In the present study it was proved that the use of continuous low-pressure oxygen insufflation through venous catheter needle after thyrocricoid puncture with assisted chest compression can ameliorate oxygenation in vivo. Moreover, it could inhibit the increase of PaCO2 and reduce the accumulation of H+ ions in blood, i.e., reduction of blood pH. It is crucial that the heart and brain should be protected from the ill-effects of asphyxia, which can eventually lead to an improved prognosis. The findings from the present study suggest a simple, safe, and effective method of managing patients with asphyxia in routine clinical and surgical settings.
The prevention of the “difficult airway,” which has a potential risk of being converted into “emergency airway,” can be closely related to the safety and quality of anesthesia. With more than 30% of serious complications, the major cause of anesthesia-related morbidity and mortality can be attributed to improper airway management, which can convert “difficult airway” to “emergency airway” and may results in hypoxia and asphyxia (7). Emergency airway can occur as anesthesia induction, maintenance, extubation, recovery, and postoperative stages can differ with a variety of influential factors. Readily accessible emergency airway facilities, which maintain adequate oxygenation during emergency airway situations, are therefore essential until definitive procedures for establishing an effective artificial airway can be instituted.
As a minimally invasive and effective technique, performing thyrocricocentesis and inserting the venous needle catheter can re-establish a temporary airway in a short time, usually within 60 seconds (8). However, whether fresh oxygen insufflation through thyrocricocentesis cannulation can provide sufficient oxygen supplement and avoid asphyxia, is still unclear. Therefore, we investigated the impact of oxygen insufflation through thyrocricocentesis cannulation on blood gases, pH, and LAC of canines without effective ventilation. We further measured serum S100β protein, cTnI, CK-MB, and moisture ratio of brain tissue to demonstrate whether oxygen insufflation can prevent or reduce damage from asphyxia in canines.
Since oxygen exchange in alveolus follows the concentration diffusion theory, the alveolar-arterial oxygen difference is the primary factor that determines direction of oxygen exchange. However, the amount of oxygen exchange is mostly influenced by the areas of oxygen exchange. Alveolus, the units for pulmonary gas exchange, have a total area of nearly 130 m2 (9). In this study, we provided positive airway pressure by using fresh oxygen insufflation through thyrocricocentesis cannulation, which prevented alveolus collapse. Additionally, the pressure gradient improved the oxygen absorption in diffusion areas, promoted oxygen exchange to enhance oxygen content in serum, which increased the oxygen reserve and helped in alleviating the hypoxia status. In this study, hypoxic canines that received continuous low-pressure oxygen insufflation survived for more than 40 minutes, demonstrating that, for urgent cases oxygen insufflation through thyrocricocentesis cannulation can be helpful until definitive procedures for achieving adequate ventilation can be instituted.
However, if effective ventilation is not achieved, such an approach will result in carbon dioxide accumulation. It is believed that chest compression can reduce CO2 accumulation by thoracic movement and subsequent passive pulmonary ventilation. Therefore, continuous oxygen insufflation with combined chest compression was performed to investigate whether this method can provide sufficient oxygenation and reduce carbon dioxide accumulation. Various physiological parameters of canines including SpO2, PaO2, PaCO2, pH value, and serum LAC were measured. In our study, we found that oxygen insufflation with or without chest compression can increase the PaO2 in circulation. Furthermore, it was shown that continuous low-pressure oxygen insufflation was more effective in improving the PaO2, while oxygen insufflation combined with chest compression was more likely to keep PaO2 in the normal range. The two methods can hamper the increase of PaCO2 and the disturbance of acid-base balance, out of which, the efficiency of chest compression was particularly evident.
Hypoxia can cause injury to vital organs, specially heart and brain. In our study, we further measured S100β protein, cTnI, CK-MB, and moisture ratio in brain tissue of subjects who were treated with these two methods to investigate the influence of the two treatments in these organs.
As one of the acid calcium binding protein, serum S100β protein has a small molecular weight, and its concentration is not affected by age, hemorrhage, temperature, or heparin. The β subunit of S100β is highly specific for central nervous system (CNS) and is a specific biochemical marker of brain injury (10). Normally, S100β protein cannot pass the blood-brain-barrier (BBB) unless the brain tissue is damaged (11). In such cases, S100β protein in cerebrospinal fluid can easily pass the BBB and is detected in blood, the concentration of which has a positive correlation with the severity of injury in CNS (12). Chaparro-Huerta et.al (13) demonstrated that in neonates with asphyxia, the concentration of serum S100β protein can reflect the severity of brain injury, can be a predictor of its progression, and is closely related to the condition and prognosis of brain injury secondary to hypoxia and ischemia of brain. In this study, serum S100β protein of hypoxic canines in group B and group C was relatively high compared with the control group, which suggested that hypoxia and hypercapnia can cause damage to the BBB. However, in similar hypoxic conditions, the level of serum S100β protein of group C was lower than that of group B, which indicated that supplemental chest compression can further relieve hypercapnia-induced brain damage.
Brain edema can, to some extent, reflect the severity of hypoxia. The principal parameter to evaluate brain edema is the moisture ratio in brain tissue (14). Hypoxia may lead to dysfunction of cerebral autoregulation, which once exceeds the tolerable limit, can cause brain edema, intracranial hypertension, and even cerebral hemorrhage (15). According to the results, hypoxia can apparently worsen the moisture ratio of brain tissue in the control group. In Group B and Group C, with the same duration of resuscitation after hypoxia, moisture ratio of brain tissue was significantly higher in Group B than that of the Group C, which suggested that continuous low-pressure oxygen insufflation combined with chest compression exhibit remarkable therapeutic effects. Besides, as shown by Group C, moisture ratio of brain tissue shows no significant increase compared with the results of 2 hours or 4 hours after resuscitation, while in some cases, the values might even decrease. This indicates that supplemental chest compression can, to a great extent, alleviate hypercapnia induced brain damage, or even reverse the brain damage secondary to hypoxia, thus improving the prognosis of patients with hypoxia, and serving to provide a valuable option for managing a patient with hypoxia in the emergency department.
Cardiac troponin I (cTnI), one of the components of the cardiac troponin complex, is expressed only in myocardium; its values do not change even in cases of skeletal muscle injury (16). Normally, it cannot penetrate the cell membrane of cardiac muscle, and hence is hardly detected in plasma. When myocardial hypoxia and ischemia occur, followed by secondary degeneration and necrosis, the highly specific biochemical marker of myocardial cTnI, can enter the interstitial tissue, and is detected at early stages in circulation. Serum concentration of cTnI above 5 g/L can be regarded as myocardial lesion (17). Our study revealed that, compared with the control group, serum level of cTnI was significantly elevated in Group B and Group C. Moreover, under the same hypoxic duration, serum level of cTnI was higher in group B than in group C, which indicates that, supplemental chest compression can alleviate myocardial damage due to hypoxia and improve the tolerance limit of survival of myocardium to hypercapnia. As for CK-MB, another biomarker for myocardial injury, is released into circulation 6 hours after myocardial injury (18). However, since its fluctuation occurred after the end of our observation period, except for a significant increase of serum CK-MB in few subjects, in most subjects, the anticipated result could not be obtained.
Several limitations need to be considered when interpreting our findings. First, as this was an animal experiment, the data and results can only serve as a clinical reference. Second, experiments were restricted by the sample size and lack of repeat tests, and hence the obtained results are correspondingly short of conviction. Third, the kidneys, like heart and brain, are also highly sensitive to acute hypoxia, and further investigations will be required to investigate kidney damage in such conditions.
Taking into account the above mentioned factors, it can be suggested that thyrocricocentesis cannulation can rapidly establish a temporary airway for ventilation, prevent the symptoms of hypoxia, and attenuate the subsequent injury of vital organs.