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Interactions between respiration and systemic hemodynamics. Part I: basic concepts

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Abstract

The topic of cardiorespiratory interactions is of extreme importance to the practicing intensivist. It also has a reputation for being intellectually challenging, due in part to the enormous volume of relevant, at times contradictory literature. Another source of difficulty is the need to simultaneously consider the interrelated functioning of several organ systems (not necessarily limited to the heart and lung), in other words, to adopt a systemic (as opposed to analytic) point of view. We believe that the proper understanding of a few simple physiological concepts is of great help in organizing knowledge in this field. The first part of this review will be devoted to demonstrating this point. The second part, to be published in a coming issue of Intensive Care Medicine, will apply these concepts to clinical situations. We hope that this text will be of some use, especially to intensivists in training, to demystify a field that many find intimidating.

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Notes

  1. A minor departure of experimental data from Eq. 1, the junction of the horizontal and steep part of actual venous return curves is smooth rather than angular, suggesting a distribution rather than a unique value of P crit.

  2. “Rightward” is enclosed in quotes for the following reason: with a true rightward shift of the venous return curve, i.e., a horizontal translation in the narrow geometric sense, P crit would increase and maximal venous return would not change. This would not be consistent with the differences between curves 1 and 2 shown in Fig. 2b.

  3. Rv is not a simple function of venous geometry and blood rheology, but depends in addition, and nonintuitively, on the distribution of blood flow between parallel vascular beds of different time constants [11]. Hence, its designation as resistance to venous return rather than venous resistance.

  4. By considering Fig. 2d, the geometrically-minded reader might note that intravascular volume expansion, translated into a “rightward” shift of the venous return curve, necessarily leads to a smaller increase in RAP than in MSFP if the heart operates on the ascending part of its function curve (i.e., if cardiac output is preload-dependent).

  5. A further factor which modulates the impact of respiration on LV filling is the influence of lung inflation on pulmonary blood volume and pulmonary venous outflow. Experiments in isolated lungs [38, 39] have indicated that, whether actuated by positive airway or negative pleural pressure, an increase in lung volume can “squeeze” blood out of the pulmonary vascular bed, provided that intra-alveolar vessels are filled at end-expiration, which usually requires a left atrial pressure >3–5 mmHg (more rigorously, West zone 3 conditions, see Sect. “RV afterload” for definition of West zones, and detailed discussion of this issue in [39].

  6. A useful simplification. More rigorously, ventricular afterload is defined as the systolic wall stress (σ), linked to transmural ejection pressure (P), chamber radius (r), and wall thickness (h) by the Laplace relationship σ = P × r/h [42]. Ejection pressure is in turn linked to arterial impedance, which measures the degree to which the arterial system opposes pulsatile blood flow [43].

  7. This is because the alveolar capillaries are in continuity with the pulmonary artery trunk, where intraluminal pressure decreases when ITP decreases, and increases when ITP increases.

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Acknowledgments

We warmly thank the reviewers for their contribution to this text, in the form of numerous thoughtful, in depth, and very constructive comments.

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Authors and Affiliations

  1. Division of Clinical Pathophysiology, University Hospital (CHUV) and Lausanne University (UNIL), 1011, Lausanne, Switzerland

    François Feihl

  2. Medical Intensive Care Unit, Regions Hospital Pulmonary and Critical Care Division, Regions Hospital, St Paul, MN, 55101-2595, USA

    Alain F. Broccard

  3. Division de Physiopathologie Clinique, Centre Hospitalier Universitaire Vaudois, BH10-701, 1011, Lausanne, Switzerland

    François Feihl

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  1. François Feihl
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Correspondence to François Feihl.

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The second part of this article is available at: doi:10.1007/s00134-008-1298-y.

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Feihl, F., Broccard, A.F. Interactions between respiration and systemic hemodynamics. Part I: basic concepts. Intensive Care Med 35, 45–54 (2009). https://doi.org/10.1007/s00134-008-1297-z

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