Heart–Lung Interactions


FIGURE 101.1 Schematic diagram of the relation between changes in lung volume and pulmonary vascular resistance, where the extra-alveolar and alveolar vascular components are separated. Note that pulmonary vascular resistance is minimal at resting lung volume or functional residual capacity (FRC). As lung volume increases toward total lung capacity (TLC) or decreases toward residual volume (RV), pulmonary vascular resistance also increases. However, the increase in resistance with hyperinflation is due to increased alveolar vascular resistance, whereas the increase in resistance with lung collapse is due to increased extra-alveolar vessel tone.



Hyperinflation-Induced Cardiac Compression

As lung volume increases, the heart is compressed between the expanding lungs (94), increasing juxtacardiac ITP. This compressive effect of the inflated lungs can be seen with either spontaneous (95) or positive-pressure–induced hyperinflation (5,40,96–98). As described above, both Ppc and ITP are increased and no pericardial restraint exists. This decrease in apparent LV diastolic compliance (93) was previously misinterpreted as impaired LV contractility, because LV stroke work for a given LV end-diastolic pressure or pulmonary artery occlusion pressure is decreased (99,100). However, when such patients are fluid resuscitated to return LV end-diastolic volume to its original level, both LV stroke work and CO also returned to their original levels (93,101) despite the continued application of PEEP (102).


HEMODYNAMIC EFFECTS OF CHANGES IN INTRATHORACIC PRESSURE


The heart within the thorax is a pressure chamber within a pressure chamber. Therefore, changes in ITP will affect the pressure gradients for both systemic venous return to the RV and systemic outflow from the LV, independent of the heart itself. Increases in ITP, by increasing right atrial pressure and decreasing transmural LV systolic pressure, will reduce the pressure gradients for venous return and LV ejection, decreasing intrathoracic blood volume. Using the same argument, decreases in ITP will augment venous return and impede LV ejection and increase intrathoracic blood volume; everything else follows from these simple truths.


Venous Return

Blood flows back from the systemic venous reservoirs into the right atrium through low pressure–low resistance venous conduits (103). Right atrial pressure is the backpressure for venous return; ventilation alters both right atrial pressure and venous reservoir pressure. It is these changes in right atrial and venous capacitance vessel pressure that induce most of the observed cardiovascular effects of ventilation. Pressure in the upstream venous reservoirs is called mean systemic pressure and is, itself, a function of blood volume, peripheral vasomotor tone, and the distribution of blood within the vasculature (104). Usually mean systemic pressure does not change rapidly during positive-pressure ventilation, whereas right atrial pressure does owing to concomitant changes in ITP. Thus, variations in right atrial pressure represent the major factor determining the fluctuation in pressure gradient for systemic venous return during ventilation (105,106). The positive-pressure inspiration increases in right atrial pressure, decreases the pressure gradient for venous return, decreasing RV filling (70) and RV stroke volume (70,105,107–115). During normal spontaneous inspiration, the opposite occurs (2,29,70,71,109,112,116,117). The detrimental effect of positive-pressure ventilation on CO can be minimized by either fluid resuscitation to increase mean systemic pressure (29,107,118,119) or by keeping both mean ITP and swings in lung volume as low as possible. Accordingly, prolonging expiratory time, decreasing tidal volume, and avoiding PEEP all minimize this decrease in systemic venous return to the RV (4,26,105,109–113,120).


However, if positive-pressure ventilation-induced increases in right atrial pressure always proportionally decreased venous return, then most patients would display profound cardiovascular insufficiency when placed on mechanical ventilator support and especially so when given increased levels of PEEP. Fortunately, when lung volumes increase, the diaphragm descends, compressing the abdominal compartment and increasing intra-abdominal pressure (121,122). Since a large proportion of venous blood exists in intra-abdominal vasculature, it is pressurized as well, increasing mean systemic pressure. Accordingly, the pressure gradient for venous return is often not reduced by PEEP (118). Inspiration-induced abdominal pressurization by diaphragmatic descent is probably the primary mechanism by which the decrease in venous return is minimized during positive-pressure ventilation (123–128). However, laparotomy, by abolishing the inspiration-associated increases in intra-abdominal pressure, makes surgery patients especially sensitive to mechanical ventilation and is one of the reasons why abdominal surgery patients often leave the operating room many liters positive.


Spontaneous inspiratory efforts usually increase venous return because of the combined decrease in right atrial pressure (2,28,110–112) and increase in intra-abdominal pressure (121,122), described above. However, this augmentation of venous return is limited (129,130) because as ITP decreases below atmospheric pressure, central venous pressure also becomes subatmospheric, collapsing the great veins as they enter the thorax and creating a flow-limiting segment (103).



FIGURE 101.2 Schematic diagram of the effect of increasing right ventricular (RV) volumes on the left ventricular (LV) diastolic pressure–volume (filling) relationship. Note that increasing RV volumes decrease LV diastolic compliance, such that a higher filling pressure is required to generate a constant end-diastolic volume. (Adapted from Taylor RR, Covell JW, Sonnenblick EH, Ross J Jr. Dependence of ventricular distensibility on filling the opposite ventricle. Am J Physiol. 1967;213:711–718.)


Ventricular Interdependence

Since spontaneous inspiration increases RV filling, it will also directly alter LV diastolic compliance by the process of ventricular interdependence. Increasing RV volume decreases LV diastolic compliance, while decreasing RV volume increases LV diastolic compliance, although the positive-pressure ventilation effect of increased LV diastolic compliance is usually minimal (Fig. 101.2) (90,131–134).


However, the spontaneous inspiration-induced RV volume increase reduces the LV diastolic compliance and is the primary cause for the inspiration-associated decrease in LV stroke volume and pulse pressure (89,91,134,135). If the pulse pressure change is greater than 10 mmHg, or 10% of the mean pulse pressure, then it is referred to as pulsus paradoxus (2). Since spontaneous inspiratory efforts can also occur during positive-pressure ventilation, the use of ventilation-associated pulse pressure variation (PPV) during positive-pressure ventilation can reflect ventricular interdependence. Presently, positive-pressure–induced changes in pulse pressure and LV stroke volume have been advocated to be a useful parameter of preload-responsiveness (136). However, in order to assess volume responsiveness using PPV, it is essential that no spontaneous inspiratory efforts be present. These points are discussed in greater detail in the next section.


Changes in ITP can directly and indirectly alter LV afterload by altering both LV end-diastolic volume and ejection pressure. LV ejection pressure can be estimated as arterial pressure relative to ITP. Since baroreceptor mechanisms located in the extrathoracic carotid body maintain arterial pressure constant relative to atmosphere, if arterial pressure were to remain constant as ITP increased, then transmural LV pressure and thus LV afterload would decrease. Similarly, if transmural arterial pressure were to remain constant as ITP decreased then LV wall tension would increase (137). Thus, under steady-state conditions, increases in ITP decrease LV afterload and decreases in ITP increase LV afterload (138,139). The spontaneous inspiration-associated decrease in ITP-induced increase in LV afterload is one of the major mechanisms thought to be operative in the wean-induced LV ischemia described in the first part of this chapter, since increased LV afterload must increase myocardial O2 consumption (MVO2). Thus, spontaneous ventilation not only increases global O2 demand by its exercise component (3–5), but also increases MVO2.


Profoundly negative swings in ITP commonly occur during forced spontaneous inspiratory efforts in patients with bronchospasm and obstructive breathing. This condition may rapidly deteriorate into acute heart failure and pulmonary edema (65), as has been described for airway obstruction (asthma, upper airway obstruction, vocal cord paralysis) or stiff lungs (interstitial lung disease, pulmonary edema, and ALI), as these swings may selectively increase LV afterload and may be the cause of the LV failure and pulmonary edema (1,51,65,66) seen, especially if LV systolic function is already compromised (13,140). Clearly, weaning from mechanical ventilation is a selective LV stress test (137,141,142). Similarly, improved LV systolic function is observed in patients with severe LV failure placed on mechanical ventilation (142).


The improvement in LV functional seen with positive-pressure ventilation in subjects with severe heart failure is self-limited, because venous return also decreases, limiting total blood flow. However, the effect of removing large negative swings of ITP on LV performance will also act to reduce LV afterload, but will not be associated with a change in venous return because, until ITP becomes positive, venous return remains constant. Thus, removing negative ITP swings on LV afterload will selectively reduce LV afterload in a fashion analogous to increasing ITP, but without the effect on CO (23,29,103,143–145). This concept has been validated to be a very important clinical approach for patients with obstructive sleep apnea. For example, the cardiovascular benefits of positive airway pressure in nonintubated patients can be seen with CPAP therapy for heart failure patients (146,147). Even low levels of CPAP, if they inhibit airway obstruction, will be beneficial (148,149). Prolonged nighttime nasal CPAP can selectively improve respiratory muscle strength, as well as LV contractile function if the patients have pre-existent heart failure (150,151); these benefits are associated with reductions of serum catecholamine levels (152). Furthermore, CPAP therapy now forms the fundamental first step in the management of acute cardiogenic pulmonary edema, because it both abolishes the negative swings in ITP during inspiration while sustaining alveolar oxygenation, and it does this from the very first breath it delivers (153,154).


USING HEART–LUNG INTERACTIONS TO DIAGNOSE CARDIOVASCULAR INSUFFICIENCY


Since the cardiovascular response to positive-pressure breathing is determined by the baseline cardiovascular state, ventilation-associated changes in arterial pulse pressure and stroke volume should be inferential for dynamic changes in venous return and the responsiveness of the heart to these transient and cyclic changes in preload (155). Both arterial pulse pressure (diastole to systole) and systolic pressure variations during positive-pressure ventilation nicely describe preload-responsiveness, with threshold values of greater than 10% variability compared to mean values in a patient on 8 mL/kg or more, adapted to the ventilation and without dysrhythmias (136). This technique can be modified to assess stroke volume variation (SVV) (156) and has profound clinical potential as newer monitoring devices allow for the bedside display of both PPV and SVV. In subjects on controlled mechanical ventilation, a PPV of more than 13% or an SVV of more than 10% accurately predict preload-responsiveness. Since a primary cardiovascular management decision in shock is whether or not to give intravascular fluids to increase blood flow (157), knowing if a patient is volume responsive before giving fluids will both prevent overhydration of nonresponsive patients and aid in monitoring the response to fluid resuscitation in responsive ones. This approach has been termed functional hemodynamic monitoring because it uses a repetitive known physiologic perturbation to drive a readout physiologic signal defining cardiovascular reserve. This application of heart–lung interactions has been validated in many prospective clinical trials, reviewed in a meta-analysis (158). This practical application of heart–lung interactions is now commonplace. Importantly, a basic understanding of the principles described in this chapter is an essential part of the training of acute care physicians. For example, the ITP-induced PPV and SVV, caused by the positive pressure breath, would be inaccurate if tidal volume were to vary from breath to breath. Similarly, if chest wall compliance were to decrease, owing to increased intra-abdominal pressure limiting diaphragmatic descent, then the accuracy of these measures would also decline.


Many functional hemodynamic monitoring approaches take advantage of these dynamic transients to measure either the capacity of the ventricles to fill as the pressure gradient for ventricular filling changes, or for the ventricles to proportionally eject this varying amount of volume (159). As described above, both spontaneous and positive-pressure breathing, by altering the pressure gradients for venous return to the right ventricle, can be used to assess both right and left ventricular preload reserve (160). For dynamic changes in venous return to alter LV stroke volume or arterial pulse pressure, then both RV and LV preload reserve need to be present. Dynamic venous flow changes during spontaneous and positive-pressure ventilation identify RV preload reserve, and can be measured indirectly by the dynamic changes in inferior vena caval (161), superior vena caval (162), and internal jugular venous diameters (163). Threshold values above 10% to 15% change in diameter define volume-responsiveness.


Because both SVV and PPV sensitivity degrade during spontaneous ventilation, low tidal volume ventilation, severe cor pulmonale and other extremes of physiology (164), alterative tests have been proposed. Specifically, performing passive leg-raising maneuvers to transiently increase venous return while concomitantly monitoring transient changes in left-sided CO is very sensitive and specific predictor of volume responsiveness under most conditions (165). It also becomes inaccurate when intra-abdominal hypertension exists because the pressure gradient for venous return is altered less (166).


Key Points




  • Spontaneous ventilation is exercise.

    • Failure to wean may connote cardiovascular insufficiency.
    • Weaning is a cardiovascular stress test.
    • Breathing loads both the heart and lungs.

  • Changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa in a fashion analogous to cardiac tamponade.

    • Low lung volumes increase pulmonary vasomotor tone by stimulating hypoxic pulmonary vasoconstriction.
    • High lung volumes increase pulmonary vascular resistance by increasing transpulmonary pressure.

  • Spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic pressure.

    • Increasing venous return.
    • Increasing LV afterload.

  • Positive-pressure ventilation increases intrathoracic pressure.

    • Decreasing venous return.
    • The decrease in venous return is mitigated by the associated increase in intra-abdominal pressure.
    • Decreasing LV afterload.
    • Abolishing negative swings in ITP selectively reduces LV afterload without reducing venous return.

ACKNOWLEDGMENTS


Supported in part by the NIH grants HL074316, HL120877 HL07820, and NR013912.


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Feb 26, 2020 | Posted by in CRITICAL CARE | Comments Off on Heart–Lung Interactions

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