In non-diabetic patients there is a modest increase in insulin secretion just before dawn which compensates for the increased glucose being released from the liver to prevent hyperglycemia. However, studies have shown that diabetic patients fail to compensate for this transiently increased blood glucose release, resulting in hyperglycemia. This resulting hyperglycemia is clinically relevant in diabetic patients as its lasting effects can lead to overall poor glycemic control. In Type 1 diabetics hyperglycemia due to the dawn phenomenon can persist despite adequate insulin compensation overnight, while in Type 2 diabetics the dawn phenomenon has been shown to be resistant to treatment with both oral medications and diet modifications. An "extended" dawn phenomenon has also been observed in which the abnormal increase in blood glucose levels continues after breakfast. This prolonged duration is thought to be caused by the compounding effects of absorbing and metabolizing breakfast carbohydrates during this period. Both the dawn phenomenon and its extended period have been shown to be significantly more difficult to control when a patients HbA1c is greater than 7%. Treatment
Management of the dawn phenomenon varies by patient and thus should be done with regular assistance from a patients physician. Some treatment options include, but are not limited to, dietary modifications, increased exercise before breakfast and during the evening, and oral anti-hyperglycemic medications if a patients HbA1c is > 7%. Insulin pumps can also be used to provide continuous subcutaneous infusions and are regarded as the gold standard for managing the dawn phenomenon in type 1 diabetics.
While some groups advocate PES for risk stratification in all individuals under 35 years old, others only offer it to individuals who have history suggestive of a tachydysrhythmia, since the incidence of sudden cardiac death is so low (less than 0.6% in some reports).Other methods of risk stratification include observing the ventricular rate during spontaneous atrial fibrillation on a 12-lead ECG. RR intervals of less than 250 ms suggest a higher risk pathway. During exercise testing, abrupt loss of pre-excitation as heart rate increases also suggest a lower risk pathway. However, this approach is hampered by the normal improvement in AV node conduction during exercise which can also mask pre-excitation despite ongoing conduction down the accessory pathway. Treatment
According to the ACLS protocol, people with WPW who are experiencing rapid abnormal heart rhythms (tachydysrhythmias) may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, medication may be used. Medications
WPW pattern with hemodynamically stability and orthodromic AVRT leading to a regular narrow complex tachycardia may be managed similarly to other regular narrow complex supraventricular tachycardias: first with vagal maneuvers followed by a trial of adenosine (first-line therapy). The 2015 ACC/AHA/HRS guidelines recommend beta-blockers or calcium channel blockers as second-line agents, electric cardioversion is reserved for refractory arrhythmias.