFFUSION IMPAIRMENT.

6. HYPOVENTILATION
• Hypoventilation is used here to refer to conditions in which
alveolar ventilation is abnormally low in relation to oxygen
uptake or carbon dioxide output.
• Alveolar ventilation is the volume of fresh inspired gas going
to the alveoli (i.e. Non–dead space ventilation).
• Hypoventilation occurs when the alveolar ventilation is
reduced and the alveolar PO2 therefore settles out at a lower
level than normal. For the same reason, the alveolar PCO2, and
therefore arterial PCO2, are also raised

7. HYPOVENTILATION
• P(A-a)O2 is normal.
• PaCO2 is elevated (hypercapnia)
• Increasing the fraction of inspired oxygen (FIO2) can alleviate
the hypoxemia and the hypercapnia can be corrected by
mechanically ventilating the patient to eliminate CO2.

8. HYPOVENTILATION
• The relationship between the fall in Po2 and the rise in Pco2
that occurs in hypoventilation can be calculated from the
alveolar gas equation if we know the composition of inspired
gas (PIo2) and the respiratory exchange ratio (R).
• A simplified form of the alveolar gas equation is –

9. CAUSES OF HYPOVENTILATION
1. depression of the respiratory center by drugs, such as
morphine derivatives and barbiturates.
2. diseases of the brain stem, such as encephalitis.
3. abnormalities of the spinal cord conducting pathways, such
as high cervical dislocation; anterior horn cell diseases,
including poliomyelitis.
4. affecting the phrenic nerves or supplying the intercostal
muscles;

10. CAUSES OF HYPOVENTILATION
5.diseases of the myoneural junction, such as myasthenia
gravis;
6.diseases of the respiratory muscles themselves, such as
progressive muscular dystrophy; thoracic cage
abnormalities (e.g., crushed chest);
7. diseases of nerves to respiratory muscles (e.g., Guillain-
Barrý syndrome);
8.upper airway obstruction (e.g., thymoma);
9. hypoventilation associated with extreme obesity
(pickwickian syndrome)
10. miscellaneous causes, such as metabolic alkalosis and
idiopathic states.

11. LOW INSPIRED OXYGEN [ PI O2 ]
• Examples-
• A decrease in barometric pressure [e.g. breathing at high
altitude].
• A decrease in FIO2 – accidental [e.g. anesthetist does not
supply enough oxygen or improper installation of oxygen
supply lines or a leak in the breathing circuit].
• P(A-a)O2 normal
• PaCO2 is decreased. This reduction in PaCO2 (hypocapnia) is
due to hyperventilation in response to hypoxemia.
• Peripheral chemoreceptors sense the low arterial PO2 and
initiate an increase in ventilation through their input to the
medullary respiratory centre

12. RIGHT TO LEFT SHUNT
• Shunt refers to the entry of blood into the systemic arterial
system without going through ventilated areas of lung.
• Shunt may be anatomical or physiological.
• P(A-a)O2 is elevated.
• PaCO2 is normal.

13. RIGHT TO LEFT SHUNT
• Anatomic shunt: when a portion of blood bypasses the
lungs through an anatomic channel.
• In healthy individuals
• i) A portion of the bronchial circulation’s (blood supply to the
conducting zone of the airways) venous blood drains into the
• pulmonary vein.
• ii) A portion of the coronary circulation’s venous blood drains
through the thebesian veins into the left ventricle.
• note: i & ii represent about 2% of the cardiac output and
account for 1/3 of the normal P(A-a)O2 observed in health.

14. RIGHT TO LEFT SHUNT
• Congenital abnormalities
• i) intra-cardiac shunt [e.g. Tetralogy of Fallot: ventricular
septal defect + pulmonary artery stenosis]
• ii) intra-pulmonary fistulas [direct communication between a
branch of the pulmonary artery and a pulmonary vein].

15. RIGHT TO LEFT SHUNT
• Physiologic shunt: In disease states, a portion of the
cardiac output goes through the regular pulmonary vasculature
but
does not come into contact with alveolar air due to filling of
the alveolar spaces with fluid [e.g. pneumonia, drowning,
pulmonary edema]
• An important diagnostic feature of a shunt is that the arterial
PO2 does not rise to the normal level when the patient is given
100% oxygen to breathe.

16. RIGHT TO LEFT SHUNT
• Examples of
intrapulmonary shunt.
(a) Collapsed and
fluid filled alveoli are
examples of
intrapulmonary shunt.
• (b) Anomalous blood
return of mixed
venous blood
bypasses the alveolus
and thereby
contributes to the
development of
intrapulmonary shunt.

17. VENTILATION PERFUSION INEQUALITY
• PaCO2 is normal
• P(A-a)O2 is elevated
• VA/Q inequality is the most common cause of hypoxemia in
disease states

18. VENTILATION PERFUSION INEQUALITY
• In normal individuals, there is a spectrum of VA/Q ratios that
range from relatively underventilated units to those lung units
which are ventilated but not perfused.
• In normal lungs, VA/Q may range from 0.6 to 3.0, with the
distribution of all units of the lung in aggregate usually
averaging a VA/Q of approximately one.

19. VENTILATION PERFUSION INEQUALITY
• The distribution of ventilation varies with common events,
such as changes in body posture, lung volumes, and age.
• Increasing age produces a gradual increase in the degree of the
VA/Q inequality.
• Ventilation–perfusion imbalance exists even in the normal
lung, depending on the region, but remains fairly tightly
regulated when assessing normal lung aggregate function

20. VENTILATION PERFUSION INEQUALITY
• In patients with obstructive or restrictive ventilatory diseases,
decreased ventilation may result from structural or functional
abnormalities of the airway and can lead to decreased VA/Q
units
• On the other hand, lung units with increased VA/Q ratios can
develop disorders that lead to over ventilation of lung units,
conditions such as emphysema,for example, in which patients
have airspace enlargement as a result of the destruction of the
alveolar sac distal to the terminal bronchiole.
• Moreover, the development of impaired perfusion through
the pulmonary vasculature, as observed in cases of
pulmonary embolism or pulmonary vasospasm, may cause
high VA/Q ratios

21. VENTILATION PERFUSION INEQUALITY

22. VENTILATION PERFUSION INEQUALITY
• Reflex mechanisms are present in the lung to minimize the
effect of VA/Q inequality, thus avoiding or minimizing the
detrimental effects of impaired gas exchange
• One mechanism is hypoxic pulmonary vasoconstriction
(HPV), whereby a fall in VA/Q leads to the development of
alveolar hypoxia which in turn causes vasoconstriction of
the perfusing arteriole.
• This effect is beneficial for pulmonary gas exchange because it
decreases the denominator of the VA/Q relationship, thereby
partially correcting regional VA/Q imbalance and improving
arterial hypoxemia

23. VENTILATION PERFUSION INEQUALITY
• HPV appears to operate over a range of alveolar PO2 values
between 30 and 150 mmHg.
• The mechanism by which alveolar hypoxia sends the message to
trigger regional vasoconstriction is unclear, but may involve the
release of humoral messengers.
• Many factors, however, can significantly interfere with HPV
1. certain drugs such as calcium channel blockers, beta-agonists,
and inhalational anesthetic agents.
• Lower respiratory tract infections or disease processes that cause
elevations in left atrial pressure can also interfere with HPV.
• In addition, although HPV may be helpful in improving arterial
hypoxemia, a progression in vasoconstrictor effect can lead to the
development of secondary pulmonary hypertension and, eventually,
right heart failure

24. DIFFUSION LIMITATION
• It is now generally believed that oxygen, carbon dioxide, and
indeed all gases cross the blood-gas barrier by simple passive
diffusion
• Fick's law of diffusion states that the rate of transfer of a gas
through a sheet of tissue is proportional to the tissue area (A)
and the difference in partial pressure (P1-P2) between the two
sides, and is inversely proportional to the thickness (T)

25. DIFFUSION LIMITATION
• The rate of diffusion is also proportional to a constant, D,
which depends on the properties of the tissue and the particular
gas.
• The constant is proportional to the solubility (Sol) of the gas,
and inversely proportional to the square root of the molecular
weight (MW)

26. DIFFUSION LIMITATION
• PaCO2 is normal.
• P(A-a)O2 is normal at rest but may be elevated during
exercise.
• a rare observation in the clinical setting

27. DIFFUSION LIMITATION
• Diffusing capacity is reduced by diseases in which the
thickness is increased, including diffuse interstitial pulmonary
fibrosis, asbestosis, and sarcoidosis.
• It is also reduced when the area is decreased, for example, by
pneumonectomy.
• The fall in diffusing capacity that occurs in emphysema may
be caused by the loss of alveolar walls and capillaries

29. DIAGNOSIS OF RESPIRATORY FAILURE
• History
• Physical examination
• Laboratory investigations

30. SYMPTOMS
• Neurologic symptoms:
• Headache
• Visual disturbances
• Anxiety
• Confusion
• Memory loss
• Hallucinations
• Loss of consciousness
• Asterixis (hypercapnia)
• Weakness
• Decreased functional performance

31. SYMPTOMS
• Specific organ
symptoms:
• Pulmonary
• Cough
• Chest pains
• Sputum production
• Stridor
• Dyspnea (resting vs.
exertional)
• Cardiac
• Orthopnea
• Peripheral edema
• Chest pain
• Other
• Fever
• Abdominal pain
• Anemia
• Bleeding

32. PHYSICAL EXAMINATION
• Physical examination of patients with hypoxemia begins with
a quick, but thorough, general assessment.
• The initial priority is to triage patients who present with severe
forms of respiratory failure from those with less severe forms.

33. PHYSICAL EXAMINATION
• General findings:
• Mental alertness
• Ability to speak in complete
sentences
• Respiratory rate > 35
breaths/min
• Heart rate > or < 20 beats from
normal
• Pulsus paradoxus present?
• Elevated work of breathing?
• Using accessory muscles
• Rib cage or abdominal paradox
• Specific organ dysfunction:
• Pulmonary:
• Stridor
• Wheezes
• Rhonchi
• Crackles.
• Cardiac:
• Tachycardia, bradycardia
• Hypertension, hypotension
• Crackles
• New murmurs

34. PHYSICAL EXAMINATION
Renal
• Anuria
Gastrointestinal
• Distended
• Pain to palpation
• Decreased bowel sounds

35. LABORATORY TESTING
Arterial blood gas:
• PaO2
• PaCO2
• pH
Chest imaging
• Chest X-ray
• Computed tomography (CT) scan
• Ultrasound
• Ventilation–perfusion scan
Respiratory mechanics:
• Spirometry (FVC, FEV1,PEF)
• Respiratory muscle pressures
• MIP (maximum inspiratory
pressure)
• MEP (maximum expiratory
pressure)
• MVV (maximum voluntary
ventilation)
Other tests:
• Hemoglobin, hematocrit
• Electrolytes, blood urea nitrogen,
creatinine
• Creatinine phosphokinase,
aldolase
• EKG, echocardiogram
• Swan–Ganz catheter
• Electromyography (EMG)
• Nerve conduction study

36. TREATMENT OF HYPOXEMIA

37. Oxygenation
• Oxygen is frequently necessary for patients who present with
hypoxemia or with conditions known to predispose to
hypoxemia.
• Most of the initial morbidity and mortality that occurs in
patients results from the consequences of untreated
hypoxemia.

38. Oxygenation
• Various types of external oxygen delivery devices are now available to
provide variable concentrations of inspired oxygen.
• The choice of a particular device depends on-
• (1) the magnitude of supplemental oxygen required by the patient to
achieve effective oxygenation;
• (2) the need for precise control of supplemental oxygen to avoid
excessive oxygenation and the development of hypercapnia.
• (3) whether airway control is needed to suction the patient for excessive
secretions.
• (4) whether other techniques are needed to increase oxygen by increasing
lung volume (externally applying positive pressure to the airway by CPAP
or PEE P.

39. Oxygenation
• Nasal prongs:
-simplest and most comfortable method.
-does not provide enriched oxygen in an extremely precise manner.
• Face mask devices:
-fit more tightly and may have non-rebreathing valves that,
coupled with an inspiratory reservoir of oxygen, provide higher
and more precise concentrations of supplemental oxygen.
-delivery of oxygen by means of a face mask with a Venturi device (a
calibrated inline device) can provide high flows of oxygen in a more
precise manner and minimize the effect of room air entrainment.

40. Medications
• The use of medications in the treatment of respiratory failure
depends on the underlying disorder.
• In patients who present with an exacerbation of airway
obstruction, bronchodilators, corticosteroids, theophylline
preparations, and possibly antibiotics, are required.
• In patients who present with pulmonary edema due to volume
overload, or with cardiac dysfunction, diuretics are in order.
• In patients who have more pronounced cardiac dysfunction,
the selected use of cardiac inotropes may be required

41. Supportive Therapy
• Acid–base or electrolyte disturbances may compromise
respiratory pump function and contribute to an elevated
ventilatory workload.
• Hypocalcemia, hypomagnesemia, hypokalemia,and
hypophosphotemia all have been identified as conditions that
lead to skeletal muscle weakness and, specifically, respiratory
skeletal muscle weakness.
•
• Correction of these abnormalities can markedly improve
ventilatory muscle strength and increase respiratory reserve.

42. Supportive Therapy
• Regardless of etiology, metabolic acidosis increases
ventilatory workload and its presence should be identified and
appropriately treated.
• The use of ancillary testing and physical examination must
appropriately diagnose the cause of metabolic acidosis
because effective therapy of this disorder is a crucial part of
the overall treatment plan for respiratory failure

43. Supportive Therapy
• Nutritional support and, in some cases, reconditioning are
also important in restoring respiratory pump function and
reversing the presence of respiratory failure.
• Renutrition increases respiratory muscle mass and restores
ventilatory muscle endurance, an important beneficial
physiologic effect that results in an improvement in respiratory
pump function.
• Moreover, rehabilitation of patients who present in a
deconditioned state, or with disuse atrophy after a critical
illness, is similarly important in restoring respiratory pump
function.

44. Reducing Ventilatory Workload
• In some patients,, ventilatory workload far exceeds capacity,
and the patient’s spontaneous effort must be augmented with
mechanical ventilation until the condition causing the higher
workload resolves or the patient’s ventilatory capacity
increases.
• Augmentation of the patient’s spontaneous breathing effort can
be achieved by either invasive or noninvasive forms of
mechanical ventilation.
• In noninvasive mechanical ventilation,a nasal or nasal oral
face mask is used to augment the patient’s spontaneous efforts
without the use of an artificial airway.
• In the case of invasive ventilation, an artificial conduit is
inserted in the patient’s airway, either an endotracheal tube or
a subglottically placed tracheotomy tube

45. Reducing Ventilatory Workload
• Invasive ventilation is the method most frequently used to
augment a patient’s spontaneous respiratory effort.
• When using invasive ventilation, endotracheal intubation is
considered mandatory for the patient’s therapy so as to-
• (1) provide airway protection.
• (2) serve as a conduit for suctioning patients with excessive
mouth or lower respiratory tract secretions.
• (3) achieve higher inspired oxygen concentrations than are
possible with a face mask.
• (4) apply positive pressure via the ventilator to increase lung
volume to treat refractory hypoxemia.

46. THANK YOU