Stroke volume variation (SVV) and pulse pressure variation (PPV) (2024)

STROKE VOLUME VARIATION (SVV) AND PULSE PRESSURE VARIATION (PPV)

Variations in stroke volume (SV) and pulse pressure (PP) occur as a result of interactions between the cardiovascular and respiratory systems. An alternative to SV optimisation is to minimise the variation in either SV or PP across the respiratory cycle. During inspiration (with positive pressure ventilation), the increase in intrathoracic pressure compresses the venae cavae. This subsequently reduces preload, and therefore the SV, once that blood has passed through the pulmonary circulation and is ejected from the left side of the heart. In theory, patients who exhibit a SVV or PPV greater than ~10-15% may be hypovolaemic and therefore may respond positively to a fluid challenge.

However, for the calculation of a valid SVV/PPV, a number of physiological/clinical criteria must be met or considered:

• Full mechanical ventilation (no spontaneous breaths)
• No arrhythmias
• Tidal volume ≥7-8 mL/kg [1, 2]; be aware that higher tidal volumes elicit higher variations [3]
• Heart rate – respiratory rate ratio (HR:RR) ≥4 [4]
• Positive end-expiratory pressure (PEEP) must be considered; a higher PEEP will result in higher variations [5]
• An open abdomen has been show to reduce SVV/PPV by 40-50% [6]
• Changes in lung or chest compliance (e.g. sick lungs), or patient position may affect readings, as may left or right ventricular dysfunction or pneumoperitoneum [7]

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Note: these criteria apply to any technology using SVV/PPV to guide fluid management.

Modified from Hofer and Cannesson.Inspiration during mechanical positive pressure ventilation results in increased intrathoracic pressure and a reduced venous return. Preload decreases, followed by stroke volume (SV) and pulse pressure (PP) once the blood transits through the pulmonary circulation. During expiration both SV and PP increase due to the reduced intrathoracic pressure.

Once the aforementioned criteria are met, uncertainty still remains about the cut-off value of SVV/PPV required for the determination of fluid responsiveness. There is a large discrepancy in the published literature about what absolute SVV/PPV deems the patient to be fluid responsive. Data from Zhang et al. [8] report the different cut-off values used in different studies, ranging from 8.5 to 15.5%.

One explanation for this variation in cut-off values is the site of measurement. In-house analysis by Deltex Medical compared simultaneous measurements of SVV flow (measured centrally by the ODM), SVV pressure (measured from arterial pressure-derived SV), and PPV, and found that SVV flow tended to operate in a higher range than SVV pressure and PPV measured from the radial artery. It seems likely that this variation is reduced when measured more peripherally. Indeed, a study by Guinot et al. [9] found that patients were likely to be fluid responsive with an SVV flow of ≥15%.

If a patient meets the clinical criteria for valid SVV/PPV measurement mentioned above, the parameters may be useful as indicators of fluid responsiveness. It is thought that PPV may be more reliable than SVV (from arterial pressure), because it is a less derived parameter. However, the reality is a large number of patients likely fall into this ‘grey area’ where it is difficult to determine whether they will respond to a fluid challenge or not. Overall, SVV and PPV have low clinical applicability, as < 10% of surgical and <3% of ICU patients meet the above requirements to rely on these measures [10-11].Oesophageal Doppler basedSV optimisation can be utilised in any patient and is supported by a large evidence base.

References