Approach to hypoxemia

APPROACH TO HYPOXEMIA

DR KALIPRASANNA CHATTERJEE2ND YEAR PGT

DEPARTMENT OF PULMONARY MEDICINEBURDWAN MEDICAL COLLEGE

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.

CLASSIFICATION OF HYPOXEMIA

This classification is based on predicted normal values for a patient who is lessthan 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.

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.

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

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.

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 –

CAUSES OF HYPOVENTILATION1. 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;

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.

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

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.

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.

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].

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.

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.

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


• 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.


• 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


• 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



• 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

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 HPV1. 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

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)

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)

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

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

DIAGNOSIS OF RESPIRATORY FAILURE

• History• Physical examination• Laboratory investigations

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

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

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.

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

PHYSICAL EXAMINATION

Renal• Anuria

Gastrointestinal• Distended• Pain to palpation• Decreased bowel sounds

LABORATORY TESTINGArterial blood gas:• PaO2• PaCO2• pHChest imaging• Chest X-ray• Computed tomography (CT) scan• Ultrasound• Ventilation–perfusion scanRespiratory 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

TREATMENT OF HYPOXEMIA

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.

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.

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.

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

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.

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

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.

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

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.

THANK YOU

Approach to hypoxemia

Health & Medicine