BY MIKE McEVOY
Your paramedic engine company responds to an 81-year-old woman who “passed out” while dining at a local restaurant. Bystanders report the patient slumped forward into her salad and remained unconscious for several minutes. The patient is alert and oriented and slightly diaphoretic and declines treatment or transport. She has a history of hypertension, is taking some “blood pressure pills,” and has never fainted before.
Across town, a rescue company responds to a reported 26-year-old man down in the bathroom at his residence. On arrival, his wife reports finding him unconscious in the bathroom after he awoke to urinate. He is awake and slightly confused. He has no past medical history and is a marathon runner.
At a funeral for a fallen firefighter, a 41-year-old brother in the honor guard passes out in a lineup where he had been standing at attention for 25 minutes. He quickly regains consciousness and is slightly dizzy when assessed by fire department paramedics.
The above scenarios involve syncope, a sudden and temporary loss of consciousness usually resulting in collapse from loss of muscle tone. It is typically followed by rapid and complete recovery. Syncope is a common problem and tends to be quite alarming for the patient, witnesses, friends, family, and health care providers. Roughly one-third of the population will have a syncopal episode at some point in their lifetime. It becomes more common with advancing age; the incidence nearly doubles at age 70. Syncope accounts for up to three percent of emergency department visits. In larger studies, men and women had equal incidences, although other studies show slightly greater occurrence in females.1 For the purposes of evaluation and treatment, work up and treat patients with presyncope exactly the same as patients with syncope. Usually, patients with presyncope present with complaints of dizziness.
A SYMPTOM, NOT A DIAGNOSIS
Syncope is a symptom, not a diagnosis. The causes of syncope can be elusive and tricky to find. For the fire EMS provider, the first step in evaluating a patient with suspected syncope is to differentiate it from other causes of loss of consciousness such as epilepsy, trauma (such as a concussion or intracerebral bleeding), hypoglycemia, hypoxia, drug overdose, and intoxication. Most of these are associated with more prolonged loss of consciousnessthat is, they are not brief and don’t tend to be followed by a rapid, spontaneous recovery. It is important to mention that transient ischemic attacks (TIAs) are rarely associated with syncope. They are more often characterized by neuro deficits without loss of consciousness.2,3
Photo by Keith D. Collum.
To cause the loss of consciousness seen with syncope requires some mechanism resulting in significant hypoperfusion to the brain. Three mechanisms that might cause this are sudden loss of cerebral blood flow for six to eight seconds, a decrease in systolic blood pressure below 60 mmHg, and a 20-percent drop in oxygen delivery to the brain. Normally, moving from a lying or seated to a standing position shifts up to a liter of blood into the venous vessels below the diaphragm. A drop in blood pressure is normally prevented by compensatory autonomic nervous system changes such as vasoconstriction. Failure of these compensatory mechanisms can result in syncope.
SYNCOPE OR SEIZURE?
Seizures are frequently mistaken for syncope; between five and 15 percent of syncope cases are actually seizures. Seizures not associated with tonic-clonic activity, those that are not witnessed, and those affecting patients for whom a good medical history is unobtainable can easily be mistaken for syncope when seizure is the actual cause of unconsciousness. (1) Adding to the diagnostic problem, anything the interrupts cerebral blood flow (i.e., all the other causes of syncope) can lead to seizure activity. Seizure activity can follow ventricular arrhythmias, cardiac arrest, and a host of other events in which syncope leads to seizure activity. There are some helpful clues for differentiating the two. The easiest is not available to EMS: an electroencephalograph (EEG) that displays a slowing pattern instead of an epileptic spike-like pattern. Recovery speed is another helpful clue. The postictal state following an epileptic seizure is longer, whereas syncope-related causes of unconsciousness typically have a quick and complete return to alertness. It is also helpful to look for soft tissue injury at multiple sites, such as the tongue or scalp, that results from tonic-clonic seizure movements. Loss of bowel or bladder control is more commonly seen in seizure than syncope.4
The second task in evaluating a patient with true syncope is to attempt to determine if there is a clear life-threatening cause. Although it might seem that it would require sophisticated testing to make such a determination, the truth is that up to 50 percent of patients with syncope have a cause readily determined by history and physical assessment alone. (4) Much of the remaining syncope cases will ultimately be determined as syncope of unknown origin. Separating syncope into causes is helpful for both treatment and prognostic purposes. Vasovagal attacks are the most common cause of syncope (18 percent) and have a fairly benign prognosis. These are followed closely by cardiac causes (14 percent), which have much poorer prognosis. Half of all patients with cardiac-related syncope will suffer a cardiac arrest and die within five years; one-third will die within the first year following their syncopal episode. (1) Note that the presence of a cardiac condition does not necessarily mean that a syncopal episode was cardiac in nature. From a risk perspective, cerebrovascular causes of syncope, although uncommon, also have a poor prognosis. Excluding cardiac and cerebrovascular causes generally points to a benign cause with little risk for bad outcomes.
Evaluating a patient for life-threatening causes of syncope should be sequential and should consider five conditions:
1 Cardiac syncope. Cardiac causes represent the most frequently occurring life threat associated with syncope. They can range from arrhythmias to valve abnormalities, tamponade, pacemaker malfunction, and ischemia. As mentioned previously, patients with cardiac-caused syncope are at high risk for sudden death. Patients with a history of heart failure (HF) who experience syncope have an even higher risk for sudden death and warrant special attention.
2 Bleeding. Hypotension induced by hypovolemia can produce syncope. Evaluate patients for traumatic blood loss, gastrointestinal bleeding, ruptured or leaking aortic aneurysm, and ruptured ectopic pregnancy or ovarian cyst. History, physical exam, and orthostatic vital signs will reveal acute blood loss from bleeding.
3 Pulmonary embolism. Although rare, shock resulting from a significant pulmonary embolus can produce syncope. Signs would include hypotension, low oxygen saturation, tachycardia, and (usually) shortness of breath.
4 Subarachnoid hemorrhage. Patients who experience syncope after complaining of headache need to be evaluated for subarachnoid bleeds. This usually requires a CT scan.
5 Anaphylaxis. Usually, anaphylaxis presents with pronounced respiratory, cardiovascular, and cutaneous (skin) symptoms. Occasionally, it may occur with only a profound drop in blood pressure and no other symptoms. This can manifest as syncope. Such a life-threatening allergic presentation occurs most frequently with venomous insect bites or stings and intravenous medication allergies, although it can be triggered by other allergens. Prompt and aggressive treatment can prevent a fatality.
Although most of these life-threatening causes can be detected by history and physical exam including vital signs, cardiac-related causes can be elusive. Rhythm disturbances most often occur without warning, unlike patients with vasovagal or other causes of syncope. Patients with bradycardias, in addition to reporting no warning symptoms, are prone to injury with their events. Patients with tachycardias often report palpitations. A 12-lead EKG should be performed and may reveal an arrhythmia but, because rhythm disturbances are common in the general population, does not always point to the cause of syncope. The most common rhythm-related cardiac causes of syncope are sinus bradycardia, AV nodal blocks, sustained ventricular tachycardia (VT), and supraventricular tachycardias (SVT).5 Syncope that occurs while sitting or lying down is particularly suspicious for arrhythmia.
Although it is uncommon to see cardiac causes of syncope in younger patients, sudden cardiac death in the pediatric population frequently happens in children with specific 12-lead EKG findings. Familiarity with 12-lead patterns reflective of long QT syndromes and prolonged QRS durations seen with hypertrophic cardiomyopathy (HCM) can be helpful when evaluating syncope in children.6
In patients without life-threatening causes, syncope results from vasovagal (also called neurocardiogenic) causes most of the time (25 to 65 percent of all syncope cases). This category includes numerous triggers, has significant bradycardia or hypotension associated with the loss of consciousness, and is usually accompanied by a prodrome prior to loss of consciousness. Patients may experience dizziness, a warm feeling, sweats, nausea/vomiting, abdominal pain, or pallor as a prodrome prior to loss of consciousness.
There are numerous triggers for vasovagal syncope including situational (e.g., from a blood draw or other emotional stressor), micturition (while urinating with a full bladder), defecation (during bowel movement), cough-mediated causes, and prolonged standing (exceeding 15 minutes in one position). A variant of neurocardiogenic syncope is carotid sinus hypersensitivity and results from external pressure to the neck from shaving, sudden head or neck turning, or a tight collar. Syncope is a reflex response from a hypersensitive carotid sinus.
Orthostasis is another benign and fairly common cause of syncope, accounting for between five and 24 percent of all cases. It is most often seen with sudden changes from a lying to a standing position and can be associated with either hypovolemia or failure of the autonomic nervous system to quickly compensate for change in position. Medications may contribute to orthostatic syncope.
Syncope is a uniquely human phenomenon; animals do not faint.7 Although common, up to half of all patients with syncope don’t seek medical care. Although up to one-third of patients who do seek medical attention will not have a clear cause of their syncope identified, the most common cause is a vasovagal event. Patients with vasovagal syncope have a very low risk of adverse outcomes. History that includes a prodrome, perhaps an identifiable trigger, an unremarkable physical exam, and normal EKG, point to low risk and little likelihood of adverse outcomes.
The risks to patients with life-threatening causes of syncope are so significant that assessment should begin with a thorough search for these causes. Several studies have examined variables that might identify patients at greater risk of adverse outcomes in attempts to stratify which patients require more thorough testing and evaluation (i.e., admission to a hospital). The most comprehensive of these to date produced the San Francisco Syncope Rule (SFSR). (4) Significant predictors of bad outcomes in the SFSR are history of heart failure, abnormal EKG (non-sinus rhythm or new changes), a hematocrit under 30, shortness of breath, or a systolic blood pressure under 90 mmHg. Other studies have also found value in advancing age and syncope without prodrome as predictors of adverse outcomes.
The three opening cases all appear to have been caused by syncope. Although two cases appear to have a classic vasovagal cause, it is prudent to consider life-threatening causes before jumping to conclusions.
Faced with any syncope patient, from a young, otherwise healthy firefighter to a stubborn elderly woman seen in the community, the assessment tips contained here can help to conduct a focused and comprehensive assessment, attempt to determine a cause, and guide appropriate treatment and transport decisions.
1. Olshansky B. “Pathogenesis and etiology of syncope.” In UpToDate Web site, Ganz L.I. (Ed), Waltham, MA (2008), www.uptodate.com.
2. Petkar S., Fitzpatrick A., Cooper P. “Transient loss of consciousness (excluding epilepsy).” Medicine, 2008; 36: 531-534.
3. Carreno M. “Recognition of nonepileptic events.” Semin Neuro, 2008; 28:298-304.
4. McDermott D., Quinn J. “Approach to the adult patient with syncope in the emergency department.” UpToDate Web site, Hockberger R.S. (Ed), Waltham, MA (2008), www.uptodate.com.
5. Olshansky B. “Management of the patient with syncope.” In UpToDate Web site, Ganz L.I. (Ed), Waltham, MA (2008), www.uptodate.com.
6. Bar-Cohen Y., Silka M.J. “Sudden cardiac death in pediatrics.” Curr Opin Pediatr, 2008; 20: 517-521.
7. van Dijk J., Sheldon R. “Is there any point to vasovagal syncope?” Clin Auton Res, 2008; 18:167-169.
MIKE McEVOY, Ph.D., REMT-P, RN, CCRN, is the fire EMS technical editor for Fire Engineering, a critical care nurse, an instructor in critical care medicine, and a member of the Pharmacy and Therapeutics Committee at Albany (NY) Medical Center. McEvoy is also the EMS coordinator for Saratoga County, New York, and chief medical officer for the West Crescent (NY) Fire Department.