Clinical background
Calculation of systemic and pulmonary vascular resistance is a central part of interpreting data from right heart catheterisation. The two resistance values answer different clinical questions: systemic vascular resistance (SVR) characterises the shock phenotype and guides the choice between vasopressor and inotropic treatment, whereas pulmonary vascular resistance (PVR) determines the classification of pulmonary hypertension and separates pre-capillary from post-capillary disease. Both depend on pressure gradients divided by cardiac output, which means that measurement uncertainty in any single variable propagates directly into the calculated resistance. Without these calculations, distributive shock cannot be distinguished from cardiogenic shock, and pulmonary hypertension cannot be classified according to current definitions.
Calculating systemic and pulmonary vascular resistance
Systemic vascular resistance (SVR)
The result is given in dyn·s·cm⁻⁵. The factor 80 converts from mmHg·min/L (Wood units) to the CGS unit dyn·s·cm⁻⁵, where 1 Wood unit corresponds to 80 dyn·s·cm⁻⁵. Mean arterial pressure is measured invasively via an arterial line, right atrial pressure via a central venous catheter or the proximal port of a Swan-Ganz catheter, and cardiac output by thermodilution or the direct Fick method.
Pulmonary vascular resistance (PVR)
PVR is given in Wood units (mmHg·min/L). To express the value in dyn·s·cm⁻⁵ it is multiplied by 80. The mean pulmonary artery pressure is obtained from the distal port of the Swan-Ganz catheter, and the pulmonary artery wedge pressure (PAWP) is measured with the balloon occluding a pulmonary artery branch.
Normal values and frame of reference
A systematic review of right heart catheterisation in healthy subjects showed that supine resting PVR in the age group 24 to 50 years was 69 ± 28 dyn·s·cm⁻⁵ (approximately 0.9 Wood units), with an age-related increase to 90 ± 39 dyn·s·cm⁻⁵ (approximately 1.1 Wood units) in subjects over 70 years [4]. This supports the practice underlying the 2022 ESC/ERS guidelines, in which a PVR above 2 Wood units together with a mean pulmonary artery pressure above 20 mmHg and a wedge pressure ≤ 15 mmHg defines pre-capillary pulmonary hypertension [1]. Normal SVR is usually given in the literature as 800 to 1200 dyn·s·cm⁻⁵, but exact limits vary between sources and should be interpreted in clinical context rather than as absolute thresholds.
Interpretation in practice
Systemic vascular resistance in shock
| SVR (dyn·s·cm⁻⁵) | Interpretation | Clinical action |
|---|---|---|
| < 800 | Low, distributive pattern | Consider septic, anaphylactic or neurogenic shock. Vasopressor (noradrenaline) is first-line. |
| 800–1200 | Normal | The shock mechanism is not primarily distributive; investigate a cardiac cause and volume status. |
| > 1200 | High, compensated or cardiogenic | Consider cardiogenic shock or late distributive shock with loss of vasoplegia. Inotropic support and possibly mechanical circulatory support. |
The concept of mixed shock has attracted increasing attention: in the modern coronary intensive care unit, mixed shock states, in which cardiogenic shock coexists with at least one additional shock mechanism, are the second commonest cause of shock [5]. SVR may in such cases show an intermediate pattern that is neither clearly low nor clearly high, and interpretation must then be weighed against the wedge pressure, cardiac output and clinical picture.
Pulmonary vascular resistance in pulmonary hypertension
According to the 2022 ESC/ERS definition, haemodynamic findings at right heart catheterisation are classified as follows [1]:
| Haemodynamic profile | Mean pulmonary artery pressure | Wedge pressure | PVR |
|---|---|---|---|
| No PH | ≤ 20 mmHg | — | — |
| Pre-capillary PH | > 20 mmHg | ≤ 15 mmHg | > 2 WU |
| Isolated post-capillary PH | > 20 mmHg | > 15 mmHg | ≤ 2 WU |
| Combined pre- and post-capillary PH | > 20 mmHg | > 15 mmHg | > 2 WU |
The PVR threshold of 2 Wood units is central to distinguishing pre-capillary pulmonary arterial hypertension (group 1) from pulmonary hypertension caused by left heart disease (group 2). It determines whether the patient should be investigated further towards PAH-specific treatment or towards optimisation of the underlying cardiac disease.
Validation and performance
The calculations are physically sound and validated in the sense that they rest on established hydrodynamic principles. The uncertainty lies not in the formula but in the measurement of cardiac output, which is the denominator in both calculations. Two large modern studies have systematically compared the two dominant methods for measuring cardiac output at right heart catheterisation: thermodilution and direct Fick.
In a Swedish retrospective study from the Karolinska comprising 852 right heart catheterisations (2014 to 2023, median age 66 years, 64% heart failure, 20% pulmonary arterial hypertension), thermodilution correlated strongly with direct Fick (r = 0.79, p < 0.001) [2]. Bland–Altman analysis showed, however, a flow-dependent bias: thermodilution overestimated cardiac output in low-flow states (+0.1 L/min) and underestimated it at normal to high flow (−0.48 L/min). Despite this, thermodilution-based PVR identified raised PVR with high diagnostic accuracy at both the 2 and the 5 Wood unit thresholds (AUC = 0.97, p < 0.001) [2]. Agreement was not affected by the degree of tricuspid regurgitation, which challenges the traditional view that thermodilution is unreliable in significant tricuspid regurgitation.
In an American study from UCLA of 116 patients with pulmonary hypertension (median age 59 years, 63% women, 75% group 1 PH), thermodilution underestimated cardiac output compared with direct Fick, with a mean bias of −0.64 L/min (p = 0.007) [3]. Median PVR differed numerically but not significantly: 5.6 Wood units with thermodilution versus 4.7 with direct Fick (p = 0.15). Eleven per cent of patients had a discordant PVR classification, that is, they fell on different sides of a threshold depending on the method. Thermodilution had a sensitivity of 97% but a specificity of 73% for identifying intermediate to high haemodynamic risk, corresponding to a false positive rate of 27% [3]. The authors recommend direct Fick at index catheterisation when strict PVR calculations are required, particularly in assessment for advanced therapies such as transplantation.
Limitations
The method used to measure cardiac output determines reliability. Thermodilution is the commonest method but carries a systematic, flow-dependent bias. At low cardiac output — precisely the situation in which PVR is often most clinically relevant (evaluation of severe PAH, assessment for transplantation) — agreement between thermodilution and direct Fick is poorest. In the UCLA study, 38% of patients with a low cardiac index by thermodilution in fact had a preserved index by direct Fick [3]. Direct Fick should be considered in these situations where resources allow.
Intracardiac shunts. Thermodilution is not reliable with intracardiac shunts, since the thermal indicator may pass through the shunt and distort the measurement. Both studies excluded patients with shunts [2, 3]. Where a shunt is suspected, direct Fick should be used, and calculations based on thermodilution should not be interpreted.
Uncertainty of the wedge pressure. PAWP may be over- or underestimated with incorrect catheter position, incomplete balloon occlusion, or in significant mitral stenosis, where the wedge pressure does not reflect the left atrial pressure. An incorrect wedge pressure directly affects the PVR calculation and can lead to misclassification of pre-capillary versus post-capillary disease.
Pressure readings and respiration. All pressures should be read at end-expiration, particularly in spontaneously breathing patients in whom intrathoracic pressure swings are large. Incorrect reading can produce systematic errors in the pressure gradient and hence in the calculated resistance.
SVR in mixed shock. An intermediate SVR in shock should not be interpreted as exclusively cardiogenic or distributive. Mixed shock states are common in modern intensive care and can produce any combination of SVR values [5]. SVR must always be interpreted together with cardiac output, filling pressures and the clinical picture.
Thermodilution versus direct Fick in a catheterisation cohort
The Swedish study from the Karolinska [2] is one of the largest modern series comparing thermodilution and direct Fick at right heart catheterisation and supports the view that thermodilution is clinically reliable for PVR classification in most cases, while confirming the need for direct Fick in low-flow states. This is consistent with the practice applied in Swedish cardiac catheterisation laboratories, where direct Fick with a metabolic cart is increasingly used at index evaluation of pulmonary hypertension.
References
- Humbert M, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022;43(38):3618–3731. PMID: 36017548
- Melin M, et al. Agreement of thermodilution and direct Fick methods for cardiac output across varying haemodynamic conditions. ESC Heart Failure. 2026;13(1):509237. PMID: 41711698
- Brownstein AJ, et al. Hemodynamic Risk Assessment by Thermodilution and Direct Fick Measurement of Cardiac Output in Pulmonary Hypertension. CHEST Pulmonary. 2024;2(3):100059. PMID: 42548471
- Kovacs G, et al. Pulmonary vascular resistances during exercise in normal subjects: a systematic review. Eur Respir J. 2012;39(2):319–328. PMID: 21885394
- van Diepen S, et al. Mixed Cardiogenic Shock: A Proposal for Standardized Classification, a Hemodynamic Definition, and Framework for Management. Circulation. 2024;150(18):1459–1468. PMID: 39466889
