FAQs about CCSV

Chest Compression Synchronized Ventilation (=CCSV) is a ventilation mode that was developed specially and exclusively for resuscitation. CCSV applies a mechanical breath synchronized simultaneously with each chest compression. With this revolutionary method, the disadvantages of conventional ventilation modes can be avoided and the gas exchange and hemodynamics improved.

The current guidelines of the European Resuscitation Council recommend a respiratory rate of 10/min with pure oxygen during professional cardiopulmonary resuscitation (Advanced Life Support, ALS) after intubation by trained staff, without interrupting chest compressions.^[1] Which type of ventilation (manual or mechanical) and which mechanical ventilation mode should be used was however not the subject matter of the currently applicable guideline reviews, so that no statement is made about this in the current guidelines.

Frequently, mechanical ventilation patterns are currently put into practice, such as Intermittent Positive Pressure Ventilation (IPPV) or BiLevel Ventilation (BiLevel), also during resuscitation, which were not developed for use during cyclical chest compressions. Through the small gas volumes in the ventilation system generated with chest compressions, the function of conventional ventilators can be significantly disrupted and preset volumes or pressures can no longer be correctly achieved. That is why the CCSV mode was developed specially and exclusively for use during resuscitation, and it demonstrates an extremely high degree of reliability in the implementation of the preset ventilation parameters. Due to the characteristic synchronization of the mechanical breaths with the chest compressions for this ventilation pattern, it succeeds in avoiding possible negative implications of the use of conventional ventilation patterns and optimizing the gas exchange and hemodynamics at the same time. As the current guidelines of the European Resuscitation Council do not issue any recommendations in favor of a specific ventilation mode, the use of CCSV during resuscitation is not contradictory to this.

Once the patient has been endotracheally intubated, CCSV with MEDUMAT Standard² can be used.

The essential mechanisms can be divided into the categories hemodynamics and gas exchange. During resuscitation, special attention is given to the restoration or maintenance of perfusion, as the functioning of vital organs directly depends on it. To this end, W. Kouwenhoven et al. (1960) describe the performance of manual chest compressions, which, in unchanged form, are nowadays still an essential part of resuscitation measures.^[2] Due to the compression of the chest, with the heart and lung organs inside it, a pressure gradient builds up, which causes an emission of blood. This mechanism later became known as the “cardiac pump mechanism”.

Chest compressions also play the key role in ventilation with CCSV. In addition, another physiological principle is utilized. In 1976, Criley et al. observed that fully conscious patients who developed ventricular fibrillation under monitoring were able to maintain consciousness by simply coughing.^[3] This discovery shows that a rapid increase in intrathoracic pressure can generate an arterial pressure. An increase in arterial pressure, in turn, causes an increase in cardiac and cerebral perfusion pressure. The mechanism described is also referred to as the “thoracic pump mechanism” and, on closer examination, can also be observed during ventilation with CCSV.

In this case, the rapid increase in intrathoracic pressure due to the delivery of the mechanical breath synchronously with the chest compressions causes a higher arterial pressure in comparison to IPPV and BiLevel. In summary, a higher cardiac and cerebral perfusion pressure and an improved organ perfusion are accordingly assumed during resuscitation with CCSV ventilation.

In the case of gas exchange, CCSV causes an improved oxygenation of the blood. Furthermore, both a normal decarboxylation of the blood and a normal pH value are observed. In several animal experiments, as well as in a randomized human study, the arterial oxygen partial pressure (PaO₂) was significantly higher than under IPPV or BiLevel.^{[5] [6] [10]}

Yes. To date, a total of 14 studies have examined the use of the CCSV ventilation pattern. Four studies on this topic have collected data on the human use of CCSV. Overall, it was demonstrated that CCSV improves both arterial and cerebral oxygenation and ensures improved CO₂ elimination compared to IPPV and bag-valve-mask ventilation. In addition, CCSV has a positive effect on hemodynamics and perfusion, particularly during prolonged resuscitation, by increasing arterial blood pressure.^{[11] [13]} There is also a trend toward improved ROSC rates and neurologically intact survival.^[12] An overview of all publications on CCSV can be found here.

High airway pressures (> 40 mbar) regularly and frequently occur during conventional ventilation under resuscitation due to the ventilation performed asynchronously to the chest compressions. Under certain circumstances, these pressures can even far exceed 60 mbar. The setting of an inspiratory pressure limit with conventional IPPV ventilation, for example, does not usually prevent these pressure peaks, as particularly at the end of the inspiratory phase, the administered tidal volume is already in the lung and is not able to escape with the very fast pressure increase at the beginning of the chest compression. This can lead to uncontrolled pressure peaks during ventilation.

In CCSV mode, the maximum airway pressures are limited to 60 mbar due to the synchronous, pressure-controlled ventilation. Furthermore, ventilation is only carried out with small tidal volumes of approx. 2 ml/kg body weight (BW). The volume load of the lungs in terms of volutrauma is therefore lower than during conventional ventilation with up to 7 ml/kg ideal body weight (IBW) and simultaneous chest compressions. 

In the studies in the porcine model with a total of more than 70 test animals, after a total of 30 minutes of resuscitation, no macroscopic or histological lung damage was observed that could be attributed to the use of CCSV or differed from the results for IPPV ventilation.^{[4] [5] [6] [7]}

In a study by Kopra et al., a higher incidence of pneumothorax was observed in the CCSV group in an animal model.^[11] This is probably due to the anatomy of the porcine thorax. Current data from human studies do not provide any indication of transferability to humans at this time.^{[10] [12]}

Another reason for this assumption is the fact that during the use of CCSV the delivery of the mechanical breath is synchronized with the compression phase of the chest compression, and consequently a defined pressure always arises in the lungs. When conventional ventilation patterns are used, asynchronous insufflation can cause a lung already filled with air to be compressed by the chest compression. In comparison to CCSV, this can even cause higher intrapulmonary pressures and potentially increase the likelihood of lung damage.

The recommendation to avoid hyperventilation is based on two hypotheses:

1. Hyperventilation during resuscitation causes a higher intrathoracic pressure during the decompression phase. This can reduce the venous return flow to the heart. Consequently, the cardiac and cerebral perfusion pressure may fall.

2. Hyperventilation produces hypocapnia, which, in turn, can have negative impacts on both the arterial pressure and cerebral perfusion.

During ventilation with CCSV, the intrathoracic pressure increases exclusively during the chest compression and not during the decompression phase, when venous return flow occurs. The feared effect of a perfusion reduction therefore does not occur. In fact, Total perfusion is even improved.

Furthermore, the calculated respiratory minute volume under CCSV actually significantly exceeds the known physiological values. Nevertheless, the effective alveolar ventilation volume is largely identical to IPPV ventilation with a tidal volume of 7 ml/kg BW and a ventilation frequency of 10/min, after deducting the dead space ventilation. This is also confirmed by data from human studies.^{[10] [12]}

The results of animal and human studies to date show that the applied minute volume leads to improved oxygenation and ventilation compared to IPPV and bag-valve-mask ventilation.^{[5] [6] [10] [12]}

Consequently, it can be assumed that CCSV results in adequate and even improved alveolar gas exchange and not only dead space being ventilated.

CCSV is only possible and approved on patients with a body weight of at least 10 kg.

During resuscitation, a high PaO₂ is preferably aimed for, as even with the best possible chest compression, the cardiac output and the tissue perfusion, particularly of the brain, are lowered significantly. Even with optimized ventilation, as with CCSV and a FiO₂ of 1.0, during resuscitation, only normal or slightly increase tissue oxygen saturation values are measured in the brain tissue. Hyperoxia is therefore not a concern. When the spontaneous circulation returns (return of spontaneous circulation, ROSC), however, tissue oxygen saturation values in the brain already rise significantly in the early reperfusion phase, which is why after ROSC, with reliably measured SpO₂ values, SpO₂ levels above 98 % should be avoided.

With CCSV, only low PEEP values of approx. 5 mbar are applied, so that there is no negative impact on venous return. Due to the exceptionally good oxygenation under CCSV, it can be assumed that PEEP under CCSV has a positive effect on therapy. 

In one of the animal experimental studies, avDO₂ was measured immediately after ROSC, which showed a significantly higher avDO₂, i.e. a higher oxygen extraction in the IPPV group compared to CCSV with similar cardiac output. This can be interpreted as an oxygen deficit, which occurred during the previous resuscitation.

Even with increased airway pressures, CCSV requires an impermeable, secured airway in order to develop its full effect. For this reason, it is only recommended to regularly use CCSV in connection with endotracheal intubation or a blocked larynx tube.

CCSV operates with a high ventilation frequency and low tidal volumes, however, these are greater than the pure dead space volume. This creates an effective alveolar respiratory minute volume that is similar to the values of IPPV, and is sufficient for eliminating enough CO₂.

By pressing the CPR button on the device, the user enters the resuscitation mode set by the operator. Depending on the presetting, CCSV mode must still be selected from the submenu. In MEDUMAT Standard², resuscitation mode (CPR mode) has the following structure:

In the absence of chest compressions, the device automatically switches from CCSV mode to IPPV mode as backup ventilation after a defined period of between 10 and 60 seconds and returns to CCSV when compressions begin again.

The trigger enables the user to change the sensitivity in detecting chest compressions. This can be set within a range from 1 to 5. With trigger level 1, the device reacts most sensitively to the chest compressions performed, while level 5 is the least sensitive setting.

• No mechanical breaths are delivered in CCSV ventilation mode despite chest compressions – what should I do?

1. Make sure that you are in CCSV ventilation mode and that all components are connected correctly.
2. Reduce the trigger level – as low as trigger level 1.
3. If mechanical breaths are still not applied, increase the PEEP.
4. If compressions are still not detected, switch to CPR-IPPV mode.

1. Make sure that you are in CCSV ventilation mode and that all components are connected correctly.
2. Reduce the trigger level – as low as trigger level 1.
3. If mechanical breaths are still not applied, increase the PEEP.
4. If compressions are still not detected, switch to CPR-IPPV mode.

The preset PEEP of 3 mbar under CCSV is used to increase the intrathoracic volume. This is especially necessary at the start of CCSV in order to generate an adequate volume flow from the lungs by means of the compressions and, consequently, an adequate trigger signal.

An increase in the functional residual capacity (FRC) by means of a moderate PEEP is useful under CCSV to recruit collapsed lung tissue through chest compressions and to ensure an adequate trigger function. This is especially the case if the FRC is reduced considerably due to obesity, significant secretion, pulmonary edema or after aspiration.

Negative impacts of a moderate PEEP are unlikely under CCSV, as an intrinsic PEEP of up to 10 mbar is reached during CCSV ventilation due to the working principle. This ensures that the alveoli are kept open at all times and that atelectasis does not occur. 

If mechanical breaths are delivered in CCSV ventilation mode without chest compressions being performed, mechanical breaths may have been wrongly triggered (autotrigger). In this case, increase the trigger level (less sensitive), e.g. from 2 to 3.

Due to the defined very low inspiratory time of approx. 200 ms and a subsequent minimum expiratory time, a correct triggering is only possible up to a maximum chest compression frequency of 140/min. If compressions are performed more frequently, only every second chest compression can be detected and synchronized. For this reason, make sure that the maximum chest compression frequency does not exceed 120/min in line with the guidelines.

Under CCSV, the tidal volumes are typically approx. 2 ml/kg (IBW). Should the tidal volumes measured by MEDUMAT Standard² significantly exceed this (> 200 ml), reduce the Pinsp from 60 mbar to 40 mbar.

If you are in CCSV resuscitation mode and the device does not detect chest compressions, the device automatically switches to backup ventilation (IPPV) and ventilation is carried out as usual.

As soon as chest compressions are no longer detected, MEDUMAT Standard² switches to IPPV back-up ventilation. As soon as MEDUMAT Standard² detects chest compressions when resuscitation becomes necessary again, the device automatically returns to CCSV mode with an inspiratory oxygen concentration of 100 % – even if the oxygen concentration has been previously manually reduced after ROSC.

Make sure that “mechanical chest compression” is set under CCSV. Should the alarm persist, increase the trigger level, e.g. from 3 to 4.

Switching is necessary, as the triggers in “mechanical” mode are optimized for mech. chest compression. In this way, an improved detection of chest compressions is possible. Furthermore, the compression frequency alarms are deactivated in the mechanical mode.

Yes, in principle, it can be used. Aspirate the airways as usual and then use CCSV. In the absence of mechanical breaths, reduce the trigger level, so that it is more sensitive, and consider raising the PEEP.

As the mechanical breaths are administered with a comparably high frequency and only small tidal volumes are used, a mixture of exhalation gas and fresh gas occurs in the ventilation system in the area of the measurement gas suction or measuring cuvette. As a result, the etCO₂ measured value of the ventilator or defibrillator is consistently lower than with conventional ventilation under resuscitation (see figure). Consequently, the value should not be used as a prognostic value.

The return of spontaneous circulation (ROSC) during chest compression and CCSV ventilation causes a significant relative rise in etCO₂, just like during conventional ventilation. A clear assessment of the actual PaCO₂ under CCSV (as is also the case with conventional ventilation under resuscitation) can only be provided by a blood gas analysis (BGA).

Aspirate the airways as usual and then use CCSV. In the absence of mechanical breaths, reduce the trigger level, so that it is more sensitive, and consider raising the PEEP.

Check the CO₂ on MEDUMAT Standard² during the analysis phase of the defibrillator. During this phase, complete expiration occurs and the device can measure the CO₂ value.