Syncope, Vertigo, and Sudden Cardiac Arrest

Amy D. DiVasta

Mark E. Alexander

SYNCOPE

Cardiac symptoms in adolescents and young adults (AYAs) are very common; true cardiac disease is not. Syncope is a frequent complaint, often raising concerns of future sudden cardiac arrest (SCA).¹ The clinician’s critical task is to distinguish between benign and significant syncope. The epidemiology almost always favors innocent causes.

Etiology

Syncope is a sudden, transient loss of consciousness and postural tone, lasting several seconds to a minute, followed by spontaneous recovery. Syncope is common, particularly among adolescent females aged 13 to 18 years.¹,² Any condition that leads to decreased cerebral perfusion may cause syncope.

Classification

There are three major categories of syncope: (1) neurocardiogenic, including vasovagal/reflex and postural orthostatic tachycardia; (2) cardiovascular, including structural and arrhythmogenic; and (3) noncardiovascular, including epileptic and psychogenic. Vertigo or seizures are generally obvious on initial evaluation, though the symptoms can overlap.

Syncope of unknown origin (i.e., simple syncope) and neurocardiogenic syncope account for 85% to 90% of events.³,⁴,⁵ Ineffective cerebral blood flow, resulting from inadequate cardiac output, leads to loss of consciousness. Only 1% to 5% of patients have significant cardiac disease. Seizures or psychiatric diagnoses account for a small minority of episodes.

History and Physical Examination

An accurate diagnosis stems from a detailed history (including family history) and thorough physical examination. Key elements of the history include (1) onset and frequency of episodes; (2) circumstances, such as exercise, posture, or other precipitating factors; (3) prodromal symptoms, including dizziness, diaphoresis, nausea, pallor, palpitations, chest pain, dyspnea; (4) complete or incomplete loss of consciousness, duration, time to recovery; (5) abnormal movements, incontinence, or injury; (6) past medical history and medications; and (7) family history of sudden death (particularly if <40 years old), similar episodes, or early onset of heart disease.

“Warning signs” that suggest a more serious etiology include syncope during exercise, syncope in a supine position, family history of sudden death, personal history of cardiac disease, or an event precipitated by a loud noise, intense emotion, or fright. The physical examination should include at least a brief neurologic assessment and a dynamic cardiac examination performed with the patient in multiple positions to evaluate for a pathologic murmur.

Table 15.1 presents a differential diagnosis for a syncopal event. Common etiologies are discussed below.

Neurocardiogenic Syncope

Neurocardiogenic syncope (i.e., vasovagal syncope) is the most common form of syncope.

Duration: Few seconds to minutes.
Onset: Gradual, typically with a prodrome.
Etiology: Precipitating factors (fear, anxiety, pain, hunger, overcrowding, fatigue, injections, sight of blood, prolonged upright posture) are usually identifiable.
Prodromal symptoms: Nausea, dizziness, visual spots or dimming, feelings of apprehension, pallor, yawning, diaphoresis, and feelings of warmth.
Syncopal event: Brief loss of consciousness with gradual loss of muscle tone.
Syncopal seizures: Rarely, a brief period of opisthotonus will occur following syncope.
Recovery: Rapid (<1 minute to consciousness), though residual fatigue, malaise, weakness, nausea, and headache are common
Pathophysiology: Neurally mediated syncope results from a combination of inappropriate peripheral vasodilation and cardiac slowing, resulting in a transient period of inadequate cerebral (and other organ) blood flow. Fainting restores cerebral blood flow and permits the reflexes to return to normal.
Specific situational syncope syndromes including needle phobia, hair brushing syncope, stretch syncope, micturition syncope, and post-tussive syncope require minimal investigation.
There is likely some decline in the preponderance of neurocardiogenic syncope and a small increase in the frequency of “adult” causes of syncope as AYAs age into their mid- to later 20s. This shift in disease frequency is subtle, but will influence diagnostic approaches.

Diagnostic Evaluation of Neurocardiogenic Syncope

AYAs with a true syncopal event should undergo a thorough history, physical examination, and electrocardiogram (ECG).⁶ A normal diagnostic screen (reassuring history, benign examination, and
normal ECG) is generally sufficient to exclude cardiac disease.⁷ Further testing is needed only if concerns of cardiac or neurologic disease continue.

TABLE 15.1 Differential Diagnosis of a Syncopal Event

	Typical/Vasovagal	Cardiac	Atypical/Conversion	Vertigo
Position	Upright	Supine or upright	Either	Change in position
Prodrome	Frequent	None	Variable	Rare
Duration	<1 min	<1 min longer really aborted arrest	Minutes	Brief, may cluster
Color	Pale	May be normal	Flushed/normal	Normal
Visual symptoms	Gradual dimming	Abrupt dimming	Variable	Room spinning
Exercise	Post exertional or no relationship	Peak exercise	Variable	Uncommon
Palpitations	Hard	Rapid, precedes faints	Variable	Uncommon
Injury/incontinence	Rare	Moderately frequent	Rare	Rare
Frequency	Isolated or episodic	Isolated or episodic	Often very frequent	Episodic
School disability	Rare	Rare	Frequent	Rare
Family history	Possibly “fainting” but otherwise negative	Often positive		Rare
ECG	Normal or nonspecific PR < 220 QTc < 460 Right atrial enlargement Borderline LVH	T wave inversion QTc > 480 WPW QRS > 120, bundle branch block	Normal or nonspecific	Normal or nonspecific
Comments	Borderline ECG findings likely nonspecific though consultation appropriate	Often established cardiac diagnosis	Typical event as a trigger

Routine laboratory investigation, electroencephalogram (EEG), or intracranial imaging is not needed.
Echocardiogram has very low yield for routine evaluation; it should be utilized to evaluate exertional syncope or syncope with high-risk features. There will be a 5% to 10% incidence of incidental, unrelated findings.⁸
Exercise testing is required if syncopal episodes occur during exercise.
Tilt table testing: Specificity is poor (35% to 100%) and sensitivity is variable (75% to 85%); 40% of healthy AYAs have a positive tilt test. Head-up tilt testing has fallen out of favor because of these poor test characteristics.
Ambulatory ECG monitoring can be useful for correlating symptoms and rhythm. The choice of monitoring (Holter monitor, external loop recorder, implantable loop recorder) requires consideration of symptom frequency, severity, and a need for more precise data.
When situational triggers are identified, either behavioral or medical therapies aimed at those triggers are appropriate. Common examples include syncope triggered by dysmenorrhea/crampy abdominal pain or events following phlebotomy.

Management of Neurocardiogenic Syncope

Management includes (1) reassurance; (2) hydration and caffeine/alcohol avoidance; (3) recognition of prodromal symptoms and preventative techniques, including assumption of supine position or postural tone (isometric contractions of the extremities, folding the arms, or crossing the legs); (4) upright, weight-bearing exercise; (5) drug therapy for refractory cases that do not respond to supportive therapy (Table 15.2). Generally, a 12-month symptom-free interval is considered a reasonable duration of treatment; subsequently, a trial off medication is warranted.

Postural Orthostatic Tachycardia Syndrome

Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous disorder of autonomic regulation. Patients complain of fatigue, dizziness, and exercise intolerance with upright position. POTS is characterized by a marked pulse change (>40 bpm) or excessive tachycardia (>120 bpm) with upright position. AYAs have sufficient tachycardia that there is typically little or no blood pressure change. POTS is likely a result of both ineffective vascular constriction with standing (hence an appropriate tachycardia) and exaggerated sympathetic response. This physiology is created in normal subjects with spaceflight or even modest periods of bed rest. Chronic fatigue syndrome and POTS overlap considerably.⁹ Treatment includes fluids and vasoconstrictors for symptom relief. β-Blockers are also commonly used. The heterogeneity of therapy options reflects the variable physiology and diagnostic criteria utilized in POTS, and the lack of clear “best practice” treatment for the condition. Though often difficult to implement, slowly progressive physical reconditioning may be the most important therapy.¹⁰

Orthostatic Hypotension

Orthostatic hypotension (drop in systolic blood pressure >20 mm Hg or drop in diastolic blood pressure >10 mm Hg with upright posture) is less common in AYAs. Etiologies of orthostatic hypotension include pregnancy, malnutrition, volume depletion, medication side effects, or neurologic disorders.

TABLE 15.2 Pharmacologic Treatment Options for Neurocardiogenic Syncope

Drug		Dose	Proposed Mechanism of Action	Side Effects	Quality of Data
Fludrocortisone		0.1-0.2 mg/d	↑ Renal Na⁺ absorption	Bloating or edema
			↑ Circulating blood volume	Hypokalemia	+
				Hypertension
Midodrine		5-10 mg q4h	α-Agonist	Piloerection
		Maximum four doses/d	↑ Peripheral vascular resistance	Scalp pruritus
				Hypertension	++
				Urinary retention
				Difficult adherence to treatment
β-Blockers			Blocks excess sympathetic response (paradoxical effect)	Fatigue
	Atenolol	25-50 mg daily		Depression	±
	Metoprolol	25-50 mg b.i.d.
SSRIs			↑ Extracellular serotonin leads to downregulation of receptor density	Headache
	Fluoxetine	20 mg daily		Insomnia	±
	Sertraline	50 mg daily		GI effects
+, moderate data to support efficacy; ++, strong data to support efficacy; ±, mixed data to support efficacy. SSRIs, serotonin reuptake inhibitors; GI, gastrointestinal.