ICU Physiology in 1,000 Words: Right Ventricular Afterload (Part 1 of 2)

ICU Physiology in 1,000 Words:

The Right Ventricular Afterload (Part 1 of 2)

By Jon-Emile S. Kenny M.D.

With my trusted-resident – Dr. Lina Miyakawa – at my side we watched as our patient could not maintain his oxygen saturation above 82%. The patient had terrible aspiration pneumonia superimposed upon horrendous methamphetamine-related pulmonary arterial hypertension [PAH]. With cardiac anesthesia preparing to intubate, Lina and I were told that paralysis was important for if the patient were to Valsalva, his pulmonary arterial pressures would shoot up, raise his right ventricular afterload and plummet his cardiac output; the reasoning didn’t sit well with me, however.

Stress on the left versus stress on the right

Trainees are commonly quizzed on the physiology of systolic wall stress or tension which is considered to be the most accurate assessment of ventricular afterload [1]. While stress is not the same as pressure, they are related. In a perfect sphere Laplace’s law tells us that the tension experienced by the wall of the sphere is directly proportional the pressure gradient across the sphere as well as its radius but inversely proportional to the thickness of the wall [1]. This approximates the wall stress of the ellipsoid left ventricle [LV] fairly well – though more specific equations have been derived [2] – because wall tension is related to a force vector acting perpendicular to the wall; in the LV, the cardiac muscle shortens circumferentially.

In the normal LV, the peak wall tension occurs at the very end of isovolumic contraction, just prior to opening of the aortic valve [3]. This is because at this point the transmural LV cavity pressure is greatest with respect to the LV radius. While LV cavity pressure does rise beyond the opening of the aortic valve, LV radius is concomitantly decreasing during ejection thereby reducing wall stress despite the rising intra-cavitary pressure.

By contrast, the relationship between right ventricular cross-sectional area [i.e. its radius] and its wall stress is more muddied. The right ventricle [RV] is not ellipsoid, but rather crescent shaped and during ejection, the RV contracts in a peristaltic fashion; the infandibular outflow tract contracts last and sees the highest ejection pressure compared to the RV free wall [4]. Thus, the force against which the RV acts does not lie perpendicular to its contraction as it does in the normal LV. Also, in significant distinction to the LV, peak wall tension of the RV is hard to define because of the RV’s different pressure-volume relationship and ventricular systolic interdependence [5, 6].

Despite this, groups have tried to define peak RV wall stress using modifications of the Laplace Law [7, 8]. As a result, there is some inherent value in the Laplace law when approaching the RV because pathophysiological events that increase RV volume [i.e. its ‘radius’] or the pressure against which the RV ejects both should augment RV wall tension to some degree; this provides a model from which one can consider the concept of RV afterload.

Pulmonary vascular resistance

The commonly-taught afterload for the right ventricle is the pulmonary vascular resistance [PVR]; there are problems with this dogma [9, 10]. Deriving resistance as a simple relationship between pressure and flow applies to non-pulsatile, non-branching, cylindrical tubes – the pulmonary vascular tree is anything but [11]. Mathematically, the PVR generates a linear relationship. If pressure is on the x-axis and flow on the y-axis, the origin is the left atrial pressure [Pla] and the slope of the line defines the PVR. But the pressure-flow relationship for the pulmonary vascular bed is not linear, it is curvilinear [12]. The reasons for the curvilinear relationship lie within the physiology of the vascular bed in totality as well as the individual vessels.

Firstly, in any vascular bed, a critical closing pressure must be surpassed prior to generation of flow. This effect serves to shift the pressure-flow relationship along the [pressure] x-axis, away from the origin. In the pulmonary vascular system, this effect can be caused by Starling Resistors, that is, vascular beds where the perivascular pressure [e.g. alveolar pressure] eclipses the intravascular pressure. This phenomenon has been called ‘Starling Resistance’ to distinguish it from classical ‘Pouiseulle’ resistance described below [9]. Because Starling resistance shifts the pressure-flow relationship in parallel along the x-axis, a PVR calculation using Pla as the downstream pressure will overestimate the true vascular ‘resistance’ faced by the RV [13].

Secondly, individual blood vessels are distensible. Consequently, as the driving pressure within a single vessel is increased, the radial pressure of the vessel enlarges and therefore its radius - the degree to which depending on the vessel's compliance. An increase in radius will lower the vessel’s resistance. Thus pressure and resistance are physiologically linked in a manner whereby flow increases in a curvilinear fashion as a function of increased driving pressure [12].

While the pressure-flow relationship is approximately linear over a limited range of physiological flows [14], ignoring both recruitment and dilation of pulmonary blood vessels in the critically-ill means that a calculated change in PVR may or may not reflect any true change in pulmonary vascular vasomotor tone. This is clinically meaningful when interventions are deemed to change pulmonary hemodynamics based only on PVR calculation. Consider a vasoactive substance that increases blood flow dramatically and because of pulmonary vascular recruitment and dilation there is only a small increase in mean pulmonary arterial pressure [mPAP]. The calculated PVR drops, but does that mean there has been a change in vasomotor tone? Will giving the same vasoactive substance to a patient in heart failure also lower the resistance to flow through the lungs? Would that medication improve pulmonary hemodynamics in severe ARDS? In WHO I PAH? The answer to all is probably no – but here’s the rub – you can’t know.

In response to these caveats, calculation of the PVR in the clinical setting has been considered ‘meaningless’ [9]. Regardless, PVR should be interpreted with caution [10]. The aforementioned also explains why testing for vasodilator response in patients with PAH has moved away from PVR and towards the response of the mPAP with respect to a change in pulmonary blood flow. When there is a clinically meaningful fall in mPAP in the context of little change – or an increase – in pulmonary blood flow, then there has likely been true change in pulmonary vasomotor tone [10]. Another interesting approach is the pulmonary arterial diastolic-pulmonary artery occlusion pressure difference [15] which, in health, is essentially 0 mmHg [16]. If this value is much higher than 5 mmHg then there is likely an increase in the resistance to flow through the pulmonary circulation. Lastly, all of the above underscore the importance of critically appraising papers that report the effect of vasopressors and inotropes on the pulmonary vascular tree – simply reporting a change in PVR does not suffice.

To be continued … part 2.

See more from Dr. Kenny on his website [www.heart-lung.org] and follow him on twitter [@heart_lung]

References:

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11. Naeije, R., Physiology of the pulmonary circulation and the right heart. Curr Hypertens Rep, 2013. 15(6): p. 623-31.

12. Mitzner, W., Resistance of the pulmonary circulation. Clinics in Chest Medicine, 1983. 4(2): p. 127-37.

13. Lopez-Muniz, R., et al., Critical closure of pulmonary vessels analyzed in terms of Starling resistor model. J Appl Physiol, 1968. 24(5): p. 625-35.

14. McGregor, M. and A. Sniderman, On pulmonary vascular resistance: the need for more precise definition. Am J Cardiol, 1985. 55(1): p. 217-21.

15. Naeije, R., et al., The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease. Eur Respir J, 2013. 41(1): p. 217-23.

16. Harvey, R.M., Y. Enson, and M.I. Ferrer, A reconsideration of the origins of pulmonary hypertension. Chest, 1971. 59(1): p. 82-94.