Effects of cpb on lung

Dr ruchi
Anesthesia and Neuromuscular Blockade
mechanical ventilation initiates atelectasis within 5 minutes .
The relaxed diaphragm is displaced cephalad by the abdominal contents.
This increases pleural pressures and compresses adjacent lung tissue, and gas flow is preferentially distributed to the
nondependent regions of the lung.

This promotes
ventilation-perfusion mismatch,
hypoventilation, and
progressive microatelectasis of the dependent lung zones.

The proximate cause of pulmonary atelectasis during CPB is cessation of ventilation and lung collapse. Th
Compression atelectasis occurs when transmural pressure distending the alveolus is reduced .

Resorption atelectasis is induced when capillary uptake of oxygen exceeds the rate of alveolar oxygen influx .
Resorption may also occur in lung zones that have low ventilation/perfusion ( ) ratios; the uptake of oxygen
increases significantly as the fraction of inspired oxygen (FIO2) increase

Surfactant depletion atelactasis

Pulmonary surfactant covers the alveolar surface and lowers surface tension to prevent alveolar and smallairway
collapse.
exposure to anesthesia impairs surfactant function and increases the permeability of the alveolar capillary barrier
Atelectasis itself promotes the production of proinflammatory cytokines, which decrease the synthesis of surfactant
Anatomic Considerations
During CPB, the heart rests on the immobile left lower lobe.
With blind bronchial suctioning, the catheter usually enters the more direct right main stem bronchus, resulting in
preferential right bronchial drainage.

Traumatic mucosal “pitting” induced by the suction catheter at the carina causes secretions to dam up and promotes
airway collapse

• When the pleural cavity is opened, blood and fluid can enter and compress the adjacent lung.
• during coronary revascularization,
dissection of the left internal mammary artery mandates entry into the left pleural space.

Together, these factors account for the 60% to 70% incidence of left lower lobe atelectasis after CPB
The right lung can be compressed during cannulation of the inferior vena cava.

The supine position is associated with a decrease in functional residual capacity (FRC) as abdominal contents push
the diaphragm cephalad and promote small-airway closure.

Significant atelectasis has been observed in the dorsal lung regions in patients after cardiac surgery
High Inspired Oxygen Concentration
High inspired concentrations of oxygen (FIO2) during the perioperative period promote atelectasis
.
When the alveolar-arterial oxygen concentration gradient (AaDO2) increases,
the capillaries rapidly absorboxygen, resulting in alveolar atelectasis.

The degree of atelectasis varies at different oxygen concentrations, and

it is most notable when the FIO2 is >0.8
Low Tidal Volume Mechanical Ventilation
The use of low tidal volumes as a component of a protective lung strategy is now the standard of care in the setting of
ARDS .

Although this protects against alveolar stretch-induced injury (volutrauma), it also promotes
atelectasis (atelectrauma).

Pressure controlled ventilation (PCV) is a ventilator mode that limits peak airway
pressures in order to decrease the risk of pulmonary barotrauma. However, if lung compliance is very poor, PCV
may result in delivery of small tidal volumes that promote the development of atelectasis
Comorbid Conditions
In heavy smokers with chronic bronchitis,Anterograde cilial clearance of mucus and debris is impaired,
surfactant production is diminished, and small airways and alveoli tend to collapse.

Obesity causes a reduction in FRC and predisposes to atelectasis before and after CPB .

An increase in extravascular lung water, whether due to congestive heart failure or pulmonary edema,
increases the tendency for small airways to collapse
Clinical Consequences of Atelectasis
FRC decreased by as much as 20% for up to a week after general anesthesia.

CPBinduced atelectasis causes more severe disruption of the broncho-alveolar tree and as a consequence FRC is decreased
by as much as 40% to 50% .

This causes a substantial impairment of lung compliance and promotes a pulmonary inflammatory response
Decreased Lung Compliance
The decline in lung compliance induced by atelectasis
increases the work of breathing required for alveolar distention.

A decrease in the expiratory reserve volume and FRC promotes further collapse because there is a
lower volume remaining in the lung at the end of a normal tidal ventilation.

.
this lead to a substantial increase in energy consumption and acute ventilatory
failure, with continued requirement for mechanical ventilation.
Acute Lung Injury
The repetitive opening of collapsing alveoli leads to surfactant inactivation and atelectrauma, and has been
implicated in the development of ventilator-induced lung injury (VILI)

. When alveoli are stretched by excessively large tidal volumes, inflammatory mediators and neutrophils are activated,
leading to increased alveolar capillary permeability and hyaline membrane formation.

Atelectrauma may be prevented or attenuated by a protective lung

strategy that limits tidal volumes to curtail inspiratory alveolar stretch and adds positive end-expiratory pressure (PEEP)
to prevent expiratory alveolar collapse