The Heart Is Not Always in Good Hands: Changes in Extracardiac Pressure

Posted by James

Lung Distension. In obstructed airflow disease, the end-tidal volume (FRC) is considerably enlarged and this volume characteristically rises further with the increase in ventilation demanded by infections or exercise. There are two important consequences of an increase in lung volume. One is the increase in right ventricular afterload, because the pulmonary vasculature is stretched and the resistance to flow through it is increased. The other is the distending force which stretches the heart and great vessels as it does the lungs (Fig 2). The pleural surfaces of the cardiac fossa and the surrounding lungs become more tense as the diaphragm descends and the rib cage expands.

Contrary to clinical lore, the average subcostal, intrapleural, or esophageal pressure does not increase much in obstructed airflow disease. The chest wall and diaphragm are still able to maintain the normal negative pressure average around the lungs. How¬ever, FRC expansion causes mediastinal pressures, particularly those around the heart in the cardiac fossa, to increase relative to subcostal intrapleural pressures. This could be because the lungs are bound together by the hilar structures and intrapulmonary ligaments so their expansion encroaches on the medi­astinal space, while they remain free to enlarge in the subcostal region (Fig 3).

The limitation of the space in the cardiac fossa has important effects on pressures around the heart. These extracardiac pressures depend upon the balance be­tween the size of the heart and the size of the cardiac fossa as well as the expansile pressures in the chest to which the cardiac fossa is exposed. This is particu­larly important for heart function when the walls of the cardiac fossa are tense. Under these conditions, an increase in cardiac size, demanded by the Frank- Starling diastolic volume increase for a rise in cardiac output, could lead to an appreciable increase in extracardiac pressure. It is interesting that the tradi­tional idea that the normal pericardial sac limits cardiac expansion is probably wrong. It is based on open-chest studies in supine animals where, of neces­sity, the cardiac fossa was retracted to get at the pericardial sac. So its effect was not seen or even thought about. buy cialis soft tabs

FIGURE 2. Effect of lung volume change on resistance of pulmonary vessels to blood flow. This increases at high and very low volumes.

Jugular Venous Pressure. Although imposed on the normal, hemodynamically determined pressure, changes in the jugular venous pressure are an excellent index of changes in extracardiac pressure, since they equal right atrial pressure changes and the right atrium acts as a pressure capsule which completely conforms to the cardiac surface. What is seen is always close to extracardiac pressure change since the Frank- Starling increase in right ventricular diastolic pressure required for any augmentation of right ventricular output is small in the normal, distensible, low pressure right heart. Thus, when jugular venous pressure rises above a horizontal line drawn through the sternal angle in any semi-reclining position (the upper limit of normal), the cause could be simply a raised extracar­diac pressure. During exacerbations of obstructive pulmonary disease, such a rise in extracardiac pressure is likely, both because the larger lung volume, (hyper- neic gas trapping) limits the space available in the cardiac fossa, and because there is cardiac enlarge­ment due to the output response to the stress. So the raised jugular venous pressure during acute exacer­bations of obstructive pulmonary disease is probably caused by this and not by right heart failure.

FIGURE 3. Gas trapping due to rapid breathing in patients with airflow obstruction increases lung volume, particularly of the lower lobes, and tenses the walls of the cardiac fossa. Pressures in the cardiac fossa become more positive relative to subcostal pressures at high lung volumes.

A better understanding of the role of the right atrial pressure as a reflection of extracardiac pressure has also clarified the jugular venous reflux test for right heart failure and the paradoxic rise in jugular venous pressure on inhalation when there is cardiac tampon­ade due to pericardial effusion (Kussmauls sign). In both conditions, the size of the heart or the heart and pericardial sac is enlarged relative to the cardiac fossa. And, in both conditions, abdominal pressure tends to augment this size by forcing an increase in venous return and volume load for the heart. The hepato- jugular venous reflux probably results from the manual compression of the splanchnic bed, particularly the engorged liver, which causes an increase in venous return, heart size, and extracardiac pressure reflected by right atrial and, therefore, jugular venous pressure. Similarly, the paradoxic increase in jugular venous pressure on inhalation with cardiac tamponade and related conditions could also be due to the increase in intra-abdominal pressure (liver compression) which acts as a self-imposed hepato-jugular reflux.
viagra plus

Wedge Pressure. Equal increases of wedge and jugular venous pressures which occur in patients with exacerbations of obstructive pulmonary disease are probably better explained as reflections of raised extracardiac pressures than as manifestations of left and right heart failure. Pressures in the cardiac fossa could be high in any condition where the heart is large and hyperpnea leads to an increase in FRC. For instance, during exercise in obstructive disease, the ventilation increases and gas trapping occurs. This particularly affects the lower lobes which form the cardiac fossa, so the walls of the cardiac fossa become tense. The extracardiac pressures go up because of the enlargement of the heart demanded by the rise in output during exercise. This could explain the raised wedge pressure that has led to the question of left heart failure on exercise. The hemodynamically de­termined pressure in the left atrium can be gauged by subtracting the right atrial pressure change from the left atrial (wedge) pressure. And, contrary to concerns of left ventricular failure, such end-diastolic left ventricular pressures are not abnormally elevated in exercising patients with airflow obstruction. Simi­larly, the increase in cardiac output and heart size due to the stress of weaning from a ventilator is associated with considerable tachypnea and gas trapping (“auto- PEEP”) in patients with airway obstruction. This could well be the cause of the elevation of wedge pressure suggesting left ventricular insufficiency at this time. The need for a measure of left heart failure in patients suspected of having ARDS is of clinical importance, since hydrostatic pulmonary edema must be excluded. Raised wedge pressures are difficult to interpret in these patients; they may be due to an increase in transmural left atrial pressure caused by left heart failure, but could merely reflect a rise in extracardiac pressure. Such an increase of extracardiac pressure occurs with positive pressure mechanical ventilation since positive airway pressures cause all the intrathoracic pressures to go up relative to atmos­pheric pressure, whether or not there is an increase in lung volume. Actually, PEEP is used to increase lung volumes in patients with ARDS, and raised lung volumes augment mediastinal and extracardiac pres­sures relative to the subcostal pressures. So the combined effect of PEEP and lung expansion could markedly elevate extracardiac and, therefore, intra­cardiac pressures. Again, subtraction of the right atrial pressure change from the wedge pressure gives the required left atrial pressure under these conditions and, when it has been done, has shown that the apparent left heart failure is spurious.

An important test for intravascular volume deple­tion is based on the measurement of the cardiac output response and wedge pressure elevation after an intra­vascular volume expansion from an acute saline load. A marked rise in wedge pressure is taken to indicate over-hydration. However, if the cardiac fossa is tense, wedge pressure may go up markedly, not because of over-hydration, but because of the expected increase in heart size with volume loading. Again, subtracting right atrial from wedge pressure changes and relating this left atrial pressure change to the cardiac output increase should give the required measure of the effect of the fluid load.