chapter 37 - hypo tension and syncope

8/14/2019 Chapter 37 - Hypo Tension and Syncope

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Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.

Copyright 2007 Saunders, An Imprint of Elsevier

CHAPTER 37 Hypotension and Syncope

Hugh Calkins Douglas P. Zipes

CHAPTER OUTLINE

DEFINITION

Syncope is a sudden transient loss of consciousness and postural tone with spontaneousrecovery. Loss of consciousness results from a reduction of blood flow to the reticular activatingsystem located in the brain stem and does not require electrical or chemical therapy for reversal.The metabolism of the brain, in contrast to that of many other organs, is exquisitely dependent onperfusion. Consequently, cessation of cerebral blood flow leads to loss of consciousness withinapproximately 10 seconds. Restoration of appropriate behavior and orientation after a syncopalepisode is usually immediate. Retrograde amnesia is uncommon. Syncope is an important clinicalproblem because it is common, costly, often disabling, may cause injury, and may be the onlywarning sign before sudden cardiac death (see Chap. 36) . [1] Patients with syncope account for 1percent of hospital admissions and 3 percent of emergency department visits. Elderly persons

have a 6 percent annual incidence of syncope (see Chap. 75) . Surveys of young adults haverevealed that up to 50 percent report a prior episode of loss of consciousness; most of theseepisodes are isolated events that never come to medical attention. The Framingham Study, inwhich biennial examinations were performed on 7814 individuals, reported the incidence of a firstreport of syncope to be 6.2/1000 person-years follow-up. [2] Patients who experience syncope alsoreport a markedly reduced quality of life. The prognosis of patients with syncope varies greatly withthe diagnosis. In the Framingham Study, for example, participants with syncope, including thosewith syncope of unknown origin, had increased mortality compared with participants withoutsyncope. The highest mortality was observed among those with a cardiac cause of syncope. In

Definition, 975

Classification, 975

Vascular Causes of Syncope, 975

Cardiac Causes of Syncope, 978

Neurological Causes of Apparent Syncope, 978

Metabolic Causes of Apparent Syncope, 978

Relationship Between Prognosis and Cause of Syncope,978

Evaluation, 978

History and Physical Examination, 978

Diagnostic Tests, 979

Approach to the Evaluation of Patients with Syncope, 981

Management, 982

Neurally Mediated Syncope, 983

References, 983

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contrast, the subgroup of participants with neurally mediated syncope (including orthostatichypotension and medication-related syncope) did not experience increased mortality. [2]

Classification

The causes of apparent syncopal episodes can be separated initially into two groupstruesyncope, in which the transient loss of consciousness results from cerebral hypoperfusion, and

nonsyncopal conditions, with real or apparent loss of consciousness from other causes.[1]

Table37-1 shows the differential diagnosis of syncope and nonsyncopal conditions, which are indicatedby an asterisk. Vascular causes of syncope are most common, followed by cardiac causes. Amongcardiac causes of syncope, arrhythmias are most common. The importance of consideringnonsyncopal conditions when evaluating a patient with apparent loss of consciousness cannot beunderestimated. These nonsyncopal conditions include conditions in which consciousness is lostas a result of metabolic disorders, epilepsy, or alcohol, as well as conditions in whichconsciousness is only apparently lost (i.e., conversion reaction). These psychogenic causes ofsyncope are now being recognized with increased frequency.

TABLE 37-1 -- Causes of Syncope

Vascular

Anatomical

Vascular stealsyndromes

Orthostatic

Autonomic insufficiency

Idiopathic

Volume depletion

Drug- and alcohol-induced

Reflex-mediated

Carotid sinus hypersensitivity

Neurally mediated syncope

Glossopharyngeal syncope

Situational (cough, sneeze, swallow, micturition,postprandial)

Cardiac

Anatomical

Obstructive cardiac valvular disease

Aortic dissection

Atrial myxoma

Pericardial disease, tamponade

Hypertrophic obstructive




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Although knowledge of the common conditions that can cause syncope is essential and allows theclinician to arrive at a probable cause of syncope in most patients, it is equally important to beaware of several of the less common but potentially lethal causes of syncope, such as the long-QT

cardiomyopathy

Myocardial ischemia, infarction

Pulmonary embolus

Pulmonary hypertension

Arrhythmias

Bradyarrhythmias

Sinus node dysfunction, bradycardia

Atrioventricular block

Tachyarrhythmias

Supraventricular arrhythmias

Ventricular arrhythmias (including long-QT and Brugadasyndromes)

Implanted pacemaker or implantable cardioverter-defibrillator malfunction

Neurological and cerebrovascular[*]

Arnold-Chiari malformation

Migraine

Seizure (partial complex, temporal lobe)

Vertebrobasilar insufficiency/transient ischemicattack

Metabolic [*]

Drugs, alcohol

Hyperventilation(hypocapnia)

Hypoglycemia

Hypoxemia

Psychogenic syncope [*]

Anxiety, panicdisorder

Somatizationdisorders

Syncope of unknown origin

* Disorders resembling syncope.




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syndrome, arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, idiopathicventricular fibrillation, catecholaminergic polymorphic ventricular tachycardia, short-QT syndrome(see Chap. 9) , hypertrophic cardiomyopathy (see Chap. 65) , and pulmonary emboli (see Chap.72) . [3] [4] [5] [6] [7] [8] [9] [10] It is also important to recognize that distribution of the causes of syncopevaries with age.

In young individuals, neurally mediated syncope is the most common, but is an unusual type of

syncope in elderly persons. [11] Common causes of syncope in elderly persons include orthostatichypotension, postprandial hypotension, medication, aortic stenosis (see Chap. 62) , carotid sinushypersensitivity, and bradyarrhythmias (e.g., sick sinus syndrome, heart block; see Chap. 35 ).

Vascular Causes of Syncope

Vascular causes of syncope, particularly reflex-mediated syncope and orthostatic hypotension, arethe most common causes, accounting for at least one third of all syncopal episodes. [1] [2] [11] Incontrast, vascular steal syndromes are exceedingly uncommon causes of syncope.

Orthostatic Hypotension

When a person stands, 500 to 800 ml of blood is displaced to the abdomen and lower extremities,resulting in an abrupt drop in venous return to the heart. This drop leads to a decrease in cardiacoutput and stimulation of aortic, carotid, and cardiopulmonary baroreceptors, which trigger a reflexincrease in sympathetic outflow. As a result, heart rate, cardiac contractility, and vascularresistance increase to maintain a stable systemic blood pressure on standing. Orthostatichypotension, which is defined as a 20-mmHg drop in systolic blood pressure or a 10-mmHg drop indiastolic blood pressure within 3 minutes of standing, results from a defect in any portion of thisblood pressure control system. Orthostatic hypotension can be asymptomatic or associated withsymptoms such as lightheadedness, dizziness, blurred vision, weakness, palpitations,tremulousness, and syncope. These symptoms are often worse immediately on arising in themorning or after meals or exercise. Syncope that occurs after meals, particularly in elderly people,can result from a redistribution of blood to the gut. A decline in systolic blood pressure of about 20

mmHg approximately 1 hour after eating has been reported in up to one third of elderly nursinghome residents. Although usually asymptomatic, it can result in lightheadedness or syncope.

Drugs that cause volume depletion or result in vasodilation are the most common cause oforthostatic hypotension ( Table 37-2 ). Elderly patients are particularly susceptible to thehypotensive effects of drugs because of reduced baroreceptor sensitivity, decreased cerebralblood flow, renal sodium wasting, and an impaired thirst mechanism that develops with aging.Orthostatic hypotension can also result from neurogenic causes, which can be subclassified intoprimary and secondary autonomic failure. [12] Primary causes are generally idiopathic, whereassecondary causes are associated with a known biochemical or structural anomaly or are seen aspart of a particular disease or syndrome. There are three types of primary autonomic failure (seeChap. 89) . Pure autonomic failure (Bradbury-Eggleston syndrome) is an idiopathic sporadic

disorder characterized by orthostatic hypotension, usually in conjunction with evidence of morewidespread autonomic failure, such as disturbances in bowel, bladder, thermoregulatory, andsexual function. Patients with pure autonomic failure have reduced supine plasma norepinephrinelevels. Multiple system atrophy (Shy-Drager syndrome) is a sporadic, progressive, adult-onsetdisorder characterized by autonomic dysfunction, parkinsonism, and ataxia in any combination.The third type of primary autonomic failure is Parkinson disease with autonomic failure. A smallsubset of patients with Parkinson disease may also experience autonomic failure, includingorthostatic hypotension. In addition to these forms of chronic autonomic failure is a rare acutepanautonomic neuropathy. This neuropathy generally occurs in young people and results inwidespread severe sympathetic and parasympathetic failure, with orthostatic hypotension, loss of




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sweating, disruption of bladder and bowel function, fixed heart rate, and fixed dilated pupils.

TABLE 37-2 -- Causes of Orthostatic Hypotension

Drugs

Diuretics

Alpha-adrenergic blocking drugsterazosin (Hytrin), labetalol

Adrenergic neuron blocking drugsguanethidine

Angiotensin-converting enzyme inhibitors

Antidepressants

Monoamine oxidase inhibitors

Alcohol

Diuretics

Ganglion-blocking drugshexamethonium, mecamylamine

Tranquilizersphenothiazines, barbiturates

Vasodilatorsprazosin, hydralazine, calcium channelblockers

Centrally acting hypotensive drugsmethyldopa, clonidine

Primary Disorders of Autonomic Failures

Pure autonomic failure (Bradbury-Egglestonsyndrome)

Multisystem atrophy (Shy-Drager syndrome)

Parkinson disease with autonomic failure

Secondary Neurogenic Causes

Aging

Autoimmune disease

Guillain-Barr syndrome, mixed connective tissue disease, rheumatoidarthritis

Eaton-Lambert syndrome, systemic lupus erythematosus

Carcinomatosis autonomic neuropathy

Central brain lesionsMultiple sclerosis, Wernicke encephalopathy

Vascular lesions or tumors involving the hypothalamus andmidbrain

Dopamine -hydroxylase deficiency

Familial hyperbradykininism

General medical disordersdiabetes, amyloidosis, alcoholism, renal failure




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Hereditary sensory neuropathies, dominant or recessive

Infections of the nervous systemhuman immunodeficiency virus infection, Chagas' disease,botulism, syphilis

Metabolic diseasevitamin B12 deficiency, porphyria, Fabry disease, Tangier disease

Spinal cord lesions

Adapted from Bannister SR (ed): Autonomic Failure, 2nd ed. Oxford, Oxford University Press, 1988, p8.

Postural orthostatic tachycardia syndrome (POTS) is a milder form of chronic autonomic failureand orthostatic intolerance characterized by the presence of symptoms of orthostatic intolerance,an increase of 28 beats/min or more in heart rate, and absence of a significant change in bloodpressure within 5 minutes of standing or upright tilt. [13] POTS appears to result from a failure of theperipheral vasculature to vasoconstrict appropriately under orthostatic stress. POTS can also beassociated with syncope related to neurally mediated hypotension (see later).

Reflex-mediated Syncope

There are many reflex-mediated syncopal syndromes ( Table 37-3 ). In each case, the reflex iscomposed of a trigger (the afferent limb) and a response (the efferent limb). This group of reflex-mediated syncopal syndromes has in common the response limb of the reflex, which consists ofincreased vagal tone and a withdrawal of peripheral sympathetic tone and leads to bradycardia,vasodilation and, ultimately, hypotension, presyncope, or syncope. What distinguishes thesecauses of syncope are the specific triggers. For example, micturition syncope results fromactivation of mechanoreceptors in the bladder, defecation syncope results from neural inputs fromgut wall tension receptors, and swallowing syncope results from afferent neural impulses arisingfrom the upper gastrointestinal tract. The two most common types of reflex-mediated syncope,carotid sinus hypersensitivity and neurally mediated hypotension, are discussed later.

TABLE 37-3 -- Differentiating Syncope Caused by Neurally Mediated Hypotension,Arrhythmias, and Seizures

ParameterNeurally MediatedHypotension Arrhythmia Seizure

Demographics,clinical setting

Female > malegender

Male > female gender Younger age (5sec)

Shorter duration (


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from a paradoxical reflex that is initiated when ventricular preload is reduced by venous pooling.This reduction leads to a reduction in cardiac output and blood pressure, which is sensed byarterial baroreceptors. The resultant increased catecholamine levels, combined with reducedvenous filling, lead to a vigorously contracting volume-depleted ventricle. The heart itself isinvolved in this reflex by virtue of the presence of mechanoreceptors, or C-fibers, consisting ofnonmyelinated fibers found in the atria, ventricles, and pulmonary artery. It has been proposed thatvigorous contraction of a volume-depleted ventricle leads to activation of these receptors in

susceptible individuals. These afferent C-fibers project centrally to the dorsal vagal nucleus of themedulla, leading to a paradoxical withdrawal of peripheral sympathetic tone and an increase invagal tone, which, in turn, causes vasodilation and bradycardia. The ultimate clinical consequenceis syncope or presyncope.

Not all neurally mediated syncope results from the activation of mechanoreceptors. In humans, it iswell known that the sight of blood or extreme emotion can trigger syncope. These observationssuggest that higher neural centers can also participate in the pathophysiology of vasovagalsyncope. In addition, central mechanisms can contribute to the production of neurally mediatedsyncope.

CAROTID SINUS HYPERSENSITIVITY.

Syncope caused by carotid sinus hypersensitivity results from stimulation of carotid sinusbaroreceptors, located in the internal carotid artery above the bifurcation of the common carotidartery. Carotid sinus hypersensitivity is diagnosed by applying gentle pressure over the carotidpulsation just below the angle of the jaw, where the carotid bifurcation is located. Pressure shouldbe applied for 5 to 10 seconds. It is important to perform carotid sinus massage in both the supineand upright positions. The main complications associated with performing carotid sinus massageare neurological. Because of this, carotid sinus massage should be avoided in patients with priortransient ischemic attacks, strokes within the past 3 months, and carotid bruits.

A normal response to carotid sinus massage is a transient decrease in the sinus rate, slowing ofatrioventricular (AV) conduction, or both. Carotid sinus hypersensitivity is defined as a sinus pause

longer than 3 seconds in duration and a fall in systolic blood pressure of 50 mmHg or more. Theresponse to carotid sinus massage can be classified as cardioinhibitory (asystole), vasodepressive(fall in systolic blood pressure), or mixed. Carotid sinus hypersensitivity is detected inapproximately one third of elderly patients who present with syncope or after falls. [1] [15] It isimportant to recognize, however, that carotid sinus hypersensitivity is also commonly observed inasymptomatic elderly patients. [16] Thus, the diagnosis of carotid sinus hypersensitivity should beapproached cautiously after excluding alternative causes of syncope. Once diagnosed, dual-chamber pacemaker implantation is recommended for patients with recur-rent syncope or fallsresulting from carotid sinus hypersensitivity. [17] [18]

Cardiac Causes of Syncope

Cardiac causes of syncope, particularly tachyarrhythmias and bradyarrhythmias, are the secondmost common causes, accounting for 10 to 20 percent of syncopal episodes (see Chap. 35) .Ventricular tachycardia (VT) is the most common tachyarrhythmia that can cause syncope.Supraventricular tachycardia can also cause syncope, although the great majority of patients withsupraventricular arrhythmias present with less severe symptoms, such as palpitations, dyspnea,and lightheadedness. Bradyarrhythmias that can result in syncope include sick sinus syndrome aswell as AV block. Anatomical causes of syncope include obstruction to blood flow, such as amassive pulmonary embolus, an atrial myxoma, or aortic stenosis.

Neurological Causes of Apparent Syncope




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Neurological causes of apparent syncope, including migraines, seizures, Arnold-Chiarimalformations, and transient ischemic attacks, are surprisingly uncommon, accounting for lessthan 10 percent of all cases of syncope. Most patients with an apparent neurological cause ofsyncope have seizures rather than true syncope.

Metabolic Causes of Apparent Syncope

Metabolic causes of syncope are rare, accounting for less than 5 percent of syncopal episodes.The most common metabolic causes of syncope are hypoglycemia, hypoxia, and hyperventilation.Establishing hypoglycemia as the cause of an apparent loss of consciousness requiresdemonstration of hypoglycemia during the syncopal episode. Although hyperventilation-inducedsyncope has been generally considered to be caused by a reduction in cerebral blood flow, thisremains an area of debate. Hyperventilation-induced syncope may also have a psychologicalcomponent. Psychiatric disorders may also cause syncope. Up to 25 percent of patients withsyncope of unknown origin may have psychiatric disorders for which apparent syncope is one ofthe presenting symptoms. [1]

Relationship Between Prognosis and Cause of Syncope

The prognosis for patients with syncope varies greatly with the diagnosis. Syncope of unknownorigin or syncope with a noncardiac cause (including reflex-mediated syncope) is generallyassociated with a benign prognosis. In contrast, syncope with a cardiac cause is associated withup to 30 percent mortality at 1 year. [1] [2]

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chapter 37 - hypo tension and syncope

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