The heart within the thorax is a pressure chamber within a pressure chamber. Therefore changes in intrathoracic pressure will affect the pressure gradients for both systemic venous return to the right ventricle and systemic outflow from the left ventricle, independent of the heart itself ( BudaeLaL 1979; Pinsky,.et...a!: 1985).
Increases in intrathoracic pressure, by both increasing right atrial pressure and decreasing transmural left ventricular systolic pressure, will reduce these pressure gradients, thereby decreasing intrathoracic blood volume. However, by the same argument, decreases in intrathoracic pressure will augment venous return and impede left ventricular ejection, thus increasing intrathoracic blood volume. Variations in right atrial pressure represent the major factor determining the fluctuation in pressure gradient for systemic venous return during ventilation ( Fessler.et.,.§L 1992). Increases in intrathoracic pressure, as seen with positive-pressure ventilation or hyperinflation during spontaneous ventilation, decrease venous return, whereas decreases in intrathoracic pressure, as seen with spontaneous inspiration, increase venous return.
Spontaneous inspiratory efforts, by decreasing intrathoracic pressure, both increase lung volume and decrease right atrial pressure, accelerating blood flow into the right ventricle (Budaefa/, 1979) and increasing pulmonary blood flow on the subsequent beat. Thus normal respiration-associated hemodynamic changes maximize ventilation-perfusion temporal matching because the spontaneous inspiration matches an increase in alveolar oxygen flux with an increase in pulmonary capillary flow. However, the augmentation of venous return is limited because, as intrathoracic pressure decreases below atmospheric pressure, the large systemic veins collapse as they enter the thorax, limiting maximal venous flow (Fesslerefa/ 1992). This 'flow limitation' is useful because intrathoracic pressure can decrease greatly with obstructive inspiratory efforts. If the increase in venous blood flow were unlimited, the right ventricle could become overdistended in volume and fail.
Left ventricular afterload or systolic wall tension is proportional to the product of transmural left ventricular pressure and left ventricular volume. Since increasing intrathoracic pressure will mechanically decrease transmural left ventricular pressure if arterial pressure is constant, increases in intrathoracic pressure unload the left ventricle, whereas decreases in intrathoracic pressure have the opposite effect ( B.ud§..et.a/: 1979). Thus, in ventricular failure states associated with fluid resuscitation, increases in intrathoracic pressure increase cardiac output ( BudaetjaJ: 1979; P.insky.§t.§/: 1.9.8,5).
Spontaneous ventilatory efforts performed against a resistive (bronchospasm) or elastic (acute lung injury) load, decrease left ventricular stroke volume via a complex mechanism collectively called pulsus paradoxus. Transient intraventricular septal shift into the left ventricular lumen combined with pericardial volume restraint decreases absolute left ventricular end-diastolic volume (T.aY.!.oL§L§/: 1.967.; B.ui!.eL.19.8.3). Increases in left ventricular afterload (left ventricular pressure minus intrathoracic pressure) increase left ventricular end-systolic volume (Buda et al. 1983).
Sudden increases in intrathoracic pressure increase arterial pressure by an amount equal to the increase in intrathoracic pressure without changing aortic blood flow. However, if the increase in intrathoracic pressure is sustained, the decrease in systemic venous return induced will eventually decrease left ventricular output, thus decreasing arterial pressure (BydaeLal 1979). In the steady state, changes in intrathoracic pressure that result in altered cardiac output also alter peripheral vasomotor tone through baroreceptor mechanisms. Baroreceptor reflexes tend to keep systemic pressure (arterial pressure) and flow (cardiac output) constant. Thus, if intrathoracic pressure increased arterial pressure without changing transmural arterial pressure, the periphery would reflexly vasodilate to maintain a constant extrathoracic arterial pressure-flow relation ( Pin..S.kY.,.et...a.l: 1985). Since coronary perfusion pressure is not increased by intrathoracic-pressure-induced increases in arterial pressure, whereas mechanical constraint from the expanding lungs may obstruct coronary blood flow, coronary hypoperfusion from a combined coronary compression and a decrease in coronary perfusion pressure is a potential complication of increased intrathoracic pressure. Although increases in intrathoracic pressure should augment left ventricular ejection by decreasing left ventricular afterload, this effect should have limited therapeutic potential, just as all afterload-reducing therapies are limited by both the minimal end-systolic volume and the obligatory decrease in venous return. Thus the potential augmentation of left ventricular ejection by increasing intrathoracic pressure is limited under most conditions because increasing intrathoracic pressure, by reducing left ventricular ejection pressure, can only decrease end-systolic volume, which is usually already small and cannot decrease much more except in markedly dilated cardiomyopathies. However, the decrease in venous return associated with the increase in intrathoracic pressure can completely arrest venous blood flow.
Mechanically speaking, there is no difference between increasing intrathoracic pressure from a basal end-expiratory level and eliminating the negative end-inspiratory intrathoracic pressure swings seen in spontaneous ventilation. For many reasons, removing negative swings in intrathoracic pressure may be more clinically relevant than increasing intrathoracic pressure. First, many pulmonary diseases are associated with exaggerated decreases in intrathoracic pressure during inspiration. In restrictive lung disease states, such as interstitial fibrosis or acute hypoxemic respiratory failure, intrathoracic pressure must decrease substantially to generate a transpulmonary pressure that is large enough to ventilate the alveoli. Similarly, in obstructive diseases, such as upper airway obstruction or asthma, large decreases in intrathoracic pressure occur owing to increased resistance to inspiratory airflow. Second, exaggerated decreases in intrathoracic pressure require increased respiratory efforts that increase the work of breathing, taxing a potentially stressed circulation. Finally, the exaggerated decreases in intrathoracic pressure can only increase venous blood flow so much before venous collapse limits blood flow. The level to which intrathoracic pressure must decrease to induce venous flow limitation is different in different circulatory conditions, but in most patients it occurs below an intrathoracic pressure of -10cmH 2O (B.U,t!e.Ll,983). Thus further decreases in intrathoracic pressure will only increase left ventricular afterload without increasing venous return. Accordingly, abolishing these markedly negative swings in intrathoracic pressure should disproportionally reduce left ventricular afterload more than venous return (left ventricular preload). These concepts of a differential effect of increasing and decreasing intrathoracic pressure on cardiac function are illustrated for both normal and failing hearts in Fig 1 and Fig, 2 using the left ventricular pressure-volume relationship during one cardiac cycle to interpose venous return (end-diastolic volume) and afterload (end-systolic volume). Using this logic, one would predict that, by endotracheally intubating and ventilating such patients, markedly negative swings in intrathoracic pressure can be abolished without any impairment in systemic venous return or any need to make the swings in intrathoracic pressure more positive. These interactions have important implications in the decision both to institute and to withdraw mechanical ventilatory support.
Fig. 1 The effect of increasing (green shading) and decreasing (gray shading) intrathoracic pressure (ITP) on the left ventricular (LV) relation with left ventricular contractility is normal. The slope of the left ventricular end-systolic pressure-volume relationship (ESPVR) is proportional to contractility. The slope of the diastolic left ventricular pressure-volume relationship defines diastolic compliance.
Fig. 2 The effect of increasing (green shading) and decreasing (gray shading) intrathoracic pressure (ITP) on the left ventricular (LV) relation in congestive heart failure when left ventricular contractility is reduced and intravascular volume is expanded. The slope of the left ventricular end-systolic pressure-volume relationship (ESPVR) is proportional to contractility. The slope of the diastolic left ventricular pressure-volume relationship defines diastolic compliance.
Spontaneous ventilatory efforts require muscular activity, consume O2, and produce CO2, and they represent a metabolic load on the cardiovascular system. Although ventilation normally requires less than 5 per cent of total O 2 delivery to meet its demand, the O2 requirements may increase to 25 per cent or more of total O2 delivery in lung disease states where the work of breathing is increased, such as pulmonary edema or bronchospasm. Furthermore, if cardiac output is limited, this level of activity (spontaneous ventilation) may not be possible even with additional cardiovascular support. The institution of mechanical ventilation for ventilatory and hypoxemic respiratory failure may reduce metabolic demand on the stressed cardiovascular system increasing SvO2 for a constant cardiac output and CaO2. Intubation and mechanical ventilation, when adjusted to the metabolic demands of the patient, may dramatically decrease the work of breathing, resulting in increased O2 delivery to other vital organs and decreased serum lactic acid levels. Under conditions in which fixed right-to-left shunts exist, the obligatory increase in SvO2 will result in an increase in PaO2, despite no change in the ratio of shunt blood flow to cardiac output.
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