Pericardial disease
ecgwaves.com · Clinical Echocardiography
Chapter 1: Constrictive pericarditis: definition, causes, diagnosis & echocardiography
This chapter is available 2 days after the completion of the previous chapter.
Constrictive pericarditis: the end stage of pericardial inflammation
Constrictive pericarditis is the result of chronic inflammation of the pericardium. In principle, all causes of pericarditis can result in constrictive pericarditis. In high-income countries, idiopathic pericarditis, radiation to the pericardium and surgical interventions are the most common causes of constrictive pericarditis. Of these three, idiopathic pericarditis is the most common cause of constrictive pericarditis. It usually takes several years to develop the constriction, but in some cases, it may appear a few months after the inflammation has occurred.
In constrictive pericarditis, the pericardium becomes fibrotic (rigid) and thickened (about 80% have thickening). The parietal and visceral leaves of the pericardium are most often fused. The process most often affects the entire pericardium. Constrictive pericarditis is most often chronic, but in some cases, the condition may be transient. Pericardiotomy can be curative, which is why it is important to detect the disease early in the course.
Hemodynamic effects of constrictive pericarditis
Diastolic heart failure and right heart failure
The rigid pericardium prevents all four heart chambers from dilating adequately during diastole. This leads to increased and equivalent diastolic pressure in all rooms. Because pressure is high in the atria, filling of the ventricles occurs fast at the beginning of diastole, but it becomes incomplete because the ventricles cannot expand normally. This leads to diastolic heart failure. The systolic function is usually unaffected, but the shock volume and ejection fraction (EF) may be reduced because the end-diastolic volume of the ventricle (EDV) is reduced. Constrictive pericarditis also leads to right-sided heart failure, which is explained by the fact that high pressure in the right atrium leads to a decrease in atrial filling.
Respiratory variations in E-wave velocity
Under normal circumstances, intrathoracic pressure decreases during inhalation, which lowers pressure in the pulmonary veins and left atrium; this facilitates blood flow from the pulmonary veins to the left atrium. In constrictive pericarditis, the pericardium is so rigid that it is not affected by pressure changes in the thorax. This leads to the fact that the pressure in the left atrium does not decrease when inhaled and, as a result, the blood flow from the pulmonary vein to the left atrium is hampered. This reduces the filling of the left atrium and, accordingly, the left ventricle. The reduced flow over the mitral valve results in reduced E-wave velocity during inhalation. Since the left ventricle is not filled normally, there is more room for the right ventricle, the filling of which increases and the septum bulges into the left ventricle. During exhalation, the conditions are the reverse; the flow increases above the mitral valve and instead decreases the pressure difference between the right atrium and the inferior vena cava, which causes the blood to flow in the retrograde direction (from the atrium to the inferior vena cava).
In constrictive pericarditis, the E wave velocity varies during inspiration and expiration. The E wave velocity is lower during inspiration.
Differential diagnosis: restrictive cardiomyopathy
It is important to be able to differentiate constrictive pericarditis from restrictive cardiomyopathy, as a result of which the myocardium is rigid and imperative, which also leads to an increase in diastolic pressure in the ventricles and atria. At present, echocardiography is the first choice in investigating suspected constrictive pericarditis. The ECG can show low voltage and nonspecific ST-T changes. Conventional thoracic X-ray sometimes reveals calcification of the pericardium. With MRI or CT, the thickness of the pericardium can be measured and in most cases, a thickening is noted. Table 1 presents the similarities and differences between restrictive cardiomyopathy and constrictive pericarditis.
Table 1. Differentiation between constrictive pericarditis and restrictive cardiomyopathy.
| Parameter | Constrictive pericarditis | Restrictive cardiomyopathy |
|---|---|---|
| Thickened pericardium and moderate pericardial effusion | Occurs | Rarely |
| Dilated vena cava inferior | Yes, with respiratory variation | Yes |
| Premature opening of pulmonary valve | Yes, due to increased right ventricular pressure | No |
| Septal bounce | Yes. Septum moves into the left ventricle during inspiration | No |
| E-wave velocity | Increased | Increased |
| Respiratory variation in E wave velocity | >25% | None |
| E/A ratio | Increased | Increased |
| Deceleration time | <160 msec | <160 msec |
| Retrograde flow in vena cava inferior during expiration | Yes | No |
| Increased pulmonary vein flow during expiration | Yes | No |
| é velocity | Normal or increased | Decreased |
| E/é ratio | Normal or decreased (max 8). High filling pressure with normal E/é ratio is patognomonous for constrictive pericarditis. | Increased (usually 15 or more) |
| Lateral é < medial é | Yes. The lateral part of the mitral annulus is attached to the pericardium, giving it slower speed in constrictive pericarditis. | No |
| Longitudinal strain (é mitral annulus). | Normal or increased | Reduced |
Symptoms of constrictive pericarditis
Symptoms of constrictive pericarditis are related to diastolic heart failure, low cardiac output, high atrial pressure, and right ventricular heart failure. This means that the patient suffers fatigue, dyspnoea, leg edema, hepatic edema, ascites, cervical vein stasis, etc.
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Chapter 2: Pericardial Effusion & Cardiac tamponade
This chapter is available 2 days after the completion of the previous chapter.
Pericardial diseases: effusion and tamponade
A long series of conditions can affect the pericardium (pericardium). The most common of these are acute pericarditis (perimyocarditis), constrictive pericarditis, pericardial effusion and tamponade. Less common are cysts and tumors of the pericardium, as well as congenital malformations leading to an incomplete or absent pericardium. In case of suspicion of pericardial disease, it is important to conduct a careful investigation as several conditions may affect hemodynamics and the underlying cause is often serious (e. g. malignancy, amyloidosis).
In case of suspicion of pericardial disease, in the first place, an echocardiographic examination is done. With echocardiography, good conditions are obtained for visualizing the pericardium, its surroundings, the myocardium and valves. ECG is recorded in all patients with suspected pericardial disease. In addition to echocardiography, ECG and clinical examination, blood tests and other radiological examinations are most often required, in particular computed tomography (DT) and/or magnetic resonance imaging (MRI).
Anatomy of the pericardium
The pericardium consists of a parietal layer and a visceral layer. The parietal layer is 2 mm thick, rich in connective tissue and envelops the entire heart and the departures of the larger vessels. The visceral layer consists of mesothelian cells, collagen and elastin and is fused with the myocardium. At the departures of the larger vessels, the visceral layer is folded back to cover the inside of the parietal layer. Between the visceral and parietal layers there is the pericardial cavity (pericardial sac) containing pericardial fluid. This fluid is produced by the mesothelian cells and consists of 25-50 mL serous fluid.
Function of the pericardium
The pericardium is considered to have several functions, despite the fact that it can be removed without affecting cardiac function or hemodynamics. The following functions are attributed to the pericardium:
The pericardium serves as a barrier to infections. The pericardium reduces friction between the ventricles and surrounding structures of the mediastinum. Friction is reduced because the fluid in the pericardial sac (pericardial fluid) reduces friction between the ventricles and surrounding structures.The pericardium provides some fixation of the heart in the mediastinum. The heart is fixed to the larger vessels and diaphragm, which stabilizes the position of the heart.The parietal layer limits the volume filling of the chambers. At normal filling volumes, the pericardium is very indulging and thus allows rapid ventricular filling. If the dilatation of the ventricles becomes pronounced, then the pericardium becomes inelastic and rigid, which limits the dilatation. It allows the pericardium to limit the filling of the chambers when the volumes become too large. Thus, the pericardium is considered to contribute to the fact that the ventricles are not overfilled in acute volume loads.
Pericardial Effusion: fluid in the pericardial space
Normally, the pericardial sac contains 25 to 50 ml of liquid. This volume is so small that the pericardial space is usually not visible on ultrasound (alternatively, a few millimeters of pericardial space can be seen). If the amount of fluid in the pericardial cavity exceeds 50 mL, there is an effusion, which is considered pathological. The effusion, as a rule, is ecolucent (ecofatical), but, depending on the etiology, may be more or less echogenic. It is important to estimate the volume, echogenicity and location of the effusion.
Regarding the location, an effusion may be general (circumferential) or localized to a specific area. The effusion itself may consist of serous fluid (transudate), protein-rich fluid (exudate) to pure blood (exudate).
Often pericardial effusion is detected randomly (for example, in CT, MRI, echocardiography). In other cases, the effusion is detected under more dramatic circumstances, as is the case, for example, in acute pericarditis or tamponade. Note that pericardial effusion is not mandatory in acute pericarditis.
Causes of pericardial effusion
A variety of cardiac conditions and systemic diseases can cause pericardial depletion. Despite careful investigation, a significant proportion of all effusions remain classified as idiopathic, which means that the etiology is unknown. Malignancy is a common cause of pericardial depletion.
TABLE 1. Causes of pericardial effusion
| ETIOLOGY | COMMENTS |
|---|---|
| Myocardial infarction with ventricular rupture Rupture | of the ventricular wall leads to hemopericard and tamponade. |
| Dressler’s syndrome | In myocardial damage (eg, myocardial infarction), inflammation may become pronounced and engage the pericardium with pericardial effusion as a consequence. |
| Infections | |
| Renal failure | |
| Hypothyroidism | |
| Malignancy | |
| Amyloidosis | |
| SLE | |
| Rheumatoid Arthritis | |
| Vasculitis | |
| Post-pericardiotomy | |
| Complications to invasive studies and treatments (pacemaker, ICD, CRT, ablation, Catheterization, electrophysiological examination) | |
| Trauma of the chest | |
| Radiation to mediastinum | |
| Bleeding | Most often a consequence of treatment with anticoagulants. |
engage the pericardium with pericardial effusion as a consequence. InfectionsRenal failureHypothyroidismMalignancyAmyloidosisSLERheumatoid ArthritisVasculitisPost-pericardiotomyComplications to invasive studies and treatments (pacemaker, ICD, CRT, ablation, Catheterization, electrophysiological examination)Trauma of the chestRadiation to mediastinumBleedingMost often a consequence of treatment with anticoagulants.
Clinical characteristics in pericardial effusion
Pericardial deffusion can be anything from asymptomatic to immediately fatal. There is a strong correlation between the extent of pericardial effusion and hemodynamic consequences. Cardiac tamponade (tamponade) means that the effusion is so pronounced that the heart flows around in the fluid. In the case of tamponade, as a rule, there are hemodynamic consequences that affect the pumping function and which can lead to hypotension and asystole.
Echocardiographic findings in pericardial effusion
Echocardiography makes it possible to assess hemodynamic consequences of the effusion, as well as assess its location and volume. Regarding the volume of effusion, a rough estimate is made according to Table 2 (measurements are made at the end of diastole).
Table 2. Grading of pericardial effusion
GRADE Effusion width Very small <0.5 cm Small 0.5 – 1.0 cm Moderate 1.0 – 2.0 cm Large
2.0 cm Very large 2.5
In most cases, the effusion is circumferential, which means that it envelops the entire heart. If the effusion is seen only in certain places, then it is localized, which is more unusual.
Spot ecotate structures in the effusion indicate that it contains coagulated blood. Blood in the pericardium is called hemopericardium and is usually seen after heart surgery, trauma and invasive interventions. Spontaneous hemopericardium is seen in acute myocardial infarction and aortic dissection. Hemopericard has greater hemodynamic consequences because the blood coagulates and solidifies, which compresses the ventricles and prevents their filling.
Cardiac tamponade and electrical alternans
In the case of massive effusions, the ultrasound image shows a heart flowing around the effusion. Because the heart flows around the pericardial sac, the distance between the heart and the chest electrodes varies, which leads to varying QRS amplitudes in the chest leads. This ECG finding is called electric alternance.
If a massive effusion leads to increased pressure in the pericardial sac, then the filling of the ventricles is aggravated, which leads to acute and potentially life-threatening heart failure. This is called cardiac tamponade (tamponade). Effusions that have developed rapidly tend to have greater hemodynamic effects. A relatively small effusion that has increased rapidly may have a greater haemodynamic effect than a large effusion that has developed slowly. Therefore, it is important to try to determine how quickly the effusion occurred.
In case of suspicion of an acute effusion etiology (ventricular rupture, aortic dissection, trauma), treatment should be carried out promptly as the effusion is likely to have haemodynamic consequences which can be expected to increase. This is due to the fact that acute effusions can not be compensated by widening the pericardium. As mentioned above, the pericardium limits the dilatation of the ventricles, as a result of which an acute effusion leads to a rapid rise in pressure in the pericardial sac. However, if the effusion develops slowly (systemic diseases, malignancy, etc.), the pericardium may be stretched gradually, allowing larger effusions (sometimes >2 litres) to occur without haemodynamic consequences.
In the case of tamponade, ventricles and atria may collapse if the pressure in the pericardium exceeds the pressure in the corresponding cardiac space. The lowest pressure is present in the right atrium, which is why the right atrium also collapses first with tamponade. Collapse is defined as the bulging of the right atrial wall during diastole. At higher pressure in the pericardium, even the right ventricle can collapse during diastole.
Collapse of the left atrium occurs. Collapse of the left ventricle is rare because the pressure in the left ventricle is high compared to the pressure in the pericardium. However, trauma and iatrogenic causes of tamponade can lead to such high pericardial pressure that the left ventricle collapses.
In tamponade, the filling of the ventricles and atria deteriorates, which causes the inferior vena cava to widen and does not coincide normally during inspiration or sniffing.
Respiratory variations in blood pressure: pulsus paradoxus
In the case of tamponade, systolic blood pressure may vary more than 10 mmHg during the respiratory cycle. The pressure falls during inhalation and this is called pulsus paradoxus. The explanation is that the filling of the right ventricle increases during inhalation and the septum can bulge into the left ventricle, which thus fills with less blood, thereby reducing stroke volume and blood pressure. During the exhalation, the reverse occurs and systolic pressure rises.
Pulsus paradoxus means that blood pressure varies >10 mm during the respiratory cycle. Blood pressure drops during inhalation and rises during exhalation.
In the case of pulsus paradoxus, echocardiography shows that the septum position varies during inhalation and exhalation. During the inhalation, the septum moves into the left ventricle and vice versa during the exhalation.
The septum position during inhalation and exhalation affects the passive blood flow from the left atrium to the left ventricle, which is represented by the E wave on the pulsed Doppler (see Assessment of Diastolic Function). When inhaled, the septum bulges into the left ventricle, which complicates the filling, and then the E wave velocity decreases. On exhalation, the reverse occurs. If the speed of the E wave varies > 30% during the respiratory cycle, it strongly indicates that the effusion has haemodynamic effects.
Pulsed wave doppler in the tricispidal valve shows reverse ratios compared to the mitral valve; the E wave velocity rises during inhalation and decreases on exhalation.
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