The highest rates of drowning globally are among children under five, and young children should be supervised, regardless of whether they can already swim. The danger increases when they are alone. A baby can drown in the bathtub, in the toilet, and even in a small bucket filled with less than an inch of water. It only takes around 2 minutes underwater for an adult to lose consciousness, and only between 30 seconds and 2 minutes for a small child to die. Choosing supervised swimming places is safer. Many pools and bathing areas either have lifeguards or a pool safety camera system for local or remote monitoring, and some have computer-aided drowning detection. Bystanders are also important in detection of drownings and in notifying them (personally or by phone, alarm, etc.) to lifeguards, who may be unaware if distracted or busy. Evidence shows that alarms in pools are poor for any utility. The World Health Organization recommends analyzing when the most crowded hours in the swimming zones are, and to increase the number of lifeguards at those moments. Learning to swim:  Being able to swim is one of the best defenses against drowning. It is recommended that children learn to swim in a safe and supervised environment when they are between 1 and 4 years old. Learning to swim is also possible in adults by using the same methods as children.
Later in the progression, a prolonged QT interval may be indicative of fibrosis. Given that diabetic cardiomyopathys definition excludes concomitant atherosclerosis or hypertension, there are no changes in perfusion or in atrial natriuretic peptide levels up until the very late stages of the disease, when the hypertrophy and fibrosis become very pronounced. Pathophysiology
Defects in cellular processes such as autophagy and mitophagy are thought to contribute to the development of diabetic cardiomyopathy. Diabetic cardiomyopathy is characterized functionally by ventricular dilation, enlargement of heart cells, prominent interstitial fibrosis and decreased or preserved systolic function in the presence of a diastolic dysfunction.While it has been evident for a long time that the complications seen in diabetes are related to the hyperglycemia associated to it, several factors have been implicated in the pathogenesis of the disease. Etiologically, four main causes are responsible for the development of heart failure in diabetic cardiomyopathy: microangiopathy and related endothelial dysfunction, autonomic neuropathy, metabolic alterations that include abnormal glucose use and increased fatty acid oxidation, generation and accumulation of free radicals, and alterations in ion homeostasis, especially calcium transients. Additional effects include inflammation and upregulation of local angiotensin systems. Diabetic cardiomyopathy may be associated with restrictive (HFPEF) and dilated phenotypes (HFREF). HFPEF results predominantly from hyperinsulinemia, hyperglycemia, lipotoxicity, AGEs and microvascular rarefication. HFREF is associated with autoimmunity, hyperglycemia, lipotoxicity, microvascular rarefication and AGE formation. Microangiopathy
Microangiopathy can be characterized as subendothelial and endothelial fibrosis in the coronary microvasculature of the heart. This endothelial dysfunction leads to impaired myocardial blood flow reserve as evidence by echocardiography.