ICU Physiology in 1,000 Words: The Right Ventricular Afterload (Part 2 of 2)
Having considered the short-comings of Laplace’s Law and the PVR with respect to the RV afterload in part 1, we will now turn to each of the following in turn: the pulmonary arterial input impedance, a measureable surrogate for detecting afterload change and the effect of Valsalva – in this second exploration of the right ventricular afterload.
As blood flow is pulsatile, pulmonary vascular resistance [PVR] does not adequately account for the right ventricular hydraulic load – as discussed in part 1 . In the early 1960s vascular input impedance was first measured and reported . Input impedance measures the relationship between pulsatile pressure and flow; it is, unfortunately difficult in terms of both acquisition and interpretation . Therefore, models have been proposed to help characterize impedance more simply. The foundation of these models was proposed by Frank well-over 100 years ago ; it is known as the Windkessel model and it takes into consideration both PVR and arterial compliance. Thus the pulmonary circulation is viewed simply as having a two biophysical properties acting in parallel – 1. Capacitance which accepts RV stroke volume during systole and is characterized by compliance and 2. Resistance which mediates vascular run-off and is described by the PVR. This is sometimes referred to as the 2-element Windkessel model and is illustrated via an ‘impedance triangle’ [4, 5]. But the 2-element Windkessel was deemed inadequate as measures of impedance took hold 50 years ago. Consequently a third element was added to better explain the relationship between pulsatile pressure and flow – the characteristic impedance [Zc] . Zc relates to the acceleration of a mass of blood against a compliant vessel. In other words, at the onset of ventricular ejection, cardiac myocytes face a continuous column of dense blood which must be ‘lifted’ against distensible vessels – Zc accounts for this property in the 3-element Windkessel model. In this model Zc acts first – in series – with compliance and resistance which act in parallel as per the 2-element model [6, 7]. The clinical relevance of the 3-element model is that highlights multiple, potentially conflicting hemodynamic variables within the pulmonary circulation. Consider the commonly encountered patient in the ICU with elevated left atrial pressure [Pla]. Study of impedance has revealed that patients with high left heart filling pressures actually have decreased PVR – presumably due to passive congestion and recruitment of the pulmonary vascular tree . However, the congestion also increases the volume of the blood vessels rendering them more stiff [i.e. having a reduced compliance]. The stiff blood vessels increase the pulse pressure which raises the mean pulmonary arterial pressure [mPAP] and, therefore, the trans-pulmonary gradient [mPAP – Pla]. This calculation may lead the clinician to spuriously think that there has been an increase in ‘resistance’ [e.g. vascular remodeling or vasoconstriction] within the pulmonary circulation when, in actuality, it is secondary to passive congestion and will resolve with salt and water removal . In such patients, the difference between the pulmonary arterial diastolic pressure and Pla is likely a better indication of changes in pulmonary vascular resistance . Pulmonary arterial transmural pressure Given the complexity of impedance, are there any methods to simply deduce the hydraulic load faced by a ventricle? This problem was elegantly explored by James Robotham’s group in the late 1980s with respect to the left ventricle [9, 10]. Simply, they reasoned that an increase in systemic impedance – whatever the cause – would raise the transmural pressure of the aorta. The transmural pressure is the pressure within a vessel less its ambient pressure. Conversely, diminution of systemic impedance would lower aortic trans-mural pressure. Most importantly, rather than measuring the transmural pressure of the aorta with invasive catheters, they ‘transduced’ its value by measuring its diameter change [9, 10]. An increase in impedance would thus raise the transmural pressure of the aorta and cause it to dilate while a decrease in systemic impedance would lead to diminished aortic volume. One must not confuse aortic dilation with decreased resistance. An extreme increase in systemic afterload is abdominal aortic cross-clamp which would undoubtedly dilate the thoracic aorta. Conversely, sodium nitroprusside infusion reduces systemic afterload and increases peripheral vascular run-off. This intervention would diminish aortic diameter . Similar reasoning has been applied to the transmural pressure of the pulmonary artery. Indeed, the distending pressure of the pulmonary artery rises in settings of increase pulmonary vascular impedance such as hyperinflation and pulmonary emboli [12-14]. Conversely, interventions known to depress pulmonary circulatory impedance reduce pulmonary arterial transmural pressure . Despite this data and the exploding interest in ICU echocardiography, there is a paucity of investigation into the effect of pulmonary arterial impedance upon echocardiographically-obtained pulmonary artery diameter. Valsalva, PVR and pulmonary arterial impedance During true Valsalva, lung volume does not change despite increased pressure within the entirety of the thorax. As a result, the pressures within the alveolus, all vascular structures, the pleural space and all chambers of the heart rise equally with respect to atmosphere. Importantly, this does not change the hydraulic load upon the RV because there is no pressure differential between the right heart and the alveolus – as occurs when lung volume changes . Of most relevance, the effect of Valsalva was studied  and erroneously concluded to raise right ventricular afterload because Valsalva augmented the calculated PVR. As discussed in part 1, this highlights one of the many problems when using mathematically derived variables as surrogates for true physiological phenomena. The calculated PVR increased because the pressure within the thorax rose relative to blood flow, but most importantly, the study documented diminished pulmonary arterial transmural pressure during Valsalva – a reduced pulmonary arterial transmural pressure with Valsalva has also been observed by Pinsky [18, 19]. As above, this demonstrates that the impedance to flow falls with Valsalva despite an increase in the calculated PVR. Because increasing intra-thoracic pressure results in a profound drop in venous return, RV wall stress – as discussed in part 1 – is actually lessened by the Valsalva maneuver. Thus Valsalva is dangerous in patients with PAH not because of augmented afterload but because these patients require preload to maintain RV output, much akin to patients with high left ventricular outflow impedance – for example, aortic stenosis.
See more from Dr. Kenny on his website [www.heart-lung.org] or follow him on twitter [@heart_lung] References: 1. Naeije, R., Physiology of the pulmonary circulation and the right heart. Curr Hypertens Rep, 2013. 15(6): p. 623-31. 2. Milnor, W.R., Arterial impedance as ventricular afterload. Circ Res, 1975. 36(5): p. 565-70. 3. Saouti, N., et al., The arterial load in pulmonary hypertension. Eur Respir Rev, 2010. 19(117): p. 197-203. 4. Rodarte, J.R. and K. Rehder, Dynamics of respiration. Compr Physiol, 1986. 5. Yanof, H.M., Biomedical electronics1972: Davis. 6. Tedford, R.J., Determinants of right ventricular afterload (2013 Grover Conference series). Pulm Circ, 2014. 4(2): p. 211-9. 7. Westerhof, N., G. Elzinga, and P. Sipkema, An artificial arterial system for pumping hearts. J Appl Physiol, 1971. 31(5): p. 776-81. 8. Naeije, R., et al., The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease. Eur Respir J, 2013. 41(1): p. 217-23. 9. Peters, J., M.K. Kindred, and J.L. Robotham, Transient analysis of cardiopulmonary interactions. II. Systolic events. J Appl Physiol (1985), 1988. 64(4): p. 1518-26. 10. Peters, J., M.K. Kindred, and J.L. Robotham, Transient analysis of cardiopulmonary interactions. I. Diastolic events. J Appl Physiol (1985), 1988. 64(4): p. 1506-17. 11. Robotham, J. and J. Peters, Mechanical effects of intrathoracic pressure on ventricular performance. Heart/Lung Interactions, 1989: p. 251-283. 12. Gelb, A.F., et al., P pulmonale in status asthmaticus. J Allergy Clin Immunol, 1979. 64(1): p. 18-22. 13. Jardin, F., et al., Mechanism of paradoxic pulse in bronchial asthma. Circulation, 1982. 66(4): p. 887-94. 14. Naeije, R., J.M. Maarek, and H.K. Chang, Pulmonary vascular impedance in microembolic pulmonary hypertension: effects of synchronous high-frequency jet ventilation. Respir Physiol, 1990. 79(3): p. 205-17. 15. Muramoto, A., et al., Nifedipine dilates the pulmonary vasculature without producing symptomatic systemic hypotension in upright resting and exercising patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease. Am Rev Respir Dis, 1985. 132(5): p. 963-6. 16. Robotham, J.L., et al., Cardiorespiratory interactions in patients with an artificial heart. Anesthesiology, 1990. 73(4): p. 599-609. 17. Charlier, A.A., P.M. Jaumin, and H. Pouleur, Circulatory effects of deep inspirations, blocked expirations and positive pressure inflations at equal transpulmonary pressures in conscious dogs. J Physiol, 1974. 241(3): p. 589-605. 18. Pinsky, M.R., Determinants of pulmonary arterial flow variation during respiration. J Appl Physiol Respir Environ Exerc Physiol, 1984. 56(5): p. 1237-45. 19. Pinsky, M.R., Instantaneous venous return curves in an intact canine preparation. J Appl Physiol Respir Environ Exerc Physiol, 1984. 56(3): p. 765-71.