Invasive hemodynamic assessment in heart failure

Abstract

Routine cardiac catheterization provides data on left heart, right heart, systemic and pulmonary arterial pressures, vascular resistances, cardiac output, and ejection fraction. These data are often then applied as markers of cardiac preload, afterload, and global function, although each of these parameters reflects more complex interactions between the heart and its internal and external loads. This article reviews more specific gold standard assessments of ventricular and arterial properties, and how these relate to the parameters reported and utilized in practice, and then discusses the re-emerging importance of invasive hemodynamics in the assessment and management of heart failure.

Fig. 1

(A) Time plot of left ventricular pressure (LVP), first derivative of pressure (dP/dt), and EKG in a patient who has heart failure with left bundle-type conduction delay. At the arrow, the patient received bi-ventricular stimulation resulting in an abrupt rise in dP/dt_max. (B) PV loops obtained at baseline and during transient caval occlusion (decreasing LV volumes—loops moving right to left). The slope of the EDSPV derived from multibeat analysis defines ventricular Ees, a load-independent measure of contractility. By measuring diastolic pressure and volume during diastasis at variably loaded beats, the end-diastolic PV relationship (EDPVR) is obtained. The shaded area subtended by the baseline loop represents the stroke work performed by the ventricle. ESP, end-systolic pressure; ESV, end-systolic volume; V₀, volume axis intercept of ESPVR. (C) The slope of the relation between systolic chamber performance (stroke work) and preload (left ventricle end-diastolic volume, LVEDV) determines the preload recruitable stroke work. This relationship shifts up and to the left, as indicated by the arrow, with an increase in contractility, as with dobutamine, or down and to the right with systolic heart failure (HF). (D) LV power (P × Q, solid line) is determined by the product of simultaneously measured pressure (P, dashed line) and flow (Q, dotted line). When indexed to preload, this calculation produces another load-independent measure of LV chamber contractility.

Fig. 2

(A) The kinetics of LV pressure decay during isovolumic relaxation (the time between aortic valve closure and mitral opening) can be modeled by various equations to derive the time constant, τ. The curve indicated by the arrow shows prolonged relaxation, often seen with heart failure, aging, and hypertension. (B) Groups of DPVR. The solid black line shows the curve in a normal person. The curve that shifts up and to the left (arrow) indicates the effects of increased passive chamber stiffness. Filling pressures (LVEDP) may be elevated because of the increased passive chamber stiffness, but similar elevations also can be seen in the absence of increased stiffness, as when there is with increased extrinsic restraint (line indicated by the asterisk). Note that the shape (stiffness) of the DPVR with enhanced restraint is similar to that in the normal patient. Finally, EDP may be elevated simply because of the overfilling of a structurally normal ventricle (dotted black line). There is evidence to support each of these possible contributors to elevated EDP in HFpEF.

Fig. 3

(A) Normal steady-state PV loop. Ea is defined by the negative slope (green line) running between the end-systolic PV point and EDV at P = 0. In healthy persons, Ees (red line) and Ea are matched to maintain optimal coupling and efficiency, with an EF of around 50% to 60% when the volume intercept is near zero. (B) In systolic heart failure, the heart is dilated (increased EDV), Ees is low (shallow ESPVR), and the EF is reduced. Acute reduction of Ea with a vasodilator (red) leads to a marked 50% increase in stroke volume (SV after) with very little reduction in blood pressure. (C) Radial artery (red), pulmonary artery (blue), pulmonary wedge (green), and right atrial (pink) pressure versus time in a patient who has dilated cardiomyopathy. There is severe pulmonary arterial and venous hypertension with borderline systemic hypotension. SV, stroke volume. (D) The same patient on a high dose (7 μg/kg/min) of sodium nitroprusside. Note the near-normalization of cardiac filling pressures with marked increase in stroke volume (SV), with little change in systolic blood pressure.

Fig. 4

(A) With aging, hypertension, and in HFpEF, ventricular (Ees) and arterial (Ea) stiffness increases. Although the Ea/Ees ratio may remain normal, combined ventricular and vascular stiffening leads to marked fluctuations in blood pressure with relatively small changes in preload or afterload. This condition is in striking contrast to heart failure with low EF (see Fig. 3B). (B) LV (black) and pulmonary artery (red) pressure tracings from an 81-year-old woman who has HFpEF demonstrating severe systemic and pulmonary artery hypertension, with markedly elevated LVEDP and wedge pressures (not shown). (C) In response to a very low dose of sodium nitroprusside (2 μg), filling pressures normalize, but severe hypotension develops. Note that there is little change in cardiac output (stroke volume) with vasodilation, again in striking contrast to heart failure with reduced EF. CO, cardiac output; PVR, pulmonary vascular resistance; PWP, pulmonary wedge pressure; WU, Wood units.

Fig. 5

Increased ventricular systolic stiffness leads to a greater rise in blood pressure for a given increase in (A) afterload or (B) preload. (C) Although isolated increases in afterload lead to a predictable reduction in stroke volume for a given level of contractility, this afterload dependence is more marked in patients who have lower Ees, as seen in patients who have heart failure with reduced EF.

Fig. 6

(A) LV (black) and pulmonary wedge (red) pressures at rest in a patient who has symptoms of New York Heart Association class II–III dyspnea and normal LV size and function on echocardiogram. Despite mild to moderate systemic hypertension, cardiac filling pressures are normal, arguing against heart failure. (B) With low-level (40 W) supine exercise in the catheterization laboratory, there is a dramatic increase in cardiac filling pressures (to 45–50 mm Hg) associated with significant dyspnea, suggesting that HFpEF indeed is the cause of the patient’s symptoms.

Fig. 7

Time varying elastance curves obtained at baseline (solid line), after β-adrenergic stimulation (dotted line), and in response to an agent that enhances myofilament calcium sensitivity (dashed line). Although the calcium sensitizer has less effect on the early rise in elastance, there is an increase in the time to peak elastance and systolic duration. See text for details.