The endotracheal tube is a guaranteed mechanism to secure a compromised airway, limit aspiration, and bring about mechanical ventilation in comatose patients. The endotracheal tube is a great method for patients who are comatose, have an obstructed airway, or need mechanical ventilation. The endotracheal tube also allows suctioning of the lower respiratory tract. Drugs that can be inserted through the endotracheal tube during cardiac arrest are discouraged. Before intubation, patients need correct patient positioning and ventilation with 100% oxygen. The purpose of ventilation with 100% oxygen is to denitrogenate healthy patients and prolong the safe apneic time. Tubes with an internal diameter of over 8mm are acceptable for most adults. Insertion technique includes visualizing the epiglottis, the posterior laryngeal structure, and not passing the tube unless tracheal insertion is ensured. Surgical airway
Surgical entry is required when the upper airway is obstructed by a foreign body, massive trauma has occurred, or if ventilation cannot be accomplished by any of the aforementioned methods. The requirement of the surgical airway is commonly known as the response to failed intubation. In comparison, surgical airways require 100 seconds to complete from incision to ventilation compared to laryngeal mask airways and other devices. During emergency cricothyrotomy, the patient lies on his back with neck extended and shoulders backward. The larynx is held in one hand by the practitioner while the other hand is holding a blade to incise the skin through the subcutaneous tissue and into the midline of the cricothyroid membrane to access the trachea.
Lown–Ganong–Levine syndrome (LGL) is a pre-excitation syndrome of the heart. Those with LGL syndrome have episodes of abnormal heart racing with a short PR interval and normal QRS complexes seen on their electrocardiogram when in a normal sinus rhythm. LGL syndrome was originally thought to be due to an abnormal electrical connection between the atria and the ventricles, but is now thought to be due to accelerated conduction through the atrioventricular node in the majority of cases. The syndrome is named after Bernard Lown, William Francis Ganong, Jr., and Samuel A. Levine. Signs and symptoms
Pathophysiology
LGL syndrome was originally thought to involve a rapidly conducting accessory pathway (bundle of James) that connects the atria directly to the bundle of His, bypassing the slowly conducting atrioventricular node. However, the majority of those with LGL in whom electrophysiological studies have been performed do not have any evidence of an accessory pathway or structural abnormality. Whilst in a minority of cases some form of intranodal or paranodal fibers that bypass all or part of the atrioventricular node can be found with subsequent conduction down the normal His-Purkinje system, in most cases the short PR interval is caused by accelerated conduction through the atrioventricular node. LGL syndrome is therefore felt to represent a clinical syndrome with multiple different underlying causes.