The Heart Is Not Always in Good Hands: Changes in Cardiac Output

Posted by James

Pulsus Paradoxus. It has long been a puzzle why intrathoracic pressure changes, as exemplified by the positive pressure Valsalva maneuver and the negative pressure Mueller maneuver, have such small effects on cardiac output in spite of the large pressures (-I-150 mm Hg to —75 mm Hg) which can be imposed. Yet, lung volume changes, which are associated with minor changes in pleural pressure (from about – 5 to about — 25 mm Hg), appear to cause rather profound effects.

A simple illustration (Fig 4) shows why the pressures in the chest, which are the same as those around the heart when the glottis is closed, have relatively little effect on cardiac output. Imagine you are holding a segment of a hose pipe about half-way along its length. It is attached to a faucet and is discharging through a sprinkler onto your lawn. The segment of the hose between your hands is the make-believe chest. The heart pump, in the hose between your hands, has been temporarily stopped. In this example, the inflow represents the venous return determined by the mean circulatory pressure. It makes no difference whether you lower the hose right down to the ground, dropping its vertical pressure, or hold it over your head—the outflow will not be changed. You could squeeze the hose upstream of one unidirectional valve with your right hand (right ventricle) and upstream of another with your left hand (left ventricle) to give a fixed impetus to the blood in each position of the hose without destroying the analogy. The pressure within the chest (the verticle pressure above ground level) does not affect flow because of the siphon effect as long as the tubing (blood vessels) are patent. The alveolar corner vessels have been shown to remain patent in spite of high alveolar pressures. They could maintain the column of blood through the chest necessary for the siphon under quite extreme collaps­ing pressures during the Valsalva maneuver.

However, in reality, intrathoracic pressure does have some effect. To mimic this, imagine that there is a distensible segment of the hose pipe made up of the intrathoracic vessels and the heart between your hands. Now, with a suitable flow rate, the distensible segment will fill as you lower the hose to the ground, temporarily reducing output. As you raise the hose above your head, the distensible segment narrows so a volume is added and there is a transiently increased output (Fig 5). If the changes in vertical height represent the large pleural pressure swings due to the airflow obstruction, they would cause a pulsus paradoxus if assessed as pressure in make-believe down­stream systemic arteries. Note that it occurs without a heart or without the need for a change in the constant flow pump representing the heart. It depends on vessels which never obstruct completely, the presence of a distensible segment, and on the extent of the vertical movement. cialis canadian pharmacy

FIGURE 4. Garden hose pipe illustration of the lack of effect of intrathoracic pressure on blood flow through the chest. The blood filled intrathoracic vessels form a siphon.

It is also likely that pulsus paradoxus is augmented by temporary mechanical changes of the real heart pump because, particularly in diastole, it is part of the compliant intrathoracic vascular segment. If the upstream, distensible right ventricle dilates with the negative intrathoracic pressures, interventricular in­terdependence, exaggerated by the limited space in the cardiac fossa, would temporarily interfere with the filling, and thus the output of the left ventricle, at a time when its load was increased by the negative pressure around it. The left ventricle must generate a pressure equal to the difference between its surround­ing pressure and the systemic blood pressure. Simi­larly, when the segment is raised (intrathoracic pres­sures high), and the distensible right ventricle decreases in volume, the diastolic left ventricle could enlarge and, with its load decreased by the more positive pressure around it, increase its output tran­siently above the usual level to augment the pulsus paradoxus.

FIGURE 5. There is a transient outflow effect (pulsus paradoxus) when distensible vessels narrow and discharge their contents at high, and widen and retain blood at low intrathoracic pressures.

Output also changes when the segment is continu­ously held high (make-believe mechanical ventilation or PEEP) because the distensible segment narrows (but always remains open) so there is an increase in resistance to flow through it (Fig 6). At the same driving pressure, flow diminishes because of this rise in the resistance of the vessels, not because of the height (intrathoracic pressure) at which the segment is held. eriacta 100 mg

FIGURE 6. The distensible segment is held high (sustained positive intrathoracic pressure) so it narrows, increases resistance to flow and therefore diminishes cardiac output. The reverse occurs when it is lowered (sustained negative intrathoracic pressure).

Severe lung distension, associated with high positive alveolar pressures, may occur in patients because PEEP is imposed therapeutically. It may also occur inadvertently, when the ventilator rate is too high to accommodate the slow exhalation through obstructed airways. This is “auto-PEEP” and is particularly dangerous because it is not shown by the ventilator pressures. Although PEEP increases all intrathoracic pressures relative to systemic pressures, it is likely, because of the siphon effect (Fig 4) that it would have but a moderate effect on cardiac output were it not for the effect of high PEEP in stretching the vessels in regions of distended lung and tensing the walls of the cardiac fossa. Such distension is much less with the widespread patchy consolidation of ARDS. Then pleu­ral and extracardiac pressures do not rise much, and, more importantly, the already high pulmonary vascu­lar resistance is little worsened by the stretching of the vessels. So the effect of PEEP is buffered and cardiac output better preserved in patients with ARDS. The usual technique of assessing auto-PEEP during mechanical ventilation—by obstructing the airway after exhalation and measuring the equilibrium pressure subsequently reached—reflects the alveolar pressure which, because of the siphon effect in the blood vessels, may not be as important in depressing cardiac output as the amount of lung distension. This is yielded by the technique of measuring the volume of a 20 to 40 s unimpeded exhalation after a tidal inflation which gives a measure of the directly deleterious volume increase due to gas trapping. In some patients with ARDS it appears that the increase in afterload of the right ventricle, because of the high resistance to blood flow through the enlarged lungs, can dominate as the cause of the low cardiac output. Then there again seems to be an effect of ventricular interdependence in restricting left ventricular per­formance, because the enlarged right ventricle, react­ing to the increased afterload, limits diastolic left ventricular distension and output.