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Principle of esCCO

Principle of esCCO

The principle of esCCO is an inverse correlation between stroke volume (SV) and pulse wave transit time (PWTT). This correlation has been confirmed by clinical experiments and data analysis, and the accuracy of SV estimation based on PWTT has been shown to be less affected by administration of drugs including vascular agents1). Based on this principle, esCCO is calculated by the following equation:
esCCO = K × (α × PWTT + β) × HR 
Where α is a fixed value which was decided experimentally by the past esCCO clinical studies. Meanwhile, constants K and β need to be individualized for each patient.

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Definition of PWTT time components

We defined PWTT as the time measured from the ECG R-wave peak to the rise point of SpO2 pulse wave. PWTT consists of the following three time components.

  1. PEP: Pre-ejection period including the electromechanical delay at the start of systole and isometric contraction time, with the R wave of ECG serving as the starting point.
  2. T1: The time it takes for pulse wave to travel from the aorta through the elastic arteries to the muscular arteries
  3. T2: The time it takes for pulse wave to travel from the muscular artery to the further distal peripheral site of SpO2 measurement.3)4).

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How can the relationship between SV and PWTT remain constant?

 

PEP is affected by cardiac contractility, preload and afterload, and is reduced as stroke volume (SV) increases. In peripheral vessels with small diameter, propagation velocity of pulse wave is reduced because the impact of viscosity becomes dominant. When there is no change in vascular diameter, T2 is less affected by viscosity. However, viscosity can have a dominant influence on T2 when vascular diameter is smaller, so T2 is affected by vascular diameter. As vascular diameter determines vascular resistance, we assume that T2 is affected by vascular resistance. Considering the relationship between SV and T2, T2 is reduced as SV is increased due to vasodilatation with increased vascular diameter.

The relationship between SV and blood pressure can be changed when blood pressure is affected by vascular resistance. However, in the course of pulse wave propagation through vessels, the relationship between SV and PWTT remains constant even when the relationship between SV and blood pressure changes. When blood pressure is increased due to vascular constriction and there is no change in SV, T1 is reduced as a result of increased blood pressure associated with increased vascular resistance. At the same time, T2 is increased as propagation velocity is decreased due to peripheral vasoconstriction. Therefore, reduction in T1 is compensated by increase in T2 and there is no change in the relationship between SV and PWTT. Additionally, in this case PEP is increased due to increased afterload, so increase in PEP also compensate the decrease in T1.

As described above, in the PWTT measurement using ECG and SpO2 peripheral pulse wave, the relationship between PWTT and SV remains constant and the relationship is less affected by vascular resistance.

1) Sugo Y, Ukawa T, Takeda S, Ishihara H, Kazama T, Takeda Z. A Novel Continuous Cardiac Output Monitor Based on Pulse Wave Transit Time. Conf Proc IEEE Eng Med Biol Soc. 2010; 2853-6

 

Impact of medication on the relationship between PWTT and SV

Impact of medication on the direction of stroke volume (SV) change, PWTT and each time component of PWTT based on clinical and animal study was evaluated in the animal study 1). In this animal study, the relationship between PWTT and SV was evaluated in different conditions of varied circulation dynamics; administration of pentobarbital, removal of blood and administration of phenylephrine (Figure 1)1). SV was measured with an electromagnetic flowmeter. 
Table 1 summarizes the study results2).

Figure 1. Relationship between SV and PWTT in varied circulation dynamics

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Table 1. Impact of drugs on time components of PWTT

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1. Phenylephrine
Although inconsistent findings have been reported about the correlation between SV and blood pressure in the administration of phenylephrine3), SV and PWTT were inversely correlated in the study.T1 changed depending on blood pressure, but this change was compensated by T2, and the inverse correlation between SV and PWTT was maintained.

2. Dobutamine/pentobarbital
The direction of change of SV and blood pressure was the same, and SV and PWTT were inversely correlated in the administration of dobutamine and pentobarbital.
- Dobutamine: T1 was inversely correlated with blood pressure and PEP was inversely correlated with SV. There was no change in T2.
- Pentobarbital: While T1 was inversely correlated with blood pressure and T2 was inversely correlated with SV, PEP was positively correlated with SV. We assumed that this was because preload and isometric contraction pressure (ICP) due to drop in blood pressure were decreased at the same time, which has not been validated.

3. Propranolol
When administering propranolol, there was a change in SV but not in blood pressure, and SV and PWTT were inversely correlated. PEP was inversely correlated with SV. There was no change in T1, as there was no change in blood pressure. Also, there was no change in T2.

1) Sugo Y, Ukawa T, Takeda S, Ishihara H, Kazama T, Takeda Z. 2010. A Novel Continuous Cardiac Output Monitor Based on Pulse Wave Transit Time. Conf Proc IEEE Eng Med Biol Soc. 2010: 2853-6

2) Sugo Y., 2013. ‘A Novel Continuous Cardiac Output Monitor Utilizing ECG and SpO2 Pulse Wave’. Proceedings of Life Engineering Symposium

3) Meng L, Cannesson M. et al. The impact of phenylephrine, ephedrine, and increased preload on third-generation Vigileo-Flotrac and esophageal Doppler cardiac output measurement. Anesth Analg 2011; 113:751-757

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