Pericardial effusion and cardiac tamponade

Cardiac tamponade results from an increase in pericardial pressure that is sufficient to impede cardiac filling, resulting in high venous filling pressures, low cardiac output, and end-organ hypoperfusion. Most often this is due to the accumulation of a pericardial effusion though there are other possible causes. Patients usually present with features of cardiogenic shock, though some may initially be normotensive or hypertensive. Echocardiography can diagnose the presence of pericardial disease, especially pericardial effusion. Any associated haemodynamic sequelae can often be inferred by static and dynamic two-dimensional echocardiographic and Doppler measured intracardiac flow velocity abnormalities. These include atrial and ventricular wall inversion or collapse, and increased respiratory phasic flow velocities in tricuspid and mitral inflow. The concepts of transmural pressure, pericardial restraint, interventricular dependence, and cardiorespiratory interactions underpin the understanding and limitations of these echocardiographic findings. However, the impact of positive pressure ventilation remains problematic with respect to the interpretation of Doppler-derived intracardiac flow velocity variation. Echocardiography can also identify conditions that may confound the interpretation of accepted echocardiographic criteria (e.g. right ventricular hypertrophy, hypovolaemia, isolated chamber compression after cardiac surgery) and diagnose conditions that may mimic or exaggerate tamponade pathophysiology such as large compressive pleural effusion. Finally, echocardiographic criteria can aid stratification of the risk of tamponade in patients with pericardial effusion, and if necessary, guide percutaneous pericardiocentesis.

P242 When there is no time for further imaging

Introduction Cardiac tamponade (CT) is a clinical syndrome characterized by hemodynamic abnormalities resulting from an increase in pericardial pressure due to accumulation of fluid. Tamponade is one of the cardiac emergencies where urgent management steps are crucial and life saving. Absolute goal of treatment in Cardiac tamponade is to relieve the intra-pericardial pressure and to reverse the hemodynamic shutdown, by removal of the pericardial fluid via pericardiocentesis or surgical drainage. As much inevitable as it is, pericardiocentesis is relatively contraindicated when the effusion is associated with aortic dissection or myocardial rupture due to the potential risk of aggravating the dissection or rupture via rapid pericardial decompression and restoration of systemic arterial pressure. Case description A 44-year-Old transit passenger was admitted after she developed sudden onset of palpitations, vomiting and epigastric pain. She was in sinus tachycardia when brought to the Emergency department, within minutes’ patient went into cardiac shock with severe metabolic acidosis. She was admitted to ICU and subsequently intubated. Chest X-ray showed evidence of Pleural effusion with enlarged cardiac shadow, which prompted an urgent transthoracic echocardiogram. Echo findings were consistent with clinical cardiac tamponade with a large left pericardial mass compressing the lateral LV wall and aortic root, with a color flow from the mass toward the left coronary system. Mean while the patient was rapidly deteriorating, with and patient was not stable to undergo further imaging (CT or MRI), urgent contrast echo was done to rule out vascular connection between the mass and pericardial fluid, The Echo contrast study showed no vascular connection from the mass to the pericardial space ,however there was a connection from the mass to the left coronary system as shown in the figure, based on these findings a pericardial drainage was done successfully. These findings were confirmed by contrast CT scan after patient is stabilized. Patient gradually improved clinically, was extubated successfully, the provisional diagnosis was suspicious of pheochromocytoma,however the final diagnosis not established as the patient travelled to home country for further management. Conclusion Some times, it may become clinically challenging to effectively rule out contraindications to a procedure by the gold standard modalities, specially when a patient is collapsing on the table and the clock is ticking. In such scenarios, immediate alternate approaches resulting in safe outcomes are indispensable. Likewise, in our case of emergent cardiac tamponade and a suspicious pericardial mass in a crashing patient, Transthoracic echo with Optison proved to be life saving to rule out vascular connections between cardiac mass and coronaries or pericardial fluid, when there was no time for definitive imaging modalities due to rapid deterioration of patient’s clinical status. Abstract P242 Figure.

Assessment of right ventricular diastolic suction in dogs with the use of wave intensity analysis

Diastolic suction (DS) can be defined as that property of the ventricle by means of which it tends to refill itself during early diastole, independent of any force from the atrium. Although thought to be significant in the left ventricle (LV), DS in the right ventricle (RV) has received little attention, probably because of RV geometry. Our recent LV studies have shown that DS is related to both decreased elastance (i.e., τ, the relaxation time constant) and end-systolic volume (VLVES), thus reconciling the two mechanisms that have been used to explain the concept of DS. We hypothesized that RV DS would similarly depend on τ and VRVES. In six anesthetized open-chest dogs, aortic, RV, right atrial (RA), pulmonary arterial (PA), and RV pericardial pressure, tricuspid velocity, and PA flow were measured. VRVES was calculated by measuring distances between eight ultrasonic crystals. An empirical index of relaxation, τ′, and VRVES were manipulated by volume loading/caval constriction and isoproterenol/esmolol. We calculated the total energy (IW−) of the backward expansion wave generated during RV relaxation and that component causing DS [IW−(DS)]; i.e., the energy remaining after tricuspid valve opening. IW− [IW−(DS) also] was found to be inversely related to τ′ and to VRVES {i.e., IW− = −8.85· e(−0.0423τ′)· e[−0.0665(%VRVES)]}. Thus, as for the LV, the energy of the backward-going wave generated by the RV during relaxation depends on both the rate at which elastance decreases and the completeness of ejection. Despite the thin wall and nonspherical shape of the RV, DS appears to be an important mechanism.

Atrioventricular nonuniformity of pericardial constraint

Physiologists and clinicians commonly refer to “pressure” as a measure of the constraining effects of the pericardium; however, “pericardial pressure” is really a local measurement of epicardial radial stress. During diastole, from the bottom of the y descent to the beginning of the a wave, pericardial pressure over the right atrium (PpRA) is approximately equal to that over the right ventricle (PpRV). However, in systole, during the interval between the bottom of the x descent and the peak of the v wave, these two pericardial pressures appear to be completely decoupled in that PpRVdecreases, whereas PpRAremains constant or increases. This decoupling indicates considerable mechanical independence between the RA and RV during systole. That is, RV systolic emptying lowers PpRV, but PpRAcontinues to increase, suggesting that the relation of the pericardium to the RA must allow effective constraint, even though the pericardium over the RV is simultaneously slack. In conclusion, we measured the pericardial pressure responsible for the previously reported nonuniformity of pericardial strain. PpRAand PpRVare closely coupled during diastole, but during systole they become decoupled. Systolic nonuniformity of pericardial constraint may augment the atrioventricular valve-opening pressure gradient in early diastole and, so, affect ventricular filling.