Transpulmonary pressure

Distinguish among atmospheric pressure, alveolar pressure, intrapleural pressure, and transpulmonary pressure... 

Transpulmonary pressure (Plp) is the pressure difference between the inside and outside of the lungs. In other words, it is the pressure difference between the alveoli and the pleural space ... 

In between breaths, the transpulmonary pressure is +5 cmH20. The transpulmonary pressure is also referred to as the expanding pressure of the... 

The entry of air into the pleural cavity is referred to as a pneumothorax. This may occur spontaneously when a "leak" develops on the surface of the lung, allowing air to escape from the airways into pleural space. It may also result from a physical trauma that causes penetration of the chest wall so that air enters pleural space from the atmosphere. In either case, the pleural cavity is no longer a closed space and the pressure within it equilibrates with the atmospheric pressure (0 cmH20). As a result, the transpulmonary pressure is also equal to 0 cmH20 and the lung collapses. 

Fig. 2. Tracings of lung airflow, transpulmonary pressure, and lung volume changes during spontaneous breathing in a rat. Airflow was measured directly using a head-out plethysmograph chamber, while pleural pressure was measured using a pressure sensitive catheter placed into the esophagus within the thoracic cavity. The functional endpoints can be automatically calculated for each breath using a data acquisition and analysis software system.

The authors concluded that inhaled nitric oxide had reduced pulmonary hypertension and pulmonary vascular resistance, but that obstruction by the atrial myxoma had caused the low cardiac output, due to a net reduction in transpulmonary pressure. 

Figure 4 Determinants of transpulmonary pressure at functional residual capacity.

The respiratory system is responsible for generating and regulating the transpulmonary pressures needed to inflate and deflate the lung. Normal gas exchange between the lung and blood requires breathing patterns that ensure appropriate alveolar ventilation. Ventilatory disorders that alter alveolar ventilation are defined as hypoventilation or hyperventilation syndromes. Hyperventilation results in an increase in the partial pressure of arterial CO2 above normal limits and can lead to acidosis, pulmonary hypertension, congestive heart failure, headache, and disturbed sleep. Hypoventilation results in a decrease in the partial pressure of arterial CO2 below normal limits and can lead to alkalosis, syncope, epileptic attacks, reduced cardiac output, and muscle weakness. 

PEEP is defined as an elevation of transpulmonary pressures at the end of expiration (17). It prevents alveoli from de-recruiting during expiration, which is beneficial, as recruited alveoli improve V/Q matching and gas exchange (12-14), patent alveoli are not exposed to the risk of injury from the stress of repeated opening and closing (17,18), and recruited alveoli prevent surfactant breakdown, thus improving CL (19). 

Figure 1 A beagle dog was anesthetized with propofol and etomidate and intubated. One 250-mL breath of ammonia vapor above an 8-M ammonia solution was administered to the dog. The end-tidal COj shows an apnea followed by rapid, shallow breathing. The arterial pressure tracing demonstrates the short-lived decrease in heart rate and attendant hypotension. The transpulmonary pressure illustrates that the apnea and tachypnea was due to the absence of ventilatory drive, rather than airway occlusion.

Figure 4 A beagle dog was anesthetized with thyamylal sodium (Surital) and intubated. The tidal volume, pulmonary artery pressure, lung resistance, dynamic compliance, trans-pulmonary pressure, and airflow are shown before and following administration of 14 breaths of an irritant. Laurie acid was heated, in a La Mer-type condensation generator (19), the vapor was condensed in a cold trap operated below 0°C. The response was due to the small particles and any vapors that were not deposited in this trap. This aerosol-vapor was administered for 14 breaths, using a time-controlled series of soleniod valves and thus only transpulmonary pressure and arterial pressure are displayed during the challenge.

All of the foregoing cardiovascular and ventilatory and respiratoiy responses—namely, apnea followed by tachypnea, bradycardia, and increased bronchial blood flow, as well as systemic hypotension—observed in the pulmonary chemoreflex are characteristic of an anaphylactic reaction (31). An example of the cardiopulmonary responses to an inhaled allergen in a spontaneously breathing dog is shown in Figure 5. There is an increase in transpulmonary pressure indicative of an increase in airways resistance and a decrease in dynamic compliance. There is a marked apnea followed by tachypnea, a marked bradycardia and hypotension. Albeit, there may be some compensatory increase in heart rate, the induced hypotension persists. This hypotension is probably, partly, mediated by the induction of nitric oxide (NO) through the parasympathetically induced activation of nitric oxide synthase (32,33). 

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