It is the involvement of the pericardium by different aspects and causes a set of signs and symptoms, some of their own, others cardiac and others corresponding to the disease of origin.
The pericardium envelops the heart like a closed bag over large vessels. It consists of a serous and a fibrous portion. The serosa has a visceral sheet over the epicardium and a perietal sheet firmly attached to the fibrous extremities. Between them there is a space known as the “pericardial reserve”, which contains between 30 and 50 cm3 of liquid with a transudate character and an intracavitary pressure of less than –2 mm Hg in expiration and –5 mm Hg in inspiration. The sac is not very extensible and mobile due to its ligaments.
There is sensory innervation in the inferior and posterior portions of the parietal pericardium, and because it is in close contact with the left diagrammatic pleura, it receives fibers from the phrenic nerve. Parasympathetic innervation is vagal, while sympathetic innervation is by cardiac branches.
Vascularization is extensive, but not systematized, from the internal mammary, upper and lower diaphragmatic, bronchial and thyroid raterias. Venous drainage is carried out through the acygos system, and the superior diaphragmatic veins, while the lymphatics are a tributary of tracheobronchial phrenic chains and infradiaphragmatic nodes.
It is practical to group pericardial diseases into four syndromes: acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis.
There are multiple causes of pericarditis: idiopathic, neoplastic (primary or secondary), infectious, traumatic, hypothyroidism, amyloidosis, cholesterol, Sarcoidosis, immunological, drug or radiation, hemodialysis, uremia, acute myocardial infarction, cardiac surgery, etc.
It is of acute onset, most often of infectious or nonspecific cause, and it can be fibrinous, hemorrhagic and with some associated effusion.
Symptoms and signs . The most frequent reason for consultation is chest pain, variable in intensity and spread, stabbing or oppressive, simulating coronary pain. It radiates to the neck, back and shoulder, increases with coughing, inspiration, swallowing and changes in decubitus, such as dorsal, lateral or chest torsion, and decreases in a sitting position, leaning forward. Its duration is variable, from days to weeks.
The most characteristic sign is the pericardial rub, but its absence does not rule it out. It should be investigated with the bell of the stethoscope in all decubitus, expiration and throughout the pericardial area. It is superficial and rough and has three components: A) presystolic component, due to atrial systole; B) systolic component, due to ventricular systole, and c) diastolic component, during rapid filling.
The last two are the most frequent and sometimes give it a swaying cadence. Systolic, sometimes unique, must be distinguished from murmurs.
Fever is very frequent, with thermal curves that vary from days to weeks in duration. It is often accompanied by effusion and superficial tachypnea, due to pain caused by breathing.
There may be palpitations due to atrial involvement, with cordants with supraventricular arrhythmias.
Complementary exams . A normal ECG does not rule out pericarditis. There may be ST elevation of superior concavity with positive T in the frontal plane and in V% and V &. With the evolution the ST is leveled and the T becomes negative, sometimes for a long time. The PR gap is common and has greater diagnostic value.
The chest radiograph may show a normal cardiac silhouette, in the absence of effusion, or of a larger size, with rectified edges, if there is a moderate increase in pericardial fluid. In Dressler's syndrome, pleurisy with or without pleural effusion and pulmonary infiltrates is added.
The echocardiography is the simplest method to detect both thickening and spill. It shows echo-free zones, only in systole, in the posterior region, if the spill is small; systolic and diastolic, if moderate; and if it is greater than 150 ml, it will appear in front of the anterior face.
The laboratory is nonspecific and depends on the etiology. There may be leukocytosis with neutrophilia and elevated erythrocyte sedimentation.
The examination of the fluid obtained by subxiphoid puncture helps the diagnosis of neoplastic pericarditis, purulent tuberculous, etc.
The biopsy of the pericardium , prior to the extraction of the liquid, allows the anatomopathological examination, culture, Immunofluorescence, etc., of the sample.
It is the presence of more than 50 ml of fluid in the pericardial cavity and can be of small or large volume, and with no or great hemodynamic repercussions; the latter depends more on the speed with which the spill is formed.
The same causes that cause pericardial disease can lead to a stroke. The existence of the latter does not imply inflammation of the pericardium, since the condition may result from intrapericardial hemorrhage due to aortic aneurysm, thoracic trauma, the use of anticoagulant drugs, or it may be a transudate due to congestive heart failure, a hypoproteinemic syndrome , chronic kidney failure or myxedema. The pericardial chyle, in turn, is due to a rupture of the thoracic duct.
In a large number of patients with chronic effusions lasting months or years, without great hemodynamic manifestations, the cause is unknown. In such cases, the anamnesis may serve as a guide if there is a history of a previous compatible condition, such as infections, trauma, heart surgery, acute myocardial infarction, etc.
Symptoms and signs . On physical examination, there are no conclusive signs, unless intrapericardial pressures are so high as to plug diastole.
In 50% of effusions with appreciable volume, neither cardiac activity nor left ventricular impulse is perceived. Percussion shows an enlargement of the matte area of the precordium. By auscultation the tones are muted or distant and sinus tachycardia is frequent. Pulmonary signs and symptoms, airways, and dysphagia may also appear. With the increase in intrapericardial pressure, signs of tamponade appear, such as a decrease in systolic blood pressure, arterial pulse pressure, increased venous pressure and a paradoxical pulse.
Complementary tests . The ECG can be normal, although the common is that the electrical complexes are of low voltage.
The chest x-ray may also be normal if the effusion is scanty, or show an enlarged cardiac silhouette in proportion to the effusion. Progressively effacement of the normal arches of the silhouette will be seen until, with a content greater than 250 ml, it adopts the shape of a pear or bottle. The lung fields will be clear and the hila normal.
The echocardiography is the most convenient, specific, sensitive method, low cost, and bloodless reproductible.mide the magnitude of the spill and classified as: a) minor b) moderate, c) severe. It can also be used to perform a targeted needle puncture to extract fluid and biopsy the pericardium.
The other methods, such as isotopic ganmagraphy, catheterization, phonocardiogram, and laboratory provide little useful data.
It is the result of such an increase in intrapericardial pressure that it hinders the diastolic filling of the heart. Therefore, cardiac output, systolic blood pressure and arterial pulse amplitude are reduced, sinus tachycardia and paradoxical pulse appear, and jugular engorgement with deep and rapid x wave will be found in the neck.
This situation occurs when the liquid accumulates rapidly and does not require large quantities to produce. A puncture wound involving the heart will cause a tamponade with only 20 or 30 ml of blood in the pericardial sac. With the first 10 ml, intrapericardial pressure increases little because it occupies the reserve volume of the pericardium; but beyond that volume, the pressure of the sac increases abruptly as the pericardium does not distend, which explains why so little fluid leads to tamponade.
The tamponade, therefore, depends on intrapericardial pressures: between 8 and 10 mm Hg the tamponade is mild; 10-15 mm Hg, moderate; and above 15 mm Hg, severe. As intrapericardial pressure increases, ventricular diastolic expansion decreases, the difficulty of atrial emptying increases, and the mean pressure in the left atrium increases, with the consequent increase in pulmonary venous pressure, pulmonary arterial pressure, and pressures in the right ventricle, right atrium, and vena cavae.
Ventricular pressure increases rapidly in early diastole, which causes early closure of the auriventricular valves and a reduction in minute volume with a decrease in aortic pressure and arterial hypotension. Here compensatory mechanisms would be set in motion that, by increasing catecholamines, increase inotropism to raise the ejection fraction, which, together with tachycardia, will attempt to restore minute volume and, through vasoconstriction, increase blood pressure.
Increased venous tone and blood volume determine the venous hypertension necessary to maintain the venoauricular gradient and preserve cardiac filling.
The paradoxical pulse consists of an abnormal decrease in systolic blood pressure during inspiration. It is normally around 10 mm Hg. It is observed in 70 to 90% of the cases of tamponade, although it is not provative of this, since it is also obtained in obstructive pulmonary disease, but by another mechanism. In tamponade the mechanisms would be: during inspiration the filling of the right heart would be greater and therefore its output rises, which does not happen with the left ventricle, whose systolic volume increases at the beginning of expiration, due to the pulmonary circulatory delay .
Greater right filling during inspiration, which is normal, persists during tamponade, increasing intrapericardial pressure further and decreasing left ventricular preload.
The transmission of intrathoracic negative pressure to the heart makes filling and emptying difficult. The descent of the diaphragm and the mediastium pulls the pericardium on inspiration, increasing the pressure within the sac.
Symptoms and signs . Physical examination findings vary according to severity, from mild signs of congestive heart failure with a paradoxical pulse to pale shock, sweating, drowsiness, and oligoanuria.
The neck veins are engorged with a venous pressure of 20 or more mm Hg, and there is a sharp x descent, recognizable as being synchronous with the carotid pulse. The jugular level drops slightly on inspiration.
Tachycardia, hypotension, and decreased pulse pressure are almost constant, as an expression of low cardiac output. The paradoxical pulse is not found in patients in shock.
Complementary exams . The ECG can be normal or of decreased voltage, but the typical is the electrical alternation of the QRS, P and T complexes.
The chest radiograph is normal or shows signs of effusion.
On ultrasound, a decrease in the diameter of the right ventricle can be observed, with early collapse of the tract and abnormal mobility of the heart, in the form of a wobble produced by electrical alternation.
The hemodynamic study by catheterization confirms the diagnosis by establishing that the intrapericardial pressures and the four chambers are equal in diastole. There will be an increase in central venous and pulmonary pressure. The right atriogram will show a prominent x collapse with decrease or disappearance of the y ball.
Pericardiocentesis has a dual purpose, a diagnostic and a therapeutic one; the extraction of small amounts of liquid for analysis quickly reverses the plugging pattern.