Links To And Excerpts From “Bedside assessment of left atrial pressure in critical care: a multifaceted gem”

Today, I review, link to, and excerpt from Bedside assessment of left atrial pressure in critical care: a multifaceted gem [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Emma Maria Bowcock 1, Anthony Mclean 2. Crit Care. 2022 Aug 13;26(1):247. doi: 10.1186/s13054-022-04115-9.

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Abstract

Evaluating left atrial pressure (LAP) solely from the left ventricular preload perspective is a restrained approach. Accurate assessment of LAP is particularly relevant when pulmonary congestion and/or right heart dysfunction are present since it is the pressure most closely related to pulmonary venous pressure and thus pulmonary haemodynamic load. Amalgamation of LAP measurement into assessment of the ‘transpulmonary circuit’ may have a particular role in differentiating cardiac failure phenotypes in critical care. Most of the literature in this area involves cardiology patients, and gaps of knowledge in application to the bedside of the critically ill patient remain significant. Explored in this review is an overview of left atrial physiology, invasive and non-invasive methods of LAP measurement and their potential clinical application.

Background

A clinician’s interest in the left atrial pressure (LAP) usually pivots around its preload contribution to cardiac output. However, the left atrium is a key component of the ‘transpulmonary circuit’ with upstream and downstream functions as reservoir, conduit and pump [1]. Increases in LAP have important consequences for gas exchange, pulmonary haemodynamic load and right ventricular performance [2]. Raised LAP may be due to pre-existing left ventricular systolic and/or diastolic dysfunction, mitral and/or aortic valve pathology; however, acute increases in LAP can be seen in critical illnesses such as sepsis, myocardial ischemia, stress-induced cardiomyopathies and volume overload states [3,4,5]. Accurate manipulation of cardiopulmonary performance using the limited tools available demands a more in-depth understanding of LA physiology and pressure measurement.

Left atrial physiology

Although the classical anatomy is that of four pulmonary veins, two superior and two inferior, draining separately into the left atrium (LA), this is only the case in 70% of individuals [6]. Around 12–25% of the population have either the two right, or the two left pulmonary veins entering through a single ostia [6]. Flow from the pulmonary veins into the left atrium is pulsatile, and the classical pressure wave form exhibits a V wave and an A wave. The V waves are passive atrial filling waves and occur during ventricular systole. The other peak, the A wave, is the left atrial pressure wave that follows active atrial contraction [78]. The relationship between the left atrial pressures and left ventricular pressures is illustrated in Fig. 1.

Fig. 1

figure 1

Relationship between the left atrial and left ventricular pressures

Blood flow from the pulmonary vein into the LA depends upon the pressure gradient, which varies throughout the cardiac cycle, i.e. the normal blood flow is both phasic and bidirectional [7]. Doppler analysis reveals four distinct waves of flow [8]. See Fig. 2. Two antegrade waves occur during the LA reservoir phase in early and mid-systole (S1 and S2, respectively), corresponding to the X descent post-A pressure wave. The V pressure wave caused by ventricular contraction reduces antegrade flow but following this during the Y descent comes the third antegrade flow during diastole, giving the pulmonary vein D wave, whose amplitude and shape mirror that of the mitral Doppler E wave. Near the end of diastole, atrial contraction occurs, resulting in a significant pressure difference between the LA and pulmonary vein creating a retrograde A wave into the pulmonary vein. This pulmonary vein Doppler A wave is related in time to the transmitral Doppler A wave and the LA pressure A wave [78].

Fig. 2

figure 2
Relationship between pulmonary vein (PV) pressure, LAP and mitral inflow Doppler waves throughout the cardiac cycle. PV Doppler D wave mirrors the mitral E wave and occurs at the time of the Y descent. PV A wave is concomitant to the mitral Doppler A wave and to left atrial contraction. The corresponding reservoir, conduit and pump functions of the left atrium are shown. MV mitral valve

What are we measuring and why?

As demonstrated in Fig. 1, there is variation throughout the cardiac cycle and the pressure at a specific time point has consequences for both incoming flow from the PV (downstream) into the LA and ongoing flow from the LA into the left ventricle (LV). It is quite difficult to express LV filling pressure (LVFP) as a single value on the LV and LA pressure tracing because the pressures fluctuate and LV filling is a complex process.

Mean LAP and LVEDP are not telling us the same thing yet are often used interchangeably. The LVEDP provides information about the LV operating compliance and is the closest estimate of LV preload as a surrogate for LVEDV. Patients with similar LVEDP can have markedly different LAP, which is determined by the operating compliance of the LA [9]. This concept is perhaps most relevant to critical care as changes to compliance can occur with fluid challenges and mechanical ventilation for example. The mean LAP integrates the atrial pressure tracing throughout systole and diastole providing a measure of the hemodynamic load determined by the LA operating compliance (and indirectly left ventricular operating compliance through atrioventricular coupling). It is the mean LAP that is reflected back to the pulmonary venous circulation impacting right ventricular performance [910].

The ‘mid A wave pressure’ (mean value of the A‐wave amplitude) is recommended in consensus statements to estimate end-diastolic LAP that correlates most closely with LVEDP [11], whereas the mean LAP is obtained by temporal integration of the instantaneous PAOP over the entire cardiac cycle (Fig. 3). Mean LAP and end-diastolic LAP can differ significantly in the presence of large ‘V’ waves that occur in severe mitral regurgitation and with reduced LA compliance [12] (Fig. 3). Some suggest that the mean LAP as opposed to the end-diastolic LAP makes more sense when wanting to differentiate pre- from post-capillary pulmonary hypertension (PH) [910]. Certainly, in the critically ill patient with hypoxic respiratory failure and RV dysfunction the more crucial question must be what the cumulative haemodynamic load on the pulmonary vascular system is. The answer to this lies with measurement of the mean LAP.

Fig 3

figure 3

PAOP trace showing the ‘mid A point’ and large ‘V’ wave (patients with mitral regurgitation or reduced LA compliance). An integrated digitised mean over the entire cardiac cycle would include the ‘V’ wave and give a higher PAOP value than a PAOP measurement taken at the ‘mid A point’. PAOP pulmonary artery occlusion pressure

LAP and ‘RV–pulmonary circuit’ dysfunction

The impact of different PH haemodynamic subgroups on RV function is increasingly recognised [13]. A higher incidence of RV dysfunction and RV–pulmonary arterial uncoupling (measured by tricuspid annular planar systolic excursion (TAPSE)/systolic pulmonary artery systolic pressure (sPAP) ratio) was found in those with pre-capillary and combined pre- and post-capillary PH than in isolated post-capillary PH [14]. ePLAR (echocardiographic pulmonary-to-left atrial ratio using tricuspid regurgitant velocity and E/e′) appears to be a simple, non-invasive ratio in differentiating pre- and post-capillary PH with reasonable accuracy, albeit in non-critically ill cohorts [15] (Fig. 4). Patients with RV dysfunction coupled with a low/normal mean LAP and high pulmonary pressures may benefit from pulmonary vasodilators, e.g. nitric oxide. In contrast, those with a high mean LAP and isolated post-capillary PH may derive benefit from diuretics, and pulmonary vasodilators in this group may worsen pulmonary oedema [16]. These diverging treatment strategies emphasise the potential benefit of amalgamating LAP measurement into categorising RV–pulmonary circuit dysfunction. Further investigation of the feasibility and utility of ePLAR in critically ill patients with RV dysfunction would be of interest.

Bedside methods for assessing LAP

Invasive: pulmonary artery occlusion pressure (PAOP)

The challenges in correlating PAOP, LAP and LVEDP when using a PA catheter have been subject to intense evaluation in previously published works [1718] and are summarised in Table 1. Table 2 summarises non-critical care studies investigating the correlation between the PAOP and LVEDP during left heart catheterisation (LHC) showing varying results [19,20,21,22]. Data comparing PAOP and LVEDP in critical care populations are scare and conflicting, and a tabulated summary is provided in Table 3 [23,24,25]. In 1974, Lozman et al. evaluated five ventilated post-operative cardiac surgical patients without ARDS and showed that the relationship between PAOP and directly measured LAP was lost at PEEP levels above 15 cm H20 [23]. Jardin et al. demonstrated that below a PEEP of 10cmH20, PAOP correlated with invasively measured LVEDP; however, this correlation was diminished at PEEP values > 10 [24]. Teboul et al. have shown that PAOP correlated strongly with invasively measured post-A wave LVEDP in patients with ARDS with PEEPs up to 20 cm H20. They suggested this observed correlation of PAOP and LVEDP is due to surrounding diseased lung preventing alveolar vessel compression [25].

Non-invasive: echocardiography and Doppler techniques

Investigation of LAP non-invasively using Doppler has been studied for over 30 years [26]. The most recent 2016 American Society of Echocardiography and the European Association of Cardiovascular Imaging (ASE/EACVI) guidelines estimate mean LAP through Doppler assessment of diastolic blood flow between the left atrium and left ventricle (mitral E to A wave ratio), tissue Doppler imaging (TDI) of the mitral annulus, the tricuspid regurgitant flow velocity and LA volumes as shown in Fig. 5 [27]. Importantly for the critical care physician who is interested in presence of raised LAP for treatment decisions, these guidelines began to differentiate between the two major objectives—LV diastolic dysfunction and LAP (Fig. 5).

Link To Full Sized Figure 5 (Much clearer)

The ratio of early diastolic mitral inflow to average mitral annular tissue velocity (E/e′) has been most extensively studied in the cardiology population [2830] and has gained some interest in the critical care literature [323436,37,38,39]. E/e′ is less load dependent and can be used to assess for raised LAP in those with atrial fibrillation (AF), making it a favoured choice in critical care. A septal E/e′ of > 11, as well as lack of mitral E velocity beat to beat variation, are suggestive of raised LAP in AF [27].

As with any haemodynamic measurement, the use of a single parameter to evaluate LAP should be avoided, and E/e′ is no exception [19]. Although a normal E/e′ does not rule out high LAP, an E/e′ > 15 does have a high specificity in identifying a high LAP [41]. This is perhaps of greatest pragmatic benefit when decisions on further fluid resuscitation are needed at the bedside: an E/e′ > 15 in this scenario would strongly favour a patient with ‘fluid intolerance’. At the other extreme, a low lateral E/e′ of < 8 has shown good diagnostic accuracy to predict PAOP < 18 mmHg [34].

A further challenge of the algorithm to identify patients with high LAP in critical care is the inability of the LA to dilate acutely (in comparison to the right atrium) [42]. Critically ill patients can have acutely high LAP despite a normal LA size, for example, those with volume overload or sepsis and acute diastolic dysfunction [3]. In summary, a dilated LA (LA volume index (LAVI) ≥ 34mls/m2) should raise suspicion for raised LAP, but a normal LA size should not exclude raised LAP. Echocardiographic evaluation of the interatrial septal (IAS) kinetics throughout the respiratory cycle may add pertinent information. Patients with fixed bowing of the IAS to the right are more likely to have raised LAP [43]. Considering right atrial pressure is important however given it is the relative pressure difference between the atria that determines position of the interatrial septum. Additional parameters, including a reduced E wave deceleration time (< 160 ms), alterations in the pulmonary venous Doppler waveform such as a reduced contribution to left atrial filling during systole (S/D ratio < 1), reduced isovolumetric relaxation time (IVRT) of < 60 ms and a mitral ‘L’ wave of > 20 cm/sec, may be additive in identifying raised LAP. An appraisal of their merits and disadvantages is discussed by Nagueh et al. [27].

Overall, when it comes to LAP measurement there exists a lack of uniformity in methods and ‘what’ is being measured. These issues are further compounded by the heterogeneity of the populations included. We shouldn’t be too hasty however in abandoning LAP measurement at the bedside altogether. A non-invasive, rapid beside screening tool to identify patients with possible raised LAP could be ‘the rule of 8’s’: lateral E/e′ > 8 [34] and a lateral e’ ≤ 8 cm/s [32]. This tool could serve as a trigger to temporarily halt further fluid resuscitation and instigate multimodal assessment of cardiopulmonary performance as proposed in Fig. 6.

 

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