Constrictive Pericarditis
A condition involving severe scarring of the pericardium leading to tightening of the pericardium around the heart and preventing adequate blood flow in and out of the heart.
A. Etiology
- 1. Idiopathic
- 2. Posttraumatic, ie following heart surgery
- 3. Tumor invasion
- 4. Chest radiation for cancer
- 5. Infections, ie tuberculosis, fungus (see figures 38a, 38b, 38c, 38d)
B. Signs and Symptoms
- 1. Heart failure with swollen feet and legs (see figures 37, 38e)
- 2. Shortness of breath, fatigue
- 3. Calcification of pericardium (figure 38a, 38b)
- 4. Possible atrial fibrillation (see figures 14, 15a, 15b, 37)
THE VENOUS PULSE WITH SPECIAL REFERENCE TO CONSTRICTIVE PERICARDITIS
The normal jugular venous pulse (JVP) reflects changes in the right atrium and consists of three positive waves and two negative troughs. The positive presystolic "a" wave is produced by the right atrial (RA) contraction and is the dominant wave in the JVP, particularly during inspiration. During atrial relaxation, the venous pulse descends from the summit of the "a" wave. This descent may continue until a plateau ("z" point) is reached just prior to RV systole. More often,the descent is interrupted by another positive venous wave , the "c" wave, that is produced by bulging of the tricuspid valve into the right atrium during RV isovolumic systole and by the impact of the carotid artery adjacent to the jugular vein. Following the summit of the "c" wave, the JVP contour declines, forming the normal negative systolic wave, the "x" wave. The "x"descent is due to the combination of atrial relaxation, the downward displacement of the tricuspid valve during RV systole, and the ejection of blood from both ventricles. The positive, later systolic "v" wave in the JVP results from the increase in blood volume in the venae cavae and and right atrium during ventricular systole when the tricuspid valve is closed. After the peak of the "v" wave is reached, the RA pressure decreases because of the diminished bulging ot the tricuspid valve opening. In the JVP, the latter occurs at the peak of the "v" wave. Following the summit of the "v" wave, there is a negative descending limb, referred to as the "y" descent or diastolic collapse, which is due to the tricuspid valve opening and the rapid inflow of blood into the right ventricle. The initial "y" descent corresponds to the RV rapid filling phase. The trough of the "y" wave occurs in early diastole and is followed by the ascending limb of the "y", which is produced by the continued diastolic inflow of blood into the right side of the heart. The velocity of this ascending pressure curve depends on the rate of venous return and the distensibility of the chambers of the right side of the heart.
Now the diastolic inflow into the RV from the RA is "super-rapid" and "short" (limited to the first 1/3 of diastole), producing a sharp "y" descent, a deep "y" trough,and a "rapid" ascent to baseline in patients with constrictive pericarditis (fig. 38f). In these patients, cardiac volume is determined by the thickened, rigid pericardium, and the heart is unable to exceed this volume, which is attained near the end of the first third of diastole. During ejection, venous return commences unimpeded,and therefore, the normal systolic surge of the venous return is preserved. Cardiac compression remains insignificant at end systole, so that when the tricuspid valve opens, blood fills the ventricles at the above referred to supranormal rate. Thus, in constrictive pericarditis, the venous return is biphasic, but with a diastolic compoment greater than or equal to the systolic component.
Rourke,R.A. and others, The History,Physical Examination,And Cardiac Auscultation ,Hurst's The Heart,10th edition,pages 226-230.
HEMODYNAMICS OF CONSTRICTIVE PERICARDITIS
The intrapericardial space is obliterated in constrictive pericarditis (fig. 38i and fig. 38j). As a result, during inspiration, the decreased intrathoracic pressure is not transmitted to the heart, venous pressure does not fall, and systemic venous return fails to increase. As a result of the faster than normal filling in constrictive pericarditis, the ventricular diastolic pressure is characterized by a dip in early diastole (fig. 38h). By the end of the rapid filling phase, the ventricles are completely filled and the ventricular diastolic pressure remains unchanged and elevated for the remainder of diastole. The resultant pattern of ventricular diastolic pressure in constrictive pericarditis is referred to as the "dip-and-plateau pattern" or the "square-root-sign"
Early diastolic filling in constrictive pericarditis is unrestrained, and only at the end of the first third of diastole does the stiff pericardium abruptly restrict ventricular filling. As a result, ventricular pressure falls rapidly in early diastole and subsequently rises abruptly to an elevated level, where it remains until the next ventricular systole. End-diastolic ventricular pressures and mean atrial pressures are elevated and nearly equal (within 5 mmHg), and end-diastolic volumes and consequently, stroke volume and cardiac output are reduced. These pathophysiologic changes are responsible for the hemodynamic and physical findings that characterize constrictive pericarditis.
Hoit,Brain D.,Diseases of the Pericardium,Hurst's The Heart,10th edition,pages 2061-2085.
Abnormal Venous Pulse In Various Conditions Including Constrictive Pericarditis
ELEVATED VENOUS PRESSURE
The most common cause of an elevated jugular venous pressure is an increased RV pressure such as occurs in patients with pulmonic stenosis, pulmonary hypertension, or RV failure secondary to left-sided heart failure or RV infarction. The venous pressure also is elevated when obstruction to RV inflow occurs, as with tricuspid stenosis or RA myxoma, or when constrictive pencardial disease impedes RV inflow. It also may result from vena cava obstruction and, at times, an increased blood volume. Patients with obstructive pulmonary disease may have an elevated venous pressure only during expiration.
KUSSMAUL'S SIGN
Normally, during inspiration, there is an increase in the a wave of the JVP but a decrease in the mean jugular venous pressure as a result of the increased filling of the right-sided chambers associated with the decrease in intrathoracic pressure. Kussmaul's sign denotes an inspiratory increase in the venous pressure, which may occur in patients with severe constrictive pencarditis when the heart is unable to accept the increase in RV volume without a marked increase in the filling pressure. Although Kussmaul's sign was first described in patients with constrictive pericarditis, its most common cause is severe rightsided heart failure, regardless of etiology. The presence of Kussmaul's sign is also useful in the diagnosis of RV infarction.
ABNORMALITIES OF THE a WAVE
The a wave in the JVP is absent when there is no effective atrial contraction, such as in atrial fibrillation (see Fig. 38f-E). In certain other conditions, the a wave may not be apparent. In sinus tachycardia, the a wave may fuse with the preceding v wave, particularly if the PR interval is prolonged. In some patients with sinus tachycardia, the jugular a wave may occur during the v or y descent and may be small or absent. In the presence of first-degree AV block, a discrete a wave with ascending and descending limbs is often completed prior to the first heart sound, and the ac interval is prolonged (see Fig. 38f-F). Large a waves are of considerable diagnostic value (see Fig. 38f-B). When giant a waves are present with each beat, the right atrium is contracting against an increased resistance. This may result from obstruction at the tricuspid valve (tricuspid stenosis or atresia, right atrial myxoma) or conditions associated with increased resistance to RV filling. A giant a wave is more likely to occur in patients with pulmonic stenosis or pulmonary hypertension in whom both the atrial and ventricular septa are intact. Cannon a waves occur when the right atrium contracts while the tricuspid valve is closed during RV systole. 20° Cannon a waves may occur either regularly or irregularly and are most common in the presence of arrhythmias (see Fig. 38f-G).
ABNORMALITIES OF THE x WAVE
The most important alteration of the normally negative systolic collapse (x wave) of the JVP is its obliteration or even replacement by a positive wave. This is usually due to tricuspid regurgitation. Although atrial relaxation may contribute to the normal x descent, the development of atrial fibrillation does not obliterate the x wave except in the presence of tricuspid regurgitation. Accordingly, the occurrence of a positive wave in the JVP during ventricular systole is strong evidence of tricuspid regurgitation (Fig. 38f-A). Mild tricuspid regurgitation lessens and shortens the downward x wave as the regurgitation of blood into the right atrium produces a positive wave that diminishes the usual systolic fall in venous pressure. In some patients with moderate tricuspid regurgitation, there is a fairly distinct positive wave during ventricular systole between the c and v waves. This abnormal systolic waveform is usually referred to as a v or cv wave, although it has also been referred to as an r (regurgitant) or an s (systolic) wave. In patients with constrictive pericarditis, the x descent wave during systole is often more prominent than the early diastolic y wave (see Fig. 38f-C ).
ABNORMALITIES OF THE v WAVE
The positive, late systolic v wave results from the increasing RA blood volume during ventricular systole when the tricuspid valve normally is closed. With mild tricuspid regurgitation, the v wave and the obliteration of the x descent result in a single, large positive systolic wave (ventricularization) (see Fig. 38f-A and fig. 38g). Normally in the JVP the v wave is lower in amplitude than the a wave. In patients with an ASD, however, the a and v waves are often equal in the right atrium and the JVP (see Fig. 38f-D). In patients with constrictive pericarditis and sinus rhythm, the RA a and v waves also may be equal, but the venous pressure is increased, which is unusual with isolated ASD. In patients with constrictive pericarditis who are in atnal fibrillation, the cv wave is prominent and the y descent rapid.
ABNORMALITIES OF THE y TROUGH
The y descent, or diastolic collapse, is produced mainly by the tricuspid valve opening and the rapid inflow of blood into the right ventricle. A rapid, deep y descent in early diastole occurs with severe tricuspid regurgitation (see Fig. 38f-A). A venous pulse characterized by a sharp y descent, a deep y trough, and a rapid ascent to the baseline is seen in patients with constrictive pericarditis or with severe right-sided heart failure. A slow y descent in the JVP suggests an obstruction to RV filling and may be the only abnormal finding in patients with tricuspid stenosis or right atrial myxoma (see Fig. 38f-B). In both constrictive pericarditis and severe right-sided heart failure, the venous pressure is elevated with a sharp y dip in the JVP. The presence of a large positive systolic venous wave favors the diagnosis of severe heart failure.
Effects of Arrhythmias on the Venous Pulse
Large a waves in the JVP during arrhythmias are present when the P wave (atrial contraction) occurs between the onset of the QRS complex and the termination of the T wave (see Fig. 38f-G). Such cannon a waves may occur regularly in junctional rhythm. More commonly, they occur irregularly when AV dissociation accompanies premature ventricular beats, ventricular tachycardia, or complete heart block. The a wave is absent in patients with atrial fibrillation, and flutter a waves at a regular rate of 250 to 300 per minute occasionally are observed in patients with atrial flutter and varying degrees of AV block. Patients with multifocal atrial tachycardia often have prominent and somewhat variable a waves in the JVP. In these patients, many of whom have pulmonary hypertension secondary to lung disease, the a wave are often very large.
Rourke,R.A. and others, The History, Physical Examination,And Cardiac Auscultation, Hurst's The Heart,10th edition,pages 226-230.
C. Heart Catheterizatioin
- 1. Shows reduced ability of heart chambers to receive blood during filling period (diastole)
- 2. Leading to decreased, limited, fixed heart output, uneffected by exercise due to scarring of pericardium.