Is it possible to faint while sleeping

While almost always frightening to the person it happens to as well as those witnessing the event, it can be caused by serious life-threatening abnormalities of the heart but often is due to conditions that, in and of themselves, are not life-threatening or are totally benign. Obviously, if or when it occurs, it is prudent to get proper medical evaluation immediately. Cardiac Causes. Arrhythmias Syncope can be due to abnormally fast, slow or irregular heart beats arrhythmia , where the heart is unable to deliver adequate blood flow to the brain.

Structural heart disease Significant heart valve disease can also lead to syncope, most commonly aortic stenosis. Primary blood pressure problems If blood pressure drops enough especially if it drops rapidly , from whatever the cause, inadequate blood flow to the brain can occur leading to syncope. Vasovagal Syncope. This is the medical term for the typical and most common type of fainting episode in an otherwise healthy and often young person in a particular situation.

Thus it is also referred to as situational syncope and when it occurs repeatedly in someone is known as vasodepressor or neurocardiogenic syncope. It classically occurs during uneasy, scary or embarrassing situations, or during blood drawing or seeing the sight of blood , coughing, urination or defecation. It might be more likely to occur if the patient is relatively dehydrated, is exposed to extreme heat, has been standing for a long period of time, is sleep deprived or is under a lot of stress.

After fainting due to a vasovagal episode, it is not uncommon for the person to have cold or clammy skin. Clinical Evaluation. The majority of syncopal episodes are either unexplained or classified as vasovagal. If the patient is otherwise healthy, they usually have a favorable prognosis.

If they have underlying cardiac disease, there is a much higher likelihood of a serious cause and the need for more extensive medical and cardiac evaluation is warranted. Cardiologists are often asked to evaluate patients with syncope. In rare instances where someone keeps fainting but goes months between episodes with previously negative medical work-ups and episodes occurring when they are not wearing any type of monitoring device , an implantable cardiac event monitor might be warranted that lasts up to 2 years so that the heart rhythm can be recorded during episodes.

What Is Fainting? Why Do People Faint? Here are some of the common reasons for fainting: Physical triggers. What Are the Warning Signs of Fainting? If you think you're going to faint, you can try to stop it by taking these steps: If possible, lie down.

This can help prevent a fainting episode, as it lets blood get to the brain. Be sure to stand up again slowly when you feel better — move to a sitting position for several minutes first, then to standing.

Sit down with your head lowered forward between your knees. This will also help blood get to the brain, though it's not as good as lying down.

When you feel better, move slowly into an upright seated position, then stand. Don't let yourself get dehydrated. Drink enough liquids throughout the day. Drink plenty of fluids before, during, and after exercise and in hot weather. Keep blood circulating. If you have to stand or sit for a long time, take breaks often and move around. Regularly tense your leg muscles or cross your legs to help improve blood flow. Avoid overheated, cramped, or stuffy environments , whenever possible.

Classic teaching is that upright posture is a prerequisite for vagally mediated syncope VMS and that syncope in the supine position has more sinister causes. We present five patients, three males and two females, with a mean age of Four patients also had a history of classic upright syncope. Based on their clinical features and thorough investigations, we excluded other causes of loss of consciousness and diagnosed these patients to be having VMS in the supine position sleep fainting.

We further describe the management and follow-up of these patients. A diagnosis can be established if there is clinical suspicion, preserved left ventricular function without evidence of coronary artery disease, no high-risk electrocardiographic evidence of pre-excitation, long or short QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia, and normal neurological work-up. Syncope is defined as a transient loss of consciousness due to cerebral hypoperfusion with recovery being spontaneous and instantaneous [ 1 - 2 ].

Of all the causes of syncope, neurocardiogenic, or vagally mediated syncope VMS is the most common [ 4 ], with syncope secondary to cardiac causes having the worst prognosis [ 5 ]. The upright posture leads to pooling of blood in the legs and the visceral circulation, reducing cardiac preload and output, thereby activating the sympathetic and inhibiting the parasympathetic system [ 6 - 7 ].

Contraction of an inadequately filled ventricle leads to stimulation of cardiac mechanoreceptors which leads to decreased sympathetic and increased parasympathetic response through the brainstem causing bradycardia, hypotension, and syncope [ 8 - 9 ]. This is classically noted in the upright posture, being rare in the supine posture due to adequate maintenance of cerebral perfusion due to gravity [ 10 ].

However, recent literature now supports the hypothesis that both vagally mediated hypotension and cardioinhibition can be noted while in a supine position. Furthermore, this phenomenon is not an uncommon observation in hospital settings in which the patient is supine, such as while venepuncture is performed and vagal symptoms are noted [ 15 ]. Similarly, during anesthesia when the patient is unconscious, similar vagal slowing is noted.

This is observed especially during pelvic and ophthalmic surgeries [ 16 ]. We report five cases where the patients experienced unexplained supine fainting — a brief unarousable state during sleep or a loss of consciousness while awake and supine. We describe the details and similarities in the clinical accounts. A year-old woman with a history of asthma on intermittent inhaler use came in with one episode of unarousable loss of consciousness.

She was noted to have irregular breathing that alarmed the mother who was sleeping next to her. She called for help and the brother then tried to wake her up but she was not arousable. According to the account, she was sweating profusely and had labored breathing. She spontaneously started breathing normally and started coming around. Her post-event recovery was less than five minutes.

She was brought to the hospital. She is a nurse by profession and was doing her normal ward duties and reports no remarkable event in her history that would have suggested volume loss or prolonged hemodynamic stress. Her examination was unremarkable and there was no postural drop in blood pressure BP. She was admitted under neurology; her blood and electrolyte work-up was normal and she underwent a complete neurological work-up. She was then referred to cardiology at which point it was noted that she had pre-excitation on the electrocardiogram ECG.

She was taken to the catheterization lab where she underwent an electrophysiological EP study that induced an orthodromic atrioventricular tachycardia. Atrial fibrillation was induced through rapid atrial pacing but could not be sustained and no ventricular arrhythmias were inducible without or with dobutamine provocation. Ablation of a left posteroseptal pathway was carried out. The earliest ventricular signal was tracked during tachycardia and ventricular pacing but ablation at the earliest position suppressed accessory pathway conduction only to recur every time.

After extensively mapping the right side and the coronary sinus, the ablation was stopped. She was put on flecainide and calcium channel blockers and was discharged. After a few weeks, she had a similar episode and was brought to the hospital. She then underwent a head-up tilt HUT test on suspicion of vasovagal mechanism of syncope, which came out positive with nitrate provocation. Her post-ictal phase was reported by her to be an exact replication of her clinical symptoms.

The flecainide and calcium channel blockers were discontinued as the mechanism of her fainting was identified to be vasovagal and not a cardiac arrhythmia. She was prescribed hydration, counter-maneuvers which she practiced inconsistently , and preventive measures. Since the last episode, she has done well but experiences recurrences. A year-old woman, married with four children, presented to the clinic with a history of four episodes of unresponsiveness. Two were in an upright posture in the morning hours while she was preparing breakfast for her children.

The other two were while she was sleeping and her husband discovered that her breathing pattern had become irregular. He tried to arouse her but could not do so. He reported that she was sweating profusely. She recovered in less than five minutes but was too weak to move and had abdominal cramps and a desire to defecate. The first such episode was short and she had not sought medical help.

After the second episode, she was seen at a cardiology tertiary care center. Her exam and basic laboratory work were unremarkable. She did not have a postural drop in BP. Her ECG showed normal sinus rhythm with frequent ventricular ectopy of the right ventricular outflow tract origin. An echocardiogram revealed structurally normal heart with preserved left and right ventricular functions. In view of ventricular tachycardia as a cause of her syncope, she was offered an EP study and ablation.

She was brought to the EP laboratory, where her rhythm was normal sinus rhythm and no ectopy could be induced despite isoprenaline provocation. She was then discharged on calcium channel blockers. At the time of her visit, she was doing well and had no ventricular ectopy.

She underwent a HUT test which was positive with nitrate provocation. She stated that her symptoms on the HUT table were consistent with the ones that she had been experiencing during the episodes. She was prescribed hydration, counter-maneuvers and preventive measures. Since the last episode, she has not had any recurrence. A year-old man who is a hospital worker came to the clinic with three successive syncopal attacks, all in the morning hours.

One was noted while he was supine and got up from sleep. He was sweating profusely according to him and it was witnessed by his wife. He felt nauseous and had an abdominal gripe and passed out while in bed. He recovered spontaneously after a few minutes while his wife tried to revive him. On examination, he did not have a postural drop in BP.

His ECG was within normal limits and an echocardiogram was conducted which was normal. His blood and biochemical work-up were normal. He underwent a HUT test which was positive with nitrate provocation. He was reassured and sent home with advice to remain hydrated, apply counter-maneuvers and exercise.

After his clinic visit, he had another episode of supine fainting and this time his wife raised his legs and he reports that despite experiencing the same symptoms, the duration of the episode was abbreviated. He has done well since the institution of regular hydration and exercising the counter-maneuvers, though he still experiences recurrent episodes.

A year-old man presented to us with three episodes of loss of consciousness. He had an aortic valve replacement with a metallic valve a few years ago and did not have any other cardiac risk factors and was fairly active.