Ebook Textbook of clinical hemodynamics (2/E): Part 2
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Ebook Textbook of clinical hemodynamics (2/E): Part 2
RIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2heart became accessible to clinical investigation, allowing the study of right-heart physiology in both normal and diseased states.1 The right heart is affected by many cardiac disease states. Recall that the primary cause of right-heart failure is left-heart failure; therefore, the myriad cardiac d Ebook Textbook of clinical hemodynamics (2/E): Part 2isorders associated with leftheart failure syndromes often impact right-heart hemodynamics. In addition, numerous congenital heart conditions as wellEbook Textbook of clinical hemodynamics (2/E): Part 2
as disorders of the pericardium affect right-heart hemodynamics. The influences these conditions have on right-heart hemodynamics are discussed in theRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2odynamics of right-ventricular failure with a focus on right-ventricular infarction.TRICUSPID VALVE STENOSISThis rare valvular lesion is most often due to rheumatic heart disease and is almost always associated with mitral stenosis; isolated rheumatic tricuspid stenosis is very rare.2 Only occasiona Ebook Textbook of clinical hemodynamics (2/E): Part 2lly is tricuspid stenosis caused by other conditions, including carcinoid syndrome, endomyocardial fibrosis, congenital tricuspid valve stenosis, endoEbook Textbook of clinical hemodynamics (2/E): Part 2
carditis, pacemaker lead-related leaflet fibrosis, or atrial myxoma. In the current era, perhaps the most commonly observed cause of tricuspid stenosiRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2ng of the right ventricle reduces cardiac output. In cases of rheumatic heart disease, the combination of tricuspid and mitral stenosis reduces the cardiac output to levels lower than expected on the basis of either valvular lesion alone. Clinical consequences of severe tricuspid stenosis include fa Ebook Textbook of clinical hemodynamics (2/E): Part 2tigue caused by low cardiac output, elevated jugular veins, peripheral edema, hepatic congestion, and ascites due to elevated right-atrial pressure. IEbook Textbook of clinical hemodynamics (2/E): Part 2
f unsuspected, the diagnosis may prove challenging because these symptoms occur in other conditions such as pericardial disease, cirrhosis of the liveRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2id stenosis have been well described.3-€ Right-atrial pressure is elevated. The a wave reaches giant proportions in patients in normal sinus rhythm and may exceed 20 mmHg. However, an enlarged a wave is not specific for tricuspid stenosis because it may be seen in the presence of pulmonary hypertens Ebook Textbook of clinical hemodynamics (2/E): Part 2ion and right-ventricular hypertrophy; although, in the absence of pulmonary hypertension, a prominent a wave supports a diagnosis of tricuspid stenosEbook Textbook of clinical hemodynamics (2/E): Part 2
is.Similar to mitral stenosis, the presence of a pressure gradient observed while simultaneously measuring pressure in the right atrium and right ventRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2ut, and the greater size of the tricuspid orifice when compared with the mitral valve, the observed gradients are correspondingly relatively small, ranging from 2-12 mmHg, with 90% of gradients less than 7 mmHg.6 A mean diastolic gradient greater than 2 mmHg is diagnostic of tricuspid stenosis. Smal Ebook Textbook of clinical hemodynamics (2/E): Part 2l gradients (2-3 mmHg) that exist only in early diastole may be observed in patients with predominantly tricuspid regurgitation without significant stEbook Textbook of clinical hemodynamics (2/E): Part 2
enosis.3 6 In patients with tricuspid stenosis and normal sinus rhythm, a small pressure gradient early in diastole increases at end-diastole because RIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2hout the cardiac cycle, and the pressure gradient is greatest in early diastole when the rinht-vpntricnlar diastolic nrpssiirp is Inwost Thp transtrici isniri valvp nrpssiirp nradiant incrpasps with144 TEXTBOOK OF CLINICAL HEMODYNAMICSFig. 7.1. Tiiese hemodynamic waveforms were obtained from a 46-ye Ebook Textbook of clinical hemodynamics (2/E): Part 2ar-old male with a history of congenital ventricular septal defect repair at age 8 and subsequent tricuspid valve replacement for severe tricuspid valEbook Textbook of clinical hemodynamics (2/E): Part 2
ve regurgitation at age 17. who then developed severe stenosis of the bioprosthetic tricuspid valve. Simultaneous right-atrial and right-ventricular pRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2pid valve orifice area has been estimated using the Gorlin formula (see Chapter 4). Similar to mitral stenosis, the mean pressure gradient across the valve, the diastolic filling period, the heart rate, and the cardiac output are the important measured variables entered into the formula; however, un Ebook Textbook of clinical hemodynamics (2/E): Part 2like the mitral valve, the coefficient has not been determined and has been arbitrarily set at 1.0 (similar to the aortic valve area). The formula hasEbook Textbook of clinical hemodynamics (2/E): Part 2
not been well validated in tricuspid stenosis, although small series have correlated the calculated valve area with the area determined at surgery.6 RIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2 the valve area because the true transvalvular flow is not known. The value of this determination is not clear, and today most assessments of the severity of tricuspid stenosis are made based upon the extent of the transvalvular gradient and its effect on right-atrial pressure.Until recently stenosi Ebook Textbook of clinical hemodynamics (2/E): Part 2s of a prosthetic tricuspid valve could only be treated surgically with another valve replacement. In the current era less invasive alternatives are aEbook Textbook of clinical hemodynamics (2/E): Part 2
vailable and transcatheter valve systems, initially designed for the aortic valve, have been employed to treat bioprosthetic tricuspid stenosis using RIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2.2 is an example of the hemodynamics obtained in a patient with bioprosthetic tricuspid stenosis treated with a SAPIEN valve (Edwards Lifesciences, Irving, CA). In this case, the gradient was reduced from a mean of 7.1 mmHg (Fig. 7.2A) to 0 mmHg at enddiastole postvalve deployment (Fig. 7.2B). While Ebook Textbook of clinical hemodynamics (2/E): Part 2 no post-implant gradient was seen in this case, residual gradients after valve-in-valve procedures for bioprosthetic tricuspid stenosis are common anEbook Textbook of clinical hemodynamics (2/E): Part 2
d may limit this approach except in patients at prohibitive risk for reoperation.TRICUSPID VALVE REGURGITATIONTricuspid regurgitation represents the mRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2ardiography and are of little to no significance. Severe tricuspid regurgitation, however, is an important valvular lesion that causes progressive right-heart failure and increased mortality.10 Among the numerous possible etiologies (Box 7.1), functional tricuspid regurgitation from right-ventricula Ebook Textbook of clinical hemodynamics (2/E): Part 2r pressure or volume overload accounts for most cases; primary regurgitation caused by organic tricuspid valve pathology is much less prevalent.11 InEbook Textbook of clinical hemodynamics (2/E): Part 2
patients with rheumatic heart disease, tricuspid regurgitation is common, with a prevalence of nearly 40% in patients with mitral stenosis. Tricuspid RIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2d regurgitation) or functional regurgitation as a consequence of pressure or volume overload of the right ventricle (often caused by associated pulmonary hypertension).12 Elucidation of the mechanism of tricuspid regurgitation seen in association with rheumatic mitral stenosis is important for prope Ebook Textbook of clinical hemodynamics (2/E): Part 2r treatment. Observation of normal nnlmnnarv nrp<ĩ<ĩiirp<ĩEbook Textbook of clinical hemodynamics (2/E): Part 2
RIGHT-SIDED HEART DISORDERS 145ABFig. 7.2. The fracings shown here were obtained in a 50-year-old male with a history of traumatic tricuspid valve injRIGHT-SIDED HEART DISORDERSMichael RagostaCHAPTER 7After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right h Ebook Textbook of clinical hemodynamics (2/E): Part 2rmed severe tricuspid stenosis. He then underwent a percutaneous valve-in-valve procedure using a 26-mm SAPIEN 3 valve (Edwards Lifesciences, Irving. CA). (B) Postvalve implantation, there is no significant end-diastolic gradient present. The white shaded area represents the pressure gradient during Ebook Textbook of clinical hemodynamics (2/E): Part 2 diastole, a, a wave; d, diastole; e. end diastole; V, V wave.Box 7.1. Causes of Tricuspid RegurgitationStructurally Normal Tricuspid Valve (FunctionaEbook Textbook of clinical hemodynamics (2/E): Part 2
l Tricuspid Regurgitation)Chronic atrial fibrillationAnnular dilatation from volume or pressure overloadAtrial septal defectRight-ventricular infarctiGọi ngay
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