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Ventilation during CPR is still an area of debate. Perhaps, like CPR, we should be tailoring to each patient.

This is a summary of a recent view on the topic.

The key points:

  1. Tidal volumes should be > 4mL/kg. Smaller volumes do not ventilate adequately.
    1. 181 mL results in chest rise, but doesn’t overcome dead space.
  2. Ventilation rate should be a maximum of 10 breaths/min, but avoid hypoventilation.
  3. Synchronous ventilation with short breaks in CPR appears to be most beneficial, without significant blood pressure drops during the short break (keep to 5 seconds)
  4. Asynchronous Ventilation, only with endotracheal tube, due to high pressures
  5. Passive oxygenation doesn’t work, even with a Boussignac endotracheal tube
  6. Impedance threshold devices don’t add anything with conventional CPR
  7. We are unsure about PEEP, during CPR, although low levels may optimise oxygen delivery
  8. Mechanical Ventilation during CPR is an unclear area, although pressure triggered ventilation should be avoided as it can lead to hyperventilation.

The Paper
van Eijk JA et al. Ventilation during cardiopulmonary resuscitation: A narrative review. Resuscitation 203 (2024). https://doi.org/10.1016/j.resuscitation.2024.110366

What is important in Respiratory Pathophysiology during CPR

During CPR the delivery of oxygen to the tissues and the elimination of CO2 depends on:

  • Cardiac output:
    • This is a direct result of the quality of our CPR. At best cardiac output is 50% of normal. The reality is that it is only 20-30% of normal cardiac output.
  • The oxygen carrying capacity of the blood and
  • Ventilation which depends on :
    • Tidal Volume
      • Current recommendation in adults, is a tidal volume of 500-600mL
      • Please note that a tidal volume of 181 mL has been found to cause the chest to rise, however this volume is not adequate for alveolar ventilation.
      • Tidal volumes of < 4mL/kg are unlikely to significantly contribute to alveolar ventilation.
      • In a recent study, using lower volumes for ventilation ie., 365mL, was associated with a lower chance or ROSC.
    • Number of breaths delivered (No ventilation means near complete desaturation within about 2 minutes. )
      • The literature on the number of breaths can be confusing:
        • It has been shown that prolonged hypoventilation (<6 breaths/min) is negatively associated with ROSC.
        • Hyperventilation defined as > 10 breaths/min have been associated with decreased survival, although other studies show a correlation between ventilation rates and good neurological outcomes.
    • Dead space
    • Shunting

Most patients experience severe hypoxaemia, hypercapnoea and acidosis during CPR.

  • Hypoxia results in:
    • decreased myocardial contraction and
    • increased susceptibility to fibrillation
  • Hypercapnoea may be both cardio and neuroprotective. However in cardiac arrest it results in:
    • acidosis
    • decreased myocardial contractility,
    • increased pulmonary vascular resistance and
    • cerebral dilatation

CPR is a source of repetitive blunt trauma to lung parenchyma. It’s usually more pronounced with mechanical rather than manual CPR. The resultant damage that occurs affects alveolar performance, resulting in reduced ventilation/perfusion ratios.

Compression-only CPR has been proposed in non-asphyxial cardiac arrest, based on the bilief that there are oxygen reserves in the lungs and oxygen is also bound to haemoglobin. Studies have shown inconsistent results here.

The belief that ‘gasping’ and that the tidal volumes created by compression only CPR provide adequate ventilation, have also been found to be less than useful in cardiac arrest. Gasping ceases soon after the arrest and the tidal volumes that CPR generates, do not provide ventilation an they do not appear to be greater than the anatomical dead space.

How to deliver Ventilation

A patent airway is important and although endotracheal intubation is considered the gold standard, it has not been found to be superior to alternative airway techniques, such as supraglottic airway and even bag-valve-mask.

Synchronous Ventilation

Synchronous ventilation occurs when we deliver breaths during compression pauses. The time taken to deliver these breaths should be approximately 5 seconds. The evidence shows that there is no post pause drop in blood pressure for the 5 seconds needed to ventilate. Blood Pressure does drop during longer pauses.

The benefits of synchronous ventilation include:

  • Low airway pressures
  • Enhanced Ventilation
  • Decreased risk of gastric insufflation
    • Gastric Insufflation occurs during CPR, with about one third of patients aspirating during cardiac arrest.

Asynchronous Ventilation

Compressions are not interrupted for ventilation. No significant increase in survival to hospital discharge has been found.

Some of the advantages are seen to be:

  • Improvement in coronary blood flow
  • Increased alveolar ventilation

This type of ventilation delivery can result in high pulmonary pressures (> 30cm H2O) and so is advised only after an advanced airway is established.

A Few Words on Other Approaches

Passive Oxygenation during CPR

Apnoeic oxygenation, although originally found to be useful in animal studies, using a Boussignac endotracheal tube, have not shown favourable outcomes in clinical trials.

End Expiratory Pressure

Posive and Negative End Expiratory pressures have been recommended to optimise delivery of oxygen during CPR.

  • Impedance Threshold Device
    • If you are a ‘thoracic-pump model’ advocate, the belief here is that these devices allow air to escape during chest compressions, but do not allow air to re-enter with chest recoil. The theory is that this increases negative intrathoracic pressure and increases venous return and cardiac output.
    • It’s effectiveness is unclear. There was a benefit shown when used with compression/decompression devices, but no benefit with conventional CPR.
  • Positive end-expiratory Pressure (PEEP)
    • PEEP prevents alveolar collapse and improves oxygenation.
    • High PEEP may decrease right ventricular output and thus venous return.
    • PEEP at lower levels ie., 0–5 cm H2O may optimize oxygen delivery.
    • No studies have have looked at the effects of PEEP on mortality during CPR.

Mechanical Ventilation during CPR

We are unsure on the use of mechanical ventilation during CPR. Some studies show a better ventilatory status with mechanical ventilation. Pressure triggered ventilation during cardiac arrest, should be avoided as it can cause hyperventialtion and haemodynamic compromise.

Chest compression-synchronised ventilations, where a small volume breath is delivered after every chest compression, by pressure controlled triggering, is one method of mechanical ventilation beeing looked at, however there are no studies to support this.

References

  1. Corp A, et al. The cardiovascular effects of positive pressure ventilation. BJA Educ 2021;21:202–9.
  2. Dorph E, et al. Oxygen delivery and return of spontaneous circulation with ventilation:compression ratio 2:30 versus chest compressions only CPR in pigs. Resuscitation 2004;60:309–18.
  3. Spindelboeck W, S et al. Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission. Resuscitation 2013;84:770–5.
  4. Ewy GA. Cardiocerebral resuscitation: the new cardiopulmonary resuscitation. Circulation 2005;111:2134–42.
  5. Hallstrom A, et al. Cardiopulmonary resuscitation by chest compression alone or with mouth-to-mouth ventilation. N Engl J Med 2000;342:1546–53.
  6. Snyder BD, et al. Association of small adult ventilation bags with return of spontaneous circulation in out of hospital cardiac arrest. Resuscitation 2023;193:109991.
  7. Aufderheide TP, et al. Standard cardiopulmonary resuscitation versus active compression- decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial. Lancet 2011;377:301–11
  8. Levenbrown Y, et al. The effect of positive end-expiratory pressure on cardiac output and oxygen delivery during cardiopulmonary resuscitation. Intensive Care Med Exp 2020;8:36.

 

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