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Heart Disease (Expert Forum)
Re: bradycardia & pacemakers
This forum is for questions and support regarding heart issues such as: Angina, Angioplasty, Arrhythmia, Bypass Surgery, Cardiomyopathy, Coronary Artery Disease, Defibrillator, Heart Attack, Heart Disease, High Blood Pressure, Mitral Valve Prolapse, Pacemaker, PAD, Stenosis, Stress Tests.
Re: bradycardia & pacemakers
by Cleveland Clinic, MD, Jan 01, 1995 12:00AM
, Jan 01, 1995 12:00AM
Posted By CCF CARDIO MD - CRC on July 14, 1998 at 10:44:13:
In Reply to: bradycardia & pacemakers posted by Howard Fischer on July 13, 1998 at 17:56:51:
my father (age 75) has historically low heart rate and blood pressure.
lately, though, his heart rate has been around 40, causing his neurologist
(separate problem) to suggest a pacemaker.
he has a bad history with surgery, including infection and suture
rejection. (some of this has to do with doctors not following instructions
and using nylon.) i am concerned that his anxiety over surgery will
cause complications.
i need some realistic information on risks related to implantation and
use of a pacemaker, as well as other, non-surgical alternatives.
fyi, he recently began taking l-dopa for parkinsons. he is not taking
beta blockers or other meds that would cause slow heart rate.
thank you.
-------------------------------------------------------------------------------------------------------------------------------
Dear Howard,
Pacemaker placement is in general a safe and simple procedure with a low complication rate. The procedure is done under local anesthesia. An area on the shoulder is numbed and a small pocket under the skin is formed where the pacemaker is placed. Small wires lead from the pacemaker to the heart chambers. The entire procedure takes about an hour. Potential complications of pacemaker placement are bleeding and infection at the site of implant (<2%), infection of the pacemaker wires requiring replacement (<1%), pneumothorax (collapse of the lung <1%) and cardiac tamponade (fluid in the heart sack <1%). Usually one stays in the hospital overnight after implant with discharge the next morning.
After implantation the pacemaker is generally checked twice a year either over the phone or as an outpatient. Be sure to discuss the individual risks and benefits of pacemaker implantation with your fathers doctor. Unless he is having symptoms due to his slow heart rate a pacemaker is not something I would rush into. Below I have attached a copy of a book chapter on bradyarrhythmis (slow heart rates) I have written for the soon to be published Cleveland Cardiology Manual. Hope this helps.
Information provided here is for general educational purposes only. Only your doctor can provide specific diagnoses and treatments. If you would like to be seen at the Cleveland Clinic, please Call 1 - 800 - CCF - CARE for an appointment at Desk F15 with a cardiologist.
Bradyarrhythmias, Atrioventricular Block, Asystole and Pulseless Electrical Activity
Bradyarrhythmias and conduction blocks are common electrocardiographic findings. Many of these arrhythmias are asymptomatic and do not require specific therapy but others can be life threatening requiring rapid action. An important cause of acute and potentially dangerous bradyarrhythmia is myocardial ischemia and emphasis will be placed on the treatment and indications for pacing of these arrhythmias.
Anatomy
The sinus beat originates in a foci of automatic cells called the sinoatrial node (SAN) located near the junction of the superior vena cava and right atrium. If the SAN fails to generate an impulse other foci in the atrium, AV node or ventricle can act as "back-up" pacemaker sites. The blood supply to the SAN is from the sinus node artery which arises from the proximal right coronary artery (RCA) in 55% of the population (Fig 1) and from the circumflex artery (CXA) in 35%. The SAN receives a dual supply of blood from both the RCA and CXA in 10% of the population. The automaticity of the SAN is affected by both the parasympathetic and sympathetic nervous systems.
The impulse generated by the SAN progresses through the atrium to the atrioventricular node (AVN) located in the anteromedial portion of the right atrium just anterior to the coronary sinus. The AVN receives its blood supply from the AV nodal artery which arises from the posterior descending artery (PDA) in 80% of the population, (Fig 1) from the CXA 10% of the time and from both arteries in 10%. In addition the AVN receives collateral blood supply from the left anterior descending (LAD) artery and is thus somewhat less prone to ischemic damage than the SAN. The AVN is also enervated by both the parasympathetic and sympathetic nervous systems.
After a delay of less than 0.2 seconds in the AVN the electrical impulse is propagated down the His bundle to the right and left bundle branches. The left bundle branch splits further into anterior and posterior fascicles. The His bundle and right bundle branch receive their blood supply from the AV nodal artery and from septal penetrating branches of the LAD. The left bundle branch receives blood for the anterior fascicle from the septal perforating branches of the LAD. The posterior fascicle has a dual blood supply from the septal perforating branches of the LAD and branches of the PDA. The autonomic nervous system does not play a major role in conduction below the AVN.
Sinus Node Dysfunction
Sinus node dysfunction (SND) is a term that encompasses any dysfunction of the sinus node and includes inappropriate sinus bradycardia, sinoatrial exit block, sinoatrial arrest and tachycardia-bradycardia syndrome.
Etiology
The etiologies of SND may be divided into intrinsic and extrinsic causes and are listed in Table 1. Idiopathic degenerative disease is the most common cause of intrinsic SND and the incidence increases with age. Acute coronary syndromes are a common cause of bradyarrhythmias occurring in 25-30% of patients with myocardial infarction (MI) (Table 2).
Clinical Presentation
The most dramatic presenting symptoms of SND are syncope and presyncope, however, there is a wide range of presentation and some patients may be asymptomatic. Fatigue, angina and shortness of breath are more subtle consequences of SND. In the tachycardia-bradycardia syndrome the primary complaint may be palpitation and documentation of the arrhythmia may be difficult due to the sporadic and fleeting nature of the problem.
ECG Findings
Inappropriate Sinus Bradycardia
Inappropriate sinus bradycardia is defined as a sinus rate of less than 60 that does not increase appropriately with exercise. The QRS complex is narrow and is preceded by a P wave. Inappropriate sinus bradycardia must be differentiated from a low resting heart rate, which may be normal in athletes and sleeping individuals.
Sinus Arrest
Sinus arrest, or sinus pause, occurs when the sinus node fails to depolarize on time. Pauses of < 3 seconds may be seen on Holter monitoring in up to 11% of normal adults (especially athletes) and is not cause for concern. Pauses longer than 3 seconds, however, are generally considered abnormal and are suggestive of an underlying abnormality.
Sinoatrial Exit Block
Sinoatrial exit block is similar to sinus arrest on the ECG tracing but may be distinguished from sinus arrest by the fact that the duration of the pause is a multiple of the sinus P-P interval. High-grade SA exit block cannot be differentiated from prolonged sinus arrest and is treated in the same manner.
Tachycardia-Bradycardia Syndrome
Also referred to as "Sick Sinus Syndrome" tachycardia-bradycardia syndrome is characterized by episodes of sinus or junctional bradycardia interspersed with atrial tachycardia, usually paroxysmal atrial fibrillation.
Diagnostic Testing
Testing for SND can be either noninvasive or invasive. Invasive testing is usually reserved for cases where noninvasive testing has failed to demonstrate an etiology.
Noninvasive Testing
The first step in evaluation of suspected SND is the 12-lead ECG followed by 24-48 hour ambulatory electrocardiographic monitoring if necessary. The use of a diary during the recording period can help to correlate symptoms with the cardiac rhythm. For less frequent events, a loop recorder or event recorder may be used to assess symptoms over a 2 -4 week period. Stress testing can be used to document the severity of chronotropic incompetence.
Autonomic Testing
Autonomic testing includes pharmacologic interventions and physical maneuvers to test the autonomic reflexes.
Physical maneuvers
Carotid Sinus Massage (CSM)
CSM is useful for distinguishing intrinsic sinus pause/sinus arrest from a pause due to carotid sinus hypersensitivity (CSH). CSH is defined as a 3-second or longer pause and/or a 50 mmHg or greater drop in blood pressure with massage of the carotid sinus (firm pressure applied to one carotid sinus at a time for 5 seconds). CSM should not normally precipitate sinus pause/sinus arrest. However, it will slow conduction in the AVN and decrease the rate of depolarization of the SAN.
Tilt Table Testing
Tilt table testing may be useful in the differentiation between syncope caused by SND and that due to autonomic dysfunction. Bradycardic episodes precipitated by tilt table are usually due to autonomic dysfunction and not SND.
Pharmacological Testing
Pharmacological intervention may be used to differentiate between SND and autonomic dysfunction. Total autonomic blockade is achieved after administration of atropine 0.04 mg/kg and propranolol 0.2 mg/kg. The resulting intrinsic heart rate represents the sinus node rate devoid of autonomic influences. The normal intrinsic heart rate in beats per minute is defined by the following formula:
Intrinsic Heart Rate = 118.1 - (0.57 x age)
An intrinsic heart rate lower than predicted by the above equation is consistent with sinus node dysfunction. An intrinsic heart rate close to the predicted rate in a patient with clinical SND is suggestive of an autonomic dysfunction as a cause of the bradyarrhythmia.
Invasive Testing
Invasive testing is used when noninvasive methods have failed to make a diagnosis but SND is still strongly suspected. The two tests most commonly employed in the electrophysiology lab to test the sinus node function are the sinus node recovery time and the sinoatrial conduction time. Both of these methods use indirect measurements of SAN function. Direct measurement of SAN function is laborious and rarely performed.
Sinus Node Recovery Time (SNRT)
SNRT is the time it takes the SAN to recover following paced overdrive suppression of the node. A delay of longer than 1400 ms is considered abnormal. This measurement may be corrected by subtracting the intrinsic sinus cycle length (in milliseconds [ms]) from the recovery time. A corrected SNRT of greater than 550 ms is suggestive of SND. The limitations of this test are that it is an indirect measurement of SAN function and reflects both SA nodal conduction time and automaticity. It may be falsely shortened by SAN entrance block during atrial pacing (due to failure of the paced impulse to "reset" the sinus node) or falsely prolonged by a SAN exit block (the sinus node is normal but the impulse cannot leave the node). Finally, the SNRT is not prolonged in all patients with SND.
Sinoatrial Conduction Time (SACT)
SACT is calculated by first determining the steady state atrial rate (A1-A1 interval or the time between P waves). Next, premature atrial extrastimule (A2) are introduced by pacing high in the right atrium starting in late diastole at progressively shorter intervals until atrial refractoriness is found (i.e. A2 does not result in a P wave). The duration before the next spontaneous atrial impulse (A3) is measured and the baseline rate is subtracted.
SACT = (A2-A3 interval) minus (A1-A1 interval)
The test assumes that SAN automaticity is not affected by pacing, that conduction time into the node is equal to the conduction time out of the node, and that there is no shift in the principle pacemaker site.
Therapy
Treatment for symptomatic sinus node dysfunction may be pharmacological, pacing or a combination of both. For patients on medication that suppress AVN automaticity, the medication should be stopped. If this is not possible it may be necessary to place a temporary or permanent pacemaker (Table 3). For patients with tachycardia-bradycardia syndrome a pacemaker is often placed for treatment of the bradyarrhythmia and antiarrhythmic drugs are added for treatment of the tachycardic episodes.
Acute treatment for patients with MI and symptomatic SND should include:
Atropine at 0.04 mg/kg iv bolus.
Temporary pacing for those patients that fail to respond to drug therapy.
Isoproterenol (starting at 1 (g/min iv) may be used as a bridge drug to pacemaker.
The indications for pacing in SND are determined by symptoms. Correlation of symptoms with a documented arrhythmia generally requires pacing (Table 3). Another common indication for pacing is when drug therapy that causes SND cannot be stopped or changed.
Atrioventricular Conduction Disturbances
Atrioventricular (AV) conduction disturbances are divided into first (1), second (2), and third (3) degree block depending on the severity of conduction abnormality.
Etiology
The causes of AV block are listed in Table 4, the most common of which is idiopathic fibrosis. Acute MI results in AV block in 14% of patients with inferior infarcts and 2% of those with an anterior infarction. The block usually occurs within the first 24 hours following MI.
Clinical Presentation
First Degree AV Block
First-degree AV block is characterized by prolongation of the PR interval beyond 0.20 seconds. This may occur as a normal variant in 0.5% of asymptomatic young adults without overt heart disease. In older individuals, it is most often caused by idiopathic degenerative disease of the conducting system.
Second-Degree AV Block
Second-degree AV block is characterized by a failure of one or more atrial impulses to conduct to the ventricles. The block may be at any level of the atrioventricular conduction system.
When more than one atrial impulse is present for each ventricular complex the rhythm may be described by the number of atrial impulses to the number of ventricular complexes (i.e. for 3 P waves preceding each QRS complex, 3:1 second-degree AV block is present). High-grade AV block (i.e. 3:1, 4:1 or greater) is typically described as Mobitz II AV block. The conducted impulse will generally have a wide QRS morphology (i.e. RBBB or LBBB pattern) and the site of block often is below the AV node. Lesser degrees of AV block (i.e. 4:3 or 3:2) with a variable P-R interval and Wenckebach periodicity are described as Mobitz I AV block. Pure 2:1 conduction patterns cannot be reliably classified as Mobitz I or II.
The conducted impulse of a Mobitz I block will generally be narrow and the site of block is often in the AV node above the His bundle. A Mobitz I block with a bundle branch block is still likely to be above the His bundle but a His bundle electrocardiogram is needed to confirm the level of block. A Mobitz II block is usually intra or infra Hisian and has an increased incidence of progressing to 3 AV block.
Third-Degree AV Block
Third-degree AV block, or complete heart block (CHB) may be acquired or congenital. Acquired AV block occurs most frequently in the seventh decade and more commonly affects males whereas 60% of patients with congenital CHB are female. Of children with congenital CHB, 30-50% of their mothers will have connective tissue disease, usually lupus errythematous.
Signs and Symptoms
1 AV block is generally not a cause of symptoms and 2 AV block seldom results in symptoms (although high grade 2 AV block may progress to 3 AV block which can cause symptoms). Depending upon the ventricular escape rate patients with 3 AV block will present with either extreme fatigue or abrupt syncope.
Physical Findings
The amplitude of the arterial pulse will vary depending on the timing of atrial filling of the ventricles. Thus in 2 AV block there will be a periodic change in the amplitude and with 3 AV block a constantly changing amplitude. In 3 block there will be periodic cannon a-waves (large amplitude waves in the venous pulsations seen in the neck when the atria contracts against a closed tricuspid valve).
The heart sounds will be similarly affected by the change in filling duration of the ventricles. The first heart sound will become softer as the PR interval is prolonged resulting in a soft S1 in 1 AV block, a progressively softening S1 in Type I 2 AV block and a constantly changing S1 in 3 AV block. Third-degree AV block may also result in a functional systolic ejection murmur.
ECG Findings
First-Degree AV Block
The diagnosis of 1 AV block is made electrocardiographically by measuring a PR interval longer than 0.20 seconds in adults (Fig 2) and 0.18 seconds in children. There is a P wave before each QRS and both the P and QRS are normal in morphology. In addition, to accurately make the diagnosis the individual should not be on any drugs that prolong the PR interval.
Second-Degree AV Block
2 AV block is divided into two subcategories, Mobitz type I and II.
Mobitz Type I
Mobitz type I, (Fig 3) also known as Wenckebach block may be diagnosed when the following criteria are met on the ECG:
Sequential and gradual prolongation of the PR interval terminated by a nonconducted P-wave
Prolongation of the R-R interval occurring in progressively shorter increments.
Duration of the pause following the nonconducted P wave less than the sum of any 2 consecutively conducted beats.
Decreased PR interval following the pause when compared to the pre-pause PR interval.
The presence of "grouped beating" may also be noted on the ECG. This pattern of repeated groups of QRS complexes is characteristic of Wenckebach block.
Mobitz Type II
Mobitz type II second-degree AV block is less common than type I. The PR interval is constant with a sudden non-conducted P wave (Fig 4). This should be differentiated from non-conducted premature atrial contractions (PAC's) which will have a varying PR interval. There may be multiple P waves to each QRS and this is designated by the number of P waves before each conducted QRS (i.e. 3:1, 4:1 etc.). The QRS complex is typically not narrow and if it is a Mobitz I block should be suspected.
Third-Degree AV Block
Third degree AV block (Fig 5) is diagnosed by identification of complete dissociation of the atrial and ventricular electrical activity. There is no temporal relationship between the P waves and the QRS complexes. With calipers one can "march" out the progression of the P waves to determine the atrial rate. Third-degree AV block is only one cause of AV dissociation and not all AV dissociation is 3 AV block.
Therapy
Patients with first-degree and Mobitz I AV block usually do not require therapy. Permanent pacing is indicated for Mobitz II AV block and 3 AV block. Complete indications for pacing are listed in Table 3. Medical therapy may be used as a bridge to pacing but has no role in the long-term treatment.
Atropine
The principle drug used as a bridge to pacing is atropine.
Reduces heart block due to hypervagotonia but not due to AVN ischemia.
More useful for AV block in inferior MI than anterior MI.
Does not increase infranodal conduction (Will not improve third-degree AV block or second-degree AV block that is below the AVN).
Ineffective in the denervated hearts of transplant patients.
Use cautiously (if at all) in Mobitz II AV block due to a possible paradoxical decrease in heart rate. ( i.e. As atrial rate increases AV conduction decreases and a 2:1 block with an atrial rate of 80 and a ventricular rate of 40 may be converted to a 3:1 block with an atrial rate of 90 and a ventricular rate of 30)
Symptomatic AV blocks that are due to digitalis may be treated with Digoxin-specific Fab fragments (2- 40 vials [40mg/vial] iv bolus).
Third-degree AV block occurring as a complication of inferior MI is usually temporary and may only require temporary pacing. When CHB occurs as a result of anterior MI however permanent pacing is often required (Table 3). Acquired third-degree AV block in adults will usually require pacing but patients with congenital third-degree AV block will often have a fast enough escape rhythm to prevent symptoms and avoid permanent pacemaker implantation.
Junctional Rhythms
Junctional rhythms arise from the area surrounding the AVN including the approaches to the node, the node itself and the bundle of His. This area has an intrinsic rate of 30-60 BPM and serves as an escape mechanism to prevent ventricular asystole in case of complete AV block. When the junctional rhythm is faster than the sinus rhythm it is referred to as accelerated junctional rhythm (AJR).
Etiology
The two major causes of AJR are MI and digitalis toxicity. AJR is seen in approximately 10% of patients with acute MI. Over half of these patients have inferior MI and about one third have anterior infarctions.
Digitalis toxicity by itself does not seem to cause AJR as evidenced in persons with normal hearts who take accidental overdoses of digoxin. It appears that concomitant heart disease is required to develop AJR.
Other causes of AJR are post operatively following valve surgery, acute rheumatic fever, direct-current cardioversion, cardiac catheterization, serious infection, COPD, systemic amyloidosis and uremia with hyperkalemia.
Clinical Presentation
Patients usually do not develop symptoms directly attributable to AJR. The physical findings of AV dissociation may be noted and are the same as those seen in third-degree AV block.
ECG Findings
Accelerated Junctional Rhythm
The P wave is normal in morphology. The QRS complex has a normal duration unless there is concomitant bundle branch block. The distinguishing characteristic of AJR is the AV dissociation and changing PR interval (Fig 6). The difference between AJR and third-degree AV block is in the fact that the ventricular rate is faster than the atrial rate in AJR and slower than the atrial rate in third-degree AV block.
Junctional Rhythm
In the absence of a sinus beat the AV node can act as a back-up pacemaker. The ECG findings are an absence of P waves, a narrow QRS complex and a rate of 30 to 60 BPM.
Therapy
For patients with a junctional rhythm secondary to SAN failure or AV block the therapy is as previously outlined for AV conduction disturbances. Patients with AJR do not usually require therapy for the arrhythmia. However, treatment of the underlying cause is indicated. Suppression of AJR may be achieved by increasing the atrial rate with drugs (i.e. atropine, adrenergics, etc.) or pacing. Digitalis induced AJR is an indication to stop digoxin but does not usually require administration of Digoxin-specific Fab fragments.
Intraventricular Conduction Disturbances
Conduction disturbances due to block below the AVN are classified based on the intraventricular conduction system. An intraventricular conduction disturbance (IVCD) does not itself cause bradyarrhythmia but may be associated with any of the other rhythms that cause bradycardia.
Etiology
The causes of IVCD are similar to those that cause AV block (Table 4) with idiopathic degenerative conduction disease and acute ischemic syndromes the most common causes. IVCD increases with age and affects up to 2% of those older than 60 years old. There is an increased incidence of IVCD in persons with structural heart disease especially those with coronary artery disease.
ECG Findings
Electrocardiographic findings of IVCD are summarized in Table 5 and examples are presented in Figures 7 - 10.
Fascicular Blocks
The IVCD may be further classified by the number of fascicles they affect. Unifascicular blocks affect only one of the three fascicles. Examples of unifascicular block would be RBBB, LAFB and LPFB. Bifascicular block is present when two of the fascicles have conduction disturbances. The most common of which is right bundle branch block (RBBB) with left anterior fascicular block. Approximately 6% of these patients will progress to complete heart block. RBBB with left posterior fascicular block is less common but the progression to complete heart block is more frequent.
"Trifascicular block" is present when there is a combination of bifascicular block and first-degree AV block (Figure 9). Pacing is indicated in those patients with bifascicular block who have intermittent symptomatic complete heart block and those patients with bifascicular or trifascicular block with asymptomatic intermittent Mobitz II AV block (Table 3).
Post-Surgical Bradyarrhythmias
Bradyarrhythmias following cardiac surgery are common. Valvular surgery and septal myectomy can cause mechanical damage to the conduction system leading to AV blocks and intraventricular conduction disturbances. Prolonged ischemic time during cardiac transplantation can lead to sinus node damage. Post-surgical bradyarrhythmias may be only temporary and the decision to proceed to permanent pacing should be made after 5 to 7 days. The same criteria (Table 3) are used to determine the need for a pacemaker. Permanent pacing is required in 2-3% of valve surgeries and upwards of 10% of transplant patients.
Pulseless Electrical Activity
Pulseless electrical activity (PEA) is defined as the absence of a pulse or blood pressure measured by usual methods with the continued presence of electrical activity of the heart. PEA may be due to a variety of rhythm disturbances such as electrical mechanical dissociation, idioventricular rhythms and ventricular tachycardias. When the electrical activity is organized and within the physiologic range the term electrical mechanical dissociation (EMD) is used. PEA may be caused by a variety of clinical situations and is a potentially treatable condition if certain actions are rapidly undertaken (Table 6).
Therapy
Specific treatment of the underlying cause of PEA is the therapy most likely to result in a successful outcome (Table 6). Emergency intervention for PEA should be initiated at once.
CPR should be started and airway management with intubation performed to treat any possible hypoxia.
Epinephrine may be given 1 mg iv push every 3-5 minutes.
Atropine 1 mg iv may be given if the rate is < 60 beats a minute and may be repeated every 3 - 5 minutes to a total dose of 0.03 - 0.04 mg/kg.
Empiric iv volume infusion should be given.
Asystole
Etiology
Asystole is the absence of myocardial electrical activity. The etiology may be due to profound paraysmpathetic suppression of both atrial and ventricular activity, "stunning" of the myocardium due to electrical defibrillation, complete heart block or prolonged myocardial ischemia. Asystole should be confirmed by switching between several leads or changing the position of the defibrillation paddles.
Clinical Presentation
Most patients with asystole present in a "code" situation. Persons outside of the hospital who are found to be asystolic by the initial responding team usually have asystole due to profound myocardial ischemia. The possibility of a successful outcome in this situation is extremely small. Patients in the hospital on a telemetry unit on the other hand may have a favorable outcome.
Therapy
Management consists of CPR, intubation and atropine to unmask the possibility of profound parasympathetic suppression of both atrial and ventricular activity. Electrical shocks have not been demonstrated to have any benefit in the treatment of asystole and may in fact produce a "stunned" myocardium leading to a delay in the return of a rhythm. Thus, routine shocking of asystole is strongly discouraged. Pacing for asystole is controversial and if it is to have any effect must be initiated early. Asystole due to myocardial ischemia is unlikely to respond to pacing but asystole due to other causes may respond.
Carotid Sinus Hypersensitivity.
Carotid sinus hypersensitivity (CSH) is common, affecting up to a third of older men with coronary artery disease. CSH is defined as a sinus pause of 3 seconds or greater and/or a drop in blood pressure of 50 mmHg or more with carotid sinus massage (CSM). CSH may be purely cardioinhibitory, purely vasodepressive or a combination of both. Carotid sinus syndrome (CSS) is present when CSH is accompanied by syncope or near-syncope.
Etiology
The cause of CSH and CSS is unknown. It is more common in older individuals, particularly those with atherosclerotic disease. CSS may be precipitated by the patient stretching their neck (such as with shaving or turning the head) or wearing a tight collar but often a precipitating event can not be found.
Sites of potential lesions causing CSH are the sternocleidomastoid muscle, central nervous system and the feedback loops between the cardiovascular and CNS. It has been demonstrated that the function of the carotid sinus is itself intact and is not "hypersensitive" in the true sense. Some investigators have suggested that CSS be renamed "carotid sinus irritability" to better reflect its pathophysiology.
Diagnostic Testing
A patient with suspected CSH/CSS should be tested lying down with ECG and blood pressure monitoring. Carotid sinus massage (CSM) is performed by placing firm manual pressure over the carotid sinus located at the bifurcation of the carotid artery for no more than 5 seconds. Only one sinus at a time should be compressed and the temporal artery should be lightly palpitated to ensure that complete occlusion of the artery does not occur. Potential risks of CSM are transient ischemic attack and stroke and CSM should not be performed if a carotid bruit is present. If a cardioinhibitory response is found, permanent pacing may be required. Tilting the patient to an upright position will increase the diagnostic yield of the test but may also result in false positives.
In Reply to: bradycardia & pacemakers posted by Howard Fischer on July 13, 1998 at 17:56:51:
my father (age 75) has historically low heart rate and blood pressure.
lately, though, his heart rate has been around 40, causing his neurologist
(separate problem) to suggest a pacemaker.
he has a bad history with surgery, including infection and suture
rejection. (some of this has to do with doctors not following instructions
and using nylon.) i am concerned that his anxiety over surgery will
cause complications.
i need some realistic information on risks related to implantation and
use of a pacemaker, as well as other, non-surgical alternatives.
fyi, he recently began taking l-dopa for parkinsons. he is not taking
beta blockers or other meds that would cause slow heart rate.
thank you.
-------------------------------------------------------------------------------------------------------------------------------
Dear Howard,
Pacemaker placement is in general a safe and simple procedure with a low complication rate. The procedure is done under local anesthesia. An area on the shoulder is numbed and a small pocket under the skin is formed where the pacemaker is placed. Small wires lead from the pacemaker to the heart chambers. The entire procedure takes about an hour. Potential complications of pacemaker placement are bleeding and infection at the site of implant (<2%), infection of the pacemaker wires requiring replacement (<1%), pneumothorax (collapse of the lung <1%) and cardiac tamponade (fluid in the heart sack <1%). Usually one stays in the hospital overnight after implant with discharge the next morning.
After implantation the pacemaker is generally checked twice a year either over the phone or as an outpatient. Be sure to discuss the individual risks and benefits of pacemaker implantation with your fathers doctor. Unless he is having symptoms due to his slow heart rate a pacemaker is not something I would rush into. Below I have attached a copy of a book chapter on bradyarrhythmis (slow heart rates) I have written for the soon to be published Cleveland Cardiology Manual. Hope this helps.
Information provided here is for general educational purposes only. Only your doctor can provide specific diagnoses and treatments. If you would like to be seen at the Cleveland Clinic, please Call 1 - 800 - CCF - CARE for an appointment at Desk F15 with a cardiologist.
Bradyarrhythmias, Atrioventricular Block, Asystole and Pulseless Electrical Activity
Bradyarrhythmias and conduction blocks are common electrocardiographic findings. Many of these arrhythmias are asymptomatic and do not require specific therapy but others can be life threatening requiring rapid action. An important cause of acute and potentially dangerous bradyarrhythmia is myocardial ischemia and emphasis will be placed on the treatment and indications for pacing of these arrhythmias.
Anatomy
The sinus beat originates in a foci of automatic cells called the sinoatrial node (SAN) located near the junction of the superior vena cava and right atrium. If the SAN fails to generate an impulse other foci in the atrium, AV node or ventricle can act as "back-up" pacemaker sites. The blood supply to the SAN is from the sinus node artery which arises from the proximal right coronary artery (RCA) in 55% of the population (Fig 1) and from the circumflex artery (CXA) in 35%. The SAN receives a dual supply of blood from both the RCA and CXA in 10% of the population. The automaticity of the SAN is affected by both the parasympathetic and sympathetic nervous systems.
The impulse generated by the SAN progresses through the atrium to the atrioventricular node (AVN) located in the anteromedial portion of the right atrium just anterior to the coronary sinus. The AVN receives its blood supply from the AV nodal artery which arises from the posterior descending artery (PDA) in 80% of the population, (Fig 1) from the CXA 10% of the time and from both arteries in 10%. In addition the AVN receives collateral blood supply from the left anterior descending (LAD) artery and is thus somewhat less prone to ischemic damage than the SAN. The AVN is also enervated by both the parasympathetic and sympathetic nervous systems.
After a delay of less than 0.2 seconds in the AVN the electrical impulse is propagated down the His bundle to the right and left bundle branches. The left bundle branch splits further into anterior and posterior fascicles. The His bundle and right bundle branch receive their blood supply from the AV nodal artery and from septal penetrating branches of the LAD. The left bundle branch receives blood for the anterior fascicle from the septal perforating branches of the LAD. The posterior fascicle has a dual blood supply from the septal perforating branches of the LAD and branches of the PDA. The autonomic nervous system does not play a major role in conduction below the AVN.
Sinus Node Dysfunction
Sinus node dysfunction (SND) is a term that encompasses any dysfunction of the sinus node and includes inappropriate sinus bradycardia, sinoatrial exit block, sinoatrial arrest and tachycardia-bradycardia syndrome.
Etiology
The etiologies of SND may be divided into intrinsic and extrinsic causes and are listed in Table 1. Idiopathic degenerative disease is the most common cause of intrinsic SND and the incidence increases with age. Acute coronary syndromes are a common cause of bradyarrhythmias occurring in 25-30% of patients with myocardial infarction (MI) (Table 2).
Clinical Presentation
The most dramatic presenting symptoms of SND are syncope and presyncope, however, there is a wide range of presentation and some patients may be asymptomatic. Fatigue, angina and shortness of breath are more subtle consequences of SND. In the tachycardia-bradycardia syndrome the primary complaint may be palpitation and documentation of the arrhythmia may be difficult due to the sporadic and fleeting nature of the problem.
ECG Findings
Inappropriate Sinus Bradycardia
Inappropriate sinus bradycardia is defined as a sinus rate of less than 60 that does not increase appropriately with exercise. The QRS complex is narrow and is preceded by a P wave. Inappropriate sinus bradycardia must be differentiated from a low resting heart rate, which may be normal in athletes and sleeping individuals.
Sinus Arrest
Sinus arrest, or sinus pause, occurs when the sinus node fails to depolarize on time. Pauses of < 3 seconds may be seen on Holter monitoring in up to 11% of normal adults (especially athletes) and is not cause for concern. Pauses longer than 3 seconds, however, are generally considered abnormal and are suggestive of an underlying abnormality.
Sinoatrial Exit Block
Sinoatrial exit block is similar to sinus arrest on the ECG tracing but may be distinguished from sinus arrest by the fact that the duration of the pause is a multiple of the sinus P-P interval. High-grade SA exit block cannot be differentiated from prolonged sinus arrest and is treated in the same manner.
Tachycardia-Bradycardia Syndrome
Also referred to as "Sick Sinus Syndrome" tachycardia-bradycardia syndrome is characterized by episodes of sinus or junctional bradycardia interspersed with atrial tachycardia, usually paroxysmal atrial fibrillation.
Diagnostic Testing
Testing for SND can be either noninvasive or invasive. Invasive testing is usually reserved for cases where noninvasive testing has failed to demonstrate an etiology.
Noninvasive Testing
The first step in evaluation of suspected SND is the 12-lead ECG followed by 24-48 hour ambulatory electrocardiographic monitoring if necessary. The use of a diary during the recording period can help to correlate symptoms with the cardiac rhythm. For less frequent events, a loop recorder or event recorder may be used to assess symptoms over a 2 -4 week period. Stress testing can be used to document the severity of chronotropic incompetence.
Autonomic Testing
Autonomic testing includes pharmacologic interventions and physical maneuvers to test the autonomic reflexes.
Physical maneuvers
Carotid Sinus Massage (CSM)
CSM is useful for distinguishing intrinsic sinus pause/sinus arrest from a pause due to carotid sinus hypersensitivity (CSH). CSH is defined as a 3-second or longer pause and/or a 50 mmHg or greater drop in blood pressure with massage of the carotid sinus (firm pressure applied to one carotid sinus at a time for 5 seconds). CSM should not normally precipitate sinus pause/sinus arrest. However, it will slow conduction in the AVN and decrease the rate of depolarization of the SAN.
Tilt Table Testing
Tilt table testing may be useful in the differentiation between syncope caused by SND and that due to autonomic dysfunction. Bradycardic episodes precipitated by tilt table are usually due to autonomic dysfunction and not SND.
Pharmacological Testing
Pharmacological intervention may be used to differentiate between SND and autonomic dysfunction. Total autonomic blockade is achieved after administration of atropine 0.04 mg/kg and propranolol 0.2 mg/kg. The resulting intrinsic heart rate represents the sinus node rate devoid of autonomic influences. The normal intrinsic heart rate in beats per minute is defined by the following formula:
Intrinsic Heart Rate = 118.1 - (0.57 x age)
An intrinsic heart rate lower than predicted by the above equation is consistent with sinus node dysfunction. An intrinsic heart rate close to the predicted rate in a patient with clinical SND is suggestive of an autonomic dysfunction as a cause of the bradyarrhythmia.
Invasive Testing
Invasive testing is used when noninvasive methods have failed to make a diagnosis but SND is still strongly suspected. The two tests most commonly employed in the electrophysiology lab to test the sinus node function are the sinus node recovery time and the sinoatrial conduction time. Both of these methods use indirect measurements of SAN function. Direct measurement of SAN function is laborious and rarely performed.
Sinus Node Recovery Time (SNRT)
SNRT is the time it takes the SAN to recover following paced overdrive suppression of the node. A delay of longer than 1400 ms is considered abnormal. This measurement may be corrected by subtracting the intrinsic sinus cycle length (in milliseconds [ms]) from the recovery time. A corrected SNRT of greater than 550 ms is suggestive of SND. The limitations of this test are that it is an indirect measurement of SAN function and reflects both SA nodal conduction time and automaticity. It may be falsely shortened by SAN entrance block during atrial pacing (due to failure of the paced impulse to "reset" the sinus node) or falsely prolonged by a SAN exit block (the sinus node is normal but the impulse cannot leave the node). Finally, the SNRT is not prolonged in all patients with SND.
Sinoatrial Conduction Time (SACT)
SACT is calculated by first determining the steady state atrial rate (A1-A1 interval or the time between P waves). Next, premature atrial extrastimule (A2) are introduced by pacing high in the right atrium starting in late diastole at progressively shorter intervals until atrial refractoriness is found (i.e. A2 does not result in a P wave). The duration before the next spontaneous atrial impulse (A3) is measured and the baseline rate is subtracted.
SACT = (A2-A3 interval) minus (A1-A1 interval)
The test assumes that SAN automaticity is not affected by pacing, that conduction time into the node is equal to the conduction time out of the node, and that there is no shift in the principle pacemaker site.
Therapy
Treatment for symptomatic sinus node dysfunction may be pharmacological, pacing or a combination of both. For patients on medication that suppress AVN automaticity, the medication should be stopped. If this is not possible it may be necessary to place a temporary or permanent pacemaker (Table 3). For patients with tachycardia-bradycardia syndrome a pacemaker is often placed for treatment of the bradyarrhythmia and antiarrhythmic drugs are added for treatment of the tachycardic episodes.
Acute treatment for patients with MI and symptomatic SND should include:
Atropine at 0.04 mg/kg iv bolus.
Temporary pacing for those patients that fail to respond to drug therapy.
Isoproterenol (starting at 1 (g/min iv) may be used as a bridge drug to pacemaker.
The indications for pacing in SND are determined by symptoms. Correlation of symptoms with a documented arrhythmia generally requires pacing (Table 3). Another common indication for pacing is when drug therapy that causes SND cannot be stopped or changed.
Atrioventricular Conduction Disturbances
Atrioventricular (AV) conduction disturbances are divided into first (1), second (2), and third (3) degree block depending on the severity of conduction abnormality.
Etiology
The causes of AV block are listed in Table 4, the most common of which is idiopathic fibrosis. Acute MI results in AV block in 14% of patients with inferior infarcts and 2% of those with an anterior infarction. The block usually occurs within the first 24 hours following MI.
Clinical Presentation
First Degree AV Block
First-degree AV block is characterized by prolongation of the PR interval beyond 0.20 seconds. This may occur as a normal variant in 0.5% of asymptomatic young adults without overt heart disease. In older individuals, it is most often caused by idiopathic degenerative disease of the conducting system.
Second-Degree AV Block
Second-degree AV block is characterized by a failure of one or more atrial impulses to conduct to the ventricles. The block may be at any level of the atrioventricular conduction system.
When more than one atrial impulse is present for each ventricular complex the rhythm may be described by the number of atrial impulses to the number of ventricular complexes (i.e. for 3 P waves preceding each QRS complex, 3:1 second-degree AV block is present). High-grade AV block (i.e. 3:1, 4:1 or greater) is typically described as Mobitz II AV block. The conducted impulse will generally have a wide QRS morphology (i.e. RBBB or LBBB pattern) and the site of block often is below the AV node. Lesser degrees of AV block (i.e. 4:3 or 3:2) with a variable P-R interval and Wenckebach periodicity are described as Mobitz I AV block. Pure 2:1 conduction patterns cannot be reliably classified as Mobitz I or II.
The conducted impulse of a Mobitz I block will generally be narrow and the site of block is often in the AV node above the His bundle. A Mobitz I block with a bundle branch block is still likely to be above the His bundle but a His bundle electrocardiogram is needed to confirm the level of block. A Mobitz II block is usually intra or infra Hisian and has an increased incidence of progressing to 3 AV block.
Third-Degree AV Block
Third-degree AV block, or complete heart block (CHB) may be acquired or congenital. Acquired AV block occurs most frequently in the seventh decade and more commonly affects males whereas 60% of patients with congenital CHB are female. Of children with congenital CHB, 30-50% of their mothers will have connective tissue disease, usually lupus errythematous.
Signs and Symptoms
1 AV block is generally not a cause of symptoms and 2 AV block seldom results in symptoms (although high grade 2 AV block may progress to 3 AV block which can cause symptoms). Depending upon the ventricular escape rate patients with 3 AV block will present with either extreme fatigue or abrupt syncope.
Physical Findings
The amplitude of the arterial pulse will vary depending on the timing of atrial filling of the ventricles. Thus in 2 AV block there will be a periodic change in the amplitude and with 3 AV block a constantly changing amplitude. In 3 block there will be periodic cannon a-waves (large amplitude waves in the venous pulsations seen in the neck when the atria contracts against a closed tricuspid valve).
The heart sounds will be similarly affected by the change in filling duration of the ventricles. The first heart sound will become softer as the PR interval is prolonged resulting in a soft S1 in 1 AV block, a progressively softening S1 in Type I 2 AV block and a constantly changing S1 in 3 AV block. Third-degree AV block may also result in a functional systolic ejection murmur.
ECG Findings
First-Degree AV Block
The diagnosis of 1 AV block is made electrocardiographically by measuring a PR interval longer than 0.20 seconds in adults (Fig 2) and 0.18 seconds in children. There is a P wave before each QRS and both the P and QRS are normal in morphology. In addition, to accurately make the diagnosis the individual should not be on any drugs that prolong the PR interval.
Second-Degree AV Block
2 AV block is divided into two subcategories, Mobitz type I and II.
Mobitz Type I
Mobitz type I, (Fig 3) also known as Wenckebach block may be diagnosed when the following criteria are met on the ECG:
Sequential and gradual prolongation of the PR interval terminated by a nonconducted P-wave
Prolongation of the R-R interval occurring in progressively shorter increments.
Duration of the pause following the nonconducted P wave less than the sum of any 2 consecutively conducted beats.
Decreased PR interval following the pause when compared to the pre-pause PR interval.
The presence of "grouped beating" may also be noted on the ECG. This pattern of repeated groups of QRS complexes is characteristic of Wenckebach block.
Mobitz Type II
Mobitz type II second-degree AV block is less common than type I. The PR interval is constant with a sudden non-conducted P wave (Fig 4). This should be differentiated from non-conducted premature atrial contractions (PAC's) which will have a varying PR interval. There may be multiple P waves to each QRS and this is designated by the number of P waves before each conducted QRS (i.e. 3:1, 4:1 etc.). The QRS complex is typically not narrow and if it is a Mobitz I block should be suspected.
Third-Degree AV Block
Third degree AV block (Fig 5) is diagnosed by identification of complete dissociation of the atrial and ventricular electrical activity. There is no temporal relationship between the P waves and the QRS complexes. With calipers one can "march" out the progression of the P waves to determine the atrial rate. Third-degree AV block is only one cause of AV dissociation and not all AV dissociation is 3 AV block.
Therapy
Patients with first-degree and Mobitz I AV block usually do not require therapy. Permanent pacing is indicated for Mobitz II AV block and 3 AV block. Complete indications for pacing are listed in Table 3. Medical therapy may be used as a bridge to pacing but has no role in the long-term treatment.
Atropine
The principle drug used as a bridge to pacing is atropine.
Reduces heart block due to hypervagotonia but not due to AVN ischemia.
More useful for AV block in inferior MI than anterior MI.
Does not increase infranodal conduction (Will not improve third-degree AV block or second-degree AV block that is below the AVN).
Ineffective in the denervated hearts of transplant patients.
Use cautiously (if at all) in Mobitz II AV block due to a possible paradoxical decrease in heart rate. ( i.e. As atrial rate increases AV conduction decreases and a 2:1 block with an atrial rate of 80 and a ventricular rate of 40 may be converted to a 3:1 block with an atrial rate of 90 and a ventricular rate of 30)
Symptomatic AV blocks that are due to digitalis may be treated with Digoxin-specific Fab fragments (2- 40 vials [40mg/vial] iv bolus).
Third-degree AV block occurring as a complication of inferior MI is usually temporary and may only require temporary pacing. When CHB occurs as a result of anterior MI however permanent pacing is often required (Table 3). Acquired third-degree AV block in adults will usually require pacing but patients with congenital third-degree AV block will often have a fast enough escape rhythm to prevent symptoms and avoid permanent pacemaker implantation.
Junctional Rhythms
Junctional rhythms arise from the area surrounding the AVN including the approaches to the node, the node itself and the bundle of His. This area has an intrinsic rate of 30-60 BPM and serves as an escape mechanism to prevent ventricular asystole in case of complete AV block. When the junctional rhythm is faster than the sinus rhythm it is referred to as accelerated junctional rhythm (AJR).
Etiology
The two major causes of AJR are MI and digitalis toxicity. AJR is seen in approximately 10% of patients with acute MI. Over half of these patients have inferior MI and about one third have anterior infarctions.
Digitalis toxicity by itself does not seem to cause AJR as evidenced in persons with normal hearts who take accidental overdoses of digoxin. It appears that concomitant heart disease is required to develop AJR.
Other causes of AJR are post operatively following valve surgery, acute rheumatic fever, direct-current cardioversion, cardiac catheterization, serious infection, COPD, systemic amyloidosis and uremia with hyperkalemia.
Clinical Presentation
Patients usually do not develop symptoms directly attributable to AJR. The physical findings of AV dissociation may be noted and are the same as those seen in third-degree AV block.
ECG Findings
Accelerated Junctional Rhythm
The P wave is normal in morphology. The QRS complex has a normal duration unless there is concomitant bundle branch block. The distinguishing characteristic of AJR is the AV dissociation and changing PR interval (Fig 6). The difference between AJR and third-degree AV block is in the fact that the ventricular rate is faster than the atrial rate in AJR and slower than the atrial rate in third-degree AV block.
Junctional Rhythm
In the absence of a sinus beat the AV node can act as a back-up pacemaker. The ECG findings are an absence of P waves, a narrow QRS complex and a rate of 30 to 60 BPM.
Therapy
For patients with a junctional rhythm secondary to SAN failure or AV block the therapy is as previously outlined for AV conduction disturbances. Patients with AJR do not usually require therapy for the arrhythmia. However, treatment of the underlying cause is indicated. Suppression of AJR may be achieved by increasing the atrial rate with drugs (i.e. atropine, adrenergics, etc.) or pacing. Digitalis induced AJR is an indication to stop digoxin but does not usually require administration of Digoxin-specific Fab fragments.
Intraventricular Conduction Disturbances
Conduction disturbances due to block below the AVN are classified based on the intraventricular conduction system. An intraventricular conduction disturbance (IVCD) does not itself cause bradyarrhythmia but may be associated with any of the other rhythms that cause bradycardia.
Etiology
The causes of IVCD are similar to those that cause AV block (Table 4) with idiopathic degenerative conduction disease and acute ischemic syndromes the most common causes. IVCD increases with age and affects up to 2% of those older than 60 years old. There is an increased incidence of IVCD in persons with structural heart disease especially those with coronary artery disease.
ECG Findings
Electrocardiographic findings of IVCD are summarized in Table 5 and examples are presented in Figures 7 - 10.
Fascicular Blocks
The IVCD may be further classified by the number of fascicles they affect. Unifascicular blocks affect only one of the three fascicles. Examples of unifascicular block would be RBBB, LAFB and LPFB. Bifascicular block is present when two of the fascicles have conduction disturbances. The most common of which is right bundle branch block (RBBB) with left anterior fascicular block. Approximately 6% of these patients will progress to complete heart block. RBBB with left posterior fascicular block is less common but the progression to complete heart block is more frequent.
"Trifascicular block" is present when there is a combination of bifascicular block and first-degree AV block (Figure 9). Pacing is indicated in those patients with bifascicular block who have intermittent symptomatic complete heart block and those patients with bifascicular or trifascicular block with asymptomatic intermittent Mobitz II AV block (Table 3).
Post-Surgical Bradyarrhythmias
Bradyarrhythmias following cardiac surgery are common. Valvular surgery and septal myectomy can cause mechanical damage to the conduction system leading to AV blocks and intraventricular conduction disturbances. Prolonged ischemic time during cardiac transplantation can lead to sinus node damage. Post-surgical bradyarrhythmias may be only temporary and the decision to proceed to permanent pacing should be made after 5 to 7 days. The same criteria (Table 3) are used to determine the need for a pacemaker. Permanent pacing is required in 2-3% of valve surgeries and upwards of 10% of transplant patients.
Pulseless Electrical Activity
Pulseless electrical activity (PEA) is defined as the absence of a pulse or blood pressure measured by usual methods with the continued presence of electrical activity of the heart. PEA may be due to a variety of rhythm disturbances such as electrical mechanical dissociation, idioventricular rhythms and ventricular tachycardias. When the electrical activity is organized and within the physiologic range the term electrical mechanical dissociation (EMD) is used. PEA may be caused by a variety of clinical situations and is a potentially treatable condition if certain actions are rapidly undertaken (Table 6).
Therapy
Specific treatment of the underlying cause of PEA is the therapy most likely to result in a successful outcome (Table 6). Emergency intervention for PEA should be initiated at once.
CPR should be started and airway management with intubation performed to treat any possible hypoxia.
Epinephrine may be given 1 mg iv push every 3-5 minutes.
Atropine 1 mg iv may be given if the rate is < 60 beats a minute and may be repeated every 3 - 5 minutes to a total dose of 0.03 - 0.04 mg/kg.
Empiric iv volume infusion should be given.
Asystole
Etiology
Asystole is the absence of myocardial electrical activity. The etiology may be due to profound paraysmpathetic suppression of both atrial and ventricular activity, "stunning" of the myocardium due to electrical defibrillation, complete heart block or prolonged myocardial ischemia. Asystole should be confirmed by switching between several leads or changing the position of the defibrillation paddles.
Clinical Presentation
Most patients with asystole present in a "code" situation. Persons outside of the hospital who are found to be asystolic by the initial responding team usually have asystole due to profound myocardial ischemia. The possibility of a successful outcome in this situation is extremely small. Patients in the hospital on a telemetry unit on the other hand may have a favorable outcome.
Therapy
Management consists of CPR, intubation and atropine to unmask the possibility of profound parasympathetic suppression of both atrial and ventricular activity. Electrical shocks have not been demonstrated to have any benefit in the treatment of asystole and may in fact produce a "stunned" myocardium leading to a delay in the return of a rhythm. Thus, routine shocking of asystole is strongly discouraged. Pacing for asystole is controversial and if it is to have any effect must be initiated early. Asystole due to myocardial ischemia is unlikely to respond to pacing but asystole due to other causes may respond.
Carotid Sinus Hypersensitivity.
Carotid sinus hypersensitivity (CSH) is common, affecting up to a third of older men with coronary artery disease. CSH is defined as a sinus pause of 3 seconds or greater and/or a drop in blood pressure of 50 mmHg or more with carotid sinus massage (CSM). CSH may be purely cardioinhibitory, purely vasodepressive or a combination of both. Carotid sinus syndrome (CSS) is present when CSH is accompanied by syncope or near-syncope.
Etiology
The cause of CSH and CSS is unknown. It is more common in older individuals, particularly those with atherosclerotic disease. CSS may be precipitated by the patient stretching their neck (such as with shaving or turning the head) or wearing a tight collar but often a precipitating event can not be found.
Sites of potential lesions causing CSH are the sternocleidomastoid muscle, central nervous system and the feedback loops between the cardiovascular and CNS. It has been demonstrated that the function of the carotid sinus is itself intact and is not "hypersensitive" in the true sense. Some investigators have suggested that CSS be renamed "carotid sinus irritability" to better reflect its pathophysiology.
Diagnostic Testing
A patient with suspected CSH/CSS should be tested lying down with ECG and blood pressure monitoring. Carotid sinus massage (CSM) is performed by placing firm manual pressure over the carotid sinus located at the bifurcation of the carotid artery for no more than 5 seconds. Only one sinus at a time should be compressed and the temporal artery should be lightly palpitated to ensure that complete occlusion of the artery does not occur. Potential risks of CSM are transient ischemic attack and stroke and CSM should not be performed if a carotid bruit is present. If a cardioinhibitory response is found, permanent pacing may be required. Tilting the patient to an upright position will increase the diagnostic yield of the test but may also result in false positives.
