Positive-pressure ventilation (PPV) alters ventricular loading conditions and compliance.
In patients who are hypovolemic, the effects of positive airway pressure on the right heart predominate, whereas in patients who have systemic ventricular systolic dysfunction, the effects of PPV on left ventricular (LV) afterload predominate.
Large changes in arterial pulse pressure over the respiratory cycle help to identify mechanically ventilated patients who may have a favorable response to the administration of fluid or who may not tolerate high levels of positive end-expiratory pressure without fluid administration.
PPV raises juxtacardiac pressure, thereby reducing LV afterload.
Respiratory effort imposes critical loads on the heart, and respiratory muscle failure from inadequate oxygen delivery (DO 2 ) is a final common pathway to death from shock.
Both spontaneous breathing and positive-pressure ventilation (PPV) affect the circulation in predictable ways. The cardiovascular system also has important effects on respiration, ventilation, and gas exchange.
Effects of ventilation on circulation
As shown by Cournand et al. in their seminal study, PPV can have important effects on the circulation. The magnitude of these effects may be accentuated by factors that compromise cardiovascular homeostatic responsiveness, such as hypovolemia, cardiac dysfunction, or disordered vascular tone.
PPV alters ventricular loading conditions and compliance. These interactions may occur simultaneously and yet not act in the same direction on cardiac output (CO). The net effect on CO depends on which interactions predominate over the course of the respiratory cycle and on underlying cardiopulmonary function. For this reason, it is often easier to rationalize an interaction than to predict it.
For clarity of discussion, wherever the terms positive pressure or mechanical ventilation are used in this chapter, the patient is presumed to respond passively, as though subjected to neuromuscular blockade. In general, the term preload dependence is used in this chapter to connote patients in whom the dominant cardiovascular effect of positive pressure breathing is to reduce right heart filling with resultant fall in stroke volume. Afterload dependence is the term applied to identify patients whose dominant effect is afterload reduction and consequent increase in stroke volume.
Right ventricular filling and stroke volume
The effects of PPV on filling of the right heart are the best understood of the various heart-lung interactions, are generally the preponderant effects on the circulation, and are mediated by changes in intrathoracic pressure (ITP) and venous return over the respiratory cycle. Spontaneous breathing and PPV have opposite effects on ITP, which largely explains their different effects on CO.
Systemic venous return
The mean systemic pressure of the circulation (P ms ) is thought to be the inflow pressure driving blood toward the right atrium. This driving pressure is not measurable in the intact patient, but it can be thought of as the static mean pressure that might exist throughout the circulation if there were instantaneously no blood flow. P ms approximates the weighted average of pressures in venous reservoirs throughout the body during the circulation of blood. The backpressure that opposes systemic venous return is the right atrial pressure (P ra ). The impact of these pressures on the return of venous blood to the heart is described by the venous return curve ( Fig. 32.1 A), which is drawn in such a way that the independent variable (Q pump ) appears on the y -axis. Picture the systemic circulation as composed of noncompliant arteries functioning largely as conductive vessels and venous reservoirs functioning as capacitive vessels, which are separated by high-resistance arterioles and a pump that receives venous return and propels it into the systemic arterial circulation ( Fig. 32.1 B). The faster the pump circulates the blood, the more blood piles up before the arterioles and the higher the arterial pressure will be; the faster the pump moves blood from venous to arterial system, the less blood resides on the venous side of the circuit and the lower the P ra will be ( x -axis). As the pump is slowed down, venous pressure rises until flow reaches zero, at which point vascular pressures equilibrate throughout the circulation at P ms . Resistance to venous return (R vr ) is the reciprocal of the slope of the linear part of the venous return curve. Simply stated,
P ms is a function of intravascular volume and vascular compliance, the vast majority of which reside within and with the venous reservoirs, respectively. The P ms can be altered by changes in venous tone and intravascular volume. P ms is an extrathoracic measurement and is less sensitive than P ra to changes in ITP. P ra , in contrast, is quite sensitive to changes in ITP.
At functional residual capacity (FRC), the thorax exerts recoil force, tending to spring outward, whereas the lung exerts recoil force (mostly as a result of alveolar surface tension), tending to collapse inward. These forces result in subambient pleural pressure. The cardiac fossa, or juxtacardiac space, which surrounds the pericardium and heart, shares in this balance of forces and has slightly negative pressure at apneic FRC. At any right atrial volume, P ra is influenced by juxtacardiac pressure because these two forces act together to oppose the right atrium’s balloon-like tendency to recoil inward. Therefore, it is not surprising that all of these pressures (pleural, juxtacardiac, and right atrial) are influenced by the respiratory cycle.
During spontaneous breathing, lung volume rises from FRC to end-inspiratory volume by expansion of the rib cage and descent of the diaphragm. This reshaping of the thorax stretches the lung, increasing its recoil tension, so that pleural pressure and juxtacardiac pressure both become more negative (subambient). At any right atrial volume, spontaneous inspiration reduces P ra by increasing its transmural pressure (P tm , inside—surrounding or juxtacardiac pressure), which distends the compliant chamber, causing the pressure within to fall. By the mathematic relationship in Eq. 32.1 , this augments venous return. Over the course of passive spontaneous expiration, all three pressures return to their values at FRC. It follows that ITP, during relaxed, spontaneous breathing, is always most negative at end-inspiration and becomes progressively less negative throughout the rest of the respiratory cycle.
Right ventricular preload and stroke volume
During spontaneous inspiration, systemic venous return to the right atrium increases. In addition, during ventricular diastole, the right ventricular (RV) P tm increases as the juxtacardiac pressure decreases, increasing its effective compliance and, for a given diastolic pressure, the extent to which it fills. The same principle applies to the left ventricle (LV). Despite a fall in right atrial and RV diastolic pressures (they are equal in the absence of tricuspid valve stenosis), the P tm increases during spontaneous inspiration and RV filling and stroke volume increase. Hence, there is a seemingly paradoxical inverse relationship between P ra and RV stroke volume over the spontaneous respiratory cycle ( Fig. 32.2 ). However, if right atrial P tm is plotted against RV stroke volume during various respiratory maneuvers and with expansion of intravascular volume, the expected strongly positive relation is found ( Fig. 32.3 ).
Positive pressure ventilation and right ventricular preload
The effects of PPV on pleural, juxtacardiac, and P ra are opposite those of spontaneous breathing. A common goal in the application of positive end-expiratory pressure (PEEP) is restoration of normal FRC. All other things being equal, pleural pressure, which opposes thoracic recoil, should be the same at end-expiration whether breathing is spontaneous or mechanical. Pleural pressure is, after all, determined by thoracic volume during passive expiration.
During spontaneous inspiration, active reshaping of the thorax by the respiratory muscles and diaphragm inflates the lungs by reducing pleural pressure. In contrast, throughout positive pressure mechanical inspiration, pleural pressure rises because the passive thorax is pushed outward (from FRC to end-inspiratory volume) by the expanding lungs. Passive expiration restores pleural pressure to that of FRC. Averaged over the entire respiratory cycle, pleural pressure is higher during positive pressure breathing than it would be during spontaneous breathing ( Fig. 32.4 ). This elevation of pleural pressure during positive pressure mechanical ventilation may be thought of as transmission of airway pressure to the pleural space. PPV, therefore, reverses the effects of spontaneous breathing on venous return and the RV diastolic P tm . RV stroke volume declines during positive pressure inspiration as P ra rises and the effective compliance of the RV decreases. Averaged over the entire respiratory cycle, P ra is raised and RV stroke volume is reduced by positive airway pressure relative to their expected values during spontaneous breathing. It is easy to argue from these observations that PPV will invariably decrease venous return to the right heart, but this is not always the case. In addition to the extent to which airway pressure is transmitted to the right heart, discussed further later, the ability of circulatory reflexes to maintain an adequate albeit elevated P ms , as well as underlying cardiac function, determines the extent to which stroke volume and CO is adversely impacted by PPV. Venoconstriction and retention of intravascular volume act to elevate the P ms and maintain an adequate pressure gradient for systemic venous return. During PPV, descent of the diaphragm may displace blood from the abdominal viscera , and positive airway pressure may displace blood from the pulmonary circulation, both of which raise P ms .
Critical illness and the effects of positive pressure breathing on RV preload
Among the effects of critical illness are inflammation-induced capillary leak, pulmonary edema, surfactant dysfunction, abnormal blood volume, and abdominal distension. Each of these modifies the effects of positive pressure breathing on RV function and loading conditions. Capillary leak alters the compliance of the atrial and ventricular chambers, modifying the responsiveness of the heart to changes in preload. Sepsis and inflammation decrease cardiac contractility, directly altering the heart’s responses to changes in loading conditions. Reduced lung compliance diminishes the transmission of alveolar pressure to the juxtacardiac space. The change in ITP that occurs with a change in static airway pressure is essentially the same as the change observed in pulmonary artery wedge pressure, which is readily measured. Recognizing this relationship in adults has made it possible to estimate percent transmission of airway pressure to the juxtacardiac space by measurement of respiratory system compliance. Lesions of the chest wall (consisting of the thoracic cage and diaphragm, the latter mechanically linking the abdominal cavity to the thorax) also impact compliance of the respiratory system and, in turn, alter pleural and juxtacardiac pressures and transpulmonary pressure. For a given airway pressure and lung compliance, as chest wall compliance decreases, the transpulmonary pressure (and lung volume) decreases, and the degree to which airway pressure is transmitted to and sensed by the heart increases. Lesions of the chest wall commonly seen in critical illness include pleural effusions, edema of the thoracic cage, ascites, and abdominal visceromegaly.
Respiration and right ventricular afterload
Respiration impacts RV afterload by modifying pulmonary vascular resistance (PVR) as a result of changes in lung volume and the distribution of blood flow within the lung, alveolar oxygen tension (P A O 2 ), and carbon dioxide clearance/blood pH. Because the unprepared RV is very sensitive to increases in RV afterload, PPV-induced changes in RV afterload may have a significant impact on RV ejection.
The alveolar septae are highly vascular ( Fig. 32.5 ). More than 90% of the alveolar surface is in contact with alveolar capillaries. These vessels can be separated into two categories according to their location or response to lung inflation. Most alveolar vessels are capillaries and lie in septa, which separate adjacent alveoli. Other alveolar vessels are termed corner vessels because they are located at the intersection of alveolar septae. These corner vessels are generally larger and most likely will divide later in their course to become alveolar capillaries located in septa between adjacent alveoli. When the lung is stretched by either spontaneous inspiration or positive pressure distension, corner vessels are pulled open by radial traction and their resistance to blood flow is reduced. When alveolar septae are stretched, alveolar capillaries are stretched and compressed, become thinner, and restrict flow. The net effect of these factors is that PVR rises as lung volume rises above FRC and approaches total lung capacity. As lung volume falls below FRC and approaches residual volume, PVR increases owing to hypoxic pulmonary vasoconstriction of extraalveolar vessels. PVR is least at FRC and rises with either atelectasis or overdistension, producing a U-shaped relationship between PVR and lung volume ( Fig. 32.6 ).
When alveolar pressure is greater than ambient, as it is during PPV, the vessels that course through alveolar septae between adjacent alveoli can be compressed. , This behavior is akin to that of a Starling resistor, a collapsible tube traversing a rigid housing ( Fig. 32.7 ). Flow (Q) is propelled through the tube by inflow pressure (P i ) and is opposed by outflow pressure (P o ). The tubing has some intrinsic resistance (R). If the housing is pressurized to a surrounding pressure (P s ), flow through the tube is determined as follows: