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Pericardium is a tough double layered membrane which covers the heart. The space between these two layers is filled with pericardial fluid which protects the heart from any kind of external jerk or shock. There are two layers to the pericardial sac: the outermost fibrous pericardium and the inner serous pericardium. The serous pericardium, in turn, is divided into two layers, the parietal pericardium, which is fused to and inseparable from the fibrous pericardium, and the visceral pericardium, which is part of the epicardium. The epicardium is the layer immediately outside of the heart muscle proper (the myocardium.The visceral layer extends to the beginning of the great vessels, becoming one with the parietal layer of the serous pericardium. This happens at two areas: where the aorta and pulmonary trunk leave the heart and where the superior vena cava, inferior vena cava and pulmonary veins enter the heart.In between the parietal and visceral pericardial layers there is a potential space called the pericardial cavity. It is normally lubricated by a film of pericardial fluid. Too much fluid in the cavity (such as in a pericardial effusion) can result in pericardial tamponade (compression of the heart within the pericardial sac). A pericardiectomy is sometimes needed in these cases
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PERICARDIUM
Dr Ramachandra
Enclosed lubricated space for the beating heart/ fix it in chest
Rule of Two’s
Double-layered: visceral=epicardium & parietal Thickness=2 mm Fibroblastic Parietal =Meshwork of 2 fibres collagen (types I and III) and elastic. Pericardial fluid volume=2x10 ml=20-30ml Two sinuses=Oblique(4PV AND IVC-SVC) & Transverse=AO and PA Pressure in pericardium 2mmHg lower than
intrathoracic pressure. Innervation :2=ANS(parasympathetic (
vagus)/sympathetic ( stellate ganglia) and somatic= the phrenic nerve.
Embryology
From mesoderm (the pleuropericardial membranes) that divide the primitive thoracic cavity of the intraembryonic coelom into pericardial and pleural compartments. The endocardial heart tube invaginates into the developing pericardial cavity, whereby the innermost serosal layer adheres to the myocardium and then folds back onto itself to create visceral and parietal layers.This process of invagination eventually results in suspending the adult heart within the developing pericardial cavity by blood vessels at its cranial and caudal attachments.The pericardium receives its blood supply via the internal mammary artery. Phrenic nerves are enveloped in the pleuropericardial membranes, and in the adult, reach the diaphragm by traveling through the fibrous pericardium .
Physiology
Pericardial fluid act as lubricant between visceral and parietal layers to facilitate frictionless beating of the heart. The intrapericardial fluid function as a reservoir of paracrine modulators, notably compounds such as prostanoids, natriuretic peptides, and endothelins, that may regulate sympathetic tone, coronary vasomotor tone, heart rate, and bloodpressure, but also immunologically active moieties, such as complement factors. Pericardial fluid is in equilibrium with pleural fluid, as there is hydraulic conductance across the parietal pericardium when intrapericardial pressures exceed pleural pressures.Numerous attachments from the pericardium to other thoracic structures secure the heart in place within the chest cavity. Cranially, the reflections on great vessels interdigitate with vascular adventitia to fasten the superior borders of the pericardium; a diaphragmatic tendon anchors the caudal end.Ventrally the pericardium connects with the interior of the sternum (superior and inferior pericaridosternal ligaments), and dorsally it affixes to the esophagus and spine.
Contd
The fibrous nature of the pericardium likely also serves as a barrier to insulate the heart from exogenous tumors and spread of infections.Despite its fibrous character, the pericardium rests at slightly lower pressures (_3 to _6 mm Hg) compared to the rest of the intrathoracic cavity and is able to transmit hanges in intrathoracic pressures with respiration.Intact pericardium is rather nondistensible and provides a strong mechanical constraint on overall heart volume and chamber enlargement. Important consequences of nondistensibility are equalizing compliance of right and left ventricles as well as interdependence of the cardiac chambers.Interdependence occurs because total intrapercardial volume (namely pericardial cavity and cardiac chamber volume) is fixed in the short term, and expansion of 1 chamber necessarily impedes expansion of another.
Contd.......
Especially as regards ventricular interdependence,acute expansion of either right or left ventricular volume will impair filling of the other chamber, at the limit resulting in signs such as the pulsus paradoxus. The same principles apply in acute pericardial effusion and tamponade physiology, because there is very little reserve volume for expansion in the pericardial space before intrapericardial pressure rises Sharply. In situations where pericardial effusion develops gradually,pericardial compliance can increase to accommodate significant fluid volumes, often a liter or more. Efferent painful stimuli (eg, inflammation, distention) are carried via phrenic nerves and stellate ganglion; however, not every surface of the pericardium is innervated. The pericardium appears insensate to temperature and vibration.
Contd
Interdependence occurs because total intrapercardial volume (namely pericardial cavity and cardiac chamber volume) is fixed in the short term, and expansion of 1 chamber necessarily impedes expansion of another. Especially as regards ventricular interdependence,acute expansion of either right or left ventricular volume will impair filling of the other chamber, at the limit resulting in signs such as the pulsus paradoxus. The same principles apply in acute pericardial effusion and tamponade physiology, because there is very little reserve volume for expansion in the pericardial space before intrapericardial pressure rises Sharply. In situations where pericardial effusion develops gradually,pericardial compliance can increase to accommodate significant fluid volumes, often a liter or more. Efferent painful stimuli (eg, inflammation, distention) are carried via phrenic nerves and stellate ganglion; however, not every surface of the pericardium is innervated. The pericardium appears insensate to temperature and vibration.
Congenital defects
Absence:“stabbing” chest pains with “heart shifting
RBBB/Clockwise loop, levoposition and posterior rotation,of the cardiac apex, as well as pathognomonic interdigitation of lung tissue between the inferior heart surface and diaphragm as well as between the aorta and pulmonary artery. “teardrop” shaped, because of atrial elongation and ventricle widening in the absence of typical pericardial tethering.
Pericardial Masses(embryonic coelomic cavity.)
Epicardial Fat
The closest D/D of pericardial effusion
Pericardial tumors
Pericardial collection
Pericardial Effusions
Mild:<5mm Moerate:5-10mm Severe(Tamponade)>10mm In acute situation even mild may cause
tamponade
Pericarditis
Infiltration is the sine qua non of pericarditis
self-limited(mostly) 80-90% of cases are idiopathic, “bread-and-butter
pericardium”=supporation Peri-infarction - 5%(TLT+) vs 10-20%
(TLT-Ve), Dressler’s < 1% Dx:At least 2 of 4 cardinal features
Contd.......
Unique pain radiation to the trapezius ridge
The pericardial friction rub
A triphasic(50%) cadence with a discrete “sandpaper” sound occurring with atrial systole, ventricular systole, and early ventricular diastole. 100% specific but evanescent ,less sensitive.
EKG changes in acute pericarditis
STAGE-I
Recurrent or Relapsing Pericarditis Latent periods of up to 6 weeks 12 weeks of therapy of NSAID in tappering CORE trial:Colchicine (1-2 mg followed by 0.5 mg daily or twice
daily for 6 months; addition to high-dose aspirin therapy for first recurrence of idiopathic,viral, or autoimmune pericarditis,24% recurrence at 18 months as compared to 51% in the control, a two-thirds reduction (10% vs 31%) in symptoms at 72 hours(CLASS I-EHA)
Steroid for auto immuno causes-0.5mg-1mg/Kg Intrapericardial corticosteroids(A single instillation of
triamcinolone (300mg/m2 to 600 mg/m2 in 100 mL isotonic saline) over 24 hours on
thebackground of maintenance colchicine therapy prevented 84%
recurrencesat 1 year Immunosuppresants:Cyclosporine /Azathioprine, remains
investigational.
Hemodynamic Consequences
Claude Schaeffer Beck (1894 – 1971) was a pioneer American cardiac surgeon, famous for innovating various cardiac surgery techniques, and performing the first defibrillation in 1947.[ He was the first American professor of cardiovascular surgery, from 1952 through 1965.
1930
Tamponade physiology
Resting intrapericardial pressure is 3 to 6 mm Hg less than the diastolic pressures in the cardiac chambers and thus does not affect intracardiac blood flows with 2-4 mmHg respiratory variation.
Pericardial pressure at which the point where cardiac filling is compromised.
Pericardial fluid becomes like a fifth cardiac chamber, occupying space within the pericardium and thus limiting the ability of atria and ventricles to expand and fill appropriately ( impaired diastolic compliance).
May be slow or fast
Contd........
Chamber-filling pressure is the ∆ between intracardiac and intrapericardial pressures
Mean diastolic pressures equalize across cardiac chambers as they need to exceed the increased pressures in the intrapericardial space
Physiologicalventricular interdependence becomes magnified due to isolation of the heart from normal respiratory ∆
Inspiration will increase right-sided flows at the expense of the left-sided chambers, thus reducing left-sided flow
Contd.......
Contd....
Left- and right-ventricular filling pressures are usually elevated at 15-20 mm Hg in tamponade. However, so-called low-pressure tamponade with much lower ventricular filling pressures can occur in patients with reduced blood volume, eg, dehydration, overdiuresis, or hemorrhage.
A pulsus paradoxus ≥10 mm Hg a likelihood ratio of 3.3 for the presence of tamponade
Value ≤10 confers a negative likelihood ratio of
0.03 PP= 20 mm Hg ≥75% Tamponade Palpable pulsus (or “total paradox”) in
almost 20%
DX of pulsus paradoxus
Pulsus suppression
RV or LV are markedly noncompliant= severe left ventricular (LV) failure, right ventricular hypertrophy, left ventricular hypertrophy, acute myocardial infarction,severe aortic insufficiency (elevated left ventricular end diastolicpressure and damping of respiratory variation), or in uremia, atrial septal defect (as venous return is offset by right to left shunting), and pericardial adhesions
QRS alternans
QRS alternans is present in 20% and total
alternans (of P, QRS, and T waves) in 8% of patients.
Low voltage complex
Echocardiographic signs of tamponade
ROVT collapse is quite consistent
Inflow and out flow doppler
Mitral 35% and aortic 25% variation and TV=80%
Pericardial Constriction
≥ 5mm echo and ≥4mm CT(N=1-2mm,<4mm)
CP Physiology with non thickened 20% Kussmaul’s sign(JVP distension in
inspiration) pericardial knock≥frequency than S3 Friedrich’s sign=Rapid Y descent of early
diastolic suction “square-root”=sign of no further filling
occurs after early diastole Equalized diastolic in all 4 chambers
Hemodynamic=CATH/ECHO
diastolic function are load-dependent
Echo Doppler
CT Scan
CT is the best imaging ≥4 mm diagnostic sigmoid-shaped ventricular septum Persistent concordance of tagged signals
between the pericardium and the myocardium during both systolic and the diastolic phases is a sign of pericardial adhesions and is a reliable sign of pericardial constriction.
CMRI+CE T1 Weighted
More soft tissue clarification at more cost
Pericardial biopsy
Add diagnostic yield only 5-6%, add 29-54% in in tamponade
Thanks, you came so long with me.....