Hemodynamics in the Cardiac Catheterization Laboratory of the 21st Century

Abstract

HomeCirculationVol. 125, No. 17Hemodynamics in the Cardiac Catheterization Laboratory of the 21st Century Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBHemodynamics in the Cardiac Catheterization Laboratory of the 21st Century Rick A. Nishimura, MD and Blase A. Carabello, MD Rick A. NishimuraRick A. Nishimura From the Mayo Clinic College of Medicine, Rochester, MN (R.A.N.), and Baylor College of Medicine, Houston, TX (B.A.C.). Search for more papers by this author and Blase A. CarabelloBlase A. Carabello From the Mayo Clinic College of Medicine, Rochester, MN (R.A.N.), and Baylor College of Medicine, Houston, TX (B.A.C.). Search for more papers by this author Originally published1 May 2012https://doi.org/10.1161/CIRCULATIONAHA.111.060319Circulation. 2012;125:2138–2150IntroductionThere has been a striking evolution in the role of the cardiac catheterization laboratory over the past decades.1 In the 1950s and 1960s, hemodynamic assessment in the cardiac catheterization laboratory was essential for understanding the physiology and pathophysiology of patients with cardiovascular diseases. With the development of surgical interventions to treat patients with valvular and congenital heart disease, it became necessary for the cardiac catheterization laboratory to provide an accurate hemodynamic assessment, laying out a therapeutic road map. Nearly all patients who had open heart surgery underwent a complete hemodynamic catheterization before surgery.In the 1980s and 1990s, the evolution of 2-dimensional echocardiography and Doppler echocardiography provided an alternative noninvasive approach for the assessment of both cardiac anatomy and hemodynamics in patients with structural heart disease.2 By measuring blood flow velocities noninvasively, Doppler echocardiography was able to provide information on volumetric flow, intracardiac pressures, pressure gradients, and valve areas, as well as diastolic filling of the heart. Furthermore, noninvasive studies could be repeated easily, allowing the practitioner to follow the progress of his/her patient's condition longitudinally. At the same time, there was growing emphasis on coronary angiography for defining epicardial coronary disease with the subsequent development of interventional approaches for coronary disease with catheter-based therapies. As the major focus in the catheterization laboratory shifted to the diagnosis and treatment of the patient with acute and chronic coronary artery disease, the hemodynamic assessment of patients with structural heart disease was left to the noninvasive echocardiographic laboratory. As a consequence, many cardiac catheterization laboratories provided neither the training nor the expertise to assess hemodynamics properly.However, the advent of procedures such as balloon valvotomy, percutaneous valve implantation, and septal ablation has revived interest in structural heart disease and provided the invasive cardiologist with an armamentarium to treat patients who previously had to undergo surgery or would have been considered inoperable.3 For the invasive cardiologist to use these new tools appropriately, he/she must fully understand the advanced principles and nuances of complex hemodynamics. Invasive hemodynamic assessment still remains of great importance in the evaluation of the patient with congenital heart disease.4 In addition, the noninvasive hemodynamic evaluation has inherent limitations, now recognized by clinicians who take care of the increasing number of patients who present with complex cardiovascular problems. The catheterization laboratory in the current era has become the place to solve the difficult diagnostic challenges that arise in patients with structural heart disease when answers are not apparent through the clinical examination and noninvasive testing.Implications of the New Cardiac Catheterization Laboratory in the 21st CenturyThe changes that have occurred in patient evaluation throughout the last 2 decades have important implications for the new cardiac catheterization laboratory. Patients now coming for hemodynamic assessment have already had a thorough noninvasive evaluation. Thus, the remaining questions are complex and pose difficult diagnostic dilemmas. It is unacceptable for the patient to leave an invasive hemodynamic assessment without a definitive answer about his/her condition. Thus, hemodynamic assessment in the cardiac catheterization now requires meticulous attention to detail. There is no longer such a procedure as routine cardiac catheterization. The operator should be constantly evaluating the accrued data, ready to perform additional diagnostic interventions if necessary such as exercise or other provocative maneuvers.Invasive cardiologists must understand the implications of the results of noninvasive testing and their correlation with the clinical examination. They need to determine the incremental information necessary for clinical decision making. Thus, a hemodynamically directed cardiac catheterization should be a goal-directed procedure, specifically individualized for each patient, based on the problem and the results of the noninvasive testing.Principles of Cardiac CatheterizationThe complex cardiac catheterization must be approached in a detailed systematic manner. First, the operator must be able to create a roadmap of what questions need to be answered. This includes assessment of the proper access and approach. For instance, in a patient who has unexplained dyspnea, a radial and internal jugular access might be appropriate instead of the standard femoral approach, so supine bicycle exercise could be implemented. Alternatively, there might be a need for direct left atrial pressure measurement, which would require a femoral approach for a potential transseptal catheterization.The operator should be constantly obtaining and analyzing data throughout the study so that additional interventions can be performed on the basis of the initial data and the clinical question. These additional interventions may include vasodilator challenge in the presence of diastolic dysfunction, nitric oxide for unsuspected pulmonary hypertension, or oxygen supplementation for arterial desaturation. In patients who might be candidates for cardiac transplantation, full evaluation of the pulmonary arteriolar resistance and (if elevated) its reversibility should be undertaken. Exercise hemodynamic assessment or fluid loading should be considered for patients with severe symptoms in whom the resting hemodynamics are not markedly abnormal.It is important to use the proper equipment for a catheterization aimed at a high-quality hemodynamic assessment. Coronary angiography has evolved to use the smallest-bore catheters, with many diagnostic angiograms using 5F or even 4F catheters to decrease vascular complications. However, proper evaluation of pressures during a complex hemodynamic catheterization is optimally performed with larger-bore catheters that yield high-quality hemodynamic data. To obtain proper hemodynamic tracings, 6F or even 7F catheters may be required if the smaller catheters do not produce high-quality pressure contours. Catheters with side holes should be used to measure ventricular pressures. Catheters with end holes should be used to measure wedge pressures. The use of high-fidelity manometer-tipped catheters might also need to be considered in those instances when intricate analysis of diastolic filling contours is required. If fluid-filled catheters are used, it is important to choose the shortest extension tubing possible to obtain optimal pressure contours. For this reason, the use of the coronary manifold with its long extenders that degrade pressure tracings should be avoided.The invasive cardiologist must continually assess pressure contours throughout the study. Overdamped and underdamped pressure tracings and whip artifact should be anticipated and corrected. Formation of small thrombi in catheters can cause significant changes in pressure contour, especially in catheters with small internal diameters (Figure 1A). Thus, all catheters should undergo intermittent flushing with heparinized saline throughout their use, with constant monitoring of the pressure contour. Rebalancing the zero baseline should also be done while the pressures are being collected. Catheter entrapment will produce erroneous pressure measurements and can be identified by unusual pressure contours. Slight changes in position of a catheter may cause abnormal pressure contours, particularly if catheters with multiple side holes are placed straddling a valve (Figure 1B).Download figureDownload PowerPointFigure 1. It is necessary to assess pressure contours continually throughout the catheterization procedure to identify pressure artifacts that may occur and lead to erroneous pressure measurements. A, The initial pulmonary artery (PA) pressure in this patient undergoing evaluation of pulmonary hypertension is 70/35 mm Hg (left). However, during the procedure, it was noted that the pulmonary artery pressure fell to 45/20 mm Hg in the absence of any other hemodynamic changes (right). This was due to the formation of a small thrombus in the small distal lumen of a thermodilution catheter. This pressure artifact should be avoided by meticulous technique, which includes constant monitoring of the pressure contour and intermittent frequent flushing of the lumen with heparinized saline. Using larger-bore catheters may be necessary to overcome this problem if damping of pressures continues despite the use of these techniques. B, In this patient with aortic stenosis, there is a pigtail catheter in the left ventricle (LV) and a separate catheter in the ascending aorta (Ao). In position 1, the contour of the left ventricular pressure is abnormal, with a marked delay in the fall of pressure during early diastole. This is due to some of the multiple side holes in the pigtail catheter straddling the aortic valve, resulting in a fusion of left ventricular and aortic pressure. Because the abnormal contour is recognized, the catheter is placed further distally so that all recording holes are in the left ventricle, as shown in position 2.Valve StenosisGeneral PrinciplesAssessment of valvular stenosis relies on measurement of the valve gradient and on calculation of valve area.5 Wiggers6 noted nearly a century ago that significant obstruction to flow occurred when a tube became limited to one third its normal area, and this principle is still in use today. Valve area is calculated in both the noninvasive and invasive laboratories with the same flow equation: F=A×V (where F is flow, A is area, and V is velocity), so A=F/V. Doppler interrogation of a valve measures flow velocity directly, whereas in the catheterization laboratory, velocity is imputed with the Torricelli law from the transvalvular pressure gradient: V=√2gh, where g is the velocity of acceleration resulting from gravity and h is the pressure gradient. The gravity acceleration term converts millimeters of mercury (the units of pressure) into the force that drives blood across the valve orifice. Thus, the invasive cardiologist has 3 basic tools to use to assess the severity of valvular stenosis: the transvalvular pressure gradient, the cardiac output, and the formula that relates the 2 variables (the Gorlin formula).The Gorlin FormulaThe Gorlins published their formula for calculating valve area in 1951. It stated that A=F/(Cc×Cv×√2gh), where Cc and Cv are the coefficients of orifice contraction and velocity loss, respectively.6a The coefficient of orifice contraction makes allowance for the fact that fluids moving through an orifice tend to stream through its middle so that the physiological orifice is smaller than the physical orifice. The velocity coefficient allows for the fact that not all of the pressure gradient is converted to flow because some of the velocity is lost to friction within the valve. These coefficients have never been determined. Instead, the Gorlins used an empirical constant to make their calculated mitral valve areas align better with actual valve areas obtained at autopsy or surgery. For the other 3 valves, not even an empirical constant has been developed. Thus, the coefficients for the aortic, pulmonic, and tricuspid valves have been assumed to be 1, a theoretical impossibility. These factors are important in understanding that calculated valve areas have clear limitations in the assessment of valvular stenosis. Valve area is one of the invasive cardiologist's tools of evaluation, but it is not the only one and must be used in conjunction with other parameters such as valve gradient, pressure contours, and the contractile state of the ventricle. In practical use, valve area is used to assess the severity of aortic and mitral stenosis. No valve area for defining severe tricuspid valve stenosis is agreed on, and pulmonic stenosis is usually assessed with gradient alone.Cardiac OutputIt is flow through the valve that generates the pressure gradient, so assessment of stenosis severity must take into account both flow and gradient together. Measurements of pressure gradients in patients with valve stenosis are discussed below and can usually be performed quite accurately. On the other hand, cardiac output measurement can be problematic. The gold standard for cardiac output determination is the Fick principle in which cardiac output is O2 consumption divided by the difference between arterial and venous O2. Although oxygen consumption can be measured quite accurately, that measurement is cumbersome, and many laboratories use standard tables for an assumed value instead of direct measurements. Such an estimation may cause an error of as much as 40% in the determination of cardiac output.5,7,8 Most laboratories now use thermodilution based on an indicator dilution methodology (a derivation of the Fick principle) to measure cardiac output. This technique is usually accurate in patients with a normal or high output who are in normal sinus rhythm. However, it becomes inaccurate in patients with intracardiac shunts, low-cardiac-output states, significant tricuspid regurgitation, or irregular rhythms, which frequently accompany advanced heart disease in severely ill patients. Calculation of the cardiac output by the Fick method can be done as an internal check to confirm the accuracy of the thermodilution method. It is critical to understand the limitations of these different methods of cardiac output measurement when assessing individual patients in the catheterization laboratory.Aortic StenosisIn evaluating the patient with aortic stenosis, the invasive cardiologist must understand the reliability of the data from the noninvasive evaluation and the diagnostic issues that might remain despite a comprehensive 2-dimensional and Doppler echocardiographic evaluation. The caveat of a Doppler-derived aortic valve gradient is that the Doppler echocardiogram cannot overestimate an aortic valve gradient unless there is a problem with the assumptions incorporated into the modified Bernoulli equation (ie, seen in severe anemia or concomitant subvalvular stenosis when the proximal velocity cannot be assumed to be negligible). However, if the Doppler beam cannot be aligned parallel to the aortic jet, the Doppler velocity will underestimate the true aortic valve gradient. Calculation of valve area by Doppler echocardiography with the continuity equation may pose inaccuracies because it is the square of a measured left ventricular outflow tract diameter that is used to calculate outflow tract area. Overall, if the patient has clinical findings of severe aortic stenosis and the mean gradient is >40 mm Hg, no further hemodynamic information is required; the diagnosis of severe aortic stenosis is established except in the unusual instance when the cardiac output exceeds 6.5 L/min. However, in those cases when there is a discrepancy between the physical examination and the elements of the Doppler echocardiogram, a meticulous hemodynamically directed cardiac catheterization must resolve the issues.The optimal technique to assess aortic valve gradient is to record simultaneously obtained left ventricular and ascending aortic pressures9–11 (Figure 2). The peak-to-peak gradient has been the conventional measurement in the past. However, it is a nonphysiological parameter in that the peak left ventricular pressure does not occur simultaneously with the peak aortic pressure. Instead, it is recommended that the mean aortic valve gradient be used, which is the integrated gradient throughout the entire systolic ejection period and the optimal indicator of severity of obstruction.12 Most catheterization laboratories now have the capability of computer analysis of the mean gradient, facilitating attainment of this measurement.Download figureDownload PowerPointFigure 2. Simultaneous left ventricular (LV) and central aortic (Ao) pressures in a patient with aortic stenosis. The optimal way to measure the gradient in a patient with aortic stenosis is to use these simultaneous pressures. The peak-to-peak gradient is the difference between the peak left ventricular and peak aortic pressures, which is a nonphysiological measurement because the peak pressures occur at different points in time. The mean pressure gradient (the integrated gradient between the left ventricular and aortic pressure throughout the entire systolic ejection period) should be used to determine the severity of the aortic stenosis.Pullback traces with a single catheter from the left ventricle to the aorta can be helpful, but only if the patient is in normal sinus rhythm with a regular rate. In patients with critical aortic stenosis, the Carabello sign may be present, in which the catheter across the valve itself will cause further obstruction to outflow.13 This sign occurs in valve areas of <0.7 cm2 when 7F or 8F catheters are used to cross the valve. Simultaneous left ventricular and femoral pressures should never be used because there can be both overestimation and underestimation of the true aortic valve gradient from either large-vessel stenosis or peripheral amplification of the distal pressures (Figure 3A). Some laboratories use dual-lumen pigtail catheters, but the operator must ensure that the small lumen in the ascending aorta is continually flushed and does not undergo “damping,” causing a falsely high gradient to appear. A crucial part of the assessment is the perfect matching of the 2 pressures (from either 2 separate catheter lumens or both lumens of a dual-lumen catheter) in the proximal aorta before the left ventricle is entered. The 2 lumens are in fact subjected to 2 identical pressures so that 2 identical pressures should be recorded, confirming the accuracy for the 2 transducers and the recording systems. Failure to follow this step may lead to a false pressure gradient caused by errors in the recording system. Ideally, the pressures in the aorta should be measured with a side-hole catheter to avoid a damping artifact (Figure 3B).Download figureDownload PowerPointFigure 3. The optimal method to measure the transaortic gradient in a patient with aortic stenosis is a simultaneous left ventricular (LV) pressure and central aortic (Ao) pressure with side-hole catheters. Shown are examples in which alternative methods are used to obtain the pressures, which produce erroneous results. A, The simultaneous left ventricular and femoral artery (FA) pressures should not be used to measure the aortic valve gradient because peripheral amplification may cause a false decrease in gradient and peripheral artery stenosis may cause a false increase in gradient. There is also a temporal delay when a femoral artery pressure is used that will affect the calculation of the mean gradient. In this patient, the use of a femoral artery pressure would significantly underestimate the peak-to-peak gradient as a result of peripheral amplification of the pressure. B, In the measurement of left ventricular and aortic pressures, catheters with side holes should be used because damping can occur with an end-hole catheter (ie, coronary artery catheters). Shown is the typical damping that may occur in the aortic pressure when an end-hole catheter (right) is used compared with a side-hole catheter (left).A visual assessment of the contours of the aortic and left ventricular pressures during catheterization adds information regarding the type of obstruction present (Figure 4). In patients with fixed valvular obstruction, there is a delay (tardus) and reduction (parvus) in the upstroke of the central aortic pressure that begin at aortic valve opening. However, in the presence of a dynamic left ventricular outflow tract obstruction (as seen in hypertrophic cardiomyopathy), the aortic contour assumes a spike-and-dome pattern with an initial rapid upstroke. There is also a late peaking left ventricular pressure resulting from the mechanism of this dynamic obstruction. The response of the aortic pulse pressure after a long pause is often diagnostic in differentiating between a fixed and dynamic left ventricular outflow obstruction by demonstrating the Braunwald-Brockenborough sign (Figure 5). These observations not only confirm the site of obstruction as assessed by noninvasive imaging but also may identify latent dynamic outflow gradients that may not have been present at the time of the echocardiogram.Download figureDownload PowerPointFigure 4. A visual assessment of the contour of the aortic (Ao) and left ventricular (LV) pressures is important during cardiac catheterization. Left, Patients with fixed obstruction (either valvular stenosis or fixed subvalvular stenosis) will demonstrate a parvus and a tardus in the upstroke of the aortic pressure, beginning at the time of aortic valve opening. Right, In patients with a dynamic obstruction (such as that found in hypertrophic cardiomyopathy), the aortic pressure will rise rapidly at the onset of aortic valve opening and then develop a spike-and-dome contour as the obstruction occurs in late systole. The left ventricular pressure also has a late peak because of the mechanism of this dynamic obstruction. LA indicates left atrium.Download figureDownload PowerPointFigure 5. Response of the aortic pressure after a long pause is useful in differentiating between the fixed obstruction of valvular aortic (Ao) stenosis and the dynamic obstruction of hypertrophic cardiomyopathy. A, In this patient with valvular aortic stenosis, the beat after the premature ventricular contraction (PVC) has an increase in pulse pressure (P-P). B, In this patient with hypertrophic cardiomyopathy, there is a reduction in the pulse pressure on the beat after the premature ventricular contraction. LV indicates left ventricle; LA, left atrium.The aortic valve area should then be calculated from a meticulous measurement of the mean gradient and cardiac output, as described previously. Although current computer systems in the modern catheterization laboratories automatically perform this calculation, it is the responsibility of the operator to do a quick ballpark calculation offline to ensure that the input into the computer is accurate. The Hakki equation (valve area equals cardiac output divided by the square root of the gradient) can be used to ensure that the more complex Gorlin equation has been calculated with the proper data input.It is always necessary to reconcile the severity of disease indicated by mean gradient and that indicated by the valve area obtained by cardiac catheterization. There is a subset of patients in whom the magnitude of the gradient will not match the severity of valve stenosis predicted by valve area, and further evaluation of these patients is necessary. Some patients present with a low gradient (<30 mm Hg) and a low output, resulting in a small calculated valve area. If severe left ventricular dysfunction is present, dobutamine stimulation is warranted to determine whether the small valve area truly is due to critical aortic stenosis or might be due to pseudo–aortic stenosis, a condition in which there is not enough momentum from a ventricle with impaired myocardium to fully open a mildly or moderately stenotic valve14,15 (Figure 6). Furthermore, the presence of inotropic reserve, defined as an increase in stroke volume >20% during dobutamine stimulation, is an important stratifier for operative risk.14,15 Although dobutamine challenge may be performed in the echocardiography laboratory, performance in the catheterization laboratory where coronary anatomy is assessed can also be quite useful in determining whether ischemia might be a cause of failed inotropic reserve. In patients at high risk for critical coronary disease, coronary angiography should be performed before dobutamine infusion. There is also a growing recognition of a population of patients who have low-output/low-gradient aortic stenosis with a preserved ejection fraction. Further evaluation of these patients may be indicated, perhaps with vasodilators to lower the high peripheral resistance seen in these patients16,17 (Figure 7).Download figureDownload PowerPointFigure 6. In patients in whom there is a low-output, low-gradient (Grad) state, it may be necessary to perform dobutamine stimulation to normalize cardiac output. This can be used to differentiate between patients with true aortic (Ao) stenosis and those with pseudo–aortic stenosis. A, With dobutamine stimulation, the gradient increases from 28 to 42 mm Hg and the valve area remains small at 0.7 cm2. This indicates that there is severe fixed valvular stenosis in this patient. B, In this patient with similar resting hemodynamics, dobutamine infusion does not change the gradient remaining at 24 mm Hg. The valve area increases to 1.2 cm2. This is an example of pseudo–aortic stenosis in which the valve area is small at baseline owing to the lack of momentum from a ventricle to fully open a mildly stenotic aortic valve. AVA indicates aortic valve area; LV, left ventricle; RV, right ventricle; and LA, left atrium.Download figureDownload PowerPointFigure 7. Low-output, low-gradient state may also be seen in patients with preserved ejection fraction. In these patients, a high additional afterload resulting from a noncompliant aortic system further contributes to the low cardiac output. Through lowering of the peripheral resistance with a vasodilator such as nitroprusside (NTP), patients with true aortic stenosis may be able to be identified by demonstrating an increase in aortic valve gradient and a fixed valve area. LV indicates left ventricular; AO, central aortic; PA, pulmonary artery; LA, left atrium; and AVA, aortic valve area.Mitral StenosisPatients with mitral stenosis frequently come to the cardiac catheterization laboratory for further hemodynamic evaluation when the noninvasive estimations of valve gradient and valve area are inconsistent with one another or when there are symptoms of pulmonary hypertension out of proportion to the apparent severity of the mitral valve disease. The transmitral gradient measured by continuous-wave Doppler echocardiography is highly accurate.18 As opposed to aortic stenosis, it is much easier to align the Doppler beam with the mitral inflow jet, providing a very reproducible method for determining mean gradient. In those rare patients in whom a transmitral gradient cannot be obtained by transthoracic echocardiography, transesophageal echocardiography should be performed. In the echocardiography laboratory, the mitral valve area may be measured by direct planimetry or by the pressure–half-time method. Poor images on transthoracic echocardiography may preclude accurate measurement of the valve area by planimetry. The valve area by half-time techniques used by Doppler echocardiography have potential limitations in that the half-time is dependent not only on the severity of stenosis but also on the compliance of the left atrium and left ventricle and concomitant mitral regurgitation.19In the cardiac catheterization laboratory, evaluation of the transmitral gradient is frequently made with a simultaneous pulmonary artery wedge pressure and left ventricular pressure (Figure 8). Although the mean pulmonary artery wedge pressure will usually reflect the mean left atrial pressure, the pulmonary artery wedge pressure/left ventricular pressure gradient frequently overestimates the true severity of mitral stenosis owing to a phase shift in the pulmonary artery wedge pressure and a delay in transmission of the change in pressure contour through the pulmonary circulation. Thus, there may be a 30% to 50% overestimation of the true gradient when conventional catheters are used, even with correction for the phase shift.18 Overestimation of the true left atrial pressure by wedge pressure can be reduced by scrupulous oximetric confirmation that the catheter is truly wedged.20,21 If necessary, a transseptal approach to obtain true left atrial pressures should be performed in patients with mitral stenosis if therapeutic decisions depend on the accuracy of these data.Download figureDownload PowerPointFigure 8. Measurement of the transmitral gradient by cardiac catheterization is frequently made with a simultaneous pulmonary artery wedge pressure (PAWP) and left ventricular (LV) pressure. However, as a result of the delay in transmission of the change in pressure contour and a phase shift, the gradient using a pulmonary artery wedge pressure will frequently overestimate the true transmitral gradient. Left, Simultaneous left ventricular and pulmonary artery wedge pressure in a patient with mitral stenosis. The measured mean gradi