Bedside Assessment of Left Atrial Pressure in Critical Care: A Multifaceted Gem | Critical Care | Full Text
Highlights
- the left atrium is a key component of the ‘transpulmonary circuit’ with upstream and downstream functions as reservoir, conduit and pump
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- a low lateral E/e′ of < 8 has shown good diagnostic accuracy to predict PAOP < 18 mmHg
- 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
- LA strain should be measured using a non-foreshortened apical-4-chamber (A4C) view of the LA where values of LA strain for reservoir, conduit and pump functions are measured
- An important concept to appreciate is that the ‘diastolic stress test’ of critical illness can shift patients from a normal ‘resting’ LAP to a high LAP state, with corresponding increases in E/e′ ratio. This is because the mitral annular velocity (e’) of the stiff left ventricle cannot increase to match the increased mitral E velocity as occurs with increased cardiac output demand [27]. This can be particularly problematic during ventilatory weaning leading to Weaning-induced Pulmonary Oedema (WiPO).
- A PAOP ≥ 18 mmHg was a commonly accepted criterion to define cardiogenic oedema in ARDS [52]. However, it was not a ‘hard’ value, was seldom measured and it was increasingly appreciated that raised LVFP could coexist with ARDS, hence it was removed from revised diagnostic criteria
Bedside Assessment of Left Atrial Pressure in Critical Care: A Multifaceted Gem | Critical Care | Full Text
Highlights
- the left atrium is a key component of the ‘transpulmonary circuit’ with upstream and downstream functions as reservoir, conduit and pump
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- a low lateral E/e′ of < 8 has shown good diagnostic accuracy to predict PAOP < 18 mmHg
- 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
- LA strain should be measured using a non-foreshortened apical-4-chamber (A4C) view of the LA where values of LA strain for reservoir, conduit and pump functions are measured
- An important concept to appreciate is that the ‘diastolic stress test’ of critical illness can shift patients from a normal ‘resting’ LAP to a high LAP state, with corresponding increases in E/e′ ratio. This is because the mitral annular velocity (e’) of the stiff left ventricle cannot increase to match the increased mitral E velocity as occurs with increased cardiac output demand [27]. This can be particularly problematic during ventilatory weaning leading to Weaning-induced Pulmonary Oedema (WiPO).
- A PAOP ≥ 18 mmHg was a commonly accepted criterion to define cardiogenic oedema in ARDS [52]. However, it was not a ‘hard’ value, was seldom measured and it was increasingly appreciated that raised LVFP could coexist with ARDS, hence it was removed from revised diagnostic criteria