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 [7, 8]. The relationship between the left atrial pressures and left ventricular pressures is illustrated in Fig. 1.

Fig. 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 [7, 8].

Fig. 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 [9, 10].

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) [9, 10]. 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.

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

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