Hemodynamics of Tamponade, Constrictive, and Restrictive Physiology



Hemodynamics of Tamponade, Constrictive, and Restrictive Physiology


Yogesh N. V. Reddy, MBBS, MSc

Mauro Moscucci, MD, MBA

Barry A. Borlaug, MD



INTRODUCTION

The pericardium is a fluid-filled sac composed of 2 layers: the visceral and parietal pericardium. Normally there is around 20 to 40 cc of fluid in the pericardial sac, which serves to lubricate the heart and minimize friction during mechanical work. The pericardium also serves to couple left- and right-sided ventricular stroke volume, such that a respiratory or positional increase in stroke volume from the right ventricle is associated with a compensatory decrease in stroke volume from the left. This ventricular interdependence, however, is exaggerated in pathological states associated with poor operating compliance of the pericardial unit, such as abnormal fluid accumulation in the pericardial sac (tamponade) or stiffening of the pericardial membrane (constriction) (FIGURE 8.1).


TAMPONADE PHYSIOLOGY

Pericardial fluid accumulation exaggerates ventricular interdependence and limits ventricular preload through enhanced pericardial restraint. Left ventricular (LV) end diastolic volume (preload) is directly proportional to left ventricular transmural filling pressure (LV diastolic pressure – pericardial pressure). Therefore an increase in pericardial pressure from accumulation of pericardial fluid can compromise LV filling, leading to hypotension and clinical tamponade. Increased pericardial pressure can also directly compress the right ventricle (which is at lower pressure) impeding right ventricular filling additionally compromising cardiac output and left ventricular preload (FIGURES 8.2, 8.3, 8.4, 8.5, 8.6 and 8.7).







FIGURE 8.1 Pericardial anatomy. Anatomy of the pericardium in the epicardial space. The left panel (A) shows a “window” of the parietal pericardium (arrow) cut away. Note the extensive epicardial fat adhered to the visceral pericardium. The right panel (B) has the heart removed, showing the visceral pericardium posteriorly and around the great vessels. The white arrow points to the oblique sinus and the yellow arrow to the transverse sinus. Reprinted with permission from Lachman N, Syed FF, Habib A, et al. Correlative anatomy for the electrophysiologist, Part I: the pericardial space, oblique sinus, transverse sinus. J Cardiovasc Electrophysiol. 2010;21(12):1421-1426.






FIGURE 8.2 Pericardial pressure-volume relationship in response to acute and chronic pericardial effusion or volume load. Pericardial pressure-volume relationship in a normal dog (left) and chronic volume loaded dog (right). The pericardial compliance adaptation (right) with rightward shift of the pressure-volume relationship in response to chronic volume load allows even large pericardial effusions to be tolerated hemodynamically without tamponade if they develop slowly. However, in the acute setting, the rapid accumulation of smaller amounts of pericardial fluid can lead to a rapid rise in pericardial pressure (left) and clinical tamponade. Adapted from Freeman GL, LeWinter MM. Pericardial adaptations during chronic cardiac dilation in dogs. Circ Res. 1984;54:294-300; Little WC, Freeman GL. Pericardial disease. Circulation. 2006;113(12):1622-1632; Circulation. 2007;115(15):e406.







FIGURE 8.3 Hemodynamic tracings in cardiac tamponade. This patient underwent evaluation for dyspnea on exertion in the setting of suspected aortic prosthetic stenosis with transseptal heart catheterization to evaluate the aortic pressure gradient. Top panel shows aortic pressure, left ventricular (LV) pressure, and left atrial pressure demonstrating mildly elevated LV end diastolic pressure with minimal aortic pressure gradient and normal left atrial pressure tracing. During the catheterization, hypotension developed abruptly with systolic blood pressures declining from 140 to 50 mm Hg along with ST elevation on the ECG leads (bottom panel). There was evidence of pulsus paradoxus along with elevation of left atrial pressure and loss of the y descent consistent with pericardial tamponade. Echocardiogram confirmed a new pericardial effusion, which was emergently drained with resolution of hypotension.







FIGURE 8.4 Stages of tamponade. Changes in heart rate (HR), mean blood pressure (BP), cardiac index (CI), left atrial pressure (LA), right atrial pressure (RA), and pericardial pressure (PP) with infusion of increasing pericardial volume (PV). Phases I, II, and III represent increasing hypotension with a decrease in CI and increase in right and left atrial pressures corresponding to rising pericardial pressures. In phase I, HR increases to compensate for declining stroke volume in an attempt to maintain cardiac output. In phase II, HR, BP and CI begin to decline with further rise in pericardial pressure. Phase III represents a preterminal phase requiring intermittent small pericardial fluid drainage to keep the dog alive and is associated with declining HR. Phase IV represents hemodynamic improvement following pericardiocentesis. Reprinted with permission from Nerlich WE. Determinants of impairment of cardiac filling during progressive pericardial effusion. Circulation. 1951;3(3):377-383.






FIGURE 8.5 Pulsus paradoxus. The aortic pressure tracing, aortic blood flow, and ratio of pressure change to flow change (ΔP/ΔV) are demonstrated along with numeric stroke volume (mL) underneath each aortic flow curve in a patient with cardiac tamponade. The top curve demonstrates the absence of aortic flow and pressure pulse with inspiration (pulsus paradoxus) due to exaggerated ventricular interdependence and ineffective LV filling with inspiration. The bottom curve demonstrates the same after prolonged expiratory hold followed by inspiration. Reprinted with permission from Ruskin J, Bache RJ, Rembert JC, Greenfield JC Jr. Pressure-flow studies in man: effect of respiration on left ventricular stroke volume. Circulation. 1973;48(1):79-85.







FIGURE 8.6 Echocardiographic findings in cardiac tamponade. A young female with metastatic lung cancer presented with hypotension and shortness of breath. The top panel shows the parasternal long axis view demonstrating a circumferential pericardial effusion (*). The lower panel shows significant respiratory variation in mitral inflow velocity consistent with intrathoracic intracavitary dissociation and exaggerated ventricular interdependence in the setting of tamponade.







FIGURE 8.7 Low-pressure cardiac tamponade. The top panel shows right atrial and pericardial pressure with low-pressure tamponade. There is pulsus paradoxus that resolves with improvement in blood pressure after pericardiocentesis despite the low right atrial and pericardial pressure. Classic tamponade is shown at the bottom with a higher pericardial pressure that resolves after pericardiocentesis. The postdrainage right atrial pressure is higher than in low-pressure tamponade, and the hemodynamic benefit obtained from drainage is often greater. FA, femoral artery pressure; RA, right atrial pressure; IP, intrapericardial pressure. Cardiac tamponade represents the extreme spectrum of hemodynamic embarrassment caused by a pericardial effusion. The hemodynamics of a significant pericardial effusion exist over a spectrum, however, and in the presence of hypovolemia, a lower pressure in the pericardial space can cause clinical symptoms, the so called low-pressure tamponade. In the classic paper by Sagrista-Sauleda et al, low-pressure tamponade was defined as a pericardial pressure <7 mm Hg, with a postpericardiocentesis right atrial pressure <4 mm Hg. Typical tamponade patients had a pericardial pressure >7 mm Hg with a postpericardiocentesis right atrial pressure >4 mm Hg. Clinical findings may be more subtle than full blown tamponade with frequent absence of jugular venous distension due to the hypovolemic state and less prominent pulsus paradoxus. However, these patients demonstrate an improvement in right atrial transmural pressure and cardiac index after pericardiocentesis proving that they have hemodynamically significant pericardial effusions. Reprinted with permission from Sagristà-Sauleda J, Angel J, Sambola A, Alguersuari J, Permanyer-Miralda G, Soler-Soler J. Low-pressure cardiac tamponade: clinical and hemodynamic profile. Circulation. 2006;1 14(9):945-952. Epub August 21, 2006.


CONSTRICTIVE PERICARDITIS

Even in the absence of pericardial fluid accumulation, inflammatory thickening of the pericardial membrane can lead to poor operating compliance of the pericardium. This can exacerbate pericardial restraint leading to decreased cardiac output and increased intracardiac pressures, with resultant fluid retention and systemic congestion. As opposed to tamponade, symptoms and clinical presentation are more chronic in constrictive pericarditis. Key findings by catheterization include ventricular interdependence and equalization of diastolic pressures due to enhanced pericardial restraint (FIGURES 8.8, 8.9, 8.10, 8.11, 8.12, 8.13, 8.14, 8.15, 8.16, 8.17, 8.18, 8.19, 8.20, 8.21, 8.22 and 8.23).

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May 3, 2019 | Posted by in CARDIOLOGY | Comments Off on Hemodynamics of Tamponade, Constrictive, and Restrictive Physiology

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