Splitting of the second heart sound in constrictive pericarditis, with observations on the mechanism of pulsus paradoxus

doi:10.1016/0002-8703(62)90175-8

American Heart Journal

Volume 64, Issue 6, December 1962, Pages 765-778

https://doi.org/10.1016/0002-8703(62)90175-8 Get rights and content

Abstract

An unusual form of inspiratory widening of the split second sound is reported in 4 cases of constrictive pericarditis with pulsus paradoxus. The widened split is due to a sharp initial movement of A₂ toward the R wave of the electrocardiogram while the R-P₂ interval remains relatively fixed.

Clinically, the split appears to be unusual in that it occurs right at the onset of inspiration and lasts for one or two beats only, but it is only by phonocardiography that the predominant movement of A₂ can be established.

The shortening of the R-A₂ interval during inspiration is related in time of onset and magnitude to the drop in systemic pressure: both events are attributed to a reduction in left ventricular stroke volume.

Catheter studies in 3 patients showed that both the wide split and the small arterial pulse occurred one beat after a sharp fall in wedge pressure and were not related to the subsequent rise in wedge pressure that occurred during a prolonged inspiration in one patient.

Right atrial pressures showed minimal respiratory fluctuations. Simultaneous wedge and left atrial tracings in one patient showed a diminution in pressure gradient between wedge and left atrium during inspiration. This confirms previous work that pulsus paradoxus occurs as a result of differential effects of the negative intrathoracic pressure on intrapericardial and extrapericardial structures.

The relatively late rise in right atrial and wedge pressures that occurs during inspiration in some cases may be due to increased intrapericardial tension produced by diaphragmatic descent but is unrelated to the fundamental mechanism of pulsus paradoxus.

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A Modern Approach to Tuberculous Pericarditis
2007, Progress in Cardiovascular Diseases
Citation Excerpt :
Rarely, there may be classic angina from compression of coronary arteries.46,47 A diastolic knock (pericardial knock) that coincides with a high-pitched early diastolic sound and sudden inspiratory splitting of the second heart sound (Vogelpoel-Beck sign)48 are subtle but specific physical signs, found in 21%, 45%, and 36% of patients with constrictive pericarditis, respectively (Table 1).39 These physical signs are often missed by the inexperienced observer.
The human immunodeficiency virus (HIV) epidemic has been associated with an increase in all forms of extrapulmonary tuberculosis including tuberculous pericarditis. Tuberculosis is responsible for approximately 70% of cases of large pericardial effusion and most cases of constrictive pericarditis in developing countries, where most of the world's population live. However, in industrialized countries, tuberculosis accounts for only 4% of cases of pericardial effusion and an even smaller proportion of instances of constrictive pericarditis. Tuberculous pericarditis is a dangerous disease with a mortality of 17% to 40%; constriction occurs in a similar proportion of cases after tuberculous pericardial effusion. Early diagnosis and institution of appropriate therapy are critical to prevent mortality. A definite or proven diagnosis is based on demonstration of tubercle bacilli in pericardial fluid or on histologic section of the pericardium. A probable or presumed diagnosis is based on proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated biomarkers of tuberculous infection, and/or appropriate response to a trial of antituberculosis chemotherapy. Treatment consists of 4-drug therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months followed by 2 drugs (isoniazid and rifampicin) for 4 months regardless of HIV status. It is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction, and their safety in HIV-infected patients has not been established conclusively. Surgical resection of the pericardium is indicated for those with calcific constrictive pericarditis or with persistent signs of constriction after a 6 to 8 week trial of antituberculosis treatment in patients with noncalcific constrictive pericarditis.
Tuberculous pericarditis
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The cineangiocardiogram in constrictive pericarditis
1974, Clinical Radiology
Selective cineangiocardiographic patterns were studied in 60 patients with constrictive pericarditis.
The venae cavae were dilated, the right atrium had a vertical, straight immobile right border, the atrio-ventricular ring was hypermobile and the apex of the right ventricle was obliterated. The pulmonary artery was normal but the pulmonary veins were distended, particularly those draining from the upper lobes. The left atrium was normal in size, but the left ventricle was small and constricted, with a visible ventricular filling halt and a normal ejection fraction.
The procedure of cine-angiocardiography was simple, uncomplicated and diagnostic.
Commentary
1972, The American Journal of Cardiology
The second heart sound in normal and abnormal conditions
1971, The American Journal of Cardiology
Changes of the second heart sound are caused by shifting in position and changes in magnitude of the aortic or pulmonary component, or both. Differences in the magnitude of each component are primarily related to changes in pressure but are also affected by structural changes of the vascular walls.
Positional changes are influenced by the time of closure of the respective valve (in turn related to time of ventricular activation, duration of systole and pressure gradient across the valve) and by the interval between valve closure and vascular vibration at the time of rebound. Normal splitting is present during inspiration and decreases or disappears during expiration. Marked differences related to age are present.
Three abnormalities may occur: wide splitting during inspiration that persists during expiration; single second sound; and reverse splitting, either occurring only during, or accentuated by, expiration (occasionally also occurring during inspiration).
Acoustic phenomena in pericardial disease
1971, American Heart Journal

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^☆: Part of the expenses of this study has been defrayed by grants from the Council for Scientific and Industrial Research and the City Council of Cape Town.

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Clinical communicationSplitting of the second heart sound in constrictive pericarditis, with observations on the mechanism of pulsus paradoxus☆

Abstract

Am. J. Cardiol.

Am. J. Cardiol.

Am. Heart J.

Am. J. Cardiol.

Am. J. Med.

Lancet

Am. J. Cardiol.

Am. Heart J.

Phonocardiography

Brit. M. Bull.

Intra and extraarterial pulse recordings in health and disease

Pulmonary capillary pressure in man

J. Appl. Physiol.

Splitting of the first and second heart sounds

Lancet

Physiologic splitting of the 2nd heart sound

Circulation

The mechanism of respiratory variation in splitting of the second heart sound

Circulation

The splitting of the 2nd heart sound in normal subjects and patients with congenital heart disease

Circulation

Determinants of duration and mean rate of ventricular ejection

Circulation Res.

The influence of the respiration on the circulation in man

Am. J. Med.

Pulmonary blood flow and venous return during spontaneous respiration

Circulation Res.

Clinical communication
Splitting of the second heart sound in constrictive pericarditis, with observations on the mechanism of pulsus paradoxus☆