SCAI/HFSA clinical expert consensus document on the use of invasive hemodynamics for the diagnosis and management of cardiovascular disease

Modern insight into the pathophysiology of the heart and circulatory system first emerged through detailed invasive hemodynamic studies performed in the cardiac catheterization laboratory. The understanding of these concepts, their evolution, and their clinical utility remain fundamental. Although noninvasive methods are now routinely used, the invasive catheter-based assessments performed in the cardiac catheterization laboratory remain the gold standard for hemodynamic evaluations of cardiovascular patients. The principal aim of this consensus document is to describe the clinical utility of invasive hemodynamics in current cardiovascular practice. Herein, we (1) define clinically relevant hemodynamic concepts and their invasive assessment; (2) describe clinical scenarios in which invasive hemodynamic assessment should be strongly considered; and (3) emphasize the need for the maintenance of quality and for continuous professional development in the field of invasive hemodynamics. The principal advantage of invasive hemodynamic assessment is the ability to directly measure pressure and flow, which is unique to studies performed in the cardiac catheterization laboratory. These studies enable the clinician to directly assess hemodynamics in multiple chambers simultaneously, both in the resting and dynamic state. With proper zero calibration and careful attention to the potential for technical errors, there is minimal observer variability for invasive hemodynamic assessments. Detailed data are gained from examination of the degree of elevation in absolute pressure(s), the contour of the pressure waveform(s), their comparative changes across multiple chambers at rest and with exercise, and the knowledge of the systemic and pulmonary flow. For the vast majority of patients, fluid-filled catheters suffice. High-fidelity micromanometers display a much higher frequency response compared with fluid-filled systems, providing more robust and accurate hemodynamic data. These systems are primarily used for research purposes, though their clinical utility has been demonstrated in situations in which higher fidelity data is required, such as invasive exercise stress testing and evaluation of heart failure 1-4. Multiple methods for measurement of flow or cardiac output (CO) exist, each with their own limitations. Although a detailed discussion of these methods is beyond the scope of this document, it is important to note certain scenarios in which these methods should not be used, or their data should at least be interpreted with caution. The thermodilution method is an indicator-dilution technique, in which saline is injected proximally in the right atrium and temperature is assessed downstream in the pulmonary artery. CO using this technique varies inversely with the area under the temperature–time curve. The thermodilution technique has limitations in the presence of valvular regurgitation, intracardiac shunt, and very low flow states. Thermodilution outputs can also show greater variability during exercise assessment. The Fick technique is generally considered the gold standard to assess CO, and is defined by the quotient of total body oxygen consumption (VO2) and arterial-venous O2 content difference, assessed by measuring hemoglobin and saturations in the systemic and pulmonary arteries. In the Fick method, caution should be exercised in high output states in which the arterial-venous O2 content difference is relatively low, and the impact of measurement errors becomes greater. It is of note that the differences between measured and assumed VO2 values derived from any of the available prediction formulas can be 25% or more 5. In addition to improved accuracy, use of directly measured MVO2 enables the clinician to assess the adequacy of flow during dynamic exercise. For exercise studies, each 1 mL/min increase in VO2 during exercise should be accompanied by a 6 mL/min increase in CO. Observed increases in CO lower than this value (<80%) indicate CO reserve impairment. Preload reflects end-diastolic ventricular stretch, and is related to maximal sarcomere length prior to systolic contraction. Because the true sarcomeric length cannot be measured clinically, atrial pressure, ventricular end diastolic volume, and ventricular filling pressures (i.e., atrial and ventricular end-diastolic pressures) are common surrogates in practice. Filling pressures are related to filling volume (preload), but this relationship varies in disease states in which there is diastolic dysfunction or pericardial restraint 6. Afterload refers to the forces opposing ventricular ejection 7. Left ventricular (LV) wall stress has been suggested as one way to quantify these forces, but this index varies with chamber size and wall thickness, and the ideal measure of afterload should be independent of ventricular structure and geometry. Aortic input impedance comprehensively describes arterial afterload, but represents a frequency-domain measurement that is cumbersome to apply to time-domain measures of ventricular mechanics 7. Effective arterial elastance (Ea) is a lumped measure of total arterial load that incorporates mean resistive and pulsatile components, varying directly with systemic vascular resistance and heart rate and inversely with total arterial compliance 8. Ea is defined by the ratio of LV end systolic pressure to stroke volume (SV) (Fig. 1). Other measures of afterload in practice are the end-systolic ventricular pressure, when ventricular pressure begins to fall to less than systemic arterial pressure, and variables of systemic (or pulmonary) vascular resistance. Pressure–volume loop. X-axis: ventricular volume; y-axis: ventricular pressure; Ea: arterial elastance; EDP: end-diastolic pressure; EDV: end-diastolic volume; Ees: end-systolic elastance; ESP: end-systolic pressure; ESV: end-systolic volume; SV: stroke volume; Vo: volume intercept at an LV pressure of zero. [Color figure can be viewed at wileyonlinelibrary.com] Similar to the effective lumped stiffness in the vasculature, the LV displays a time-varying stiffness or elastance 9. During diastole, LV elastance is low, allowing for adequate LV filling without untoward elevation in filling pressures. During systole, LV elastance increases markedly due to cross-bridge interaction with contraction. LV end-systolic elastance (Ees) is defined by the LV end-systolic pressure divided by the difference between the end-systolic volume and the volume intercept at an LV pressure of zero (V0, Fig. 1) 6, 7. Ees is defined in experimental conditions by the linear relationship between LV end systolic pressure and volume (end-systolic pressure–volume relationship [ESPVR]) measured during acute changes in preload volume, such as during inferior vena cava occlusion. Ea and Ees share common units and provide a convenient way to conceptualize ventricular-arterial interaction or coupling 7. Based upon a qualitative understanding of these elastances, one can predict how a given patient will respond to alterations in loading conditions. When contractility is depressed (such as with heart failure and reduced ejection fraction [HFrEF]), the ESPVR slope is shallow and Ees is low (Fig. 2). Under these circumstances, even modest reductions in arterial afterload or Ea can lead to dramatic in with a very high which is with and heart failure and ejection fraction will relatively greater reductions in arterial pressure with the of with less increase in even with the degree of (Fig. These with can high of with at much lower The assessment of diastolic stiffness in the cardiac catheterization laboratory is it is in the pressure–volume clinical hemodynamics are the of these are and are by and The end-diastolic pressure volume relationship describes the concepts of stiffness and is with at low and at greater (Fig. 2). of the of this are the chamber pericardial and ventricular or has a a has a (Fig. 2). in ventricular load and contractility and the pressure–volume or in contractility the slope of the end-systolic pressure volume in chamber stiffness the of the end-diastolic pressure volume with less or more compliance Ees: end-systolic elastance; ESP: end-systolic pressure; ESV: end-systolic volume; Vo: volume intercept at an LV pressure of zero. [Color figure can be viewed at wileyonlinelibrary.com] Pressure–volume in with with In with the LV volume is and the slope of the end-systolic pressure volume relationship systolic elastance is in arterial elastance in this to in in end systolic with minimal in arterial In with not display heart volume, but display Ees In this the degree of is with much more dramatic pressure with less increase in used in the catheterization will be to much greater in with and much greater in CO with less in with from [Color figure can be viewed at wileyonlinelibrary.com] In addition to in the right and share a common area the pericardial and one in describes this relationship between the right and Under the ventricular to from the right during with minimal impact LV When the is the of the is during and LV filling is to a relatively greater to a in LV lower pressure, pressure, in the of of ventricular can also with when there is relatively compliance from valvular disease or chamber In pressures can ventricular end-diastolic pressure and lead to in the LV pressure These important when acute or failure the clinical ventricular has important in the of with ventricular In these patients, can in LV and of the and In patients, and right heart catheterization can be used to and is an of cardiac that the of in response to ventricular it reflects the of and of and a preload and afterload, contractility increases the and of sarcomeric is by the and or an increase in heart rate contractility in the this relationship is or even in the In the clinical ventricular contractility is to The used such as ejection fraction and rate of of ventricular pressure are load and not the of the heart 9. The use of the end-systolic pressure–volume relationship to Ees has been suggested as a method of contractility (Fig. 1). The of pressure–volume for an of contractility is with noninvasive and invasive though these assessments are primarily performed for research (Fig. output is a less used of and can be as mean arterial pressure has been to be a of clinical hemodynamics and a of in with heart failure or (Fig. in is as the of mean arterial pressure to units into of In the a higher with lower with from In pulmonary hemodynamics are assessed using a of continuous flow and resistance. pulmonary arterial pressure is by CO through the pulmonary in to the resistance (i.e., a of flow and (Fig. the resistance can be low, the volume of the right with low the increase in flow during exercise, pulmonary vascular resistance through of in the increase in flow the in resistance. of flow and in and with In and with without the mean pressure a increase in flow. 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