Ebook Practical cardiovascular hemodynamics: Part 2

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Ebook Practical cardiovascular hemodynamics: Part 2

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(BQ) Part 2 book Practical cardiovascular hemodynamics has contents: Assessment of mixed valvular disorders, pulmonary hypertension, hemodynamics in shock and fluid responsiveness, hemodynamics of left ventricular support devices and left ventricular pressure volume loop in various cardiac conditions,... and other contents.

XIII Tamponade XIII.1 OVERVIEW OF THE HEMODYNAMICS OF TAMPONADE In tamponade, intrapericardial pressure usually increases to ~10 to 25 mmHg and compresses the cardiac chambers until the pressure inside these chambers equalizes with the intrapericardial pressure (Figure XIII.1).1-5 This leads to equalization of diastolic pressures of the 4 cardiac chambers Because the rightsided chambers have thin walls, they tend to collapse when intrapericardial pressure is equal to or larger than their intracavitary pressure FIGURE XIII.1 Pressure-volume curve of the pericardium showing the intrapericardial pressure in rapidly and slowly developing effusions or cardiac dilatation In acute conditions, the pericardium cannot stretch, and its pressure rises markedly with small volume changes This explains how tamponade may develop with small acute effusion and how the pericardium may be stretched in case of acute RV dilatation leading to a “functional” CP Once the pericardial pressure exceeds a stretch limit (bar), it increases exponentially with any change in volume Even when intrapericardial pressure is lower than right-sided pressure, the RV or RA transmural pressure (RA pressure or RV pressure minus intrapericardial pressure) is reduced, which impairs RV outward expansion and filling; in addition, at this point, pericardial pressure is at a steep slope, and there is at least a threatened tamponade Although fluid administration may initially increase RV pressure and RV transmural pressure, intracardiac volume can stretch the pericardium and further increase intrapericardial pressure even if intrapericardial volume is unchanged; this explains how fluid administration in euvolemic or hypervolemic patients may be harmful This graph also shows that patients with high intrapericardial pressure resulting from CP or severe RV dilatation stretching the pericardium may have LVEDP >20 mmHg, yet the transmural LV pressure is almost nil and the LV volume cannot expand These patients have low LV volume yet increased pulmonary capillary pressure The amount of fluid in the pulmonary veins is modest, and thus, the lungs are almost always clear despite sometimes severe dyspnea Modified from Spodick DH Acute cardiac tamponade N Engl J Med 2003; 349: 684–690 The equalization of diastolic pressures is similar to what is observed in CP As opposed to CP however, the respiratory changes of intrathoracic pressure are transmitted to the cardiac chambers.1,2 This explains why RA pressure decreases during inspiration and thus venous flow from the SVC to the RA increases during inspiration (absence of the Kussmaul’s sign) Left-sided flow does not increase because pulmonary veins and LV are both exposed to the negative intrathoracic pressure; actually, the pulmonary veins are more affected by this negative pressure The increased venous flow to the right cavities makes the RV push against the LV in diastole, rather than push against the pericardium since the high pericardial pressure prevents that This reduces LV filling in inspiration and explains the reduction of systolic arterial pressure by more than 10 mmHg with normal inspiration (pulsus paradoxus) (Figure XIII.2) FIGURE XIII.2 Sequence of events during inspiration in tamponade (−) sign adjacent to a structure signifies there is tramsmission of the negative intrathoracic pressure to this structure, whereas (0) corresponds to the lack of transmission of the intrathoracic pressure to this structure Gray arrows signify increased flow between 2 chambers, whereas the blue arrows signify reduced flow between 2 chambers During inspiration, the negative pressure is transmitted to PV and SVC and to the intracardiac chambers (this is different from constriction) This increases flow between both IVC and SVC on the one hand and the RA then RV on the other hand, which pushes the septum to the left and reduces LV filling from LA and PV X descent is deep especially during inspiration, but Y descent is flat because of impeded RA-to-RV flow throughout all diastole, including early diastole E: mitral inflow Doppler wave; PV: pulmonary vein; S: systolic flow wave of IVC, SVC, and PV on Doppler, corresponds to X descent; D: diastolic flow wave of IVC, SVC, and PV on Doppler, corresponds to Y descent Although ventricular interdependence is present in both CP and tamponade, a different mechanism is incriminated in each case: during inspiration, RV pushes LV in tamponade, whereas RV is sucked by LV in CP As opposed to CP, LV flow is reduced in tamponade because of RV compression, not because of a lack of transmission of the negative intrathoracic pressure to LV In addition, because of the uniform pericardial fluid, the constraint is more uniform across both LV and RV in case of tamponade As a result of this different mechanism, ventricular interdependence is more prominent in tamponade and leads to pulsus paradoxus, which is only present in one third of cases of CP Furthermore, as opposed to CP where the heart briefly expands in early diastole before getting constrained, the heart is compressed throughout all diastole in tamponade, including early diastole Thus, RA-to-RV flow is impeded throughout all diastole, including early diastole, and there is no deep Y on the RA tracing and no diastolic dip on the RV tracing There is a deep X in early systole as RV annulus moves down and stretches out the compressed RA XIII.2 SUMMARY OF HEMODYNAMIC FINDINGS IN TAMPONADE Cardiac tamponade is defined as a pericardial effusion compressing the cardiac chambers and leading to hemodynamic compromise This compromise manifests clinically as any or all of the following: elevated JVP, systemic blood pressure alteration with pulsus paradoxus early on, tachycardia, and tachypnea/dyspnea/orthopnea with clear lungs (PCWP is increased, but the intracardiac and pulmonary venous volume is low, hence the lack of pulmonary edema) On invasive hemodynamics, the following 3 findings are characteristic of tamponade: 1-On RA and SVC tracings: elevated mean pressure with a deep X descent (mainly during inspiration) and a flat Y descent (Figure XIII.3) 2-Elevation and equalization of diastolic pressures of the 4 cardiac chambers and equalization of PA diastolic pressure with RV end-diastolic pressure (RVEDP), similarly to CP: CVP = mean RA pressure = RVEDP = PA diastolic pressure = mean PCWP = LVEDP (normally, RVEDP < PA diastolic pressure = PCWP = LVEDP) FIGURE XIII.3 Note the deep X and the blunted Y descents in a patient with tamponade 3-Although the systolic aortic pressure is initially normal or even elevated as a result of adrenergic release, pulsus paradoxus is present and pulse pressure is abnormal early on On any arterial or aortic tracing, pulsus paradoxus means that systolic pressure decreases >10 mmHg with normal inspiration In addition, the aortic waveform is narrow, and the pulse pressure is reduced (aortic tracing is “short” and narrow) (Figure XIII.4) Ultimately, the systolic pressure decreases as well However, an increase in systolic pressure up to 150 to 210 mmHg and diastolic blood pressure up to 100 to 130 mmHg is frequent in tamponade and occured in up to one third of tamponade cases in one report, particularly in patients with a history of hypertension who are sensitive to the catecholamine surge.6,7 Hypertension does not mean preserved cardiac output; in fact, cardiac output is as low as in cases of normal arterial pressure, but increased peripheral vascular resistance preserves blood pressure (pressure = flow × resistance) Patients with tamponade and hypertension had a reduction in blood pressure, reduction in SVR, and increase in cardiac output following pericardiocentesis FIGURE XIII.4 Typical arterial pressure in tamponade Tachycardia at 120 bpm The arterial pressure is reduced, the tracing is narrow based, and the pulse pressure is reduced The systolic pressure and the pulse pressure decline with inspiration (blue arrow), and the tracing almost collapses at end inspiration (vertical arrow) Note: Besides respiratory variation of arterial pressure, pulsus paradoxus manifests as exaggerated respiratory variation of RV and LV systolic pressures in low-output aortic stenosis, 85, 87f, 88f, 212, 213 in mitral stenosis, 104 Doppler tracings and RA pressure, 8–9 Doppler velocities and HOCM, 129f, 137f Doppler velocities and left ventricular dysfunction, 68, 69 Doppler velocities and prosthetic valves, 122t Doppler velocities of hepatic and pulmonary veins, in constrictive pericarditis, 142f, 143f, 147f, 149t, Dynamometer, 67 Dyssynchrony, 160f E E wave, 10f, 25f, 71f in constrictive pericarditis, 142f, 143f, 149t ECG and cardiac cycle, 7–8 Echocardiographic valve area calculation pitfalls, 92t, 93t, 98–99 Echocardiography, 54, 68–72, 69t, 70f, 71f, 72f, 90, 92t, 93t, 172, 179 constrictive pericarditis and restrictive cardiomyopathy, 149t left-sided filling pressure, 68–72, 69t, 70f, 71f, 72f LV diastolic function, 68–72, 69t, 70f, 71f, 72f for mitral stenosis, 98–102, 99f, 100f, 101f, 102f in pulmonary hypertension, 172 in shock, 179 Effective orifice area (EOA), valvular prosthesis, 121, 122t Effusive-constrictive pericarditis, 167–168 Eisenmenger syndrome, 56, 58, 171, 308–309, 348 Ejection fraction (EF), 72f, 188f, 189f End-diastolic pressure volume relationship (EDPVR), 188f, 190f End-systolic pressure volume relationship (ESPVR), 188f, 190f Epoprostenol, 170, 174 F Femoral arterial pressure, in AS, 93 FFR See Fractional flow reserve Fick equation, 49–51, 54, 277 Filling pressures, left ventricular, 68, 70f Fluid administration in LV dysfunction, 67 in tamponade, 163f, 166 Fluid responsiveness, 178–180, 178f Forward stroke volume, 112f, 115f Fractional flow reserve (FFR), 193–207, 194f, 195f, 196f acute coronary syndrome, 200–201 after PCI, 205 bifurcation disease, 200 and bypass grafts, 202 comparison with IVUS, 204–205 diffuse disease, 199, 199f in multivessel disease, 202 vs nuclear perfusion imaging, 202 in previously infarcted myocardium, ischemia and viability, 201–202 left main assessment, 205, 206f left ventricular hypertrophy, 201 microcirculatory dysfunction, 201 ostial disease, 200 performance of, 196–197 pitfalls, 203 serial stenoses, 197–199, 197f, 198f viability and, 201–202 Frank-Starling curve, 27f, 167, 178f, 179 superimposition with pressure-volume curve, 27f G Gorlin equation, 75–77, 216f, 221, 224, 276, 313 in atrial fibrillation, 76 in mixed valvular disease, 76–78, 116f, 125f, 275 H Hakki’s equation, 75, 216 Heart failure, See also Left ventricular failure diastolic, 23–26, 69–72, 72f high-output, 301 left, 63–72, 188, 189f, 190f, 191f LVEDP in left, 23–28 PCWP in left, 20, 22 pulmonary hypertension in, 169, 170, 170f right, 13, 15t Heart failure with normal EF (HFNEF), 23–26, 69–72, 72f High output heart failure, 301 in mitral stenosis, 311 HOCM, see Hypertrophic obstructive cardiomyopathy Hyperemia, 194f, 196 Hypertrophic cardiomyopathy, 129 Hypertrophic obstructive cardiomyopathy (HOCM), 79, 79f, 129–139, 247–248, 349–350, 351–352 asymmetric septal hypertrophy, 129 correction of, 138 features of, 130–131, 130f, 131f, 132f hypertrophy pattern, 129 LVOT obstruction, causes of, 133–137, 134f, 135f, 136f, 137f provocative maneuvers, 132–133, 136f severe LV hypertrophy, other causes of, 137–138 Hypotension, see Shock Hypovolemia, 166, 177, 177t, 179 See Fluid responsiveness Hypoxemia, and PCWP, 18t I IABP, See Intra-aortic balloon pump Idiopathic effusive-constrictive pericarditis, 155 Impact artifact, 39 Impaired relaxation, 25f Impella, 185–186, 185f, 191f contraindications, 186 on pressure-volume (PV) loop, 191f Inferior vena cava pressure, 144 Inspiration constrictive pericarditis during, 142–144, 142f in tamponade, 164, 164f Intra-aortic balloon pump (IABP), 181–184, 385–386 aortic pressure (unassisted and assisted), 182f, 386 augmented pressure, 181, 386 contra-indications, 184 inappropriate timing, 184f overview of, 181, 181f pressure augmentation, lack of, 184t timing, 182–184 triggering, 182–184, 182f, 183f Intracavitary pressure effect of respiration, 44–46, 142–144, 150f, 154t Intracoronary papaverine, 197 Intrapericardial pressure, 163, 163f Intrathoracic inspiratory pressure, 11f Intrathoracic pressure, 143f, 164f Intravascular ultrasound (IVUS), 204–205 Ischemia assessment in an infarcted myocardium, FFR and, 201–202 Isometric exercise, 67 Isovolumic contraction, 68, 188 Isovolumic relaxation, 188 time, 25f IVUS See intravascular ultrasound K Kussmaul’s sign, 142, 153, 163 L L wave, 71f LA-LV diastolic pressure gradient vs PCWP-LV diastolic pressure gradient, 98, 99, 100f, 101f, 243, 245f, 276f Laplace’s law, 187 Left atrial pressure, 16, 17 pulmonary capillary wedge pressure and, 16–17, 98, 99, 100f, 101f, 245f, 276f Left heart failure, 63–72, 188, 189f, 190f, 191f Left main disease, 205, 206f Left ventricular-aortic pressure gradient, 79–83, 211, 217, 219, 337, 341 in HOCM, 131f, 132f, 133f pullback, 82f, 83f, 84f, 130f, 131f, 228 Left ventricular assist devices, 185, 187, 191f Left ventricular cavity size, and afterload, 64, 66f, 187 in aortic insufficiency, 115f in left ventricular failure, 63 in mitral regurgitation, 112f Left ventricular contractility, 68, 188, 188f, 189f Left ventricular diastolic dysfunction, 23–27, 25f, 63–72, 190f Left ventricular diastolic failure, 23–27, 25f, 63–72, 190f, 227–229, 279–284, 322, 326, 328, 371, 372 Left ventricular diastolic pressure, 27f Left ventricular ejection fraction (LVEF), 70f, 72f Left ventricular end-diastolic pressure (LVEDP), 23–28, 63, 64, 64f, 65f, 66–67, 67f, 102f, 116, 146f, 151f, 220, 221, 224, 228, 229, 234, 236, 238, 240, 242, 244, 280, 322, 326, 371, 372 atrial fibrillation and, 67f measuring, 29–30 and PCWP, 29 pitfalls in determination, 30–31 response to exercise and pacing, 355, 356 transmural, 45–46 Left ventricular failure, 23–27, 25f, 27f, 63–72, 355–356 afterload, 65f diastolic, 23–28, 69–72, 70f, 71f, 72f, 188, 190f, 191 diuresis, 63 echocardiographic parameters, 68–72, 69t, 70f, 71f, 72f index of contractility, 68 with normal LVEDP/PCWP at rest, 66–67, 67f overview of, 63–66, 64f pulmonary artery pressure, 63 systolic, 27f, 28, 65f, 66f, 188, 191 Left ventricular-femoral arterial pressure tracing, 83, 85f, 341 Left ventricular hypertrophy and FFR, 201 severe, 137–138 Left ventricular pressure tracing, 23–31 Left ventricular pressure-volume loop, 188–192, 188f, 189f, 190f, 191f superimposition with Starling curve, 27f Left ventricular relaxation, 25f Low-pressure tamponade, 166 Low systemic vascular resistance (SVR) shock, 177, 177t Lung zones, and PCWP, 17 LVEDP See Left ventricular end-diastolic pressure LVEDP-left ventricular failure, interpretation of, 23–31 M Maximal hyperemia, 200 Microcirculatory dysfunction, 201 Microcirculatory vasodilation, 193 Micromanometer-tipped catheters, 39, 68 Minimal luminal area, 204 Mitral balloon valvuloplasty, 105–107, 105f, 106f, 107f, 127 Mitral commissurotomy, 106f Mitral inflow Doppler wave, 16, 142f, 164f Mitral regurgitation (MR) acute, 112f, 375 chronic severe, compensated, 112f chronic severe, decompensated, 111f, 112f, 229, 242–245, 275, 276 functional, 113 hemodynamics of, 111–113, 111f, 112f, 119f severity of, 111 V wave, 19f, 20, 111, 111f, 112f Mitral stenosis (MS) anatomically mild, functionally severe, 101, 311–313 atrial fibrillation, 103, 103f, 104f β-blockade, 312 cardiac output effect, 101, 311–313, 366 echocardiographic determination of, 98–102, 99f, 100f, 101f, 102f, 312 echocardiographic pitfalls, 99, 312 false impression of, in case of large V wave, 101f left atrial pressure waveform, 97 LVEDP in, 312–313, 372 mild, 100f, 104 mitral balloon valvuloplasty, 105–107, 105f, 106f, 107f overestimation, in case of large V wave, 98, 101f overestimation, with the use of PCWP, 97, 98, 100f, 101f pulmonary hypertension, 102 severity of, 100t stress testing for, 104–105 transmitral pressure gradient in, 97, 102f, 103f, 104f, 105f V and A waves in, 97 Mitral prosthesis, obstruction, 237–242 Mitral valve area (MVA), 75, 100t, 233, 313 Mixed aortic stenosis and insufficiency, 116f, 126f, 223–224 Mixed mitral stenosis and regurgitation, 101f, 125f, 243–245, 275, 276 Mixed single valve disease, 125–127, 125f, 126f moderate, 127 Mixed venous O2 saturation, 53, 273 difference between SVC and IVC O2 saturation, 53, 273 in septic shock, 273 Monophasic flow, peripheral arterial disease, 35 Multiple valvular disease, 127 MVA See mitral valve area Myectomy, 138 Myocardial blood flow, 193 Myocardial contractility, 188, 188f, 190f Myocardial O2 demands, 188 Myocardial perfusion imaging versus FFR, 202 N Nitric oxide, 174 Nitroprusside, in aortic stenosis, 87 in mitral regurgitation, 112, 112f in pulmonary hypertension testing, 170f, 174 Nuclear perfusion imaging versus FFR, 202 O Obstructive hypertensive cardiomyopathy, 133 Obstructive shock, 177, 177f Ostial disease and FFR, 200 O2 therapy and shunt calculations, 55, 249, 250 Overwedging, 18 Oximetry, for shunt evaluation, 56–57, 59 P Parenchymal pressure, pulmonary, 44–46 Patent ductus arteriosus (PDA), 54t, 305, 348 diagnosis, 307–309, 348 Eisenmenger syndrome, 308, 348 LV dysfunction, 308 PA-aortic recording, 306 right-to-left and left-to-right shunt calculations, 309 severe pulmonary hypertension, 308 PCWP See pulmonary capillary wedge pressure PCWP-LV diastolic gradient in constrictive pericarditis, 148, 156f, 381 in mitral stenosis, 98, 99, 100f, 101f, 243, 245f, 276f PDA See Patent ductus arteriosus PEEP, and transmural pressure, 45 Percutaneous LV assist device See Impella and TandemHeart Pericardial pressure, 163 pressure-volume relationship, 163f Peripheral arterial pressure, 34–36, 32f, 35f, 388 Peripheral pulmonary arterial stenosis, 120, 383–384 PH See Pulmonary hypertension Phonocardiogram, 117f PISA method, mitral valve area calculation, 99 Poiseuille law, 195f Post-capillary pulmonary hypertension, 169–170, 219, 262, 279–284, 372 Postextrasystolic pause in aortic insufficiency, 117f in aortic stenosis, 134f in HOCM, 133f in mitral stenosis, 103f, 104f, 313 Potential energy, 91, 188f Precapillary pulmonary hypertension, 170–171, 285–290 Preload, 188f, 189f differentiation of PCWP, LVEDP, and CVP from, 17, 19, 27f, 178f Pressure augmentation, lack of, 184t Pressure damping, 38–40 Pressure half-time (PHT), 98, 102f Pressure measurements, zero reference, 40–43 Pressure pullback curve, 82f, 199f Pressure recovery, 91–93, 91f, 92t, 93t, 121t Pressure transducer, 38, 39, 42f, 43f Pressure tracing, chamber identification, 15t, 315, 317, 323, 331, 333, 339, 343, 353 Pressure ventricularization, 36–38, 329 in FFR assessment, 196f, 200, 203t Pressure-volume area, 188f Pressure-volume loop, 188–192, 188f, 189f, 190f, 191f superimposition with Starling curve, 27f Prostanoids, in pulmonary hypertension, 174 Prosthetic valves, 120–123, 121t, 122t mitral, thrombosis, 237–242 Provocative maneuvers, in HOCM, 132 Pseudonormalized hypertension, 89 Pseudosevere AS, 88f Pseudostenoses, coronary, 203 Pulmonary artery hypertension, see Pulmonary hypertension oxygen saturation, 49, 53 pressure, 14–15 differentiation from PCWP, 19 Pulmonary capillary hydrostatic pressure (Pcap), 18–19 Pulmonary capillary wedge pressure (PCWP), 16–22, 59, 61, 64f, 97, 98, 125f, 158f, 169, 170f, 172, 173f abnormalities of, 20–22 case examples, 220, 226, 227–230, 234, 243–244, 317, 339, 345, 371–372, 375 differentiating PA pressure from, 19 and LA pressure, 16–17 in mitral stenosis, 97–98, 100f, 101f and LVEDP, 29 pitfalls in interpreting, 17–20 in pulmonary hypertension, pitfalls, 17–18, 18f, 98 in right ventricular failure, 171, 264 Pulmonary embolism, 148–149, 172 Pulmonary hypertension (PH), 15, 169 cardiac catheterization, goals for, 172–175, 173f cases of, 226–229, 234, 248, 249, 251, 262 defined, 169, 169t evaluation of, 172 in mitral stenosis, 98, 102 PCWP assessment in, 17–18, 18f, 98 post-capillary, 169–170, 219, 262, 279–284, 372 precapillary, 170–171, 285–290 in congenital heart disease, 171 pulmonary veno-occlusive disease, 171 secondary to left heart failure, 169, 170f secondary to lung disease, 171 secondary to thromboembolic disease, 171 vasoreactivity testing, 174 Pulmonary regurgitation (PR), 54t, 120 Pulmonary vascular resistance (PVR), 51, 56, 58, 63, 170f in shunt cases, 56, 58, 249 Pulmonary vasodilator, 174, 250 Pulmonary vein (PV) Doppler, 9f, 10f in pericardial disease, 142f, 143f, 148f, 149t, 164f stenosis, 98 Pulmonary veno-occlusive disease, 18, 171 Pulmonary venous hypertension, see Post-capillary pulmonary hypertension Pulmonary venous O2 content, 249 Pulmonary venous O2 saturation, mixed, 348 Pulmonic insufficiency, 120 Pulmonic stenosis, 11, 120, 254 Pulse oximetry, waveform analysis and fluid responsiveness, 180 Pulse pressure, 33f, 34, 35t, 80, 166f Pulse wave velocity, 35 Pulsus alternans, 33f, 34 Pulsus bisferiens, 32f, 240 Pulsus paradoxus, 33 lack of, in tamponade, 167 Q Qp/Qs shunt ratio calculation, 55, 58, 249–251, 298, 309 R RA myxoma, 390 RA/RV/PA pressure, chamber identification, 15t cases, 315–316, 317–318, 323–324, 331–332, 379, 383 Regional tamponade, 167 Regurgitant volume, 77f, 112f Respiration, effect on intracardiac pressure, 44–46 in constrictive pericarditis, 142f, 143f, 147f, 148f PCWP, 16f right atrial pressure, 8 Restrictive cardiomyopathy, 9, 13, 144–147, 145t, 149t, 154t, 158f echocardiography and, 147–148 PCWP in, 27f, 64 Right atrial O2 saturation, 53, 57 Right atrial pressure, 7–12 abnormalities, 9–12, 10f, 11f, 12f in constrictive pericarditis, 9, 141f, 156f, 158f in tamponade, 165f, 354f ventricularized, in tricuspid regurgitation, 12f, 119f, 277f, 315, 380f Right ventricular end-diastolic pressure (RVEDP), 151f, 153f, 165 Right ventricular failure, severe, 15t, 148–151, 149t, 150f, 151f, 154f PCWP in, 171, 264 Right ventricular pressure tracing, 12–14 dip-plateau pattern, 141, 144, 145t, 157f, 257f Ringing artifact, 39 Ross procedure, 253 RVEDP See Right ventricular end-diastolic pressure RV/LV end-diastolic pressures, equalization, 263 RV-LV simultaneous pressure recording, 145, 146f, 151f, 157f, 260f, 262–263, 266–267 RV-LV systolic discordance, 145, 146f, 157f, 266–267 RV-PA simultaneous pressure recording, 254, 256 RV relaxation, 13 S S wave (hepatic or pulmonary venous Doppler), 8, 9, 9f, 147–148 Scimitar Syndrome, 347–348 SEP See Systolic ejection period Sepsis and PCWP, 18t Septic cardiomyopathy, 177 Serial stenosis, and FFR, 197–199, 197f, 198f Shock, 177 diagnosis, 238, 272–273 dicrotic aortic pulse, 241, 274 types of, 177t Shunt bidirectional, 54, 55, 58, 250–251 evaluation mixed venous O2 saturation (SvO2), 53 shunt flow ratio, 54 step-up location, 54t left-to-right, 54, 55, 58, 250–251 and pulmonary hypertension, 56 right-to-left, 54, 55, 58, 250–251 Shunt ratio calculation, 55, 58, 249-251, 298, 309 Simultaneous LV-aortic pressure, 83f, 84f, 86f Sinus tachycardia and RA pressure tracing, 12f Stress testing for left ventricular dysfunction, 66 for mitral stenosis, 104–105 Stroke volume, 65f, 66f, 86, 90f, 133, 178f, 188, 188f, 214 Subaortic gradient, 130, 131f, 132f, 133f, 136f, 361–362 Subvalvular aortic stenosis, 361–362 Supravalvular aortic stenosis, 359–362 SVC flow, in constrictive pericarditis vs COPD, 153 SVC pressure, respiratory variations in constrictive pericarditis, 142f, 143f SVC O2 saturation, correlation with mixed venous O2 saturation, 53, 273 in septic shock, 273 Swan-Ganz catheter, 59–61, 60f Systemic vascular resistance (SVR), 51, 56, 58 shock, 177, 177t Systolic anterior motion (SAM), 93, 129 Systolic dysfunction, left ventricular, 188, 191 Systolic ejection period (SEP), 75, 76f, 77f, 216, 336–337 Systolic left ventricular failure, decompensated, see Left ventricular failure, systolic T Tachycardia aortic insufficiency and, 114 effect on coronary blood flow, 193 left ventricular failure and, 28 right atrial pressure and, 12f transaortic pressure gradient and, 84 transmitral pressure gradient and, 97 Tamponade, 163–168 arterial pressure in, 33f, 166f, 370f atrial pressure, 10–11, 165f, 354f diastolic pressures equalization, 163, 165 effusive-constrictive pericarditis, 167–168 fluid administration, 166 hemodynamics of, 163–166, 163f, 164f, 166f inspiration in, 164f intrapericardial pressure, 163, 163f low-pressure, 166 pulsus paradoxus, lack of, 167 regional, 167 systolic pressure in, 165, 166f ventricular pressure in, 370 TandemHeart, 186–187, 191f Tau index, 24f Temporary balloon occlusion, testing before ASD closure, 56 Thermodilution, 49–50, 58, 60f, 77f Thrombolysis, for prosthetic valve thrombosis, 240 Thrombosis, prosthetic valve, 240 Transaortic pressure gradient, 79f, 80–84, 80f, 81f, 82f, 83f, 84, 84f, 116f , 126f Transducer miscalibration, 83f Transient constrictive pericarditis, 153 Transmitral Doppler flow velocity, in mitral stenosis, 102f Transmitral pressure gradient, See Mitral stenosis Transmural LVEDP, 45–46 Transmural pressure, 44–46 Transpulmonary gradient, 170, 170f Transvalvular LV assist device See Impella Tricuspid regurgitation (TR), 118, 119f right atrial pressure, ventricularized, 12f, 119f, 277f, 315, 380f Tricuspid stenosis, 120, 390 Triphasic flow, peripheral arterial Doppler, 35f Tunnel aortic obstruction, 360 U Underdamping, 39, 39f, 40f V V wave, 7, 10, 11 large, PCWP, 19–22, 19f, 21f, 119f, 230f, 245f, 339f, 375f large, RA pressure, 9, 12f, 119f, 277f, 316f, 380f Valsalva maneuver, in HOCM, 136 Valvular area calculation, 75–77, 216f, 221, 224, 276, 313 in atrial fibrillation, 76, 77f coexisting regurgitation, 76–78, 77f, 116f, 125f, 276f Valvular regurgitation, 119f Valvulopasty, mitral, 106f Vasodilator testing, 174, 289–290 in post-capillary PH, 282–284 Venous O2 saturation (SvO2), mixed, 53, 273 in septic shock, 273 Ventricularization of coronary pressure, 36–38, 200, 329 of RA pressure, 10, 12f, 119f, 277f, 315, 380f Ventricular septal defect (VSD), 54t, 56 cases of, 291–300, 357–358 Ventricular systolic discordance See RV-LV systolic discordance Ventricular wall tension, afterload, 187 Ventriculography, 77f VSD See Ventricular septal defect W Whip artifact, 39 Wood unit, 170f X X descent, deep, 9, 10, 11f, 165f, 262f shallow, 10, 12f, 118, 119f, 353f Y Y descent, RA pressure, deep, 9, 11, 11f, 12f, 141f, 152f, 156f, 262f, 267f, 316f, 324f shallow, 10, 11, 165f Z Zero the pressure, 40, 41, 42f, 43f, 83f ... pulmonary hypertension J Am Coll Cardiol 20 09;54:S43–S54 Oudiz RJ Pulmonary hypertension associated with left-sided heart disease Clin Chest Med 20 07 ;28 :23 3 24 1 Costard-Jackle A, Fowler MB Influence of preoperative pulmonary artery pressure on... Clinical signs in medicine: pulsus paradoxus J Post Grad Med 20 02; 48:46–49 XIV Pulmonary hypertension XIV.1 DEFINITION Pulmonary hypertension (PH) is defined as a mean PA pressure 25 mmHg at rest.1 ,2 An increase in mean PA pressure to >30 mmHg with exercise used to be... N Engl J Med 19 92; 327 :463–466 Spodick DH Threshold of pericardial constraint: the pericardial reserve volume and auxiliary pericardial functions J Am Coll Cardiol 1985;6 :29 6 29 7 Hashim R, Frankel

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  • Contents

  • Preface

  • Abbreviations

  • Acknowledgements

  • BASIC AND ADVANCED HEMODYNAMICS Elias B. Hanna

  • Pressure tracings

    • I.1. RIGHT ATRIAL PRESSURE TRACING

      • Pressure contour

      • Timing in relation to the ECG and the ventricular tracing

      • Respiratory variations

      • Correlations between the RA pressure tracing and the Doppler tracings of the inferior vena cava, hepatic veins, and trans-tricuspid flow

      • Description of some abnormalities

      • I.2. RIGHT VENTRICULAR PRESSURE TRACING—CHARACTERISTICS OF RV FAILURE

      • I.3. PULMONARY ARTERY PRESSURE TRACING

      • I.4. PULMONARY CAPILLARY WEDGE PRESSURE

        • Description of PCWP waves—correlation of PCWP with LA pressure

        • Pitfalls in interpreting PCWP

        • Key points in differentiating PA pressure from PCWP (Figure I.11)

        • Abnormalities of PCWP tracing

        • I.5. LEFT VENTRICULAR PRESSURE TRACING AND INTERPRETATION OF LVEDP-LEFT VENTRICULAR FAILURE

          • LV systolic pressure

          • LV diastolic pressure and evaluation of LV failure

          • Patients with high early diastolic LA-LV pressure gradient: Differentiate pusher from sucker

          • Correlation between LVEDP and PCWP

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