Cardiovascular complications and arrhythmias account for high mortality in cardiopulmonary patients in intensive care unites (ICU) and critical care unites. Patients in ICU are often administered with 100% oxygen for treatment with many diseases. According to American Heart Association (AHA), more than 2200 deaths related to cardiac failure are reported every day with an average of 1 in every 39 seconds. Cardiomyopathy is also reported in many diseased conditions including acute lung injury, diabetes, obesity, hypertension, and cancer. Recent studies indicate that hyperoxia induces cardiac injury due to dysfunctional lung and compromised pulmonary functioning. The exact mechanism of cardiovascular complications in ICU/ critical care remains unknown. This review will discuss the effect of hyeproxia on cardiac remodeling with more emphasis on ventricular and electrical remodeling. Understanding the exact mechanism of hyperoxia induced cardiomyopathy is not only important to understand the disease development and progression but also open new avenues for targeted therapy.
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Administration of 100% oxygen (O2) is widely used intervention in critically ill patients at Critical care or Intensive Care Units (ICU). Although O2 administration is supported by many guidelines for the patients with various medical emergencies (Anderson et al., 2007; Dickstein et al., 2008; O'Driscoll et al., 2008), the clinical implication of hyperoxia remain an important subject of debate (Altemeier & Sinclair, 2007). Recent studies indicate that hyperoxia induces cardiac injury due to dysfunctional lung and compromised pulmonary functioning (Visser, Walther, Laghmani el, Laarse, & Wagenaar, 2010). As pulmonary and cardiovascular systems are known to be in cooperative regulation, changes in cardiovascular systems may influence pulmonary function and vice versa (Howden et al., 2012b). Furthermore, smoke inhalation induced lung injury has been shown to have cardiovascular changes in previous study (Demling, Lalonde, Youn, & Picard, 1995) and continuous exposure of rabbits to hyperoxia for 72h caused elevated heart rate and low blood pressure (Sventek & Zambraski, 1988) indicating a close regulation between cardiovascular and pulmonary systems. More recent studies exploring the functional implications of hyperoxia from a cardiovascular stand point identify functional changes in heart rate and heart rate variability and linked it to polymorphisms and candidate gene loci (Howden et al., 2012b). Although the damage caused by delivering 100% oxygen treatment is to the lung and pulmonary system, patients supplemented with 96% of oxygen (hyperoxic), causes accumulation of lung fluid leading to pulmonary dysfunction causing oxidative stress in the heart. Additionally, many clinical reports indicating that hyperoxia was independently associated with increased in-hospital mortality in ICU following resuscitation from cardiac arrest, stroke, and traumatic brain injury (Damiani et al., 2014; Helmerhorst et al., 2014; Kilgannon et al., 2010; Nelskyla, Parr, & Skrifvars, 2013; Rincon, Kang, Maltenfort, et al., 2014; Rincon, Kang, Vibbert, et al., 2014).