Use of Oxygen Supplementation Therapy on Acute Coronary Syndrome

Answer

Use of Oxygen Supplementation Therapy on Acute Coronary Syndrome

For more than 100 years, inhaled oxygen (O₂) has been administered to patients who have been suspected of having acute myocardial infarction (MI). The basis for this practice has been informed by the fact that oxygen supplementation increased usually-deficient arterial oxygen content in patients to better their individual myocardial oxygenation, thus minimizing infarct size (Cabello et al., 2016). Studies have, however, shown that this assumption is not proof-based and conditional. Whereas such physiological changes in patients may relate to some patients who are hypoxemic, substantial data suggests that oxygen therapy may have some harm on people. Thus, current acute coronary syndromes (ACS) guidelines, supplementary oxygen should only be initiated on a patient if a patient is breathless, a condition referred to as hypoxemia( SpO2 < 94%), or when a patient exhibits signs of shock or heart failure ( Level IV evidence ANZCOR Guideline 14.2, 2016). It is against this background that this study aims at discussing published evidence regarding oxygen administration therapy to ACS and determine whether it would be justifiable to change or maintain the oxygen administration therapy to both Mr. Hertz and Mika’s management.

One of the widely accepted therapies for hypoxaemic patients is oxygen supplementation. This is attributed to the fact that oxygen therapy increases the delivery of oxygen to a person’s cells and is, therefore, believed to reverse the impacts of hypoxia (Nakashima & Tahara, 2018). However, the worth of oxygen therapy in patients having preserved oxygen saturation is yet not known; further, it may even be dangerous under some circumstances (Cabello et al., 2016). Hypoxaemic patients benefit from insufflation of oxygen since hypoxia can minimize brain and general ischemia (Stone et al., 2015).

Notwithstanding the fact that the elevation of in a person’s dissolved oxygen can raise the supply of oxygen to their tissues, it can as well better the formation of reactive oxygen species (ROS) (Kone, 2011). Stone et al. (2015) explain that these highly reactive molecules, which are outcomes of a person’s normal oxygen metabolism, can result in substantial damages to a person’s cells. In the case of ischaemia, ROS has been shown to be a crucial factor in post-ischaemic harm, since they trigger inflammation and leucocyte chemotaxis (Sukumalchantra et al., 2012). ROS can also destroy a person’s electron transport intricacies in their mitochondria (Conti, 2009), and an increased level of ROS in experimental ischaemia along with reperfusion effect a person’s cell death (Bodetoft et al., 2016).

Regarding the interaction between a person’s cardiac myocytes and vascular smooth muscle cells, myocytes that are left exposed to high concentrations of oxygen produce considerably increasing amounts of angiotensin I, thus enhancing a person’s vascular tone (Burls et al., 2011). Nonetheless, myocytes that are exposed to low concentrations of oxygen secret adenosine, thus minimizing a person’s vascular tone (Bodetoft et al., 2016). These studies suggest that myocytes in a person’s blood functions as oxygen sensors as well as help in the modulation of a person’s vascular tone in accordance with the needs of the person’s myocardium, thus restricting adverse impacts of hypoxia along with the widespread formation of ROS. Other harmful effects of ROS, according to Nakashima and Tahara (2018), are associated with their electrophysiological implications, oxidative stress with hydrogen peroxide enhances early after-depolarization as well as triggered activity, thus induces lethal kinds of arrhythmia, like ventricular fibrillation and ventricular tachycardia.

Clinically, medical data regarding the value of administration of oxygen in MI. Experiments in this regard that used animals showed a beneficial impact of high oxygen in MI. For instance study found out that an inspired oxygen fraction of o.4 resulted in a decrease in ST-segment elevation, ischaemic injury, and myocardial creatine phosphokinase levels in animals. Evidently, higher fractions of inspired oxygen was not found to further better a person’s myocardial injury (Nakashima & Tahara, 2018). In another study using animals, it was shown that oxygen reduced the animals’ infarct size by 39% and also increased their post-reperfusion ischaemia ejection fraction (EF), and these findings  led the research’s authors to postulate that high-oxygen tension minimizes myocardial ischaemia, notwithstanding the danger of exacerbating the animal’s reperfusion injury via lofty free radical levels (Gao et l., 2011).

Recent clinical researches have examined the impacts of very high levels of oxygen suing hyperbaric oxygen, which entails the intermittent inhalation of 100 oxygen at > 1 atmosphere of pressure. Treatment functions to elevate a person’s plasma oxygen concentration, an effect that can increase or normalize oxygen tension in an animal to hyperoxic levels in ischaemic tissues (Stone et al., 2015). Two randomized experiments in MI patients have shown conflicting results concerning the impacts of oxygen, despite both being treated with thrombolysis. One of the studies, which enrolled 74 patients, showed a substantial fall in the end-systolic volume index by 21% and bettered cardiac output by 11% (Sukumalchantra et al., 2012). Contrarily, a study that enrolled 112 patients showed a shorter time to pain-relief as well as a non-substantial increase in ejection fraction (EF), with no substantial fall in CPK levels (Shuvy et al., 2013). The study also indicated that left ventricular stiffness and diastolic properties were equally unaffected by oxygen administration therapy.

Along with medical efficacy of oxygen administration therapy in patients with ACS, its haemodynamic and cardiovascular effects have been studied, with most studies showing that oxygen therapy does not have beneficial haemodynamic impacts and is even dangerous. In normoxaemic patients with MI, oxygen therapy minimizes people’s cardiac output and stroke volume (SV) besides increasing systematic vascular resistance (SVR) (Nakashima & Tahara, 2018). According to Burls et al. (2011), in hypoxaemic patients with ACS or MI, oxygen therapy increased their cardiac output, while another study indicated that the administration of 100% oxygen in ACS or coronary artery disease (CAD) patients resulted in a rise of the patients’ lactate production presumably as a result of decreased coronary flow.

Let us now consider the management of Mr. Hertz and Mika. From the foregoing literature, it is evident that there is no clear evidence between when supplementary oxygen or no oxygen is administered to a patient with reference to mortality.  Bodetoft et al. (2016) suggest withholding routine high oxygen concentration supplementation (8L/min) in normoxic patients with ACS except for patients with MI, severe respiratory failure, chronic obstructive pulmonary disease, central cyanosis, or dyspnea resulting from any other cause. Additionally, according to Level IV evidence ANZCOR Guidline 14.2 (20016), oxygen administration is to be initiated only on patients who in hypoxemia state. However, from the medical report regarding Mika, it was noted that he only had mild shortness of breath, with a respiratory rate of 20 breaths per minute. Similarly, it was noted that Mika’s evaluation showed no evidence of jugular venous distention and that Mika’s lung examination was normal. Without the administration of oxygen, the case reveals that Mika responded well to the treatment that he was offered at the care facility’s emergency department. Based on the aforementioned Level IV evidence ANZCOR Guidline 14.2 (20016) and Bodetoft et al. (2016)’s findings, there is no compelling reason to administer oxygen therapy to Mika.

Further, despite registering mild shortness of breath and respiratory rate 20 breaths minute, being well perfused, having pulse, and registering capillary return 2 seconds, along with a blood pressure of 122/52, oxygen therapy is completely not administered to Mika even though he was presented with chest radiating to his back. While oxygen, through nasal cannula or face mask, is usually administered to patients who are suspected to have ACS or AMI in attempts to increase the patients’ myocardial oxygenation as well as to minimize their infarct sizes (Gao et l., 2011), there is no justified reason to administer oxygen to Mika since he is not in the hypoxemia condition.

Considering the case Hertz, after being administered with oxygen therapy for pain relief, it is reported that he again suffered pain the same night even when under the oxygen administration. This implies that oxygen therapy was ineffective in managing Hertz’s pain condition. Having been subjected to other treatment options, Hertz is finally better and thus released. Since he is to stay at home as he further recuperates, oxygen therapy would not be a good choice for the management of his condition because the treatment requires an intensive care provision that cannot practically be achieved when a patient is at home (Bodetoft et al., 2016). Lastly, since Hertz is not in the hypoxia condition, it is against the Level IV Guidelines on oxygen administration to patients. For these reasons, it is justifiable to change Hertz’s oxygen administration therapy to another therapy, especially now that he has been discharged to his home where he cannot be able to get the oxygen therapy. Similarly, I would change the therapy because from literature and evidence from Hertz’s management, it can be seen that the therapy may reduce a patient’s perfusion and cardiac blood flow, minimize the patient’s cardiac output, as well as increases the patient’s coronary vascular resistance (Shuvy et al., 2013). If myocardial reperfusion in a patient is attained, oxygen may in some cases have a paradoxical impact by triggering reperfusion harm via generation of oxygen free radicals (Cabello et al., 2016).

To conclude, there is sufficient justification for changing oxygen administration therapy to both Mr. Hertz and Mika’s management. It has been shown that acute oxygen therapy may raise a person’s blood pressure as well as lowering cardiac index, cardiac oxygen consumption, heart rate, and blood flow in the person’s renal and cerebral beds. Additionally, oxygen may as well lower an individual’s capillary density as well as redistribute blood in the person’s microcirculation. Several studies also show that these changes happen in human beings. In patients with ACS and stable coronary disease, the administration of oxygen may constrict the patient’s coronary vessels, worsen ischemia, and lower the person’s myocardial oxygen. This explains why other studies have appeared to change in favour of oxygen administration only in hypoxemic patients.