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FCA 1 Anaesthetic Refresher Course
Cardiopulmonary interactions
Southern African Journal of Anaesthesia and Analgesia | Vol 29, No 6 | a1439 |
DOI: https://doi.org/10.36303/SAJAA.3023
| © 2023 M. Ngwenya
| This work is licensed under Other
Submitted: 30 November 2025 | Published: 30 December 2023
Submitted: 30 November 2025 | Published: 30 December 2023
About the author(s)
M. Ngwenya, Department of Anaesthesia, School of Clinical Medicine, Faculty of Health Sciences, Charlotte Maxeke Johannesburg Academic Hospital, University of the Witwatersrand, South AfricaFull Text:
PDF (232KB)Abstract
The goal of the heart and lungs is to deliver oxygen at a tissue level, and this is determined by cardiac output (CO) and the oxygen
content of arterial blood (CaO2), DO2 = CO × CaO2.1 The heart and lungs share the same intrathoracic space: mechanically this is akin
to having a pump within a pump.2 Cardiopulmonary interactions refer to the relationship between airway pressures, lung volumes,
and CO.3 In health, the effect of cardiopulmonary interactions is minimal. It is important to look at each part of the heart separately
as phasic changes in intrathoracic pressures (ITP) have differing effects.
In a spontaneously breathing person, a negative ITP is transmitted to the right atrium. The flow of blood to the right atrium is
governed by Ohm’s law, flow = P/R, where P is the driving pressure to the right atrium and R is the resistance of the capacitance
vessels.4 With positive pressure ventilation (PPV) the increased ITP is transmitted to the right atrium, which results in a reduction
of the driving pressure and ultimately the venous return (VR). The right ventricle afterload is the pressure that the heart must work
against to eject blood during systole, and this is determined by the pulmonary vascular resistance (PVR).
PVR is determined by the extra-alveolar vessels and the intra-alveolar vessels. The total PVR is the addition of the two and lowest
at functional residual capacity.5 The left ventricle preload is essentially equal to the right ventricle output. There is a time lag
as blood must traverse the pulmonary circulation. Left ventricle afterload can be expressed as left ventricular (LV) wall stress.
Afterload increases as transmural pressure and vascular resistance increase. Positive pressure reduces the transmural pressure
needed for the ejection of the stroke volume. With negative ITP there is a pressure pulling outwards as the ventricle attempts to
eject its stroke volume, therefore higher transmural pressures are needed.4 Knowing how the heart and lungs work in the normal
physiological state will help guide decision-making about heart-lung interactions in critically ill patients therefore mitigating any
adverse consequences.
content of arterial blood (CaO2), DO2 = CO × CaO2.1 The heart and lungs share the same intrathoracic space: mechanically this is akin
to having a pump within a pump.2 Cardiopulmonary interactions refer to the relationship between airway pressures, lung volumes,
and CO.3 In health, the effect of cardiopulmonary interactions is minimal. It is important to look at each part of the heart separately
as phasic changes in intrathoracic pressures (ITP) have differing effects.
In a spontaneously breathing person, a negative ITP is transmitted to the right atrium. The flow of blood to the right atrium is
governed by Ohm’s law, flow = P/R, where P is the driving pressure to the right atrium and R is the resistance of the capacitance
vessels.4 With positive pressure ventilation (PPV) the increased ITP is transmitted to the right atrium, which results in a reduction
of the driving pressure and ultimately the venous return (VR). The right ventricle afterload is the pressure that the heart must work
against to eject blood during systole, and this is determined by the pulmonary vascular resistance (PVR).
PVR is determined by the extra-alveolar vessels and the intra-alveolar vessels. The total PVR is the addition of the two and lowest
at functional residual capacity.5 The left ventricle preload is essentially equal to the right ventricle output. There is a time lag
as blood must traverse the pulmonary circulation. Left ventricle afterload can be expressed as left ventricular (LV) wall stress.
Afterload increases as transmural pressure and vascular resistance increase. Positive pressure reduces the transmural pressure
needed for the ejection of the stroke volume. With negative ITP there is a pressure pulling outwards as the ventricle attempts to
eject its stroke volume, therefore higher transmural pressures are needed.4 Knowing how the heart and lungs work in the normal
physiological state will help guide decision-making about heart-lung interactions in critically ill patients therefore mitigating any
adverse consequences.
Keywords
cardiopulmonary interactions, intrathoracic pressure, spontaneous ventilation, positive pressure ventilation, pulmonary vascular resistance
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