Near-Syncope After Exercise

Home , Carotid bruit, Syncope (medicine)

GRAND ROUNDS CLINICIAN’S CORNER AT THE JOHNS HOPKINS BAYVIEW MEDICAL CENTER

Roy C. Ziegelstein, MD Syncope and near-syncope are great diagnostic challenges in medicine. On CASE PRESENTATION the one hand, the symptom may result from a benign condition and pose A 72-year-old man complained of near- little or no threat to health other than that related to falling. On the other syncope after exercise that had been oc- hand, syncope or near-syncope can be the manifestation of a serious un- curring for several months. Every morn- derlying condition that poses an imminent threat to life. Patients with a car- ing, he walked at 3.5 mph for about half diac cause of syncope are at far greater risk of dying in the first year after an an hour on his treadmill in the well- ventilated basement of his home. After episode of syncope or near-syncope than individuals with a noncardiac cause. exercising, he would step off the tread- A cardiac cause of syncope should be considered in every patient with syn- mill, check his pulse, and become light- cope or near-syncope, but it is particularly common in older patients or in headed immediately afterward. This feel- patients with known structural heart disease, arrhythmia, or certain electro- ing lasted a few minutes and he would cardiographic abnormalities. Although many diagnostic tests may be help- then go upstairs to eat breakfast and take ful in the evaluation of syncope and near-syncope, the history, physical ex- his medications. amination, and electrocardiogram pinpoint the cause in many circumstances. The patient was referred to me shortly after a very severe episode that almost re- Syncope after exercise may be due to left ventricular outflow tract obstruc- sulted in loss of consciousness. During tion from aortic stenosis or hypertrophic obstructive cardiomyopathy but can that episode, he stepped off the tread- also suggest the diagnosis of postexercise hypotension in which an abnor- mill and tried to feel his pulse as usual. mality in autonomic regulation of vascular tone or heart rate results in va- He then felt that he was losing his pe- sodilation or bradycardia after moderate-intensity aerobic activity. The pa- ripheral vision and thought he would fall. tient discussed in this case highlights the importance of the clinical history He stopped feeling his pulse and eased in the evaluation of this condition, since the diagnosis was revealed as the himself down to the floor without los- patient’s story was described and eventually acted out. ing awareness of his surroundings. Af- ter a few minutes, he felt better and JAMA. 2004;292:1221-1226 www.jama.com walked around the room to “cool down.” amination results were entirely unre- ties during the recording and exercised During the initial evaluation, the pa- markable. Notably, his blood pressure normally on his treadmill in the morn- tient said that he was otherwise well. He and pulse were normal and there was no ing. He reported that he thought every- denied headache, difficulty with speech, significant change in either when he as- thing was the same that day as always, weakness, chest discomfort, shortness of sumed the upright posture. Electrocar- although he did deviate from his rou- breath, palpitations, or lightheaded- diogram results were also normal. tine slightly and did not take his pulse ness either during exercise or at other The patient was sent home with a 24- after exercise because he knew his heart times except immediately after exer- hour ambulatory electrocardiogram rate was already being monitored elec- cise. His medical history was remark- (Holter monitor), and plans were made tronically. He also noted that he did not able only for hypertension. Four years for an exercise treadmill test in the very experience lightheadedness after exer- earlier, a stress test and echocardio- near future. The patient was asked to per- cise on that occasion. gram, performed as part of a routine car- form all his usual activities while wear- diovascular evaluation, were both nor- ing the Holter monitor. Specifically, he Author Affiliation: Department of Medicine, Divi- mal. He was regularly taking vitamin E sion of Cardiology, Johns Hopkins Bayview Medical was asked to exercise on the treadmill in and a combination of hydrochlorothia- Center, Johns Hopkins University School of Medi- his basement as usual. The Holter moni- cine, Baltimore, Md. zide and triamterene. His physical ex- Corresponding Author: Roy C. Ziegelstein, MD, De- tor recording was completely normal and partment of Medicine, Division of Cardiology, Johns demonstrated the expected increase in Hopkins Bayview Medical Center, 4940 Eastern Ave, CME available online at heart rate with exertion. The patient said Baltimore, MD 21224-2780 ([email protected]). www.jama.com Grand Rounds Section Editor: David S. Cooper, MD, that he engaged in all his usual activi- Contributing Editor, JAMA.

sciousness. Given the importance of the tality of patients with a cardiac cause of Box 1. Causes of Syncope clinical history in the evaluation of syn- syncope is 2 to 5 times that of patients 2,3 Cardiac or Cardiopulmonary cope and near-syncope and sensing that with noncardiac syncope. In particu- Causes a clue was revealed by the absence of lar, it is important to consider poten- Arrhythmias symptoms during Holter monitoring, I tially lethal or imminently lethal condi- Aortic stenosis asked the patient to describe his epi- tions like ventricular tachycardia, rapid Hypertrophic obstructive sodes in detail again and the diagnosis supraventricular tachycardia, torsades de cardiomyopathy became apparent. pointes in the setting of congenital or ac- Aortic dissection quired long QT syndrome, myocardial Myocardial ischemia DISCUSSION ischemia, or critical aortic stenosis. A car- Pericardial tamponade Syncope is one of the greatest diagnos- diac cause of syncope is particularly com- Pulmonary embolism tic challenges in medicine. While the mon in older patients or in patients with Pulmonary hypertension cause is often benign with no imminent structural heart disease, a history of ar- Noncardiac Causes threat to the patient other than that due rhythmia, or who have certain electro- Neurally mediated reflex syndromes to physical injury as a result of falling, it cardiographic abnormalities (BOX 2).4,5 Vasovagal faint is sometimes a sign of a potentially le- Given this, older patients like the 72- Micturition or defecation syncope thal condition such as critical aortic ste- year-old man or patients with a history Postprandial hypotension nosis, hypertrophic obstructive cardio- of heart disease should be considered to Orthostatic hypotension myopathy, or ventricular tachycardia. have a cardiac cause of syncope until Cerebrovascular steal Syncope is a sudden loss of conscious- proven otherwise. Although the his- Conditions Frequently ness, usually accompanied by falling due tory, physical examination, electrocar- Misdiagnosed as Syncope to loss of postural tone, with subse- diogram, and normal stress test and echo- Hypoglycemia quent spontaneous recovery. It is typi- cardiogram from 4 years earlier made a Epilepsy cally due to a transient global decrease cardiac cause less likely in this patient Cataplexy in blood flow to the brain for more than despite his age, the patient was sent home Vertebrobasilar transient ischemic 8 to 10 seconds. The inadequate blood with a 24-hour ambulatory electrocar- attacks flow to the brain is most often caused by diographic recording device and plans systemic hypotension resulting from in- were made for an exercise treadmill test adequate vasoconstriction, hypovole- in the near future, given the relation- mia, decreased venous return, an abrupt ship of his symptoms to exercise. Exer- Box 2. Electrocardiographic change in heart rate, or an acute de- cise stress testing is a particularly valu- Features Suggesting a Cardiac crease in cardiac contractility. “Near- able part of the evaluation of patients Cause of Syncope syncope” or “presyncope” are terms used with exertional syncope or near- Atrial fibrillation or flutter when the patient feels as if loss of con- syncope. The normal response to tread- Multifocal atrial tachycardia sciousness is about to occur but does not. mill exercise is a progressive increase in Paced rhythm The major causes of syncope are systolic blood pressure and no change or Frequent premature ventricular listed in BOX 1 and may be separated a decrease in diastolic blood pressure; a contractions into conditions that are primary car- drop of the systolic blood pressure dur- Ventricular arrhythmia diac or cardiopulmonary and those that ing exercise below the standing pre- Bundle branch block 1 Left ventricular hypertrophy are noncardiac. Some conditions are exercise value typically defines exercise- 6 Pathologic Q waves indicative of frequently misdiagnosed as syncope induced hypotension. Exercise- prior myocardial infarction (Box 1) since they also produce a tem- induced hypotension during treadmill Mobitz II or higher atrioventricular porary disturbance of consciousness testing often reflects left ventricular dys- block that may result in loss of postural tone. function or myocardial ischemia. When Wolff-Parkinson-White syndrome Although an individual with one of associated with either of these 2 factors, these conditions may resemble a pa- it indicates a significantly increased risk tient with true syncope, the impaired for cardiac events.6 Echocardiography to Although I was still concerned about consciousness in these disorders does rule out structural heart disease was also a cardiac cause of near-syncope, one of not result from sudden transient global considered in this patient, but was not the leading diagnostic considerations at cerebral hypoperfusion.1 performed as the initial diagnostic test this point was postexercise hypoten- One of the first tasks when evaluat- because his echocardiogram was com- sion (PEH), a condition in which a pa- ing someone like this patient is to deter- pletely normal 4 years earlier and his tient’s blood pressure falls rapidly and mine whether there is a cardiac cause of physical examination and electrocardio- significantly after exercise, resulting in the patient’s symptoms. This distinc- gram were normal during the current lightheadedness or even loss of con- tion is important because the 1-year mor- evaluation.

The patient history is of critical impor- not completely offset by an increase in tance in determining the cause of syn- cardiac output. The hypotension that re- Box 3. Conditions Producing cope and can often obviate the need for sults may last several hours.12,13 The Effort Syncope extensive diagnostic testing. The his- mechanism of the peripheral vasodila- Left ventricular outflow tract tory, physical examination, and base- tion occurring after exercise is not clear, obstruction line electrocardiogram provide a diag- although various factors have been im- Aortic stenosis nosis in 50% of patients with syncope.7 plicated including impaired sympa- Hypertrophic obstructive When approaching a patient like the man thetic vasoconstriction,14,15 resetting of cardiomyopathy presented in this case, it is important to the arterial baroreflex control of heart Right ventricular outflow tract clarify the relationship of symptoms to rate after exercise,16 and increased ni- obstruction 17 Pulmonary valve stenosis exertion. Exertional syncope usually tric oxide production. Infundibular stenosis indicates one of the cardiac or cardio- Less commonly, PEH may result from Pulmonary hypertension 8 pulmonary causes shown in BOX 3. Left marked bradycardia or asystole after Arrhythmia or right ventricular outflow tract obstruc- exercise in otherwise healthy individu- Myocardial ischemia tion and pulmonary hypertension pro- als.18-20 This appears to be due to a va- duce effort syncope because in these con- sovagal reaction that relates to activa- ditions, cardiac output is unable to tion of the so-called Bezold-Jarisch as if on a treadmill, then stopped and im- increase in response to the increased reflex.21 During exercise, the vigorous mediately put his hand on his neck to peripheral demand of exercise. This, contractions of an underfilled heart may check his pulse. He was asked to stop the coupled with the fall in peripheral resis- initiate an inhibitory vasovagal reac- demonstration. The patient was then tance during exercise, may lead to effort tion by stimulating ventricular mecha- asked to lie on the examining table and syncope.9 However, in some circum- noreceptors whose nonmyelinated C- continuous electrocardiographic and stances, a patient with one of the con- fibers carry afferent inputs to the blood pressure monitoring was initiated. ditions shown in Box 3 may have few or medulla. The efferent response slows the After recording a rhythm strip, gentle ca- no symptoms during exercise if sympa- heart rate and counteracts the sympa- rotid sinus pressure was applied by the thetic tone increases sufficiently dur- thetic response by increasing parasym- examiner.Thisresultedina5-secondven- ing effort to limit or prevent the fall in pathetic neural input to the heart via the tricular pause. The patient said he felt the peripheral vascular resistance that ordi- vagus nerve. After exercise and with- same way during this maneuver as he did narily occurs at this time. Symptoms may drawal of the sympathetic response, a after exercise. His blood pressure mea- then only begin after exertion, once the person with this type of PEH may have sured 15 seconds after initiation of the ca- increase in sympathetic tone is with- significant slowing of the heart rate or rotid sinus pressure was normal. drawn. Although a cardiac cause of syn- asystole and lose consciousness. cope was initially suspected in this Postexercise hypotension was an im- Carotid Sinus Hypersensitivity patient, significant cardiac or cardiopul- portant consideration in this patient be- The history and examination in this pa- monary disease was considered very cause of the constant and predictable tient provided the diagnosis of carotid si- unlikely because of the complete absence relationship between the onset of his nus hypersensitivity (CSH), which was of symptoms during exercise and his nor- symptoms and the cessation of exer- first reported as a cause of syncope by mal physical examination results. cise, and because this diagnosis is more Weiss and Baker more than 70 years common in older individuals with ago.22 Carotid sinus hypersensitivity has Postexercise Hypotension chronic hypertension. However, there been reported as the cause of syncope in The patient presented in this case did not was a particular feature of this pa- 5.8% of patients in one study23 and 14% experience symptoms during exertion tient’s near-syncope that was striking. in another.24 These studies may overes- and only noted any problems after ex- After interviewing the patient again, the timate the role of CSH as a cause of syn- ercise. This initially suggested a diag- consistent temporal relationship of his copal events and may more accurately re- nosis of PEH. Lightheadedness after ex- symptoms to the act of taking his pulse flect the prevalence of an abnormal ercise may be caused by hypovolemia or after exercise became apparent. Just as response to carotid sinus massage (CSM) by antihypertensive medications; this striking was the absence of symptoms in patients with otherwise negative evalu- can usually be easily identified by his- after exercise the day he wore the Holter ations for syncope. The prevalence of tory. Postexercise hypotension is a con- monitor, when he did not take his pulse CSH in patients with an abnormal re- dition that is caused by an abnormality knowing that it was already being response to CSM in whom the history re- in autonomic regulation of vascular tone corded by the device. veals a close relationship between syn- or heart rate. Individuals with PEH de- The patient was asked to demonstrate cope or near-syncope and accidental velop a marked fall in peripheral vascu- his recent severe episode that almost re- pressure on the carotid sinus (as in the lar resistance immediately after moder- sulted in loss of consciousness. He began case presented herein) has been esti- ate-intensity aerobic exercise10,11 that is walking in place in the examining room mated at about 1%.25 Carotid sinus hy-

stretch (FIGURE 1). Sensory impulses should be monitored continuously with Figure 1. Location of the Carotid Sinus from these stretch receptors are car- an electrocardiogram and, ideally, with ried via branches of the glossopharyn- a blood pressure monitor that is ca- Anterior Margin of geal nerve to vasomotor and cardio- pable of beat-to-beat recording. Two in- Sternocleidomastoid Muscle External inhibitory centers in the medulla. dividuals should be present, one to evalu- Carotid Artery Stimulation of these centers inhibits ate the patient and perform CSM and the sympathetic impulses to peripheral other to obtain the electrocardiogram and Internal Angle of Carotid Artery Mandible blood vessels and increases vagal stimu- to record symptoms and blood pres- lation of the heart. A patient with CSH sure. It is recommended that a defibril- Carotid may experience lightheadedness or syn- lator and an advanced cardiac life sup- Sinus cope when these stretch receptors are port crash cart be available in the unlikely Common simulated by abruptly turning the head, event that they will be needed. Carotid Artery Superior Border of by wearing a tight collar, by shaving, The carotid sinus (initially on the Thyroid Cartilage or by compression or invasion of the right) should be identified at the mid- carotid sinus or of the glossopharyn- point between the angle of the man- geal nerve by a head and neck tumor. dible and the superior border of the thy- There are 2 types of CSH, each of roid cartilage right along the anterior The carotid sinus is a small dilatation of the internal which is related to the respective med- margin of the sternocleidomastoid carotid artery immediately above the bifurcation of the common carotid artery that contains specialized sen- ullary center from which the efferent muscle (Figure 1). The area should be sory nerve endings sensitive to pressure or stretch. To limb of the reflex originates (FIGURE 2). initially touched with firm but gentle perform carotid sinus massage, firm but gentle pressure is applied to the area at the midpoint between The vagal or cardioinhibitory type of pressure with careful attention to the the angle of the mandible and the superior border of CSH results from reflex slowing of the electrocardiogram. This should be done the thyroid cartilage along the anterior margin of the sternocleidomastoid muscle. heart and may produce sinus arrest or even before massage is performed be- asystole, as it did in the patient in this cause some patients, as the man pre- case. The other, known as the vasode- sented herein, have hypersensitivity of persensitivity may cause unexplained pressor type of CSH, produces hypoten- the carotid sinus that is evoked merely falls in older individuals. In one study of sion without bradycardia due chiefly to with gentle pressure. If a positive re- 26 consecutive patients older than 65 inhibition of sympathetic vasoconstric- sponse (see below) does not result from years who presented to an emergency de- tion. About one third of individuals with this alone, the area should be massaged partment with unexplained falls (mean CSH demonstrate both responses. with a similar degree of pressure for age, 79 years), the prevalence of an asys- about 5 seconds. All actions by the ex- tolic response to CSM was 46%.26 In a Carotid Sinus Massage aminer should be marked on the elec- larger study, CSH was found in 65 (23%) Carotid sinus massage is recommended trocardiogram and the patient’s symp- of 279 unexplained or recurrent fall- as part of the evaluation of patients older toms should be recorded elsewhere. The ers.27 To determine the effective treat- than 40 years who have syncope of un- blood pressure should be recorded ment for CSH, older patients with this clear cause.1 The procedure is contrain- within 15 seconds of CSM. A positive re- condition were randomized to receive a dicated in individuals with an acute myo- sponse is generally defined as a de- dual-chamber permanent pacemaker or cardial infarction or in a patient with a crease in systolic blood pressure of 50 no pacing. Falls were reduced by two recent stroke or transient ischemic at- mm Hg or greater (vasodepressor thirds in the group that received a pace- tack, known carotid artery occlusion, or response), a ventricular pause of more maker.28 In another randomized study, with a history of a serious ventricular ar- than 3 seconds (cardioinhibitory 32 patients with symptomatic CSH re- rhythmia. Before considering CSM, the response), or a combination of these ceived pacemakers and 28 did not. Af- examiner should listen for a carotid bruit (mixed response). The diagnosis of CSH ter an average follow-up of 3 years, syn- and if one is found, the maneuver should is enhanced if CSM elicits symptoms con- cope recurred in 9% of the pacing group, probably be avoided. For patients with sistent with the diagnosis, even if the clas- whereas it recurred in 57% of those who a carotid bruit, some have recom- sic hemodynamic response is not ob- did not receive a pacemaker.29 mended Doppler ultrasound prior to tained. Repeating CSM with the patient Syncope in patients with CSH is CSM to exclude critical stenosis30 even upright, typically using a tilt table, has caused by pressure on the carotid si- though the risk of neurological compli- also been recommended as a more use- nus, a small dilatation of the internal cations resulting from the procedure is ful procedure to evaluate the vasode- carotid artery immediately above the bi- exceptionally low,31-33 and significant ca- pressor response to CSM.1 furcation of the common carotid ar- rotid stenoses may still exist when no tery in which the adventitia contains a bruit is heard.34 CASE RESOLUTION large number of sensory nerve end- To perform CSM (BOX 4), the patient The patient underwent placement of a ings that are sensitive to pressure or should lie supine for several minutes and dual-chamber permanent pacemaker

Figure 2. Types of Responses to Carotid Sinus Massage in Carotid Sinus Hypersensitivity

A Cardioinhibitory Response

Electrocardiogram (Schematic) Carotid Sinus Massage (5 s)

>3 s Pause

Systolic Blood Pressure (Schematic) 150

100 mm Hg 50

B Vasodepressor Response Electrocardiogram (Schematic) Carotid Sinus Massage (5 s)

Systolic Blood Pressure (Schematic) 150

≥50-mm Hg 100 Decrease mm Hg 50 0102030 Time, s

A, A pure cardioinhibitory response produces a reflex slowing of the heart and may produce sinus arrest or asystole. A fall in systolic blood pressure typically occurs deriving from and proportional to the extent and duration of the decrease in heart rate. During carotid sinus massage, a positive cardioinhibitory response is defined as a ventricular pause of more than 3 seconds. If the slowing of the heart is prevented (for example with a pacemaker), individuals exhibiting a pure cardioinhibitory response will not experience a decline in blood pressure. B, A pure vasodepressor response produces hypotension without bradycardia due chiefly to inhibition of sympathetic vasoconstriction. A pure vasodepressor response results in a decline in systolic blood pressure that is of longer duration than that observed in a pure cardioinhibitory response. During carotid sinus massage, a positive vasodepressor response is defined as a decline in the systolic blood pressure of 50 mm Hg or greater. Note that about a third of individuals demonstrate both types of hypersensitivity responses. and returned to regular treadmill exercise with no difficulty. It was sug- Box 4. Carotid Sinus Massage gested that he check his pulse in his Who? wrist rather than his neck and that he Patients with unexplained syncope, especially those aged 40 years and older drink water or an electrolyte solution Contraindicated if acute myocardial infarction, recent stroke or transient before exercising to minimize dehy- ischemic attack, history of ventricular fibrillation/ventricular tachycardia dration. He has had no recurrent lightheadedness or near-syncope now al- How? most 2 years later. This is the expected Patient should be supine and monitored continuously with an electrocardiogram Two individuals are needed: one to massage, the other to record outcome in a patient in whom the car- A defibrillator and cardiac drugs should be in the room dioinhibitory type of CSH predomi- Gently but firmly touch the carotid sinus (see text) for 5 seconds nates. Although many individuals with If no response, massage carotid sinus for 5 seconds, no more than 10 seconds the cardioinhibitory type of CSH also What Is a Positive Response? have some vasodepressor symptoms Ն and signs,35 dual-chamber cardiac pac- Positive response= decrease in systolic blood pressure 50 mm Hg, ventricular pause of Ͼ3 seconds, or both ing is curative in the majority28,29 and is recommended for patients with recurrent syncope caused by carotid sinus stimulation in whom minimal cation.36 Since pacing does not alter the have a mixed cardioinhibitory and va- rotid sinus pressure induces ventricular vasodepressor response, those indi- sodepressor response may need addi- asystole of more than 3 seconds’ dura- viduals with this type of CSH or who tional or alternative treatment. This may

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