In adult cardiac surgical patients, pulmonary hypertension is frequently the result of left-sided heart disease (all causes associated with pulmonary venous congestion).1 An increase in left atrial pressure will cause pulmonary venous congestion, which may lead to increased pulmonary vascular reactivity and pulmonary vascular resistance (PVR) and reduced pulmonary vascular compliance.2–4 Chronic increases in left atrial pressures may also cause a “congestive vasculopathy” resulting in medial hypertrophy and endothelial fibrosis of the vessel walls.2,4 Cardiopulmonary bypass may further lead to elevated PVR through several mechanisms including endothelial dysfunction, systemic inflammatory syndromes, pulmonary reperfusion injury, and protamine reactions.5–7 Excessive afterload may negatively impact the right ventricle and, when acute, may result in right ventricular failure. The importance of right ventricular failure in cardiac surgery has been reviewed and, when coupled with a low cardiac output, it carries a significant mortality burden, up to 44%.8,9
Pulmonary artery (PA) Doppler imaging may be helpful in assessing the overall vascular forces opposing right ventricular ejection. We will briefly review hydraulic principles relevant to the normal and diseased pulmonary vasculature that will facilitate the understanding of alterations in the PA Doppler profile.
FORCES OPPOSING FLOW
The pressure in a conduit remains constant in a system with constant flow. Similar to Ohm’s law, pressure (P) is equal to the product of resistance (R) and flow (Q) (P = R × Q). If the flow in a system is not constant, neither is pressure. PVR does not completely describe the constraints acting on the right ventricle, as it assumes a constant flow, pressure, and static load. In oscillatory systems, pressure is equal to the product of impedance (Z) and flow (P = Z × Q). Impedance is a term that represents the forces opposing pulsatile flow and is expressed as: Z = P/Q.10,11 Elevations in pulmonary impedance may impose an excessive burden on right ventricular ejection.
The distal vessels (capillaries and arterioles) are the largest contributors to resistance (R), where R = η × L/r4 (Poiseuille’s law), where η is the viscosity, L is the length of the vessel, and r is the vessel radius. Vasoconstriction, increases in alveolar and pleural pressures (e.g., positive end-expiratory pressure causing compression of the pulmonary microcirculation), will increase vessel resistance. Conditions that increase blood viscosity may also alter resistance by increasing viscous friction (η, mentioned earlier).12 Most therapies for pulmonary hypertension targeted the distal vessels.13,14 Left-sided ventricular or valvular diseases are common in the adult cardiac surgical population. Venous congestion, with or without alterations in precapillary or capillary resistance, will result in increased PA pressure (PAP). PAPs may further be exacerbated by exercise or an increase in cardiac output.11,12 Indeed, in these situations, most therapies are targeted toward improving left ventricular function (systolic or diastolic) or valvular function. Reductions in left atrial pressure will result in a reduction in pulmonary venous congestion and resistance to outflow.
The pulmonary circulation is pulsatile and operates at lower pressures than the systemic circulation. This is because of its large distributed compliance (see Compliance section below), which “buffers” the pulsatile load.15 Yet, the proportion of pulsatile to total work (pulsatile plus steady) is larger in the pulmonary circulation than in the systemic circulation (~25%–30% vs ~10%–15%), and this proportion is maintained in patients with idiopathic pulmonary hypertension.15–18 Pulsatile (oscillatory) work represents wasted energy that is not useful in the net forward movement of blood. In the pulsatile vascular system, pressure waves will “oscillate” around the mean pressure. In the systemic circulation, the ratio of pulse pressure to mean pressure is approximately 0.4; however, in the pulmonary circulation, it is approximately 1.0.15 In other words, in the pulmonary system, the pulse pressure is as large as the mean pressure. Exaggerated pulsatility may be observed in patients with chronic thromboembolic pulmonary hypertension where strong proximal reflectors (see below) will cause an increase in pulse pressure and a ratio >1.0 may be seen.19
In summary, the right ventricle operates at lower pressures but with higher pulsatility than the left ventricle. In pulmonary hypertension, the overall amount of work (oscillatory and steady) will increase.16 Conditions that result in exaggerated pulsatile work will result in a further elevated burden on right ventricular ejection.
During systole, the mitral valve is closed and the PA system must accommodate stroke volume without incurring excessive pressure. Vascular compliance may be understood as the system’s ability to “absorb” volume through vessel elasticity and capacity. A system with good compliance (C) will admit volume without large changes in pressure (C = ΔV/ΔP). When compared with the pulmonary circulation, the systemic circulation has comparatively fewer distal arterioles that have higher resistance, and the compliance is situated more proximally.15,20 In the pulmonary system, the compliance is distributed throughout the entire pulmonary tree. The larger main PA and the proximal right and left PAs provide approximately 15% to 20% of the compliance because of their size and distensibility.15,21 Contrary to the systemic circulation, pulmonary vessel distensibility extends distally to small vessels of approximately 1 mm in size.21 As a result of their large numbers and high distensibility, the more distal vessels contribute to the remaining portion of total pulmonary vessel compliance. The relationship between the systolic PAP and the vessel distensibility is exponential.22 In other words, as the pulmonary system becomes pressurized, vessel compliance decreases as it becomes stretched. However, in disease, direct alterations in vessel elasticity that reduce compliance may occur independent of PA pressure.22
Capacitance is a measure of the total arterial compliance based on the pulse pressure method. It is measured as the ratio of stroke volume to pulse pressure.20 The relationship between capacitance and resistance is hyperbolic where the product of the 2 describes a constant that is maintained throughout disease and treatment (Fig. 1).3,15,21,23 This important relationship is the result of the distribution of compliance. Changes in distal vessel resistance will be closely associated with changes in capacitance. Furthermore, an elevated PA capillary wedge pressure (PCWP), frequently seen in adult cardiac surgery, will shift the PVR-capacitance relationship to the left, resulting in a decreased PVR × capacitance constant (Fig. 1).3 From Figure 1, we see that capacitance is reduced early in disease.
Capacitance has been shown to be a good predictor of adverse outcome in patients with congestive heart failure and idiopathic pulmonary hypertension.3,24 Because an increase in PAP is a relatively later event in the progress of disease, more attention should be placed on the assessment of capacitance.25 A decrease in capacitance may be an early indicator of pulmonary vascular disease.3,15,22,23,26
A contributing factor to increases in systolic pulmonary pressure is wave reflection, where forward pressure waves “collide” with backward (reflected) pressure waves (Fig. 2, A and B). These waves are not to be confused with blood flow. Their presence augments the hydraulic load of the right heart.27 Wave reflections (pressure and flow) are a precapillary phenomenon; they occur at arterial branch points, sites of change in vessel caliber, and high-resistance arterioles. In the normal state, reflections are small, diffuse, and often cancel each other. Compliant vessels further attenuate any returning wave. However, in PA disease, reflected waves return quicker and maintain more energy because they are reflected within stiff, noncompliant vessels.28 Their fusion with forward waves will result in systolic pressure augmentation, directly increasing afterload (Fig. 2, A and B). Simultaneously, flow waves are reflected inverted and consequently cause a premature reduction in flow (or flow velocity) (Fig. 2, C and D). Slower reflected pressure (or flow) waves that return in diastole are of little importance to right ventricular ejection.
ASSESSING PULMONARY VASCULAR DISEASE THROUGH PRESSURE AND DOPPLER FLOW VELOCITY
The interplay between input (stroke) volume, resistance, compliance, and the generation of wave reflections can be appreciated by examining both the PAP and the Doppler velocity traces. In the normal pulmonary circulation, pressure and flow traces display similar contours.29 In disease, these similarities disappear. The PAP trace provides useful information on the amplitude of the pulsatile load such as the pulse pressure.19,30 Pressure augmentation may also be inferred from the PAP trace, seen as a secondary pressure increase in systole (Fig. 2, A and B). However, its precise assessment requires the use of high-fidelity catheters not routinely used in the clinical setting.30,31 Pressure augmentation may also be indirectly measured using Doppler echocardiography (discussed later). The pulmonary Doppler velocity trace may provide further important information. The changes in velocity contour, flow reversal, and the role of the pulmonary acceleration time (AT) in disease will be discussed in more detail later.
PA Doppler Acquisition
PA Doppler measurements have been performed using transthoracic echocardiography by sampling in the right ventricular outflow tract (RVOT) at the pulmonary valve. Using transesophageal echocardiography (TEE), the sampling location that provides the best Doppler alignment with pulmonary flow is in the midesophageal ascending aortic short-axis (SAX) view (Fig. 3A). To interrogate at the pulmonary valve, the upper esophageal aortic arch SAX view, optimized for the PA, may be used (Fig. 3B). Alternatively, the transgastric right ventricular inflow–outflow view may be used to sample in the RVOT close to the pulmonary valve (Fig. 3C). The views demonstrated in Figure 3, B and 3C may occasionally prove difficult to obtain.
Pulmonary Doppler Patterns
The normal pulmonary velocity flow profile is broad and rounded as peak velocity is attained (Fig. 4A).32 Increased resistance, decreased compliance, and pressure augmentation result in a pattern that demonstrates a more rapid increase and a premature cessation of flow velocity.30,33 As impedance increases, the flow velocity contour progresses from a rounded peak to a more triangular appearance (Fig. 4, B and D) and in some cases it may be notched (Fig. 4C).34,35 Flow reversal may be observed when interrogating in the midesophageal ascending aortic SAX view (Fig. 4, B–D).
AT and Doppler Estimates of Pulmonary Pressure and PVR
Systolic and mean PAPs may be derived from the tricuspid regurgitant (TR) jet and the pulmonary regurgitant jet using continuous wave Doppler (CWD).36,37 Estimating PVR using the ratio of peak TR jet velocity divided by RVOT velocity time integral has also been described.38 PA AT is measured using pulsed wave Doppler in the RVOT (using transthoracic echocardiography) at the pulmonary valve (Fig. 3, B and C for TEE). It is defined as the time interval from the onset to the peak of pulmonary flow velocity (Fig. 4A). Normal values range from 134 ± 20 milliseconds to 153 ± 32 milliseconds.29,32 The relationships between AT and PAP or PVR have yielded good correlations.29,32,39–41 Overall, an AT < 100 milliseconds predicts an increased mean PAP > 25 mm Hg and a PVR > 3 Woods Units. An increased PVR is unlikely when AT is >110 milliseconds.27 AT may also be affected by increases in PCWP. Reductions in AT from a normal value of 136 ± 41 milliseconds to 117 ± 29 milliseconds have been found in the presence of a normal PVR with an elevated PCWP.41
The AT may also be significantly affected by large-amplitude wave reflections, the result of strong proximal reflectors.19,42,43 AT values <100 milliseconds have predicted pressure augmentations of at least 8 mm Hg.29 Notching of the Doppler velocity profile may be observed in embolic disease (Fig. 4C). In a group of patients undergoing pulmonary embolectomy for chronic thromboembolic pulmonary hypertension, a longer time interval from onset of flow to notching, compared with that from notch to end of flow (a later appearing notch), was thought to reflect more distal disease that would persist after embolectomy, resulting in increased in-hospital mortality and disease progression.43
Using TEE, measurements of AT are ideally made near the pulmonary valve (Fig. 3, B and C) because flow disturbances (see below) observed in the main PA (Fig. 3A) may significantly affect AT values. According to current American Society of Echocardiography guidelines, mean PAP may be estimated from the pulmonary AT according to the following relationship: PAP mean =72 − (0.42 × AT) (used when AT < 120 milliseconds).32,44 However, measurements based on the TR jet are preferred. At present, echo-derived methods, including the AT in the Doppler determination of PVR, are not supported under the current American Society of Echocardiography Guidelines.44
Doppler Assessment of Pressure Augmentation
Pressure augmentation may be appreciated directly from the PAP trace (Fig. 2B). Doppler echocardiography may also be helpful. Bech-Hanssen et al.27,29 described an echo-derived method to measure pressure augmentation using the CWD trace of the TR jet. Unlike the AT, the time to peak velocity is measured from the QRS to the peak velocity of the PA pulsed wave Doppler trace (Fig. 5A). A pressure gradient is obtained from the TR velocity profile using this time interval (QRS to peak pulmonary flow velocity), the PA systolic pressure at the point of flow reduction. The peak pressure gradient is then measured from the peak velocity of the TR Doppler trace. The difference between the 2 represents the pressure augmentation (Fig. 5B). There are some shortcomings; this technique requires a very clear CWD trace of the TR velocity, which may not always be possible to achieve by using TEE. Furthermore, it is not possible to make both Doppler measurements simultaneously, which may lead to errors resulting from unmatched data sets.
Pulmonary Flow Patterns
Using color flow Doppler, it is not uncommon to see some degree of flow reversal characterized by blue color in the main PA in the midesophageal ascending aortic SAX view (Supplemental Digital Content 1, Video 1, http://links.lww.com/AA/B157). Flow reversal has been associated with elevated pulmonary pressure and enlarged PAs.45 Flow vortices, the swirling of blood in the main PA, have also been observed in patients with overt pulmonary hypertension (Supple mental Digital Content 2, Video 2, http://links.lww.com/AA/B158, and Supplemental Digital Content 3, Video 3, http://links.lww.com/AA/B159).46 Using magnetic resonance imaging, Reiter et al.46 reported large and persistent flow vortices in the main PA of patients with pulmonary hypertension. Vortex intensity, persistence, and onset correlated with severity of disease. The authors speculate that a PA vortex might be a method of preserving kinetic energy, whereas others consider it the result of PA geometry.45,46 Vortices may also be involved in the efficient transport of blood in disease.47
NOVEL ASSESSMENTS: THE FREQUENCY DOMAIN
A Fourier transformation can be used to mathematically decompose periodic biological events such as a blood pressure trace (the time domain) into a collection of sinusoids (the frequency domain). The signal must repeat regularly, where starting and ending values are the same, and the system must be in a steady state.48,49 Pulmonary flow velocity and pressure waves obtained at the same location using Doppler echo and a PA catheter may therefore be deconstructed into their component waves (Fig. 6, A and C). Each sinusoid of ascending frequency (harmonic) will have a distinct amplitude and phase (e.g., starting point of sinusoid shifted from zero degrees, Fig. 6E). As the frequency increases (multiples of the fundamental frequency such as the heart rate), the amplitude decreases (Fig. 6, A and C). Pulmonary impedance in the frequency domain (Fig. 7) may be expressed as a series of sinusoidal pairs of P and Q for each harmonic or multiple of the fundamental frequency (Zn = Pn/Qn, where n is the harmonic number). The result is a more complete representation of the forces opposing right ventricular ejection in the pulmonary system.
Frequency domain analysis of pulmonary impedance (Fig. 7) may be divided into 2 parts: the zero harmonic (steady flow component) and the subsequent harmonic numbers (1, 2, 3 …). The latter may be further divided into 2 parts: the lower harmonic numbers that contain the wave reflections and the subsequent “reflectionless” harmonics that define the characteristic impedance (Zc). The y-intercept (zero harmonic or Z0) is the total PVR and largely represents the contribution of peripheral resistance vessels.50 The pulmonary input impedance spectrum for the subsequent harmonics reflects the properties of approximately the first 5 orders of vessels in the pulmonary tree (proximal to the distal resistors).51 In the presence of significant wave reflections, an increased impedance will be observed at the lower harmonics (Fig. 7, Z1, Z2 upper trace). The lower harmonics will also reflect the degree of divergence between the sinusoidal harmonic pairs of pressure and the flow waves, represented as the phase difference (Pphase angle − Qphase angle) for each harmonic number (Fig. 6E). In the highly compliant pulmonary system, there will be an early negative phase at the low harmonics (flow precedes pressure). In the presence of significant wave reflections, the phase difference (divergence of P and Q) will be sustained into the following higher harmonics. At the higher harmonics, impedance may be assessed free from the influence of significant wave reflections. The average of the higher harmonic impedances (from the first minimum value for Z or from Z3 to Z10 in Fig. 7) is termed the characteristic impedance (Zc). Zc may also be appreciated in the time domain from the relationship of the slopes of the pressure and flow traces early in ejection (e.g., dP/dQ, Fig. 8).52 It may be easier to understand if Zc is modeled as a resistor (R = P/Q). Zc is dependent on the caliber and compliance of the proximal vessels.51–53
In summary, the impedance modulus in the frequency domain provides in 1 plot the information on total PVR (zero frequency, distal resistors) and the properties of the more proximal vessels, either free from wave reflections (characteristic impedance, higher harmonics) or in the presence of wave reflections when present (lower harmonics).50–53
PULMONARY IMPEDANCE AND DOPPLER ECHOCARDIOGRAPHY
In the clinical setting, pulmonary impedance has been measured in the adult and pediatric population using a PA catheter and Doppler echocardiography.54,55 Evaluation of the impedance modulus displayed in the frequency domain (Fig. 7) was found to be reliable and feasible in a clinical setting.54,55 However, the lower harmonic values remain the most reliable.56 Assessment of impedance in the frequency domain may help guide therapy in patients who present with significant vascular disturbances of the pulmonary tree. It may also provide opportunities to appreciate reductions in resistance (Z0) and wave reflections (lower harmonics) in response to various interventions, such as alterations in heart rate, stroke volume, and vasopressor and vasodilator therapy.54,55,57,58
Conditions that generally increase volume in the normal pulmonary system (e.g., exercise) do not normally result in significant increases in PAPs. In cardiac patients, elevated left-sided pressures with or without alterations in precapillary resistance result in a “pressurization” of the pulmonary tree. This results in increased stiffness and, in the presence of reflectors, sets in motion dynamic changes such as pressure augmentation that will negatively impact right ventricular function. A comprehensive echocardiographic assessment of the right-sided system necessitates multiple measurements that are not always feasible in the perioperative setting.59 Alterations in the pulmonary Doppler profile can provide global insight into the sum of the vascular constraints that may impact right ventricular function.
Name: Claude Tousignant, MD, FRCPC.
Contribution: This author contributed in a significant way toward the design, writing, redaction, as well as drafting, and revisions of all versions before submission.
Attestation: Claude Tousignant approved the final draft.
Name: Jordan R. Van Orman, MD, PhD.
Contribution: This author contributed in a significant way toward the design, writing, redaction, as well as drafting, and revisions of all versions before submission.
Attestation: Jordan R. Van Orman approved the final draft.
This manuscript was handled by: Martin J. London, MD.
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