# Calculation of V’alv, VDaw and VDaw/VTe

Article

Author: Clinical Experts Group, Hamilton Medical

Date of first publication: 05.10.2020

Last change: 05.10.2020

(Originally published: 25.08.17) SW versions updated
How do Hamilton Medical ventilators calculate V`alv and VDaw/VTE, and what are these parameters used for?

### Calculating V`alv

Alveolar minute ventilation in l/min:  V'alv = RR * Vtalv = RR * (VTE - VDaw)

V'alv:     Alveolar minute ventilation
RR:       Respiratory rate
Vtalv:    Alveolar tidal volume
VDaw:  Anatomical dead space volume, calculated using the Vds-PIE slope method (Wolff G, X. B. J. , Weibel W., Bowes C.L. , Muchenberger R., Bertschmann W. (1989). Anatomical and series dead space volume: concept and measurement in clinical practice. Applied cardiopulmonary pathophysiology, 2, 299-307.1​)
VTE:     Expiratory tidal volume

In short, the alveolar minute ventilation (V`alv) reflects Area X in Figure 1 (below) multiplied by the respiratory rate.

### Calculating the dead space fraction

Dead space fraction in %: VDaw/VTE = 100 x VDaw/VTE

VDaw:  Anatomical dead space volume, calculated using the Vds-PIE slope method (Wolff G, X. B. J. , Weibel W., Bowes C.L. , Muchenberger R., Bertschmann W. (1989). Anatomical and series dead space volume: concept and measurement in clinical practice. Applied cardiopulmonary pathophysiology, 2, 299-307.1​)
VTE:    Expiratory tidal volume
The dead space fraction puts the expiratory tidal volume VTE in relation to the anatomical dead space volume VDaw.

### What do they tell us?

Alveolar minute ventilation:

An increase in V‘alv can be seen after an effective recruitment maneuver and induces a transient increase in V‘CO2.
A decrease in V‘alv can indicate that fewer alveoli are participating in the gas exchange, for example, due to pulmonary edema.

The dead space fraction gives you an indication of how effective the ventilation is. A rising VDaw/Vte ratio may be an early sign of ARDS. In a normal lung, the VDaw/Vte ratio is between 25% and 30%. In patients with ARDS, a dead space fraction ≥ 60% was associated with higher mortality (Kallet RH, Zhuo H, Liu KD, Calfee CS, Matthay MA; National Heart Lung and Blood Institute ARDS Network Investigators. The association between physiologic dead-space fraction and mortality in subjects with ARDS enrolled in a prospective multi-center clinical trial. Respir Care. 2014;59(11):1611-1618. doi:10.4187/respcare.025932​).

Relevant devices (Standard on the HAMILTON-S1A​)​: HAMILTON-G5/S1 (SW v2.8x and later); HAMILTON-C2/C3/C6 (SW v2.2.x and later / SW v2.0.x and later / SW v1.1.x and later); HAMILTON-C1/T1 (SW v2.2.x and later)

#### Footnotes

• A. Standard on the HAMILTON-S1

#### Anatomical and series dead space volume: concept and measurement in clinical practice

Wolff G, X. B. J. , Weibel W., Bowes C.L. , Muchenberger R., Bertschmann W. (1989). Anatomical and series dead space volume: concept and measurement in clinical practice. Applied cardiopulmonary pathophysiology, 2, 299-307.

#### The association between physiologic dead-space fraction and mortality in subjects with ARDS enrolled in a prospective multi-center clinical trial.

Kallet RH, Zhuo H, Liu KD, Calfee CS, Matthay MA; National Heart Lung and Blood Institute ARDS Network Investigators. The association between physiologic dead-space fraction and mortality in subjects with ARDS enrolled in a prospective multi-center clinical trial. Respir Care. 2014;59(11):1611-1618. doi:10.4187/respcare.02593

BACKGROUND

We tested the association between pulmonary dead-space fraction (ratio of dead space to tidal volume [V(D)/V(T)]) and mortality in subjects with ARDS (Berlin definition, P(aO2)/F(IO2) ≤ 300 mm Hg; PEEP ≥ 5 cm H2O) enrolled into a clinical trial incorporating lung-protective ventilation.

METHODS

We conducted a prospective, multi-center study at medical-surgical ICUs in the United States. A total of 126 ALI subjects with acute lung injury were enrolled into a phase 3 randomized, placebo-controlled study of aerosolized albuterol. V(D)/V(T) and pulmonary mechanics were measured within 4 h of enrollment and repeated daily on study days 1 and 2 in subjects requiring arterial blood gases for clinical management.

RESULTS

At baseline, non-survivors had a trend toward higher V(D)/V(T) compared with survivors (0.62 ± 0.11 vs 0.56 ± 0.11, respectively, P = .08). Differences in V(D)/V(T) between non-survivors and survivors became significant on study days 1 (0.64 ± 0.12 vs 0.55 ± 0.11, respectively, P = .01) and 2 (0.67 ± 0.12 vs 0.56 ± 0.11, respectively, P = .004). Likewise, the association between VD/VT and mortality was significant on study day 1 (odds ratio per 0.10 change in V(D)/V(T) [95% CI]: 6.84 [1.62-28.84] P = .01; and study day 2: 4.90 [1.28-18.73] P = .02) after adjusting for V(D)/V(T), P(aO2)/F(IO2), oxygenation index, vasopressor use, and the primary risk for ARDS. Using a Cox proportional hazard model, V(D)/V(T) was associated with a trend toward higher mortality (HR = 4.37 [CI 0.99-19.32], P = .052) that became significant when the analysis was adjusted for daily oxygenation index (HR = 1.74 [95% CI 1.12-3.35] P = .04).

CONCLUSIONS

Markedly elevated V(D)/V(T) (≥ 0.60) in early ARDS is associated with higher mortality. Measuring V(D)/V(T) may be useful in identifying ARDS patients at increased risk of death who are enrolled into a therapeutic trial.