(BQ) Part 2 book “Textbook of clinical hemodynamics” has contents: Right-sided heart disorders, pulmonary hypertension and related disorders, pericardial disease and restrictive myocardial diseases, left-ventricular hemodynamics, heart failure, and shock, congenital heart disease,… and other contents.
Michael Ragosta CHAPTER RIGHT-SIDED HEART DISORDERS After Werner Forssmann boldly inserted a urological catheter into his own right atrium, the right heart 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 disorders associated with leftheart failure syndromes often impact right-heart hemodynamics In addition, numerous congenital heart conditions as well as disorders of the pericardium affect right-heart hemodynamics The influences these conditions have on right-heart hemodynamics are discussed in their respective chapters This chapter will focus on disorders unique to the right heart, including tricuspid and pulmonic valvular diseases and the hemodynamics of right-ventricular failure with a focus on right-ventricular infarction TRICUSPID VALVE STENOSIS This 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 occasionally is tricuspid stenosis caused by other conditions, including carcinoid syndrome, endomyocardial fibrosis, congenital tricuspid valve stenosis, endocarditis, pacemaker lead–related leaflet fibrosis, or atrial myxoma In the current era, perhaps the most commonly observed cause of tricuspid stenosis is dysfunction of a prosthetic tricuspid valve Tricuspid stenosis impairs right-atrial emptying and elevates right-atrial pressure Diminished filling 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 fatigue caused by low cardiac output, elevated jugular veins, peripheral edema, hepatic congestion, and ascites due to elevated right-atrial pressure If unsuspected, the diagnosis may prove challenging because these symptoms occur in other conditions such as pericardial disease, cirrhosis of the liver, and pulmonary hypertension; the latter may, in fact, be present due to associated mitral stenosis The hemodynamic abnormalities observed in tricuspid stenosis have been well described.3–6 Rightatrial 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 hypertension and right-ventricular hypertrophy; although, in the absence of pulmonary hypertension, a prominent a wave supports a diagnosis of tricuspid stenosis Similar to mitral stenosis, the presence of a pressure gradient observed while simultaneously measuring pressure in the right atrium and right ventricle during diastole characterizes tricuspid valve stenosis (Fig 7.1) Because of the lower right-sided pressures, the relatively lower cardiac output, 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 mmHg.6 A mean diastolic gradient greater than mmHg is diagnostic of tricuspid stenosis Small gradients (2–3 mmHg) that exist only in early diastole may be observed in patients with predominantly tricuspid regurgitation without significant stenosis.3,6 In patients with tricuspid stenosis and normal sinus rhythm, a small pressure gradient early in diastole increases at end-diastole because of the rise in atrial pressure from atrial contraction For patients with atrial fibrillation, right-atrial pressure remains uniformly elevated throughout the cardiac cycle, and the pressure gradient is greatest in early diastole when the right-ventricular diastolic pressure is lowest The transtricuspid valve pressure gradient increases with inspiration, predominantly caused by a fall in the ventricular diastolic pressure with inspiration The gradient increases with exercise because of an increase in the right-atrial pressure An increase in volume will also increase the gradient 143 144 TEXTBOOK OF CLINICAL HEMODYNAMICS Fig 7.1. These hemodynamic waveforms were obtained from a 46-year-old male with a history of congenital ventricular septal defect repair at age and subsequent tricuspid valve replacement for severe tricuspid valve regurgitation at age 17, who then developed severe stenosis of the bioprosthetic tricuspid valve Simultaneous right-atrial and right-ventricular pressure waveforms are shown The right-atrial pressure is markedly elevated and there is a large diastolic pressure gradient Calculation of the tricuspid 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, unlike 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 has not been well validated in tricuspid stenosis, although small series have correlated the calculated valve area with the area determined at surgery.6 Similar to mitral stenosis with associated mitral regurgitation, if there is associated tricuspid regurgitation, the Gorlin formula will underestimate 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 stenosis of a prosthetic tricuspid valve could only be treated surgically with another valve replacement In the current era less invasive alternatives are available and transcatheter valve systems, initially designed for the aortic valve, have been employed to treat bioprosthetic tricuspid stenosis using a “valve-in-valve” approach Case reports and small series demonstrate the feasibility of this approach with an improvement in hemodynamics.7–9 Fig 7.2 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 mmHg at enddiastole postvalve deployment (Fig 7.2B) While no post-implant gradient was seen in this case, residual gradients after valve-in-valve procedures for bioprosthetic tricuspid stenosis are common and may limit this approach except in patients at prohibitive risk for reoperation. TRICUSPID VALVE REGURGITATION Tricuspid regurgitation represents the most commonly encountered right-sided valvular heart lesion Mildto-moderate degrees of tricuspid regurgitation are very commonly detected on 2D echocardiography 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-ventricular pressure or volume overload accounts for most cases; primary regurgitation caused by organic tricuspid valve pathology is much less prevalent.11 In patients with rheumatic heart disease, tricuspid regurgitation is common, with a prevalence of nearly 40% in patients with mitral stenosis Tricuspid regurgitation is due to several potential mechanisms in these patients, including rheumatic involvement of the tricuspid valve (i.e., primary tricuspid 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 proper treatment Observation of normal pulmonary pressures suggests primary valve disease In patients with pulmonary hypertension, echocardiography can help distinguish functional regurgitation from organic tricuspid valve disease Tricuspid regurgitation causes volume overload of the right ventricle and atrium Over time, the right ventricle dilates further, worsening the degree of regurgitation In the presence of pulmonary hypertension, Chapter 7 Right-Sided Heart Disorders 145 s v s v a v a d v a e e s s v a e d d d A s a s s s a v v a v a e e v e d d d d B Fig 7.2. The tracings shown here were obtained in a 50-year-old male with a history of traumatic tricuspid valve injury who had a bioprosthetic tricuspid valve replacement 19 years earlier (A) Simultaneous right-atrial and right-ventricular pressure waveforms confirmed severe tricuspid stenosis He then underwent a percutaneous valve-in-valve procedure using a 26-mm SAPIEN 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 diastole a, a wave; d, diastole; e, end diastole; v, v wave Box 7.1. Causes of Tricuspid Regurgitation Structurally Normal Tricuspid Valve (Functional Tricuspid Regurgitation) Chronic atrial fibrillation Annular dilatation from volume or pressure overload Atrial septal defect Right-ventricular infarction Congestive heart failure Pulmonary hypertension Post–heart transplantation Structurally Abnormal Tricuspid Valve Rheumatic heart disease Carcinoid Radiation-induced valvular regurgitation Endocarditis Trauma Right-ventricular biopsy induced Pacemaker-lead induced Myxomatous degeneration severe tricuspid regurgitation causes both volume and pressure overload and is less well tolerated, leading to earlier onset of symptoms Signs of severe tricuspid regurgitation reflect right-heart failure and include lower extremity edema, ascites, distended neck veins, and cachexia Symptoms include dyspnea, anorexia, abdominal distension, and profound fatigue from decreased cardiac output The observed hemodynamic abnormalities of severe tricuspid regurgitation are preload and afterload dependent and include elevation of right-atrial pressure, decreased cardiac output, and abnormalities of the right-atrial pressure waveform.13 Because the jugular veins mirror the abnormalities present in the right atrium, it is no surprise that the characteristic atrial waveform abnormalities attributed to tricuspid 146 TEXTBOOK OF CLINICAL HEMODYNAMICS SM c 1st TR 2nd y Fig 7.3. Venous pressure waveform in severe tricuspid regurgitation demonstrating a large c-v wave (From Messer AL, Hurst JW, Rappaport MB, Sprague HB A study of the venous pulse in tricuspid valve disease Circulation 1950;1:388–393.) c, c wave; y, y descent c-v a Fig 7.4. Right-atrial waveform from a patient with secondary tricuspid regurgitation from associated severe left-sided heart failure and right-sided heart failure Attenuation of the x descent is present, seen after the a wave (left arrow), leading to a prominent c-v wave (right arrow) a, a wave; RA, right-atrial regurgitation were first observed on analysis of jugular venous pressure waveforms (Fig 7.3).14 Normally, an x descent exists on the right-atrial waveform, reflecting descent of the base of the heart during systole Classically, in tricuspid regurgitation, the x descent is attenuated (Fig 7.4) The x descent ultimately disappears and is replaced by a systolic wave with a peak-dome contour often termed the c-v wave.1,15–17 The v wave is classically prominent, and the y descent is very rapid (Fig 7.5) Ventricularization of the right-atrial pressure waveform may occur (Fig 7.6) In some cases, the right-atrial pressure wave is nearly indistinguishable from the right-ventricular pressure contour (Fig 7.7) The v wave may increase further during exercise Unfortunately, these hemodynamic findings are not always helpful in diagnosing tricuspid regurgitation The findings are dependent on the preload and afterload status; thus they may be absent in the event of excessive diuresis or more prominent when volume is overloaded Atrial fibrillation without tricuspid regurgitation may distort the atrial waveform in a fashion similar to that observed with severe regurgitation, with absence of the x descent (because no atrial contraction is present) causing the c-v wave to appear prominent.17,18 Finding a normal right-atrial pressure, normal x descent, and absence of prominent v waves does not necessarily exclude significant tricuspid regurgitation.18–20 Ventricularization of right-atrial pressure is very specific for severe tricuspid regurgitation but is seen in only 40% of patients.20 Similar to mitral regurgitation, the size of the v wave in tricuspid regurgitation depends upon the volume status and compliance of the right atrium and does not necessarily correlate with the presence or severity of tricuspid regurgitation.21 A subtle hemodynamic finding is perhaps more sensitive for tricuspid regurgitation Instead Chapter 7 Right-Sided Heart Disorders 147 Fig 7.5. Right-atrial waveform in severe tricuspid regurgitation demonstrating absence of the x descent and a large c-v wave with a prominent y descent RA, Right-atrial of the normal fall in right-atrial pressure with inspiration, one study found that all patients with tricuspid regurgitation demonstrated either a rise or no change in right-atrial pressure during deep inspiration.20 This finding was very sensitive for tricuspid regurgitation but was also apparent in several patients with severe (>90 mmHg) pulmonary hypertension; thus in the absence of severe pulmonary hypertension, this sign may help diagnose tricuspid regurgitation In contrast to mitral regurgitation, angiographic assessment of tricuspid regurgitation is problematic and rarely used, because the presence of a catheter across the tricuspid valve in order to perform right ventriculography may interfere with tricuspid valve function and cause regurgitation; however, this method is useful for proving the absence of tricuspid regurgitation Some of the clinical and hemodynamic aspects of severe tricuspid regurgitation may be confused with constrictive pericarditis.22 The predominant symptoms of both conditions (edema, ascites, prominent neck veins, and fatigue) are very similar In addition, the right-atrial pressure waveform may appear similar with a prominent y descent, particularly if the patient’s rhythm is atrial fibrillation The finding of ventricular interdependence is an important clue that may distinguish these two conditions (see Chapter 9).23 Cardiac output determination using the thermodilution method may be problematic in patients with tricuspid regurgitation because severe degrees of regurgitation underestimate the cardiac output.24 The Fick methodology is more accurate in this setting. PULMONIC VALVE STENOSIS Pulmonic stenosis is the most common abnormality of the pulmonary valve and nearly always has a congenital cause It may be seen in association with other congenital heart defects or exist in isolation Often detected in childhood, pulmonic stenosis rarely presents in adults In the majority of cases, the valve leaflets are fused and amenable to balloon or surgical valvotomy The 10%–15% of pulmonic valves stenosed from dysplastic conditions (as seen in association with Noonan syndrome) are often not treatable by valvotomy Obstruction causes a pressure gradient across the pulmonic valve, with right-ventricle systolic pressure exceeding pulmonary artery systolic pressure (Fig 7.8).25 Pressure overload and subsequent hypertrophy of the right ventricle ensues The hemodynamic abnormalities depend upon the severity of stenosis and the cardiac output In mild cases, the pressure gradient across the pulmonic valve is less than 20 mmHg and the cardiac output increases normally with exercise.25,26 With severe pulmonic stenosis, the pressure gradient exceeds 40 mmHg and may reach very high levels (>100 mmHg), causing the right-ventricular pressure to equal systemic arterial pressures The right-ventricular stroke volume is fixed and unable to augment with exercise.26 In addition, because of diminished right-ventricular compliance from concentric hypertrophy of the right ventricle, severe pulmonic stenosis elevates right-ventricular end-diastolic pressure, both at rest and with exercise An elevated right-ventricular end-diastolic pressure may raise right-atrial pressure and cause right-to-left shunting if there is a patent foramen ovale leading to cyanosis 148 TEXTBOOK OF CLINICAL HEMODYNAMICS A B Fig 7.6. These tracings were obtained from a patient with severe tricuspid regurgitation due to profound biventricular heart failure (A) The right-atrial waveform shows ventricularization Compare this with (B), the right-ventricular waveform from the same patient RA, Right-atrial; RV, right-ventricular or paradoxical embolism Furthermore, right-ventricular diastolic pressure rises have been associated with elevations in left-ventricular end-diastolic pressures, likely from interactions via the septum.27 Interestingly, many individuals are asymptomatic even with severe stenosis Symptoms of severe stenosis include dyspnea, fatigue, syncope, and exercise intolerance Valve area can be calculated using the Gorlin formula, as described in Chapter 4, and adapted to the pulmonic valve.28 However, most clinicians classify the severity of pulmonic stenosis and base treatment decisions upon the extent of the transvalvular gradient alone Current guidelines recommend either surgical or balloon valvuloplasty for asymptomatic patients with a peak instantaneous gradient greater than 60 mmHg or mean gradient greater than 40 mmHg and for symptomatic patients with a peak instantaneous gradient greater than 50 mmHg and mean gradient greater than 30 mmHg.29 Outcomes with balloon valvuloplasty are excellent with little chance of recurrence (Fig 7.9) Chapter 7 Right-Sided Heart Disorders 149 A B Fig 7.7. Severe tricuspid regurgitation may result in complete ventricularization of the right-atrial waveform (A) The rightventricular pressure wave (B) Note the nearly indistinguishable appearance of the right-atrial waveform RA, Right-atrial; RV, right-ventricular Related conditions that cause similar physiologic and hemodynamic effects on the right heart include peripheral pulmonary artery stenosis (discussed in Chapter 11) and right-ventricular infundibular stenosis Infundibular stenosis is commonly associated with severe pulmonic stenosis because compensatory right-ventricular hypertrophy narrows and obstructs the outflow tract With relief of valvular obstruction, hypertrophy regresses and the extent of infundibular stenosis regresses.30 PULMONIC VALVE REGURGITATION Pulmonary insufficiency is uncommon It is most often seen in association with congenital heart disease, typically because of either surgical or balloon valvotomy for pulmonic stenosis or from repair of tetralogy of Fallot Other causes include rheumatic heart disease, endocarditis, dilatation of the pulmonary artery (either idiopathic or from pulmonary hypertension), traumatic disruption of the pulmonic valve, syphilis, or an isolated congenital defect.31,32 The low-pressure circuit of the right heart causes pulmonary regurgitation to behave differently than aortic regurgitation.33 Right-atrial contraction can maintain forward pulmonary blood flow despite severe regurgitation, and the pulmonary resistance is typically very low, allowing blood to easily pass through the lungs and preventing significant backward flow during diastole Thus the volume overload on the right ventricle is substantially less than that seen in severe aortic regurgitation and allows this lesion to be tolerated for longer periods Conditions that increase pulmonary vascular resistance, however, will increase the regurgitant volume and may lead to detrimental effects Eventually, the right ventricle dilates and becomes dysfunctional, leading to reduced exercise capacity and right-heart failure 150 TEXTBOOK OF CLINICAL HEMODYNAMICS s s d s s s d d s s s d d d s s s d d d d d A s s s s s s d d d e d e d e s s s s s s d d d de s s s s d d d d e e B Fig 7.8. Right-heart pressures obtained in an infant with severe, congenital pulmonic stenosis (A) The systolic pulmonary artery pressure measured 15 mmHg (B) Right-ventricular pressure reached systemic levels at nearly 80 mmHg d, Diastole; PA, pulmonary artery; RV, right-ventricular; s, systole Chapter 7 Right-Sided Heart Disorders 151 r r r r s s r s s s dd r s r s s s s dd dd r s s s s r s s dd dd r r dd dd A r r s s e d d r s s s s r d de e d d s s s s s s s ed d r e d e d d r s s s d r s s ed e d d e B Fig 7.9. Balloon valvuloplasty performed in the patient shown in Fig 7.8 resulted in elimination of the pressure gradient between (A) the pulmonary artery and (B) the right ventricle d, Diastole; e, end diastole; PA, pulmonary artery; r, R wave; RV, right-ventricular; s, systole 152 TEXTBOOK OF CLINICAL HEMODYNAMICS The hemodynamic abnormalities reflect the severity of pulmonic regurgitation Patients with severe pulmonary regurgitation demonstrate an increased pulmonary arterial pulse pressure, a rapid dicrotic collapse, and early equilibration of the diastolic pressures between the pulmonary artery and right ventricle or “diastasis”31,32,34 (Figs 7.10–7.11) The pulmonary artery pressure becomes “ventricularized” (Fig 7.12).35 Milder forms of pulmonary regurgitation affect the pulse pressure to a lesser degree, and equilibration of the pressure between the right ventricle and pulmonary artery occurs only at end-diastole. RIGHT-VENTRICULAR FAILURE The right ventricle is subject to failure, most commonly from associated left-heart failure Isolated right-heart failure can occur in a variety of settings including severe pulmonary hypertension, chronic severe pulmonic insufficiency, right-ventricular infarction, chronic, severe lung disease, acute massive pulmonary embolism, myocardial contusion from trauma, focal myocarditis, or inadequate cardiopreservation during heart surgery or from acute rejection after cardiac transplantation (Fig 7.13) Several of these conditions are discussed elsewhere in this text, and the remaining discussion will focus on the hemodynamics of right-ventricular infarction. RIGHT-VENTRICULAR INFARCTION Infarction of the right ventricle may present with dramatic hemodynamic consequences and is one of the major causes of cardiogenic shock in patients with acute myocardial infarction Initially described as a mmHg 30 24 18 12 PA RV Fig 7.10. Diastasis of pressure between the right-ventricular and pulmonary artery pressure is a hemodynamic finding of severe pulmonic insufficiency (From Nemickas R, Roberts J, Gunnar RM, Tobin JR Isolated congenital pulmonic insufficiency Differentiation of mild from severe regurgitation Am J Cardiol 1964;14:456–463.) PA, Pulmonary artery; RV, right-ventricular s s e d d Fig 7.11. This is an example of severe pulmonic valve regurgitation in a 10-year-old with a history of tetralogy of Fallot with pulmonary atresia and multiple complex surgeries in the past Shown here is diastasis between right-ventricular and pulmonary artery pressures; there is also a modest gradient consistent with stenosis d, Diastole; e, end diastole; PA, pulmonary artery; RV, right-ventricular; s, systole INDEX A a wave in left-ventricular pressure wave, 30f in mitral stenosis, 68f in patient with a pacemaker, 52f in pulmonary capillary wedge pressure waveform, 27f in right-atrial waveform, 21f in right-ventricular waveforms, 23f Absolute flow reserve, 275–276 Doppler-derived, 276, 277f Acquired left-ventricular outflow tract obstruction, 131–135, 137f–138f Acute coronary syndromes, fractional flow reserve in, 285 Acute mitral regurgitation, aortic waveform in, 224f Acute myocardial infarction, in cardiogenic shock, 222b Acute valvular regurgitation, in cardiogenic shock, 222b Adenosine, infusion of, 280–281, 294–295 Adults, with peripheral pulmonary artery stenosis, 264–265 Afterload, on pressure-volume loop, 220, 221f Alcohol septal ablation, for hypertrophic cardiomyopathy, 131 Alveolar hypoxia, 52 Alveolar pressure, schematic representation of, 28f Ambrisentan, for PAH patients, 174–176 American College of Chest Physicians, 174 Amlodipine, for PAH patients, 174–176 Anacrotic notch central-aortic pressure waveform with, 31–32, 32f–33f in chronic severe aortic regurgitation, with turbulence, in abnormal valve, 90–91, 90f in severe aortic stenosis, 104, 106f Angina chest pain, in aortic stenosis, 96 Angiogram of coarctation of aorta, 256f of tetralogy of Fallot, 262f Angiographic method, for cardiac output determination, 60 Angiographic stroke volume, 95 Angiography in aortic valve regurgitation, 93–95, 95b coronary, 270 hemodynamics related to, 295, 297f–298f selective, 270 Aorta coarctation of, 253–257 angiogram of, 256f complications in, 256–257 etiology of, 253–254 hemodynamic tracings of, 257f hemodynamics of, 255 infants with, 255 presentation of, 255 treatment of, effects of, 255–257 gradient in, TAVR and, 110, 112f Aortic balloon valvuloplasty, 109, 109f–110f Aortic pressure central, left-ventricular pressure and, 33f, 34 diastolic, low, chronic aortic regurgitation and, coronary perfusion and, 93 Aortic pressure tracing in acute aortic regurgitation, 93, 95f in severe aortic stenosis, 106f Aortic pressure wave in hypertrophic cardiomyopathy, 121f–122f valvular aortic stenosis from, fixed obstruction and, 121f Aortic pressure waveform central, 31–32 with anacrotic notch, 31, 32f components of, 32 femoral artery sheath pressure and, 33f normal, 31, 31f with ventricular bigeminy, 46f Aortic regurgitation, regurgitant fraction in, 303 Aortic regurgitation index (AR index), 111, 113f, 303 Aortic stenosis, 95–114 angina chest pain in, 96 atrial fibrillation and, varying systolic pressure gradients, 97, 97f calcific, 104–105, 107f calculated valve area in, 103 coexisting aortic regurgitation and, 105–107 critical, 103 Note: Page numbers followed by “b,” “f,” and “t” indicate boxes, figures, and tables, respectively 305 306 INDEX Aortic stenosis (Continued) fluid dynamic theory and, 96–97 hemodynamic findings in, 103–105 invasive techniques for, 97 low gradient-low output, 105, 108t mild, 103–104 moderate, 103 physiology of, 95–97 pressure gradient in, 96–97, 96f in prosthetic aortic valves, 107–109, 108f severe, 105 after transcatheter aortic valve replacement, 112f anacrotic notch in, 104, 106f with calcific aortic stenosis, 104–105, 107f determination of, 97–98 in preserved left-ventricular function, 105 pseudo, 105 pulsus alternans in, 104, 107f sign of, 104, 105f sudden cardiac death in, 96 supravalvular, 139, 140f transcatheter aortic valve replacement for, 110–114 transvalvular pressure gradient in, 97, 97f measurement of, 100–103, 100f–104f, 100b valvular, 48f fixed obstruction and, from aortic pressure wave, 121f Aortic valve area Gorlin’s formula for, 303 application of, 98–100, 99f estimation of, 98 Hakki formula for, 303 Aortic valve disease, 88–117 Aortic valve regurgitation, 88–95 acute, 89 aortic pressure trace in, 93, 95f chronic vs., 88–89 hemodynamic findings of, 93, 94f–95f left-ventricular end-diastolic pressure (LVEDP), 93, 94f angiography in, 93–95, 95b aortic balloon valvuloplasty and, 109, 110f causes of, 89b chronic, 88 acute vs., 88–89 anacrotic notch in, 90–91, 90f aortic diastolic pressure affected by, coronary perfusion and, 93 femoral artery pressure in marked peripheral amplification in, central aorta pressure vs., 90–91, 91f hemodynamic findings in, 90–91 left-ventricular end-diastolic pressure (LVEDP), 92, 92f peripheral manifestation of, 89t Aortic valve regurgitation (Continued) systolic hypertension in, 90f wide pulse pressure, 93, 93f chronic severe after transcatheter aortic valve replacement, 113f anacrotic notch in, with turbulence, in abnormal valve, 90–91, 90f elevated right-ventricular end-diastolic pressure, 92–93 wide pulse pressure, 90–91, 90f coexisting, 105–107 effect of heart rate on, 113f grading the severity, 94, 95b hemodynamic findings in, 90–93, 90f–95f paravalvular, 111, 112f regurgitant volume in, 94 vasodilators in, 88 Aortic waveform in acute mitral regurgitation, 224f in heart failure, 229f during shock, 224f central, 222–224 normal, 223f Apical variant, of hypertrophic cardiomyopathy, 131 Arrhythmia in cardiogenic shock, 222b effects, on hemodynamic measurements, 43–51 transvalvular pressure gradient and, 97, 97f Arterial elastance (Ea), 218–220 Arterial hypotension, pericardial effusion and, 187 Arterial hypoxemia, tamponade and, 188–189 Arterial waveforms, in Impella percutaneous left-ventricular assist device, 238–239, 239f Arteriovenous concentration difference, 56 Arteriovenous oxygen (AV-O2), 56–57 Artifacts, 34–43, 38f catheter entrap, 39–43, 43f overshoot, 39, 40f ring, 39, 39f whip or fling, 39, 41f–42f Atrial bigeminy, 49f Atrial fibrillation, 44–48, 50f–51f aortic stenosis and, varying systolic pressure gradients, 97, 97f chronic, right-atrial waveform in, 21f Atrial flutter, with mitral regurgitation, 70f Atrial septal defect, 249–251 hemodynamic tracings of, 251f hemodynamics of, 250 treatment of, effects, 250–251, 252f Atrial septostomy, 174–176 Atrioventricular (AV) junction, block, 20–21, 22f first-degree, 53f with pacemaker, 52f Austin Flint murmur, 88–89 Automated computer analysis, by Gorlin’s formula, 99–100, 99f INDEX 307 Autoregulation, 275f Average peak velocity (APV), measurement of, 276 B Balancing, of transducers, 18–19 Balloon valvuloplasty aortic, 109, 109f–110f in pulmonic valve stenosis, 151f Beck triad, 187 Berman catheter, 10–11, 11f Bernard, Claude, Bernheim effect, 92–93 Beta blockers, for hypertrophic cardiomyopathy, 130 Bifurcation, fractional flow reserve for assessment in, 285 Bigeminy atrial, 49f ventricular, 46f Blalock-Taussig shunt, 261–263 Block AV, 20–21, 22f first-degree, 53f with pacemaker, 52f complete heart, 48–51 Blood flow coronary, stenosis severity relationship to, 275f pulmonary, in cardiac output, 56 systemic, 61–62 Blood sampling, 62f locations for, in complete saturation run, 62f Bosentan, for PAH patients, 174–176 Brockenbrough sign, in hypertrophic cardiomyopathy, 122, 124f C Calcific aortic stenosis, 104–105, 107f Calcium channel blockers, for hypertrophic cardiomyopathy, 130 Calibration, of transducers, 18–19 Cannon wave, 48–51, 52f Carabello sign, 104, 105f Cardiac catheterization for atrial septal defect, 250 contraindications for, 14–15 core elements of, early, 2, 2f for Eisenmenger syndrome, 266–267 equipment for, 10–13 laboratory, 57 hemodynamic assessment in, 1–16 protocols, 13–15 in two or more chambers, 32 Cardiac chambers, 183, 184f respiratory cycle and, 185f Cardiac cycle, 216, 217f changes in pressure in, 17, 18f Cardiac output, 56–65, 302 determination of angiographic method of, 60 Fick method for, 56–58 indicator-dilution method for, 58–59 thermodilution method for, 59–60, 60f measurement of, 56–60 oxygen consumption in, 56–57 pulmonary blood flow in, 56 pulmonary hypertension and, 167–168, 174–176 Cardiac power output (CPO), 225, 304 Cardiogenic shock aortic waveform in, 224f causes of, 222b definition of, 220–222 diagnostic criteria for, 221t downward spiral of, 223f hemodynamics of, 222–225, 223f–224f intra-aortic balloon pump in, 233–237 pathophysiology of, 220–222 pressure-volume loops in, 226f therapies for, hemodynamics of, 230–247 Cardiomyopathy, restrictive, 206–207, 209b Cardiopulmonary laboratory, 4–5 Cardiovascular system functions of, hemodynamics and, Catheter dual lumen pigtail, 102, 102f Langston, 102, 102f malposition of, 39–43, 46f pigtail, 126f retrograde, 100f, 101–102 Catheter entrapment artifact, 39–43, 43f Catheterization left-heart, protocols for, 13, 14b risks of, 15b protocols for, 13–15 right-heart, indications for, 10 protocols for, 14, 14b risks of, 15b Catheter-tip pressure, ventricularization of, 270, 271f–273f, 274b Central-aortic pressure in aortic stenosis, 100–101, 100f–101f, 103f left ventricular pressure and, 33f, 34 Central-aortic pressure waveform, 31–32 with anacrotic notch, 31, 32f, 90–91, 90f components of, 32 femoral artery sheath pressure and, 33f normal, 31, 31f during shock, 222–224 Chest irradiation, hemodynamic consequences of, 210, 214f Chronic obstructive lung disease (COPD), associated with PH, 169, 179 308 INDEX Chronic thromboembolic pulmonary hypertension (CTEPH), 163, 165b, 172 group 4, 179–180 Circular shunt, 258 Clinical practice FFR in, 282–285, 283f–284f modern, hemodynamic assessment in, 10 Coarctation of the aorta, 253–257 angiogram of, 256f complications in, 256–257 etiology of, 253–254 hemodynamic tracings of, 257f hemodynamics of, 255 infants with, 255 presentation of, 255 treatment of, effects of, 255–257 Coefficient of orifice contraction (Cc), 73 Coexisting aortic regurgitation, 105–107 “Combustion,” Compensatory mechanisms, in mitral regurgitation, 79–80 Computer analysis, automated, by Gorlin’s formula, 99–100, 99f Computer systems, for hemodynamic waveforms, 12–13, 13f Congenital heart disease, 249–269 atrial septal defect, 249–251 coarctation of the aorta, 253–257 Ebstein anomaly, 257–258 Eisenmenger syndrome, 265–267 peripheral pulmonary artery stenosis, 263–265 tetralogy of Fallot, 258–263 ventricular septal defect, 251–253 Constrictive pericarditis, 195 diagnosis of, 205 hemodynamic findings in, 199–205, 200b, 201f, 203f–204f physiology of, 196–199, 200f restrictive cardiomyopathy and, 207, 210f–213f tricuspid valve regurgitation vs., 147 ventricular interdependence in, 204f Constrictive physiology, 199 Contractility, on pressure-volume loop, 220, 221f Contraction, coefficient of orifice, 73 Contrast aortography, in aortic regurgitation, 94 Cor pulmonale, 52 CORAL trial, 295–297 Coronary angiography, 270 selective, 270 Coronary artery FFR assessment, 288f hemodynamics, 270–301 left main, atherosclerotic narrowing of, 285 Coronary blood flow, intra-aortic balloon pump in, 234 Coronary catheter pressure waveforms, in coronary hemodynamics, 270–273, 271f–273f Coronary disease diffuse, FFR for, 287, 291f multivessel, FFR for, 285–287 Coronary flow coronary stenosis effects on, 274–275, 275f reserve, 275–276, 275f Coronary hemodynamics, 273–274 Coronary physiology, 274 Coronary pressure, measured by fractional flow reserve (FFR), 286f–287f Coronary stenosis, effects, on coronary flow, 274–275, 275f Corrigan pulse de Musset sign, 89t Cournand, André F., 4–5, 5f CPO see Cardiac power output (CPO) CTEPH see Chronic thromboembolic pulmonary hypertension (CTEPH) c-v wave, 164 D Damping pressure, 270, 271f, 274b in pressure waveforms, 17 Defects atrial septal, 249–251 outlet, 251 sinus venosus, 250 ventricular septal defect, 251–253 Deflation, timing of, 235 Diastasis, 92, 92f Diastole, in cardiac cycle, 216 Diastolic dysfunction, in hypertrophic cardiomyopathy, 120, 120f–121f Diastolic pressure left-ventricular, pulmonary capillary wedge and, 71b low, chronic aortic regurgitation and, coronary perfusion and, 93 during respiratory cycle, 184–185, 186f Diastolic pressure gradient (DPG), 163, 302–303 Diffuse coronary disease, FFR for, 287, 291f Diltiazem, for PAH patients, 174–176 Dip and plateau, 158f Disopyramide, for hypertrophic cardiomyopathy, 130 Distal lesion pressure (Pd), to proximal pressure (Pa), in wave free period, 294–295 Dobutamine, 231–233, 232f Doppler-derived absolute flow reserve, 276, 277f Downward spiral, of cardiogenic shock, 223f DPG see Diastolic pressure gradient (DPG) Dual lumen pigtail catheter, 102, 102f Duroziez sign, 89, 89t Dye, indocyanine green, 58–59 Dye curve, 63–65 Dynamic obstruction, in hypertrophic cardiomyopathy, 122, 124f Dyspnea, pericardial effusion and, 187 INDEX 309 E Ebstein anomaly, 257–258 hemodynamic tracings of, 259f–260f hemodynamics of, 258 neonates with, 258 treatment for, effects of, 258 Echocardiography, 303 mitral annular calcification on, 72f ECMO see Extracorporeal membrane oxygenation device (ECMO) EDPVR see End-diastolic pressure-volume relationship (EDPVR) Effusive-constrictive pericarditis, 205–206, 206f–209f Eisenmenger syndrome, 265–267 heart schematic for, 266f hemodynamics of, 266–267 treatments for effects of, 267 phlebotomy for, 267 Electrical mechanical dissociation, localized, 227–229 End-diastolic pressure-volume relationship (EDPVR), 218–220, 219f in heart failure, 229–230 End-hole catheter, 10–11 End-systolic pressure-volume relationship (ESPVR), 218–220, 219f in heart failure, 229–230 Epoprostenol, for PAH patients, 174–176 Equipment, for cardiac catheterization, 10–13, 11f ESPVR see End-systolic pressure-volume relationship (ESPVR) European Society of Cardiology, 174 Ewart sign, 187 Expiration, pericardium during, 183–184, 185f Extracorporeal membrane oxygenation device (ECMO), veno-arterial, 243–247, 245f–246f synopsis of, 247b F FAME trial, 282–284 Fatigue, pericardial effusion and, 187 Femoral artery pressure, in chronic aortic regurgitation marked peripheral amplification in, central aorta pressure vs., 90–91, 91f Femoral artery sheath pressure errors in, 102 simultaneous, 33f FFR see Fractional flow reserve (FFR) Fick, Adolph, 2, 56 Fick method, 58f, 302 for cardiac output determination, 56–58 error in, 57 Fick’s principle, 302 Fifth World Symposium on PH, 163 Fixed obstruction, in hypertrophic cardiomyopathy, 121f, 122 Flamm formula, 302 Flow reserve absolute, 275–276 coronary, 275–276, 275f Doppler-derived absolute, 276, 277f pressure-derived fractional, 276–278, 278f relative, 275–276 Fluid mechanics and flow, through stenotic orifice, 96–97 Fluid-filled systems, 12 Force-tension curve, 216–218, 218f dobutamine on, 231–233, 232f norepinephrine on, 231–233, 233f phenylephrine on, 231–233, 231f in pressure-volume loop, 220 Formula, hemodynamic, 302 Forssmann, Werner, 3, 4f, 143 Forward flow, diminished, in acute aortic regurgitation, hemodynamic findings in, 93 Fractional flow reserve (FFR), 275–276, 304 acute coronary syndromes, 285 for ambiguous lesions, 284f, 286f–287f bifurcation, 285 clinical applications, 282–285, 283f–284f coronary pressure measurement, 286f–287f for diffuse coronary disease, 287, 291f greater than 0.75, outcome of, 282–284 hyperemia during, 278 ischemic, 290–294 left main disease, 285 limitations of, 290–294 measurement errors with, 281f for multivessel coronary disease assessment, 285–287, 289f–290f pressure-derived, 276–278 derivation of, 278f side branches, 285 technique, 279–282, 279f–280f theory, criticisms, 290–294 transducer pressure drift during, 281 at various stenosis severities, 283f–284f Frank-Starling mechanism, 226–227 Free pulmonary regurgitation, 261f, 265f French femoral arterial sheath, 103f French (Fr) catheter, 295, 296f G Gorlin’s formula for aortic valve area, 303 application of, 98–100, 99f estimation of, 98 automated computer analysis by, 99–100, 99f for mitral valve area, 73–75, 302 for prosthetic valve area, limitations of, 76–77 for pulmonic valve stenosis, 148 Guidewire, 298f–299f 310 INDEX H Hakki formula, for aortic valve area, 303 Hales, Stephen, 1–2 Hamilton, William, 7–8 Hamilton manometer, Heart, schematic of for Eisenmenger physiology, 266f with restricted ventricular septal defect, 254f–255f of tetralogy of Fallot, 262f Heart block, complete, 48–51 Heart disease congenital, 249–269 atrial septal defect, 249–251 coarctation of the aorta, 253–257 Ebstein anomaly, 257–258 Eisenmenger syndrome, 265–267 peripheral pulmonary artery stenosis, 263–265 tetralogy of Fallot, 258–263 ventricular septal defect, 251–253 left, pulmonary hypertension due to, 164, 165b Heart disorders, right-sided, 143–162 pulmonic valve regurgitation, 149–152, 152f–154f pulmonic valve stenosis, 147–149, 150f–151f right-ventricular failure, 152, 155f right-ventricular infarction, 152–160, 156b, 157f–161f tricuspid valve regurgitation, 144–147, 145b, 146f–149f tricuspid valve stenosis, 143–144, 144f–145f Heart failure, 216–248 aortic waveform in, 229f left, impact, on right-heart hemodynamics, 143 left-ventricular waveform in, 228f–230f with reduced ejection fraction hemodynamics of, 226–230, 228f pressure-volume loop in, 229–230, 230f systolic, pathophysiology of, 226, 227b right, 143 right-ventricular waveform in, 230f therapies for, hemodynamics of, 230–247 Heart failure with preserved ejection fraction (HFpEF), 174 Heart rate, impacting transmitral gradient, 76f Hemodynamic abnormalities in chronic lung disease, 54 of hypertrophic cardiomyopathy, 120–125 in tricuspid regurgitation, 145–146 in tricuspid stenosis, 143, 144f Hemodynamic assessment in cardiac catheterization laboratory, 1–16 computer systems for, 12–13, 13f core elements of, equipment for, 10–13, 11f history of, 1–8, 2f indications for, 10 Hemodynamic assessment (Continued) in modern clinical practice, 10 specific challenges in, of hypertrophic cardiomyopathy, 125–129, 126f–130f Hemodynamic data artifacts for, 34–43 errors in, 34–43, 37b Hemodynamic equations, 302 Hemodynamic findings, in aortic valve regurgitation, 90–93, 90f–95f of left ventricular function, 92, 92f Hemodynamic measurements effect of arrhythmia on, 43–51 effect of obesity on, 51–52, 54f effect of pulmonary disease on, 52–54 during peripheral arterial disease evaluation, 295–297 Hemodynamic monitoring system, 9f, 10 Hemodynamic study, goal of, 17 Hemodynamic tracings of atrial septal defect, 251f of coarctation of the aorta, 257f of Ebstein anomaly, 259f–260f for peripheral pulmonary artery stenosis, 264f–265f for tetralogy of Fallot, 261f “Hemodynamically significant,” 295–297 Hemodynamics, angiography related to, 295, 297f–298f assessment, instantaneous wave free ratio and, 294–295, 294f of atrial septal defect, 250 of coarctation of the aorta, 255 of constrictive pericarditis, 199–205, 200b, 201f, 203f–204f coronary, 270–301 coronary catheter pressure waveforms in, 270–301 of Ebstein anomaly, 258 of Eisenmenger syndrome, 266–267 of mitral balloon valvuloplasty, 77–78, 77f–78f of mitral regurgitation, 80–83, 83f severe, 84f of mitral valve stenosis, 67–73 of pericardial effusion, 188–193 peripheral, 270–301 of peripheral pulmonary artery stenosis, 263 in right-ventricular infarction, 159f–160f of tamponade, 188–193, 189f–191f of tetralogy of Fallot, 260–261 pregnancy with, 260–261 of ventricular septal defect, 252–253 High-fidelity left-ventricular pressure waveform, 29f Hill sign, 89t Hybrid tracings, 39–43, 44f–45f Hyperemia, during FFR, 278 INDEX 311 Hypertrophic cardiomyopathy, 118–142 alcohol septal ablation, 131, 132f–135f aortic pressure wave in, 121f–122f apical variant of, 131, 136f Brockenbrough sign in, 122, 124f diastolic dysfunction in, 120, 120f–121f dynamic obstruction in, 122, 124f fixed obstruction in, 121f, 122 hemodynamic abnormalities of, 120–125 hemodynamic assessment of, specific challenges in, 125–129, 126f–130f left ventricular outflow tract obstruction in, 120–125, 121f–125f mitral regurgitation in, 119f outflow tract obstruction in, 127f–129f pathophysiology of, 118–119, 119f, 119t post-PVC beat in, 122, 124f treatment of beta blockers in, 130 calcium channel blockers in, 130 disopyramide in, 130 effects of, 130–139 Hypertrophic obstructive cardiomyopathy, PVC with, 48f Hypoxia alveolar, 52 pulmonary hypertension due to, 165b I IABP see Intra-aortic balloon counterpulsation (IABP) Iliac stenosis, pressure measurements in, 296f Iloprost, for PAH patients, 174–176 Impella percutaneous left-ventricular assist device, 237–239, 237f–240f synopsis of, 241b Impulse gradient, 95 Indicator substance application technique of, 58 concentration of, 58 limitations of, 58–59 Indicator-dilution method for cardiac output determination of, 58–59 of shunt detection, 63–65 thermodilution method vs., 59, 59f Indocyanine green dye, 58–59 Infants, with coarctation of the aorta, 255 Inferior vena cava (IVC), calculations of, 61, 62f Inflation, timing of, 235 Infundibular stenosis, 149 Inotropes, 231–233, 231f–233f Inspiration, pericardium during, 183–184, 185f Instantaneous wave free ratio, hemodynamic assessment and, 294–295, 294f Intra-aortic balloon counterpulsation (IABP), 233–237, 234f–236f Intra-aortic balloon pump, 235–237 synopsis of, 237b Intracardiac shunt full oxygen saturation for, 61 screening for, 61 Intracoronary adenosine, 279–280 Irradiation, chest, hemodynamic consequences of, 210, 214f Isolated postcapillary pulmonary hypertension, 164t Isovolumic contraction, occurrence of, 216 K Korotkoff sounds, 190–191 Kussmaul sign, 196 L Langston catheter, 102, 102f LaPlace, law of, 88 Last-drop effect, 183 Left heart failure, impact, on right-heart hemodynamics, 143 Left main disease, fractional flow reserve in, 285, 286f–288f Left ventricular dysfunction, severe, in leftventricular pressure waveform, 227, 228f Left ventricular end-diastolic pressure (LVEDP), 29, 30f–31f, 165 in acute aortic regurgitation, 93, 94f in chronic aortic regurgitation, 92, 92f in heart failure, 226–227 Left ventricular function hemodynamic findings in, in aortic valve regurgitation, 92, 92f obstruction of, 95 Left ventricular outflow tract obstruction, in hypertrophic cardiomyopathy, 120–125, 121f–125f acquired, 131–135, 137f–138f Left-atrial pressure, PCWP calculation errors and, 74f–75f Left-heart catheterization, protocols for, 13, 14b risks of, 15b Left-to-right shunt, 61, 64f Left-ventricular assist device Impella percutaneous, 237–239, 237f–240f, 241b mechanical, 233 TandemHeart percutaneous, 240–243, 241f–244f, 244b Left-ventricular diastolic pressure, pulmonary capillary wedge and, 71b Left-ventricular hemodynamics, 216–218, 217f–218f Left-ventricular pressure in aortic stenosis, 100–101, 100f–101f central-aortic pressure and, 33f, 34 combination of, with pulmonary capillary wedge, 33–34, 36f–37f PCWP and, 33–34, 36f–37f PCWP simultaneous with, in mitral regurgitation, 81f in prosthetic valve patient, 108 312 INDEX Left-ventricular pressure waveform in heart failure, 230f severe left ventricular dysfunction in, 227, 228f Left-ventricular systole, 216 Left-ventricular waveform, 29 a wave in, 30f high-fidelity, 29f normal, 29 respiratory variation on, 31f Lesions ambiguous, FFR for, 282–284, 284f renal artery, pressure measurements in, 295, 296f tandem, 287–289, 292f–293f Localized electrical mechanical dissociation, 227–229 Low gradient-low output aortic stenosis, 105, 108t Low-pressure tamponade, 192, 197f Lung disease chronic, hemodynamic abnormalities in, 54 pulmonary hypertension due to, 164, 165b, 169 Lung zones, 28, 28f LVEDP see Left ventricular end-diastolic pressure (LVEDP) M Macitentan, for PAH patients, 174–176 Marked peripheral amplification, in central aorta pressure, femoral artery pressure vs., in chronic aortic regurgitation, 90–91, 91f McConnell sign, 170 Mean gradient, 100 Mean pulmonary artery pressure (mPAP), 163, 168f, 179f Mechanical left-ventricular support devices, 233 Mechanical recorder, for hemodynamics, 9f Micromanometer, 12 Microvascular resistance, 290–294 Midaxillary line, as zero position, 18 Midcavity obstruction, 127f MitraClip procedure, for mitral regurgitation, 83–84, 85f Mitral annular calcification, severe, 71, 72f Mitral balloon valvuloplasty, hemodynamics of, 77–78, 77f–78f Mitral regurgitation, 78–84 acute, 81–82 acute severe, 81f, 83f hemodynamics of, 84f atrial flutter with, 70f causes of, 79b compensatory mechanisms in, 79–80 hemodynamics of, 80–83 in hypertrophic cardiomyopathy, 119f pathophysiology of, 79–80 percutaneous mitral valve repair for, 83–84 pulmonary artery waveform with, 82f severity grading of, 79b Mitral regurgitation (Continued) simultaneous pressure in, with PCWP and left-ventricular pressure, 81f v wave correlation with, 80–81, 81f, 85f Mitral stenosis, 66–78 a waves in, 68f causes of, 67b hemodynamics of, 67–73 pathophysiology of, 66–67 PCWP in, 68–71, 71f pressure gradient in, 66, 68, 70f causes of, 71b pressure tracing of, 68f rheumatic, pathology of, 67f v wave in, 69f y descent in, 69f Mitral valve area, 303 calculation using Gorlin’s formula, 73–75 Mitral valve disorders, 66–87 mitral balloon valvuloplasty, 77–78 mitral regurgitation, 78–84 mitral stenosis, 66–78 prosthetic mitral valves, 76–77 Mitral valves prosthetic, 76–77 repair of, for mitral regurgitation, 83–84 Mixed venous oxygen content, Muller sign, 89t Multivessel coronary disease assessment, FFR for, 285–287, 289f–290f Myocardial oxygen demand, 274, 275f Myocardial resistance, 290–294 N Nifedipine, for PAH patients, 174–176 Noise, 17 Norepinephrine, 231–233, 233f O Obesity, effect, on hemodynamic measurements, 51–52, 54f Obstruction in cardiogenic shock, 222b dynamic, in hypertrophic cardiomyopathy, 122, 124f fixed, in hypertrophic cardiomyopathy, 121f, 122 left ventricular outflow tract, in hypertrophic cardiomyopathy, 120–125, 121f–125f acquired, 131–135, 137f–138f midcavity, 127f Ohm’s law, Wood units and, 167–168 Optical manometer, 7, 8f Optimal catheter, 10–11 Outflow tract obstruction, in hypertrophic cardiomyopathy, 127f–129f Outlet defects, 251 Overdamping, in pressure waveforms, 17 Overshoot artifact, 39, 40f INDEX 313 Oximetric technique, limitations of, 63 Oxygen consumption, in cardiac output, 56–57 myocardial demand of, 274, 275f saturation, full, for intracardiac shunt, 61 P Pacemaker, hemodynamics and, 52f PAH see Pulmonary arterial hypertension (PAH) Pain, chest, pericardial effusion and, 187 Paravalvular aortic regurgitation, 111, 112f Parietal pericardium, 183 Parvus, 255 Pathophysiology, of hypertrophic cardiomyopathy, 118–119, 119f, 119t PCWP see Pulmonary capillary wedge pressure (PCWP) PE see Pulmonary embolism (PE) Peak instantaneous gradient, 100 Peak-to-peak gradient, 100 Percutaneous balloon pericardiotomy, 193–195 Pericardial anatomy, normal, 183–185 Pericardial calcification, 205, 205f Pericardial constriction, 195–196 pericardial calcification in, 205, 205f physiology of, 196–199, 200f Pericardial disease, 182–183, 182b constrictive pericarditis as, 195 diagnosis of, 205 hemodynamic findings in, 199–205, 200b, 201f, 203f–204f physiology of, 196–199, 200f restrictive cardiomyopathy and, 207, 210f–213f ventricular interdependence in, 204f pericardial effusions in hemodynamic sequelae of, 187, 188f hemodynamics of, 188–193 tamponade and, 185–188 tamponade in advanced phases of, 189 hemodynamics of, 188–193, 189f–191f, 193f–196f low-pressure, 192, 197f pericardial effusions and, 185–188, 188f pulmonary edema and, 188–189 pulmonary hypertension and, 192, 193f–196f pulsus paradox with, 190–191, 192f right-ventricular hypertrophy and, 192, 193f–194f treatment of, 193–195 Pericardial effusions hemodynamic sequelae of, 187, 188f hemodynamics of, 188–193 tamponade and, 185–188 Pericardial reserve volume, 183, 184f Pericardiocentesis, 193f–194f, 195, 198f–199f Pericardiotomy, percutaneous balloon, 193–195 Pericarditis constrictive, 195 diagnosis of, 205 hemodynamic findings in, 199–205, 200b, 201f, 203f–204f physiology of, 196–199, 200f restrictive cardiomyopathy and, 207, 210f–213f tricuspid valve regurgitation vs., 147 ventricular interdependence in, 204f effusive-constrictive, 205–206, 206f–209f Pericardium functions of, 183 parietal, 183 pressure-volume relationship for, 184f visceral, 183 Peripheral arterial disease evaluation, hemodynamic measurements during, 295–297 translesional pressure gradient, 295 Peripheral artery, hemodynamics, 270–301 Peripheral pulmonary artery stenosis, 263–265 adults with, 264–265 hemodynamic tracings for, 264f–265f hemodynamics of, 263 syndromes associated with, 263 treatment for, effects of, 263–265 PH see Pulmonary hypertension (PH) Phenylephrine, 231–233, 231f Phlebostatic axis, 18, 19f Phlebotomy, for Eisenmenger syndrome, 267 Pigtail catheter, 10–11, 126f dual lumen, 102, 102f Pink tet, 260 Postcapillary pulmonary hypertension, 163, 164t Post-PVC beat, in hypertrophic cardiomyopathy, 122, 124f Potts shunt, 261–263 Precapillary pulmonary hypertension, 164t see also Pulmonary capillary wedge pressure (PCWP) Pregnancy, with tetralogy of Fallot, hemodynamics of, 261 Preload, on pressure-volume loop, 220, 220f Premature ventricular beat (PVC), 43–44 aortic pressure with, 46f with hypertrophic cardiomyopathy, 48f systolic pressure with, 47f with valvular aortic stenosis, 48f Pressure damping, 270, 271f, 274b Pressure gradient in aortic stenosis, 95–97, 96f left-ventricular diastolic, pulmonary capillary wedge and, 71b in mitral stenosis, 66 causes of, 71b pullback, 296f in pulmonic valve stenosis, 147–148, 150f in renal artery lesions, 295, 296f 314 INDEX Pressure gradient (Continued) translesional, in peripheral arterial disease, 295 transvalvular, in aortic stenosis, 97, 97f measurement of, 100–103, 100f–104f, 100b in tricuspid stenosis, 143, 144f Pressure guidewire, 298f–299f Pressure measurements iliac stenosis, 296f renal artery lesions, 295, 296f Pressure recovery, in aortic stenosis, 96–97, 96f Pressure tracing ideal, 17 of mitral stenosis, 68f Pressure transducer, 17 Pressure waveforms, generation of, 17, 18f Pressure wire, 101, 101f Pressure-derived fractional flow reserve, 276–278, 278f derivation of, 278f Pressure-volume loop, 218–220, 218f–221f dobutamine on, 231–233, 232f in heart failure with reduced ejection fraction, 229–230, 230f by Impella percutaneous left-ventricular assist device, 238–239, 238f norepinephrine on, 231–233, 233f in normal heart, and various causes of cardiogenic shock, 226f phenylephrine on, 231–233, 231f by TandemHeart percutaneous left-ventricular assist device, 242–243, 243f by veno-arterial extracorporeal membrane oxygenation device, 245–246, 246f of ventricular support devices, 235f Pressure-volume relationship, for pericardium, 184f Prostaglandins, for coarctation of the aorta, 254–255 Prosthetic aortic valves aortic stenosis in, 107–109, 108f deteriorating, TAVR for, 114, 114f–116f left-ventricular pressure in, 108 Prosthetic mitral valves, 76–77 Prosthetic valve area, limitations of, 76–77 Proximal pressure (Pa), distal lesion pressure (Pd), to, in wave free period, 294–295 Pseudoconstriction, 199, 201b, 202f–203f pattern, 158f Pullback, for measuring transvalvular gradient, 102–103, 104f Pullback pressure gradient, 296f Pulmonary angiogram, 170, 172f Pulmonary arterial hypertension (PAH), 163, 165b, 178f Pulmonary artery pressure estimation, schematic representation of, 28f Pulmonary artery pulsatility index (PAPi), 168 Pulmonary artery stenosis, peripheral, 263–265 adults with, 264–265 hemodynamic tracings for, 264f–265f hemodynamics of, 263 syndromes associated with, 263 treatment for, effects of, 263–265 Pulmonary artery waveform, 24–25 in mitral regurgitation, 82f normal, 24, 24f novel methods for, 25–26, 26f respiratory variation in, 24f–25f Pulmonary blood flow, in cardiac output, 56 Pulmonary capillary hemangiomatosis, 165b Pulmonary capillary wedge, left-ventricular diastolic pressure and, causes of gradient between, 71b Pulmonary capillary wedge pressure (PCWP), 163, 165–167, 168f–169f, 173f, 175f, 224–225 calculation, errors in, 74f–75f left-ventricular pressure simultaneous with, in mitral regurgitation, 81f in mitral stenosis, 68–71, 71f v waves in, 75f Pulmonary capillary wedge pressure waveform, 26–29 a waves in, 27f correlation to, 29 high-quality characteristics of, 28 obtaining, 28 left-atrial waveform and, 27f left-ventricular pressure and, 33–34, 36f–37f mean, 29 normal, 26–27, 27f in patients on a ventilator, 29 v waves in, 27f Pulmonary disease, effect, on hemodynamic measurement, 52–54 Pulmonary edema, tamponade and, 188–189 Pulmonary embolism (PE), hemodynamic effects of, 170–172, 172f–173f Pulmonary endarterectomy, 179–180 Pulmonary flow to systemic flow ratio (Qp/Qs), 254f–255f, 266–267 Pulmonary hypertension (PH), 149 classification of, 165b criteria of, 163, 164t definition of, 163, 164t diagnosis of, 163–164, 166f group 5, 180 hemodynamic effects of, 169–170 findings in, 164–169, 167f–171f treatment and effects on, 174–180, 178f–179f mitral stenosis and, 66 prevalence of, 169–170 and related disorders, 163–181 right atrial waveform in, 164, 167f INDEX 315 Pulmonary hypertension (PH) (Continued) right ventricular pressure waveform in, noncompliance in, 164, 167f right-ventricular waveform in, 22–24, 23f tamponade and, 192, 193f–196f v wave in, 164 vasodilator challenge and, 172–174, 174t, 175f–177f Pulmonary insufficiency, 149, 152f–154f in tetralogy of Fallot, 263 Pulmonary regurgitation, free, 261f, 265f Pulmonary vascular resistance (PVR), 52, 163, 303 Pulmonary venoocclusive disease, 165b, 172–173 Pulmonary venous pressure, schematic representation of, 28f Pulmonic valve regurgitation, 149–152, 152f–154f Pulmonic valve stenosis, 147–149, 150f–151f balloon valvuloplasty in, 151f Gorlin’s formula in, 148 pressure gradient in, 147–148, 150f valve area, calculation of, 148 Pulsatility index, 303 Pulsus alternans, 227–229, 229f with severe aortic stenosis, 104, 107f Pulsus bigeminus, 227–229 Pulsus paradox, 183–184, 185f, 227–229 accurate measurement of, 190–191 causes of, 191b physiologic, 186f with tamponade, 190–191, 192f Pump failure, in cardiogenic shock, 222b Pump flow, 243 PVC see Premature ventricular beat (PVC) PVR see Pulmonary vascular resistance (PVR) Q Quincke sign, 89t R RAP see Right-atrial pressure (RAP) Reduced ejection fraction, heart failure with hemodynamics of, 226–230, 228f pressure-volume loop in, 230f systolic, pathophysiology of, 226, 227b Reflected waves, 32, 33f Regurgitant fraction, 94–95, 303 Regurgitant volume, in aortic valve regurgitation, determination of, 94 Relative flow reserve, 275–276 Renal artery lesions, pressure measurements in, 295, 296f Resistance vessels, 274 Respiratory cycle cardiac chambers and, 185f diastolic pressure during, 184–185, 186f systolic pressure during, 184–185, 187f Respiratory variation on left-ventricular waveform, 31f in pulmonary artery waveform, 24f–25f Restrictive cardiomyopathy, 206–207, 209b constrictive pericarditis and, 207, 210f–213f Restrictive myocardial diseases, 182–215 Restrictive ventricular septal defect, 253, 254f–255f Retrograde catheter, 100f, 101–102 RHC see Right-heart catheterization (RHC) Rheumatic mitral stenosis, pathology of, 67f Right atrial waveform, in pulmonary hypertension, 164, 167f Right heart failure, 143 Right ventricular pressure, in chronic severe aortic regurgitation, 92–93 Right-atrial pressure (RAP), 164 Right-atrial waveform, 20–22, 21f with chronic atrial fibrillation, 21f normal, 21–22, 21f in tamponade, 189f in tricuspid valve regurgitation secondary, 146f severe, 147f Right-heart catheterization (RHC), 5, 163 in cardiogenic shock, 224–225 indications for, 10 protocols for, 14, 14b risks of, 15b Right-sided heart disorders, 143–162 pulmonic valve regurgitation, 149–152, 152f–154f pulmonic valve stenosis, 147–149, 150f–151f right-ventricular failure, 152, 155f right-ventricular infarction, 152–160, 156b, 157f–161f tricuspid valve regurgitation, 144–147, 145b, 146f–149f tricuspid valve stenosis, 143–144, 144f–145f Right-ventricular end-diastolic pressure (RVEDP), 164 in chronic aortic regurgitation, 92–93 Right-ventricular failure, 152, 155f Right-ventricular hypertrophy, tamponade and, 192, 193f–194f Right-ventricular infarction, 152–160, 156b, 157f–161f Right-ventricular pressure, combination of, leftventricular pressure and, 32–33, 34f–35f Right-ventricular waveforms, 22–24 a wave in, 23f in heart failure, 230f normal, 22–24, 23f in patient with pulmonary hypertension, 22–24, 23f in right-ventricular infarction, 158f Ring artifact, 39, 39f Riociguat, for PAH patients, 174–176, 179–180 316 INDEX Risks for left-heart catheterization, 15b for right-heart catheterization, 15b Roentgen, Wilhelm, 2, 3f RR intervals, 51f RVEDP see Right-ventricular end-diastolic pressure (RVEDP) S SAM see Systolic anterior motion (SAM) Saturation run, complete, blood sampling locations for, 62f Selective coronary angiography, 270 Selexipag, for PAH patients, 174–176 Senile aortic stenosis, 95 Serial lesions, 287–289 Shock, 216–248 aortic waveform in, 224f causes of, 222b definition of, 220–222 diagnostic criteria for, 221t downward spiral of, 223f hemodynamics of, 222–225, 223f–224f pathophysiology of, 220–222 pressure-volume loops in, 226f therapies for, hemodynamics of, 230–247 Shunt calculation, 302 left-to-right shunt size, 302 Shunt detection, indicator-dilution method of, 63–65 Shunt flow, calculation of, 63 “Shunt run,” 61 Shunt size, calculation, 61–63 Shunts, 56–65 Blalock-Taussig, 261–263 calculation of, 61–65 circular, 258 intracardiac, screening for, 61 left-to-right, 61, 63, 64f Potts, 261–263 Qp/Qs for, 63 Side branches, fractional flow reserve for assessment in, 285 Sildenafil, for PAH patients, 174–176 Simultaneous pressure in aortic stenosis, 100f–103f with left-ventricular and left-atrial pressure, mitral balloon valvuloplasty and, 77f measurement of with central-aortic and left-ventricular pressure, 33f, 34 with left-ventricular and right-ventricular pressure, 32–33, 34f–35f with pulmonary capillary wedge, and leftventricular pressure, 33–34, 36f–37f in two or more chambers, 32 with PCWP and left-ventricular pressure, in mitral regurgitation, 81f in transcatheter aortic valve replacement, 113f Sinus venosus defects, 250 Sleep disordered breathing, associated with PH, 169 Small caliber (4 French [Fr]) catheter, 295, 296f Sphygmograph, Square root sign, 158f, 199, 201f Starling curve, 216–218, 217f dobutamine on, 231–233, 232f norepinephrine on, 231–233, 233f phenylephrine on, 231–233, 231f in pressure-volume loop, 220 Starling’s Law of the Heart, 216 Stenosis coronary, effects of, on coronary flow, 274–275, 275f iliac, pressure measurements in, 296f infundibular, 149 mitral, 66–78 a wave in, 68f causes of, 67b hemodynamics of, 67–73 pathophysiology of, 66–67 PCWP in, 68–71, 71f pressure gradient in, 66, 68, 70f, 71b pressure tracing of, 68f rheumatic, pathology of, 67f v wave in, 69f y descent in, 69f peripheral pulmonary artery, 263–265 adults with, 264–265 hemodynamic tracings for, 264f–265f hemodynamics of, 263 syndromes associated with, 263 treatment for, effects of, 263–265 pulmonic valve, 147–149, 150f–151f balloon valvuloplasty in, 151f Gorlin’s formula in, 148 pressure gradient in, 147–148, 150f valve area, calculation of, 148 sequential, 288–289, 292f–293f severity of coronary blood flow relationship to, 275f at various stenosis severities, 283f–284f, 297f–298f tricuspid valve, 143–144, 144f–145f hemodynamic abnormalities in, 143, 144f pressure gradient in, 143, 144f Stenotic orifice, fluid flow in, 96–97, 96f Stroke volume, angiographic, 95 Subaortic membrane, hypertrophic cardiomyopathy and, 136, 139f Sudden cardiac death, in aortic stenosis, 96 Superior vena cava (SVC), calculations of, 61, 62f Supravalvular aortic stenosis, hypertrophic cardiomyopathy and, 139, 140f SVR see Systemic vascular resistance (SVR) Swan, Harold JC, 6, 6f Swan-Ganz catheter, 10–11, 11f INDEX 317 Systemic blood flow (Qs), 61–62 Systemic vascular resistance (SVR), 224–225, 304 calculation of, 225 Systole, in cardiac cycle, 216 Systolic anterior motion (SAM), 119f Systolic ejection period (SEP), in Gorlin’s formula, 98–99, 99f Systolic heart failure, with reduced ejection fraction, pathophysiology of, 226, 227b Systolic hypertension, in chronic aortic regurgitation, 90f Systolic pressure with PVC, 47f during respiratory cycle, 184–185, 187f T Tachycardia, pericardial effusion and, 187 Tadalafil, for PAH patients, 174–176 Tamponade advanced phases of, 189 hemodynamics of, 188–193, 189f–191f, 193f–196f low-pressure, 192, 197f pericardial effusions and, 185–188, 188f pulmonary edema and, 188–189 pulmonary hypertension and, 192, 193f–196f pulsus paradox with, 190–191, 192f right-ventricular hypertrophy and, 192, 193f–194f treatment of, 193–195 Tandem lesions, 287–289, 292f–293f TandemHeart percutaneous left-ventricular assist device, 161f, 240–243, 241f–244f synopsis of, 244b Tardus, 255 TAVR see Transcatheter aortic valve replacement Tet spells, 260 Tetralogy of Fallot, 258–263 abnormalities associated with, 260 angiogram of, 262f clinical features of, 260 heart schematic for, 262f hemodynamic tracings for, 261f hemodynamics of, 260–261 incidence of, 258–260 natural history of, 260 therapy for, 261–263 Thebesian vessels, 61 Theophylline, in FFR, 282 Thermodilution method for cardiac output determination of, 59–60, 60f indicator-dilution method vs., 59, 59f technique for, 59 Three lung zones of West, 28, 28f Transcatheter aortic valve replacement, 110–114 gradient in the aorta and, 110, 112f hemodynamic assessment in, 110 paravalvular leaks in, 111, 112f Transcatheter aortic valve replacement (Continued) severe aortic stenosis after, 112f subvalvular gradient in, 110, 111f “valve-in-valve” approach in, 114, 114f–116f wide pulse pressure after, 112f Transducer pressure drift, during FFR, 281 Transducers, 11, 12f, 17 balancing of, 18–19 calibration of, 18–19 previous generations of, 18 zeroing of, 18–19 Translesional pressure gradient, in peripheral arterial disease, 295 Transmitral gradient heart rate impacting, 76f quantification of, 74f from severe mitral annular calcification, 72f Transpulmonary gradient, 304 Transvalvular pressure gradient aortic balloon valvuloplasty in, 109, 109f in aortic stenosis, 97, 97f measurement of, 100–103, 100f–104f, 100b Traube sign, 89t Treatments for atrial septal defect, effects of, 250–251, 252f for coarctation of the aorta, effects of, 255–257 for Ebstein anomaly, effects of, 258 for Eisenmenger syndrome, effects of, 267 for hypertrophic cardiomyopathy alcohol septal ablation in, 131 beta blockers in, 130 calcium channel blockers in, 130 disopyramide in, 130 effects of, 130–139 for peripheral pulmonary artery stenosis, effects of, 263–265 for ventricular septal defect, effects of, 253 Treprostinil, for PAH patients, 174–176 Tricuspid valve, structurally normal, 145b Tricuspid valve regurgitation, 144–147, 145b, 146f–149f causes, 145b constrictive pericarditis vs., 147 hemodynamic abnormalities in, 145–146 secondary, right-atrial waveform in, 146f severe right-atrial waveform in, 147f venous pressure waveform in, 146f ventricularization in, 148f Tricuspid valve stenosis, 143–144, 144f–145f hemodynamic abnormalities in, 143, 144f pressure gradient in, 143, 144f Tubing, 11 U Unclear multifactorial mechanisms, pulmonary hypertension with, 165b 318 INDEX V v wave, 21–22, 21f mitral regurgitation correlation with, 80–81, 81f, 85f in mitral stenosis, 69f with PCWP, 27f error calculation for, 75f Valsalva maneuver, 125f Valve area aortic, Gorlin’s formula for application of, 98–100, 99f estimation of, 98 calculated, in aortic stenosis, 103 pulmonic valve stenosis with, 148 Valvular aortic stenosis, PVC with, 48f Valvuloplasty, mitral balloon, hemodynamics of, 77–78, 77f–78f Vardenafil, for PAH patients, 174–176 Vasoactive drugs, 231–233, 231f–233f Vasodilator agents, for pressure gradient, 295–297 Vena contracta, 96–97, 96f Veno-arterial extracorporeal membrane oxygenation device, 243–247, 245f–246f synopsis of, 247b Venous pressure waveform, in severe tricuspid valve regurgitation, 146f Ventricular bigeminy, aortic pressure waveform with, 46f Ventricular filling, phases of, 216 Ventricular interdependence, in pericardial constriction, 204f Ventricular septal defect, 251–253 classification of, 251 hemodynamics of, 252–253 restrictive, 253, 254f–255f treatment for, effect of, 253 Ventricular stroke work, 219f Ventricular wall tension, 219f Ventricularization, in tricuspid valve regurgitation, 148f Ventricularization of catheter-tip pressure, 270, 271f–273f, 274b Vessels resistance, 274 Thebesian, 61 Visceral pericardium, 183 Volume overload, acute, in acute aortic regurgitation, hemodynamic findings in, 93 W Wave free period, 294–295, 294f Waveforms, 17–55 aortic pressure, central, 31–32 with anacrotic notch, 31, 32f components of, 32 femoral artery sheath pressure and, 33f normal, 31, 31f with ventricular bigeminy, 46f central aortic pressure, with anacrotic notch, 90–91, 90f Waveforms (Continued) characteristics of normal physiology of, 19–32, 20f systematic approach to, 20b collection of, 17 coronary catheter pressure, in coronary hemodynamics, 270–273 interpretation of, 17 left-ventricular, 29, 29f a wave in, 29f high-fidelity, 29f normal, 29 respiratory variation on, 31f pressure, generation of, 17, 18f pulmonary artery, 24–25 in mitral regurgitation, 82f pulmonary capillary wedge pressure, 26–29 a waves in, 27f correlation to, 29 left-atrial waveform and, 27f mean, 29 normal, 26–27, 27f in patients on a ventilator, 29 v waves in, 27f in pulmonary hypertension, 164, 167f noncompliance in, 164, 167f right-atrial, 20–22, 21f a wave in, 21f with chronic atrial fibrillation, 21f normal, 21–22, 21f right-ventricular, 22–24 a wave in, 23f normal, 22–24, 23f in patient with pulmonary hypertension, 22–24, 23f in tricuspid valve regurgitation, right-atrial secondary, 146f severe, 147f Wide pulse pressure after transcatheter aortic valve replacement, 112f chronic, severe aortic valve regurgitation, 90–91, 90f in chronic aortic regurgitation, 93, 93f Wiggers manometer, 7, 8f Wood units, 163, 164t, 168, 173–174 X x descent, 20–21, 21f–23f Y y descent, 20–21, 21f, 23f in mitral stenosis, 69f Z “Zero” position, 18, 19f midaxillary line as, 18 Zeroing, 11 of transducers, 18–19 Fast answers and trusted evidence Drive better outcomes with a clinical search engine nd and apply relevant knowledge Fast Anticipates your query, recognizing ering shortcuts Complete Draws relevant answers from a wide range of current, comprehensive content across 30+ medical and surgical specialties ckey.co/books Convenient Accessible at the patient’s bedside or on the 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Cardiol 20 03;41: 127 3– 127 9 42 Cintron GB, Hernandez E, Linares E, et al Bedside recognition, incidence and clinical course of right ventricular infarction Am J Cardiol 1981;47 (2) :22 4 22 7 43 Lopez-Sendon... Intensive Care Med 20 02; 28:1117–1 121 25 Dow JW, Levine HD, Elkin M, et al Studies of congenital heart disease: IV Uncomplicated pulmonic stenosis Circulation 1950;1 :26 7 28 7 26 Moller JH, Rao... venous filling 1 72 TEXTBOOK OF CLINICAL HEMODYNAMICS A B C Fig 8.9. (A–B) Pulmonary angiogram of a 52- year-old woman with acute pulmonary embolism (C) Computed tomography angiogram of the same patient