Airway Resistance vs. Lung Compliance
When pressure waveform slope increases, lung compliance has decreased. When the step-up (pressure at which flow begins) is elevated, airway resistance has increased. Alveoli are protected when resistance has increased (thus one can safely crank up the vent), whereas changes in compliance do not protect alveoli.
Conditions associated with low compliance (pneumonia, pulmonary edema) can lead to increased transmural pressure because more of the ventilatory force is transmitted to the central vasculature.
Positive-pressure ventilation 1) decreases the venous return gradient in the right heart 2) decreases venous return to the left heart by compressing the pulmonary vessels, which sometimes overloads the RV which pushes into the LV (ventricular interdependence) and 3) decreases ventricular distensibility/filling.
Generally, PPV decreases cardiac output due to the above mechanisms, but in cases when ventricular filling is not compromised, the increased transmural pressure can facilitate cardiac output, ie in hypovolemic patients CO is decreased by PPV, and in normovolemic patients it is increased.
CBF changes approximately by 3% for each 1 mm Hg change in PaCO2 over the clinically important range of 20 to 60 mm Hg in patients with TBI [J Trauma 39: 1091, 1995]. Compensatory mechanisms return CSF and brain pH to normal in a matter of hours ( lactate production, changes in bicarbonate), thus according to Andrews CBF will return to normal within 4-6 hours of hyperventilation.
In vitro, the middle cerebral artery constricts when it is exposed to raised extracellular pH. In contrast, in vivo, large intracranial vessels (carotid, MCA, vertebral) are not significantly affected by changes in PaCO2, whereas the ACA and M2 are [Neurosurgery 32: 737, 1993]. Vessel caliber follows changes in arterial CO2 by responding to the pH in the perivascular space without molecular CO2 and bicarbonate ions acting independently on cerebral vessels [Acta Neurochir Suppl (Wien) 71: 62, 1998]. Nevertheless, changes in pH may exert their effect on smooth muscle tone through second messenger systems or by altering the calcium concentration in vascular smooth muscles directly.
The goal of positive end-expiratory pressure (PEEP) is to provide sufficient transpulmonary pressure (defined as the difference between airway and pleural pressure) to prevent or reverse atelectasis. Thus, PEEP, which by definition measures airway pressures, completely neglects an important component of this physiologic approach. Measurement of esophageal pressure, which is a reasonable estimate of pleural pressure [Higgs BD et al. Anesthesiology 59: 340, 1983], allows the clinician to optimize transpulmonary pressure. A recent prospective trial of PEEP-guided versus esophageal pressure-guided ventilatory management in patients with ARDS showed improvements in PaO2 as well as respiratory compliance in the esophageal pressure-guided group [Talmor D et al. NEJM 359: 2095, 2008; FREE Full-text at NEJM].