LEARNING OUTCOMES
After completing this module the paramedic will be:
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You are called to attend an adult female patient who has suddenly collapsed in the reception of a GP surgery. When you arrive, staff are performing chest compressions on the patient. You are working as a single responder and begin to lead the resuscitation attempt, using the surgery staff as part of your team.
Introduction
The resuscitation of a patient who has suffered a cardiac arrest in the out-of-hospital setting is a fundamental challenge in paramedic practice, and can indeed be seen as the foundation on which the profession has developed in recent decades. Although the overall management of patients suffering from cardiac arrest is becoming increasingly complex as our understanding of the nuance and variability of each patient develops, chest compressions remain a core treatment. This CPD article aims to focus on this treatment to help develop your understanding of why it remains such an important treatment and how it may vary in the future.
A brief history of chest compressions
In 1960, a seminal publication was released by Kouwenhoven and Knickerbocker that detailed the use of ‘external transthoracic cardiac massage’. Following multiple animal experiments and human case reports, they suggested a human survival rate of 70% in 20 patients who received the treatment. Their advice for the universal implementation of chest compressions now resounds clearly, almost 60 years on:
“Anyone, anywhere, can now initiate cardiac resuscitative procedures. All that is needed are two hands.”
However, evidence of chest compressions dates back much further when in 1868 a surgeon named John Hill working in the Royal Free Hospital in London detailed closed chest compressions. In 1892 Friedrich Maass working in Goettingen, Germany published details of performing chest compressions successfully on patients that had suffered a cardiac arrest during anaesthesia involving chloroform. This complication was usually unequivocally associated with death until interventions such as chest compressions were identified. However, the use of chest compressions dwindled as consensus recommended not using it as a treatment. It wasn't until the 1950s and 60s where it became high profile once again, remaining so today throughout healthcare systems around the world.
Cardiac arrest
Cardiovascular disease remains the leading cause of death worldwide (WHO 2012) and is the leading cause of Sudden Cardiac Arrest (SCA). This presents the majority of modern ambulance systems with a demographic of cardiac arrest patients which are typically unpredictable with presenting rhythms of Ventricular Fibrillation (VF) in approximately 25–50% of cases (Cobb et al, 2002).
A range of evidence informs modern resuscitation guidelines that recognise that prompt recognition, early and effective compressions and defibrillation are the cornerstones of all resuscitation attempts (Khalifa et al, 2015). When either of these are delayed, omitted or incorrectly provided, the likelihood of reversing the cardiac arrest falls proportionally to the length of delay.
Understanding a typical model of the cardiac arrest patient reveals the possibility of three phases following a cardiac related sudden arrest, where a shockable rhythm may present. This is more typical of the cardiac patient and less likely in patients that have experienced cardiac arrest from other causes, such as trauma, hypoxia or poisoning.
Gilmore et al (2006) detail the three phases and how they overlap following the initial arrest and relate to the possibility of a Return of Spontaneous Circulation (ROSC) in Table 1.
| Phase 1 | Phase 2 | Phase 3 |
|---|---|---|
| 0–4 minutes | 6–10 minutes | >10 minutes |
| Minimal tissue hypoxia. Early and rapid defibrillation most important intervention. Associated with greatest possibility of ROSC | Chest compressions increasingly important. Ventilation now required. Combined can lead to higher ROSC rates following defibrillation. | Likely reperfusion injury, translocation of gut bacteria, inflammation, poor survival outcome. |
However, in paramedic practice this cannot always be relied upon as a strict guide. The exact collapse time, onset of arrest, cause of arrest and the varying health status of each patient makes it unpredictable. It is useful to consider that the most effective treatment is early defibrillation when an arrest is witnessed, but if this is not possible then the use of chest compressions can lengthen the second phase and potentially delay the third phase of cardiac arrest.
The aims, phases and objectives of delivering chest compressions
Exactly how chest compressions work is not necessarily as simple as it may seem at first. It is apparent that the motion of pressing on the centre of the chest and allowing full recoil can be split into two distinct phases. Compression phase: Where pressure is applied to the chest, usually causing the chest wall to move inwards and raising intra-thoracic pressure. Decompression phase: Where the pressure is released, allowing the chest wall to naturally recoil back to its resting formation, thus reducing intra-thoracic pressure.
We also have to consider time when compressions are not being applied in resuscitation efforts. Often when small staff groups such as ambulance crews or single responders are managing the cardiac arrest patient, delays performing chest compressions may be necessary in order to manage the scene or patient safely. Even small delays associated with ventilations are associated with significantly reduced coronary artery filling due to dropping preload volumes and pressures (Berg et al, 2001). This has largely influenced modern guidelines where early, continuous and effective chest compressions with early defibrillation are now the main focus of resuscitation efforts for most patients (Khalifa et al , 2015). The exact haemodynamic process is often split between two suggested models.
Cardiac pump model
This model suggests that the heart if effectively pressed between the sternum and the spine during the compression phase of CPR. This motion squeezes blood out of the left ventricle, into the aorta and around the systemic circulation. Eventually this will lead to blood returning to the right side of the heart and pulmonary circuit. During the decompression phase, the heart is allowed to expand which causes a sucking action, drawing blood back into the ventricle. Research that has been critical of this model suggests that there is no pressure difference observed in animal models during compressions and you often have little valve closure, which would usually be expected in such flow states.
Studies on human patients experiencing cardiac arrest have been carried out following animal models. Pell et al (1994) carried out an early study using Transoesophageal Echocardiography (TOE) and found haemodynamic shifts more associated with the cardiac pump model in 18 human patients. This was also found in a similar early study of comparable size by Redberg et al (1993), who also highlighted that mitral regurgitation (with apparently healthy valves) occurred in five patients which suggests that compressions can ultimately force blood in a retrograde direction, which would be associated with poorer overall effective flow.
Thoracic pump model
The thoracic pump model is a more complex suggestion where the explanation lies with changing aortic pressures. When compression is applied, the thoracic space is reduced and a more 3 dimensional model of pressure is exerted throughout the thoracic cavity, applying force on the great vessels. There then exists a see-sawing motion of pressure gradients where it is higher in the compression phase aortic site compared to the lower pressure decompression phase. This causes a shift of blood from the chest into the extra-thoracic spaces during compressions, and then reversed with a subsequent return of blood flow during decompression. Although this same principle also applies to the venous system, the pressure gradients are less severe due to higher capacitance and the presence of valves to prevent retrograde flow.
There are a small number of studies that suggest the thoracic pump mechanism is more dominant than the cardiac pump model. Haas et al (2003) found evidence of flow consistent with the thoracic model in patients with cardiac tamponade, where direct compression of the heart may have been impeded. The likely conclusion is that a combination of both models occurs, dependant on the individual's physical thoracic shape and resistance, venous and arterial capacitance and blood volume.
Faults, challenges and errors
There are a number of factors that can contribute to ineffective resuscitation attempts. Rarely is the perfect resuscitation attempt performed, particularly in paramedic practice when resourcing, environment, training and experience of rescuer can vary enormously. Table 2 is a summary of some of those factors relating to chest compressions identified by the European Resuscitation Council's 2015 guideline update, adapted to consider specific paramedic practice.
| Error or fault | Factors | Solution |
|---|---|---|
| Bystanders starting compressions | Anxiety, delays starting with ventilations | Advise to start with chest compressions. In paramedic practice, this can often allow for the single responder to gather their thoughts and plan their management. |
| Compression depth | Muscle strength limitations, fatigue | Guide of 5-6cm to avoid under compressing. ERC recognise difficulty. |
| Hand position | Incorrect placement | Lower chest target associated with better flow - heel of hand on centre of chest, which is towards the lower chest. |
| Compression rate | Too fast or slow – anxiety, lack of pacing system | Use of metronomes. |
| Interruptions | Need to ventilate, distraction, lack of support | Emphasis on need to reduce pause to less than 10 seconds to ventilate. |
| Obese patients | Increased rescuer fatigue | Consider external compression device, requesting additional support. |
| Increased thoracic resistance | Increased rescuer fatigue | Consider external compression device, consider reversing increased resistance (air, fluid, tissue injury etc.). |
| Scene management | Lack of experience, exposure or feedback | Increased time spent in regular simulation, dedicated specialists that are targeted towards cardiac arrests. Involvement in debrief or clinical case review after the event. |
| Alternative approach | Advantages | Disadvantages |
|---|---|---|
| Mechanical Chest Device: once set up generates air or battery driven compressions to a patient | Frees up clinicians, prevents fatigue and deteriorating compression quality in prolonged arrest. | Cost and availability. No clear evidence in large trials to support its use in improving outcomes. |
| Open Chest CPR: surgical chest opening to elicit hand compression of the ventricles | Associated with improved flow and coronary perfusion in traumatic arrest or during surgery. | Skill and training issue to perform an invasive surgical intervention on a relatively rare patient group. |
| Active compression-decompression (ACD-CPR): hand held suction device that actively causes decompression on lifting | Promotes decompression filling of the great arteries. | Mixed evidence with some studies reporting improved outcomes, and others showing no difference to standard CPR. |
| Impedance threshold device (ITD): a valve that limits air entry to the lungs during the decompression phase | Promotes filling with lower intrathoracic pressure in decompression phase. | Combination of ITD & ACD showed improved but yet to be recommended in routine use. |
| Ventilation-only resuscitation | When hypoxia is the cause of arrest, such as drowning, early ventilation only may reverse cardiac arrest. | Cause of arrest not always immediately apparent. May only be useful in the early stages of resuscitation. |
| Interposed Abdominal Compression (IAC) | During chest decompression, abdominal compression is applied to promote thoracic filling. | Some mixed evidence, with the emergence of some small, positive randomised trials. |
Alternative delivery
There are a number of alternatives available to paramedics carrying out resuscitation attempts on the cardiac arrest patient. An appreciation of the importance of the quality of research is fundamental is evaluating how these alternatives might best be used in future. Ideally large sample, multi-site, randomised control trails are crucial to support or refute changes to practice as the field of resuscitation research is prone to unmeasured confounding bias or error given the chaotic nature of the events themselves. Case reports and animal studies are a useful start, but until therapies can be proven with higher levels of evidence it is sensible for the individual paramedic approaching novel or exciting changes with an open mind, until sufficient research is available to fully support its use. Below is a summary of some of the alternatives available in particular circumstances:
Conclusion
Chest compressions, together with defibrillation, are one of the few well supported interventions available to paramedics attending cardiac related sudden arrests. The exact mechanism of how they work may be unknown to many clinicians. An awareness of the factors that can reduce the effectiveness of compressions can make paramedic practice more robust. As the evidence base for high quality clinical trials increases with time, we may see alternatives either refuted or supported which may change our view further still.