Cardiac Tamponade
Karim Ratib, Gurbir Bhatia, Neal Uren, James Nolan in Emergency Cardiology, 2010
Patients typically present with cardiogenic shock, with hypotension, cold-clammy peripheries, oligo-anuria and associated agitation. Untreated, this condition can be rapidly fatal. In the setting of a more slowly developing tamponade, patients appear less ill and may present with anorexia, weakness and signs of biventricular failure such as shortness of breath, peripheral oedema and hepatomegaly. There may be an accompanying tachycardia, and the presence of pulsus paradoxus (an inspiratory decrease in amplitude of the palpated pulse or measured blood pressure) is supportive of the diagnosis. The jugular venous pressure (JVP) is markedly elevated with a prominent x descent and absent y descent. A positive Kussmaul’s sign (an inspiratory increase in the JVP) is rare in cardiac tamponade. Its presence suggests that an organizing process and epicardial constriction is present, in addition to an effusion. The apex beat may not be palpable and the heart sounds are soft or even absent. There may be a pericardial friction rub.
Haemodynamics: flow, pressure and resistance
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
This is a condition in which pulse pressure falls by more than 10 mmHg during each inspiration. This is not really a ‘paradox’ at all; it is an exaggeration of the normal inspiratory fall (see ‘Traube-Hering waves’, next section). Pulsus paradoxus >20 mmHg is generally caused by cardiac tamponade (pressure around the heart), due to an accumulation of fluid in the pericardial cavity. Tamponade sets a fixed limit to the combined volume of the two ventricles inside the pericardial sac. During inspiration, the fall in intrathoracic pressure increases the flow of venous blood into the right ventricle, increasing the right ventricular volume. Since the total volume is limited by the tamponade, the rise in right ventricular volume reduces the left ventricular volume. Thus, left ventricular stroke volume and systolic pressure decline excessively during inspiration. Pulsus paradoxus can also be caused by severe bronchospasm during an asthma attack.
Pericardial disease in the elderly
Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich in Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Urgent echocardiography is often needed in a case of suspected cardiac tamponade. Typical echocardiographic findings in tamponade include late diastolic collapse of the RA and early diastolic collapse of the RV, especially when the intrapericardial pressure exceeds the intracavitary pressure (38). The maximal pericardial pressure in tamponade occurs during end-diastole, when the RA volume is minimal, causing right atrial buckling. Persistence of RA collapse for more than one-third of the cardiac cycle is highly sensitive and relatively specific for tamponade (5,6). Left ventricular collapse, which can also occur in tamponade, is highly specific (though not as sensitive) for tamponade. Reciprocal changes occur in the RV and LV during respiration which indicate ventricular interdependence are quite simple to be detected as increased respiratory variability of transmitral E velocity >25% or tricuspidal E velocity >40% (5–7). The interventricular septum bulges into the LV during inspiration due to an increased systemic venous return to the RV and limited expansion of the RV free wall due to the increased intrapericardial pressure. The transmitral pressure gradient increases during expiration and subsequently, the systemic venous return decreases with reversal of diastolic flow in the hepatic veins. These findings contribute to pulsus paradoxus. Other echocardiographic findings in tamponade include inferior vena cava (IVC) dilatation (with less than a 50% reduction in its diameter during inspiration) (Figure 28.10), and the “swinging motion of the heart” within the pericardial sac.
Extrapulmonary tuberculosis
Published in Expert Review of Respiratory Medicine, 2021
Surendra K Sharma, Alladi Mohan, Mikashmi Kohli
The onset is insidious. Constitutional symptoms like fever, malaise, and weakness are present. Vague chest pain, dyspnea, cough, and weight loss are common. Pericardial TB can present acutely as acute pericarditis, cardiac tamponade, pericardial effusion, effusive constrictive pericarditis, or chronic constrictive pericarditis. Concurrent pleural involvement with effusion may be present. Pulsus paradoxus, raised jugular venous pressure, ascites, and dependent edema are common physical signs. A classical pericardial rub may also be heard; sometimes, it may be triphasic (audible in the atrial, ventricular systole, and ventricular diastole phases), heard over the left sternal border louder at inspiration and on bending forward [2]. Myocardial TB presents with idiopathic ventricular tachycardia or unexplained heart failure [17]. Myocardial TB is an underdiagnosed entity as the diagnosis of myocardial TB is difficult. Due to patchy distribution of the lesions, it may be missed even on endomyocardial biopsy.
Constrictive pericarditis decades after aortic valve repair
Published in Baylor University Medical Center Proceedings, 2020
Pericarditis can be acute or chronic. Acute pericarditis lasts <6 weeks; common etiologies include medications, postmyocardial infarction, and viral infections. Chronic pericarditis lasts >6 months and can lead to development of constrictive pericarditis. Etiologies of constrictive pericarditis include past cardiac surgeries, viral infections, radiation, trauma, or uremia. Our patient had no recent viral infections and no history of radiation, trauma, or uremia. Signs and symptoms of chronic pericarditis include elevated jugular venous pressure, pulsus paradoxus, and right heart failure symptoms, such as dyspnea, ascites, hepatomegaly, pitting edema, and pleural effusions.3 In patients with constrictive pericarditis, the pericardium becomes fibrotic and thickened. This leads to a decrease in compliance of the atria and ventricles, which decreases the blood return, subsequently causing the signs and symptoms described above. While ventricular interdependence is always present, constrictive pericarditis leads to a marked increase of ventricular interdependence due to the increase in right ventricular pressure, causing a decrease in left ventricular end diastolic volume.4
Multimodality imaging for the diagnosis and treatment of constrictive pericarditis
Published in Expert Review of Cardiovascular Therapy, 2019
Michael Chetrit, Natalie Natalie Szpakowski, Milind Y. Desai
The clinical presentation of effusive-constrictive pericarditis may contain elements of pericardial effusion or constriction, or a combination of both. Patients can present with pulsus paradoxus, a finding that is not typically associated with isolated constrictive pericarditis. Recent hypotheses suggest effusive-constrictive pericarditis is a transitional state wherein pericardial inflammation or effusion is resolving, and a fibrosing pericardium is beginning to form. Of note, in a recent series by Kim et al., from among 33 patients with the diagnosis effusive constrictive pericarditis, 31 patients had complete resolution of constrictive physiology either with anti-inflammatory medications or spontaneously, suggesting an overall favorable prognosis [6].
Related Knowledge Centers
- Blood Pressure
- Pulse
- Inhalation
- Signs & Symptoms
- Pericardial Effusion
- Physical Examination
- Heart Sounds
- Radial Artery
- Jugular Venous Pressure
- Kussmaul'S Sign