That includes mariners [and] even many (most) rescue professionals: It is impossible to die from hypothermia in cold water unless you are wearing flotation, because without flotation – you won’t live long enough to become hypothermic. Submersion into cold water can induce cardiac arrhythmias (abnormal heart rates) in healthy people, sometimes causing strong swimmers to drown. The physiological effects caused by the diving reflex conflict with the bodys cold shock response, which includes a gasp and uncontrollable hyperventilation leading to aspiration of water. While breath-holding triggers a slower heart rate, cold shock activates tachycardia, an increase in heart rate. It is thought that this conflict of these nervous system responses may account for the arrhythmias of cold water submersion.Heat transfers very well into water, and body heat is therefore lost extremely quickly in water compared to air, even in merely cool swimming waters around 70 °F (~20 °C). A water temperature of 10 °C (50 °F) can lead to death in as little as one hour, and water temperatures hovering at freezing can lead to death in as little as 15 minutes. This is because cold water can have other lethal effects on the body. Hence, hypothermia is not usually a reason for drowning or the clinical cause of death for those who drown in cold water. Upon submersion into cold water, remaining calm and preventing loss of body heat is paramount.
Complications
Children with this condition are at a higher risk of developing the following complications:
Failure to thrive
Recurrent chest infections
Endocarditis
Epilepsy
Stroke
Arrhythmia
Heart failure
Premature deathChildren whose PAVSD is caused by DiGeorge syndrome (also known as 22q11.2 deletion syndrome) are more likely to suffer from the post-surgical complications (especially respiratory ones) associated with surgeries that treat this defect.Women with PAVSD are at a slightly higher risk of being infertile and having miscarriages or children with a congenital heart defect.Airway hyperresponsiveness is a commonly seen co-morbidity among those afflicted with PAVSD. Pathogenesis
Pulmonary atresia in PAVSD takes place during the first 8 weeks of fetal life, when the pulmonary valve that is supposed to form, fails to form, this doesnt allow blood to flow through the pulmonary artery from the right ventricle. The ventricular septal defect associated with PAVSD lets the right ventricule form.In some cases of PAVSD, major aortopulmonary collateral arteries develop; in a normal fetus, these arteries usually develop but then start deteriorating after pulmonary arteries grow, in fetuses with PAVSD, the pulmonary arteries dont develop, and this gives a chance to the major aortopulmonary collateral arteries to develop fully. Pathophysiology
The mildest variant of pulmonary atresia with ventricular septal defect involves pulmonary atresia with normally developed main pulmonary artery and branch pulmonary arteries, the blood that flows to the lungs from the right side of the heart goes to the left side of the heart through the ventricular septum which then flows through the patent ductus arteriosus.