“Science is nothing but trained and organized common sense” Thomas Huxley [1]
Over 1,250,000 incidents of sudden cardiac arrest (SCA) occur yearly, in North America and Europe, most often due to cardiac arrhythmia, rather than other cardiomyopathies which are usually preceded with symptoms and signs [2-6].
Etiologically, SCA can be identified by the abrupt discontinuity of organs’ perfusion following sudden asystole of the systemic ventricle, whether fibrillated or knocked-out, due to pathophysiological cardiac-extracardiac disorders, physiopathological events or intentionally induced; In-hospitals (IHCA) or Out-of-hospitals (OHCA) [7-14].
Current cardiopulmonary resuscitation (CPR) combines four therapeutic modalities, namely, mid-sternal chest compressions, whether manually or mechanically; mouth-to-mouth ventilation; DC shock; and invasive-CPR which includes injection of epinephrine, mechanical ventilation, extracorporeal membrane oxygenation (ECMO) known as E-CPR, implantable cardioverter defibrillators (IDC), and direct cardiac massage with cardiopulmonary bypass (CPB) under certain circumstances [15-23].
Despite progress and medical advances, the therapeutic impacts of CPR remain quite poor with a 30-day survival rate of approximately 2% [24, 25]. Most of the CPR survivors succumb within 24h after the return of spontaneous circulation (ROSC), due to multiple organs failure as result of inadequate organs’ perfusion during the procedure [26].
On the other hand, cardiac arrest has become a safe procedure, performed daily by cardiac surgeons, and in almost 100% of cases the heart defibrillates and beats again after being knocked-out for a significant length of time in patients with cardiomyopathy.
This makes CPR one of the most controversial therapeutic concept in modern medical history, which requires an entire overhaul of the concept with extensive scientific research.
Previously, we have demonstrated the benefits of prioritizing immediate restoration of circulatory flow dynamics over exhorting return of heartbeat, using a noninvasive low-pressure extracorporeal pulsatile device [27], applicable in refractory and postarrest [28].
The goal of this study is to present a new technique of chest compressions to be used in the early onsets of cardiac arrest, adaptable to cardiovascular pathophysiology and thoracic biomechanics promoting potential improvements of current CPR outcome. A safer, less traumatic, more effective procedure, which can be used by a bystander and/ or a rescuer in less exhaustive efforts, outside or inside hospital environments.
INSUFFICIENCY OF CURRENT CPR
The main goal of CPR is rapid ROSC while ensuring adequate perfusion of vital organs during the procedure. In other words, we need to create an action potential at the conducting system, particularly in the walls of the right atrium (RA) and septum, while hypothetically delivering sufficient stroke volume through the aorta by compressing / decompressing the left ventricle (LV), which is almost impossible for several reasons.
As a reminder, CPR has been adopted at random in the early 1960s, following successful experiments of a pioneering engineer while proving the concept of external defibrillators on canine models [29]. However, morphologically, dogs are sorely different from humans, which makes CPR incompatible with the pathophysiology and biophysics of our cardiovascular system. For example, with a more obtuse sternocostal angle in dogs, chest compressions are performed through the left chest wall while the canine model is placed on the right side and DC shocks are delivered in anterolateral position. Besides, dogs have a well-developed coronary network promoting more frequent ROSCs in canine models unlike human and porcine models [30].
Yet, this clinical discrepancy in CPR raises a quaternary therapeutic dilemma that must be meticulously analyzed and resolved.
For example, CPR which is supposed to effectively manage throughout four phases of cardiac arrest, namely, early onset; refractory; postarrest, and prophylaxis, collides with four concomitant pathophysiological barriers that must be overcome, which are: hemostatic state; electrophysiology; cardiotorsal anatomy; and thoracic biomechanics.
First, following the hemostatic condition, within 30 seconds of cardiac arrest, the left-heart side which normally contains ≤10% of blood volume (BV) becomes almost empty with an aortic pressure (AP) =0 mm Hg. Similarly, the adult heart which roughly contains ≤ 400 mL of BV, unequally divided between its chambers, becomes nearly empty as part of the intracardiac blood moves backward–forward through the low-pressure valveless vena cavae and the pulmonary artery. Consequently, the stagnant venous capacitance increases, and the venous pressure rises from ≤ 0mm Hg to ≥20 mm Hg [31].
Second, a heartbeat starts from within the heart by the action potential at the conducting system, particularly inside the right atrium (RA) and septum. In other words, blood flow dynamics control heartbeats, biochemically, with the combinations of neurohumoral factors that create polarization- depolarization activities at the pacemaker cells of the conducting system, and mechanically, via the pulsatile impacts of shear stress and wall stress, since the 21st day of gestation [32]. The superiority of blood flow dynamics in controlling heartbeat over the autonomic nervous system is demonstrated with the denervated hearts transplant patients [33]. Likewise, disturbed RA wall stress can induce variant types of arrhythmias, e.g., post Mustard arrhythmias [34].
Third, anatomically, the heart is anchored in the body by the great vessels (Dr. Claude Beck) [35]. As depicted in Fig.1, several centimeters separate the sternum from the free wall of the right ventricle (RV), which is followed by the interventricular septum and then the left atrium (LA) and LV. And then in case of cardiac arrest and placing the victim on a supine position the heart becomes further distant from the sternum, pushed backward by the mediastinum*.
And finally, it is also fundamental to consider, the cylindrical shell-shape thoracic cage, particularly the ribs’ orientations and their movements on the axis of their attachments between 2 hard and fixed boney structures (sternum and spines) helped by the sternocostal, costochondral, costovertebral, and costotransverse joints [36,37].
Although victims of SCA are quite diverse (e.g., gender, age, etiology, ...), however, they all share the same abovementioned pathophysiological barriers, which must be overcome.
DISADVANTAGES OF CURRENT CPR
Hemorheologically, at least a stroke volume ≥ 140 mL, delivered by the LV, in pulse pressure (syst. BP ≥80 mm Hg) and shear rate (≥ 40 / min) with a coronary perfusion pressure ≥ 15 mm Hg, are required to ensure adequate organs perfusions and promote ROSC [38]. Hence, it becomes an impossible task to achieve with CPR causing serious complications in the victims.
For example, manual or mechanical mid-sternal chest compressions are performed vigorously and strongly (e.g., ≥ 8 to 16 bar / in2), in total disregard of thoracic biomechanics, hoping to deliver stroke volumes from the distant near-empty LV through the hard bony sternum to compress movable soft mediastinal and cardiac structures. Also, the high frequency of chest compressions (≥100 bpm) restricts recoil of the thorax as well as venous return during decompression and does not adapt the capillary pressure cycle (40 bpm) [39-41]. In addition to the fact that the thoracic cage becomes more fragile, prone to trauma due to the loss of muscle tone of the intercostal muscles. As a result, mechanical CPR devices are contraindicated in pediatrics and less frequent in females due to mammary glands trauma.
Likewise, while mouth-to-mouth ventilation provides insufficient tidal volume for victims [42], the entire concept of ventilation during cardiac arrest has no substantial benefit due to the lack of gas exchange at the alveolar level.
Similarly, due to the anterolateral position of the AED electrodes, which is effective in dogs unlike humans, most DC shocks deviate from the electric field and nearly 4% reach the heart requiring more powerful energy (≥ 300 joules) for compensation. Consequently, skin burns occur in more than 25% of patients, in addition to other complications such as tachyarrhythmia, thromboembolic events and pulmonary edema have also been reported after strong DC shocks [43]. It is also important to remind that the prolonged depolarization period after strong DC shocks promotes myocardial necrosis and electroporation of the precious pacemaker cells which represent approximately 1% of cardiomyocytes [44,45].
Apart from the employment of ECMO, the benefits of the invasive-CPR procedures, remain controversial because of the hemostatic condition [46]. For example, attempts to improve cerebral perfusion with intravenous hypertonic saline and/or nitrates [47-49], did not change the significant numbers of brain damage in postarrest victims [50]. However, ECMO requires skilled squads guided by ultrasounds for its installation via empty flattened arteries, which makes its use in OHCA more difficult [51, 52].
* Cardiac surgeons used to switch-off the ventilation to avoid hurting the still beating heart during sternotomy.