Fluid sac around heart2/11/2024 ![]() This leads to a compression of the right heart, increasing the right heart pressure. When fluid accumulates in the pericardial space, the intrapericardial pressure increases. During expiration, the intrathoracic pressure increases which leads to less right heart filling and augments filling of the left heart chambers. Conversely, the left heart filling decreases during inspiration, as the intrapericardial volume is fixed. ![]() Normally, the intrathoracic pressure decreases during inspiration which allows blood to flow easily into the right heart. Pulsus paradoxus is an abnormal decline (>10 mmHg) in systemic arterial pressure during inspiration. Since the filling pressure in the right side of the heart is lower than in the left side of the heart, filling pressure increases more rapidly in the right than in the left side of the heart. The decreased preload accounts for the reduced stroke volume and compensatory increased contractility, and tachycardia is not enough to maintain stroke volume, thus leading to reduced cardiac output. Thus, pericardial pressure dictates intracavitary pressure leading to a progressive decline in cardiac volumes. The equalisation is closest during inspiration. ![]() The pathophysiological and haemodynamic explanation for the above-mentioned findings is as follows.ĭuring fluid accumulation, left- and right-sided atrial and ventricular diastolic pressures rise, and equalise the pressure similar to the pericardial sac (20-25 mmHg). Other clinical signs in a patient with cardiac tamponade include tachycardia, pulsus paradoxus, decreased electrocardiographic voltage with electrical alternans and an enlarged cardiac silhouette on chest X-ray with slow-accumulating effusions. The classic signs in cardiac tamponade are included in Beck’s triad of hypotension, jugular venous distension, and muffled heart sounds. Several signs may be present during examination depending on the time of fluid accumulation. The left-hand panel shows the pressure-volume curve with rapidly increasing pericardial fluid whereas the right-hand panel shows a slower rate of pericardial effusion. When the elastic limit is reached the intrapericardial pressure rises. Pericardial strain-stress curves illustrating that the pericardium has some degree of elasticity. A compliant pericardium can allow considerable fluid accumulation over time without haemodynamic compromise. This is due to adaptive stretching of the pericardium over time. ![]() In contrast, 1,000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. Thus, rapid accumulation of as little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output. There is a slow phase and a steep rise, leading to critical cardiac compression. The pericardial strain-stress curve is depicted in Figure 1. The stiffness of the pericardium determines fluid increments precipitating tamponade. Thus, cardiac tamponade comprises a continuum from an effusion causing minimal effects to one causing circulatory collapse. The key element which determines the clinical presentation is the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms. For all patients, infectious diseases are still the most common cause of pericardial tamponade but, due to an increasing number of cardiac interventional procedures (cardiac ablation, device lead implantation and percutaneous coronary intervention), the incidence of haemopericardium seems to be increasing. Causes of effusion with a high incidence of progression to tamponade include bacterial, fungal, human immunodeficiency virus-associated infections, bleeding, and cancer involvement. More rare causes are collagen diseases (systemic lupus erythematosus, rheumatoid arthritis, scleroderma), radiation, aortic dissection, uraemia, post-myocardial infarction and bacterial infection. The most common causes of tamponade are pericarditis (infection and non-infection), iatrogenic (cardiac invasive procedures and post-surgery), and malignancy. The causes of pericardial fluid accumulation leading to cardiac tamponade are idiopathic, infectious, immune-inflammatory, neoplastic disease, post-cardiac surgery, trauma, renal failure, aortic dissection and miscellaneous (chronic renal failure, thyroid disease, amyloidosis). Pericardial diseases may be isolated or part of a systemic disease. Cardiac tamponade is a life-threatening condition due to slow or rapid pericardial accumulation of fluid with subsequent compression of the heart. It provides lubrication and protection from infection. The pericardial space enclosed between the two serosal layers normally contains up to 50 mL of serous fluid. The pericardium is a double-walled sac containing the heart and the roots of the great vessels and is composed of a visceral and parietal component.
0 Comments
Leave a Reply.AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |