The Heart Is Not Always in Good Hands

Posted by James

The Problems

TJecently there have been considerable advances in our understanding of the role of the “hands that hold the heart” —the lungs which form the cardiac fossa in which the heart lies in the chest —in affecting cardiovascular function in health and in disease (Fig 1). I shall try to use this new knowledge to clarify some of the clinical problems of cardiopulmonary interactions that have puzzled physicians dealing with chest diseases.

Atrial Pressures

Is right or left ventricular failure caused by acute exacerbations of chronic obstructive pulmonary dis­ease?

A raised jugular venous pressure occurs during exacerbations of obstructed airflow disease and has been regarded as a sign of right ventricular failure. It is more evident when there is a worsening of airflow obstruction attributable to a flare-up of respiratory infection. The possibility of right heart failure is often supported by the presence of a palpable liver and peripheral edema. However, these patients do not have heart failure by the usual criteria since they have a normal or increased cardiac output and are able to augment blood flow on exercise.

The puzzle of the raised jugular venous pressure, mentioned above, is made even more challenging by the demonstration that the wedge pressure, measured relative to atmospheric pressure at the mid-thoracic level, is also high, leading to the impression that there is left heart failure, as well as right heart failure. Exercise also appears to cause a raised wedge pressure even when there is stable obstructive pulmonary disease. viagra 10 mg

Figure 1. The cardiac fossa.

Does left heart failure occur in patients when they are ventilated with positive pressures?

Inexplicable rises in wedge pressure, greater than can be accounted for by the positive intrathoracic pressures, are common during mechanical ventilation and important when the adult respiratory distress syndrome (ARDS) is treated by positive end-expira­tory pressure (PEEP) since hydrostatic pulmonary edema must be excluded. Such pressures cause particular alarm about left heart failure when they occur with spontaneous breathing during attempts at weaning from mechanical ventilation.⁷

Cardiac Output

Does pulsus paradoxus signify cardiac dysfunction in patients with airway obstruction?

Pulsus paradoxus is an inspiratory fall in left ventricular output at the time when venous return to the heart should be increasing—hence the “paradoxus” and the puzzle about its cause. This sign was first described in pericardial effusion, although now an exacerbation of chronic obstructive pulmonary disease or an attack of asthma is particularly associated with pulsus paradoxus. The puke pressure, reflecting out­put, is decreased on inhalation and increased on exhalation and the extent of this swing from inhalation to exhalation is very useful clinically as a reflection of the severity of the airflow obstruction. Why is cardiac output less depressed by PEEP when ARDS is present?
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A fall in cardiac output with positive pressure breathing is an important problem. However, in very sick patients with ARDS, quite high levels of PEEP can be tolerated. These findings have been the subject of considerable controversy since the description of the syndrome and its treatment. Why, when there is heart failure, is cardiac output maintained during periods of very positive intratho­racic pressure?

A “square wave” (maintained blood pressure) re­sponse to a positive intrathoracic pressure (Valsalva maneuver) has been used as a clinical test for the presence of heart failure. Normally, after an initial rise, there is a fall in systemic blood pressure and cardiac output during a voluntary squeeze of the chest. This is followed by a characteristic overshoot of pressure and a bradycardia after release of the pres­sure. Surprisingly, in heart failure, pressure and output are maintained during the Valsalva maneuver and there is no overshoot.

Why does the right ventricle hypertrophy in chronic obstructive pulmonary disease?

Cor pulmonale and the presence of right heart failure in obstructive pulmonary disease have been attributed to an increase in the right ventricular afterload, measured as pulmonary artery pressure, as a result of hypoxic vasoconstriction or loss of pulmo­nary vessels. In reality, the pulmonary artery pressure is but little increased in chronic obstructive pulmonary disease, typically into the 20-30 mm Hg range, while pulmonary artery pressures up to systemic levels appear to be tolerated without overt right heart failure in congenital heart disease or primary pulmonary hypertension. The concept that the hypertrophy is due to intermittent hypoxic vasoconstriction (during sleep, for instance), has also been challenged because oxygen breathing, while it may reduce the pulmonary artery pressure, does not restore it to normal either short-term or after long-term oxygen breathing at home. Also, the idea that the cor pulmonale is due to high pulmonary vascular resistance because of obstructions in, or a loss of, pulmonary vessels in regions where there are emphysematous changes is even more unlikely because these are irreversible vascular conditions and it has been shown repeatedly that there is an improvement in right ventricular (unction with recovery from an exacerbation of airflow obstruction.
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Why does the left ventricle hypertrophy in chronic obstructive pulmonary disease?

Perhaps most surprising of all, since lung disease should affect only the right heart, is that left ventric­ular hypertrophy is present in up to Уз of patients with cor pulmonale due to airflow obstruction. This is not just the left ventricular septal hypertrophy which might be associated with an increase in right ventricular muscle mass, but an overall thickening involving the free wall of the left ventricle. Why should the left ventricle be enlarged so frequently when, according to some (although not all) reports, there is no evidence of systemic hypertension or other known causes?