Synchronizing lungs and heart during CPR
The new CCSV (Chest Compression Synchronized Ventilation) ventilation mode from WEINMANN Emergency is revolutionizing ventilation during resuscitation.
This innovation is the result of our longstanding experience in the field of emergency and transport ventilation and participation in various scientific research projects.
During chest compression, the heart and the pulmonary vessels in the lung are compressed, which also results in gas volume escaping from the lung below. Surrounded by soft tissue, the heart can thus compress only to a limited extent. The CCSV ventilation mode revolutionizes this decades-old procedure. CCSV modifies the principle of cardiopulmonary resuscitation as follows: The synchronized mechanical breath causes the thoracic pressure to additionally increase during the compression phase. As a result, no gas volume can escape, increasing the circulation of the blood. In the subsequent decompression phase, the device switches to expiration to avoid hindering venous return to the heart.
Scientific studies have shown that the principle of resuscitation with CCSV leads to an in-crease in arterial blood pressure and an improvement in oxygenation and decarboxylation in comparison to conventional ventilation under resuscitation (IPPV).
The CCSV ventilation mode can be easily integrated in the resuscitation process and is com-patible with automatic chest compression devices. This is unique in the world.
CCSV is a real innovation in emergency ventilation during resuscitation. The mode can be easily integrated in the ventilator MEDUMAT Standard² from WEINMANN Emergency and retrofitted to existing equipment.
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What is CCSV?
Chest Compression Synchronized Ventilation (=CCSV) is a ventilation mode that was devel-oped exclusively for resuscitation. CCSV applies a mechanical breath synchronized with each chest compression. With this revolutionary method, the disadvantages of conventional venti-lation modes can be avoided and the exchange of gas and hemodynamics improved.
The guidelines of the European Resuscitation Council  recommend a respiratory rate of 10/min during ongoing chest compressions and a secured airway with volume-controlled ventilation. Overall, however, the evidence for IPPV during resuscitation is limited. Furthermore, there is also a lack of specific instructions for selecting the ventilation pattern and precisely setting the ventilation parameters.
The asynchronous ventilation currently carried out with Intermittent Positive Pressure Ventila-tion (IPPV) or bilevel ventilation (BiLevel) could increase the intrathoracic pressure at the wrong moment and thus have negative impacts on hemodynamics. In this case, it should be borne in mind that neither IPPV or BiLevel were designed for use during continuous chest compressions. Accordingly, the influence of chest compressions on the feasibility of the pre-set ventilation parameters is unclear. Furthermore, the question remains whether chest com-pressions cause damage to a lung that is already filled with ventilation gas.
Chest Compression Synchronized Ventilation (CCSV) mode was developed specially and ex-clusively for use during resuscitation, and it demonstrates an extremely high degree of reliability in the implementation of the preset ventilation parameters. The synchronization of the mechanical breaths with the thoracic compressions, which is characteristic of this ventilation mode, succeeds in minimizing the above negative effects. In addition, CCSV has several positive features when compared to IPPV and BiLevel, including an improvement in gas exchange and hemodynamics, which speak to the advantages of CCSV in resuscitation. There is no conflict with the current recommendations of the ERC.
For what types of resuscitation is CCSV suitable and how does the mode work?
As soon as the patient is intubated endotracheally, CCSV can be used with MEDUMAT Standard² (with purchased and enabled flow measurement and CCSV software options).
The essential mechanisms can be divided into the categories hemodynamics and gas ex-change. 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 . Due to the compression of the chest and, subsequently, the heart between the sternum and the spi-nal column, a pressure gradient builds up, which causes an emission of blood. This mecha-nism later became known as the “heart pump mechanism”.
Chest compressions also play the key role in ventilation with CCSV. In this case, yet another principle is utilized. In 1976, Criley et al. observed that fully conscious patients who devel-oped ventricular fibrillation under monitoring were able to maintain consciousness by simply coughing . This discovery shows that a rapid increase in intrathoracic pressure can gener-ate 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 “chest 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 com-parison to IPPV and BiLevel. In summary, a higher cardial 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. Further-more, both a normal decarboxylation of the blood and a normal pH value are observed. In several animal experiments, the arterial oxygen partial pressure (PaO2) was significantly higher than under IPPV or BiLevel  .
Has CCSV already been examined in studies?
Yes. To date, a total of four studies have examined the use of the CCSV ventilation pattern. Three studies were conducted in a pig model (phase I), and another was conducted in a spe-cially developed simulation model (phase II):
Phase I: data from animal experiments (pig model)
Study 1: IPPV/BiLevel/CCSV (n=24): Exploratory study of feasibility and safety 
Study 2: IPPV-CCSV crossover (n=12): Examination of 3 CCSV settings regarding gas exchange and hemodynamics 
Study 3 IPPV-CCSV group comparison (n=44): Gas exchange, hemodynamics, cere-bral oxygenation, ROSC, post-resuscitation phase, histology 
Phase II: simulation model
• Study 4 IPPV/BiLevel/CCSV (n = 90 paramedic): feasibility of preset ventilation pa-rameters 
How does the device detect the chest compressions and in which phase are mechanical breaths delivered?
A defined low expiratory gas flow, as typically occurs at the start of each chest compression on intubated patients, is a trigger for the beginning of inspiration. The sensitivity of the trigger can be manually adjusted by the user. In this way, any necessary adaptation to particular lung characteristics is made possible.
In the novel ventilation mode CCSV, the mechanical breaths are applied simultaneously with the automatically or manually performed chest compressions. The ventilation frequency is thus identical with the compression frequency (100-120/min). Consequently, very short inspira-tory times (Tinsp = 205 ms) are observed. To achieve the positive effect on the hemodynam-ics described above, comparatively high inspiratory pressures of 60 mbar or 40 mbar are necessary (cf. figure 1). As a result, depending on the condition of the lungs, tidal volumes of 100 ml to 200 ml are achieved.
Figure 1: How Chest Compression Synchronized Ventilation (CCSV) works: Ventilation is pressure-controlled with Pinsp = 60 mbar during the compression phase of the chest com-pression (Tinsp = 205 ms). No ventilation takes place during the decompression phase.
Relatively high ventilation pressures arise during resuscitation. Are these harmful to the patient?
High airway pressures (> 40 mbar) frequently occur during conventional ventilation under re-suscitation due to the ventilation performed asynchronously to the chest compressions. Un-der certain circumstances, these pressures can even exceed 60 mbar.
In CCSV mode, the maximum airway pressures are limited to 60 mbar due to the synchro-nous, 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. Furthermore, no macroscopic or histological lung damage was observed during the use of CCSV in the animal model. 
In the studies in the pig model [4, 5, 6, 7] with a total of more than 70 test animals, after a to-tal of 30 minutes of resuscitation, no macroscopic or histological lung damage was observed that could be attributed to the use of CCSV. Accordingly, it is currently assumed that the high inhalation pressures applied do not lead to lung damage in humans.
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 ventila-tion 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 Guidelines say that hyperventilation is to be avoided. Isn't that exactly what CCSV does?
The recommendation to avoid hyperventilation is based on two hypotheses:
1. Hyperventilation during resuscitation causes a higher intrathoracic pressure during the de-compression phase. This can reduce the venous return flow to the heart. Consequently, the cardial 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, perfusion can even be improved.
Furthermore, the calculated respiratory minute volume under CCSV actually significantly ex-ceeds the known physiological values. Nevertheless, after deducting the dead space, the ef-fective ventilation volume is significantly lower. The results of studies so far show that the applied respiratory minute volume leads to normocapnia due to the low tidal volumes (ap-prox. 12 ml/kg body IBW). 
Is there then not a risk that CCSV results in only dead space being ventilated?
The results of studies so far show that the applied respiratory minute volume leads to im-proved oxygenation and normocapnia.  
Consequently, it can be assumed that CCSV results in adequate and even improved alveolar gas exchange and strong>not only dead space being ventilated.
During CCSV ventilation, the tidal volumes are actually only slightly higher than the dead space. The standard physiological understanding of ventilation is not suitable for understand-ing the gas exchange in the alveoli as a result of such small volumes. Other mechanisms are of significance in this regard. To get a better understanding of this, a comparison with High Frequency Jet Ventilation (HFJV) is most appropriate. Evans et al. state that the applied tidal volumes for HFJV are frequently less than the dead space volume of the patient being treated. 
The principles contributing to the transport of oxygen-rich gas into the alveoli and to the discharge of carbon dioxide from the alveoli in spite of low tidal volumes were described as far back as 1984 by Chang . He states that various mechanisms contribute to the transport and distribution of gas, resulting in alveolar gas exchange in spite of extremely low tidal volumes. According to Evans, the three most important mechanisms are:
- Laminar flow in the small airways, meaning that the molecules in the middle of the airways flow at a high rate, but those close to the airway walls flow only slowly
- Turbulent flow in larger airways, which can result in wider dispersion of the gas flow and improved intermingling (Taylor type dispersion)
- Pendelluft as balancing gas flow between alveolar areas with high and low time stabilizer (“fast” and “slow” alveoli) 
How is CCSV switched on in the device?
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 (image).
In the absence of chest compressions, the device automatically switches from CCSV mode to IPPV mode as back-up ventilation after a defined period of between 10 and 60 seconds and returns to CCSV when compressions begin again.
What is the effect of setting the trigger?
No mechanical breaths are delivered in CCSV ventilation mode despite chest compressions – what should I do?
Why is a PEEP required under CCSV?
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 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 inherently reached during CCSV ventilation.
Consecutive mechanical breaths are delivered in CCSV ventilation mode without chest compressions – what should I do?
In CCSV ventilation mode, only every second chest compression is followed by a mechanical breath – what should I do?
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.
Hyperventilation is suspected under CCSV – what should I do?
What happens if MEDUMAT Standard² does not detect chest compressions despite the trigger setting being corrected?
What happens if chest compressions are no longer performed due to ROSC?
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.
Can mechanical resuscitation devices also be used with CCSV?
Yes, compatibility with LUCAS, corpuls CPR and the AutoPulse has been verified. If a mechanical chest compression device is used, the setting on the device must be changed from manual chest compression to mechanical chest compression. The frequency tachometer is then gray and the frequency alarms are deactivated.
During the use of CCSV with a mechanical resuscitation device, the “Frequency high” alarm appears – what should I do?
Why does the device have to be switched from manual to mechanical resuscitation or vice-versa?
The patient has aspirated. Is it possible to use CCSV?
The CO₂ (etCO₂) value measured at the end of exhalation is relatively low, but all other measurement pa-rameters are within the standard range – why?
In principle, normocapnic values are achieved by the use of CCSV.  Because the mechanical breaths are administered at a very high frequency, the etCO2 value measured by the ventilator or defibrillator is regularly lower than during conventional ventilation under resuscitation or, under certain circumstances, cannot be measured. Consequently, it should not be interpreted 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).
 Jasmeet Soar, Jerry P. Nolan, Bernd W. Böttiger, Gavin D. Perkins, et al. (2015): European Resuscitation Council Guidelines for Resuscitation 2015. In: Resuscitation 95 (2015) 100–147
 JUDE JR, KOUWENHOVEN WB, KNICKERBOCKER GG. (1960): Clinical and experimental application of a new treatment for cardiac arrest. In: Surg Forum. 1960;11:252-4.
 J. Michael Criley, Arnold H. Blaufuss, Gary L. Kissel (1976): Cough-Induced Cardiac Compression Self-administered Form of Cardiopulmonary Resuscitation. In: JAMA. 1976;236(11):1246-1250. doi:10.1001/jama.1976.03270120022018
 Dersch, Wolfgang; Wallot, Pascal; Hahn, Oliver; Sauerbrei, Christopher; Jerrentrup, Andreas; Neuhaus, Christian et al. (2012): Resuscitation and mechanical ventilation with Chest Compression Synchronized Ventilation (CCSV) or Intermitted Positive Pressure Ventilation (IPPV). Influence on gas exchange and return of spontaneous circulation in a pig model Category: CPR Systems. In: Resuscitation 83, e3. DOI: 10.1016/j.resuscitation.2012.08.010.
 Kill, Clemens; Hahn, Oliver; Dietz, Florian; Neuhaus, Christian; Schwarz, Stefan; et al. (2014): Mechanical Ventilation During Cardiopulmonary Resuscitation With Intermittent Positive-Pressure Ventilation, Bilevel Ventilation, or Chest Compression Synchronized Ventilation in a Pig Model. In: Critical Care Medicine: February 2014 - Volume 42 - Issue 2 - p e89–e95. doi: 10.1097/CCM.0b013e3182a63fa0
 Kill, Clemens; Galbas, Monika; Neuhaus, Christian; Hahn, Oliver; Wallot, Pascal; Kesper, Karl et al. (2015): Chest Compression Synchronized Ventilation versus Intermitted Positive Pressure Ventilation during Cardiopulmonary Resuscitation in a Pig Model. In: PloS one 10 (5), e0127759. DOI: 10.1371/journal.pone.0127759.
 Speer, T., Dersch, W., Kleine, B. et al. Adv Ther (2017) In:34:2333. https://doi.org/10.1007/s12325-017-0615-7
 Evans, Elen; Biro, Peter; Bedforth, Nigel (2007): Jet ventilation. In: Continuing Education in Anaesthesia, Critical Care & Pain 7 (1), S. 2–5. DOI: 10.1093/bjaceaccp/mkl061.
 Chang, H. K. (1984): Mechanisms of gas transport during ventilation by high-frequency oscillation. In: Journal of Applied Physiology 56 (3), S. 553–563. Online verfügbar unter jap.physiology.org/content/56/3/553.