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Name of patient



35 yrs


C/o saradha
Panickal House

Marital status




Date of Admission


I P Number


Ward and unit


Chief complaints on

: sudden weakness with syncope


: Sick Sinus syndrome


Mr.Jalesh was apparently normal till 4/5/2016 after that he got admitted in the general hospital
followed by weakness and syncope from there ECG was taken it was shown abnormality in the
rhythm and patient was transferred to TDMCH Vandanam, on Admission the vital signs was
pulse -32 b/mt ,BP-130/80,respiration-24 and ECG was repeated which showed Sick sinus
syndrome and patient got admitted in ward 12. Now he is on beta adrenergic agonist and under


Patient has no significant past history of diseases like hypertension and diabetes. History of
septal defect in the childhood . Relevant medical data not available
There is no history of any heart disease or other congenital disorders in the family
Family Tree




Diet pattern :- Non-vegetarian, lack of appetite in recent period

Bowel and bladder habits :- Normal and irregular bowel and bladder habits
Sleeping habits :-Regular, but now decreased sleep due to pleuritic chest pain , cough &

mild hemoptysis
Unhealthy habits :- History of alcoholism and smoking

Patient comes from a middle class family.he is married and has 1 children,she maintains good
inter-personal relationship with family members and neighbours. He is the breadwinner of the


1. General Appearance



52 kg

General hygiene :


Body built

Moderately built

2. Vital Signs
Temperature :


Pulse rate


Respiration rate :


Blood Pressure :

130/ 70 mmHg

3. Head to foot examination

Head -

Normal in shape, no abnormalities, black hair


Symmetrical facial features ,no facial puffiness.


Pupils equal and reacting to light P0E0E0R0L0A0

Nose -

no deviation in nasal septum, nasal flaring absent +

Mouth -

oral mucosa is pink, tongue in midline

Neck -

No tracheal shift, cervical lymph node enlargement present,

Chest -

Air entry is bilaterally equal and Bilateral,

Respiratory rate = 28/minute

Inspection: Bilaterally expanding chest, no enlarged tumours

Palpation: No enlarged lymph nodes,decreased tactile fremitus.

Percussion: Increased diaphragmatic excursion,

Auscultation: bronchial and broncho-vesicular sound , apical pulse 40b/mt

Soft, no distention or tenderness

Inspection: no distension,symmetrical in appearance

Auscultation: decreased bowel sounds,no borborgomi
Palpation: no tenderness, hepatosplenomegaly HSMPercussion: no fluid/thrill

no abnormalities or discharge in genital area, no indwelling catheter present

Extremities- No bilateral pitting edema present, cold extremities, moving all four limb, two
cannula present on left hand
4. System wise examination
Central Nervous Examination
Patient is conscious,GCS Scale E4V5M6
Higher mental function- Client is conscious,oriented to time, place and person
Sensory function intact
Reflexes intact
Cardio-vascular system
Pulse rate 40/min, regular
Blood pressure 130/70 mmHg
Capillary refill within 2 seconds
Heart sounds S1 S2 heard,
Peripheral pulses palpable
Extremities cold,no edema

JVP not elevated,

Respiratory system
Inspection Respiratory rate is 28/breath/min
Palpation: No enlarged lymph nodes, normal tactile fremitus.
Percussion: normal diaphragmatic excursion,
Auscultation: no adventitious breath sounds
Gastro-intestinal system
Oral mucosa moist
Bowel sounds - norml bowel sounds
Musculo-skeletal system
Moving all four limbs
Integumentary system
Skin moist
Edema not present
Genito-urinary system
No abnormal discharges, no foul smell

Sinus Node Dysfunction(sick sinus syndrome)

Sinus node dysfunction is a common clinical syndrome, comprising a wide range of
electrophysiologic abnormalities from failure of impulse generation, failure of impulse
transmission to the atria, inadequate subsidiary pacemaker activity, and increased susceptibility
to atrial tachyarrhythmias.4 This disorder has also been variably termed the sick sinus
syndrome,tachycardia-bradycardia syndrome,SA disease, and SA dysfunction.
Etiology of Sinus Node Dysfunction
Although the exact etiology of SND is usually not identified, most cases are believed to be
attributable to a combination of various intrinsic (processes that directly affect the anatomy and
physiology of the sinus node and/or the surrounding atrial tissue) and extrinsic factors
(processes that affect sinus node function in the absence of structural abnormalities). The most
common intrinsic causes are cardiac age-related SN changes and coronary artery disease. The
most common extrinsic causes are medications and autonomic hyperactivity.

The idiopathic form of SND is degenerative, with fibrosis and fatty infiltration of the SN and
consequent decrease of functional nodal cells.

Intrinsic SND
Age-related changes
Age-related changes are believed to be the most common cause of SND and are related to
fibrosis in the SN. These fibrotic changes also occur in the atrium and the conduction system of
the heart and are believed to contribute to the association among SND, tachy-brady syndrome,
conductive system disease, and an inappropriately slow escape rhythm.
The pacemaker activity in the SN has been found to be related to voltage and calcium
clocks. Age-related down-regulation of calcium channel expression in the SN has been suggested
as a potential cause of SND with aging.
Coronary artery disease
Coronary artery disease is believed to be a common contributory cause of SND, probably
through atherosclerotic changes in the SN artery.
Genetic causes
SND may be familial an autosomal dominant pattern of inheritance has been described.
Several molecular defects in human hearts (defects in the sodium channel, calcium channel,
hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel, ankyrin-B, and
connexin have been associated with familial sick sinus syndromes.
In addition, SND is seen in children with congenital and acquired heart disease, particularly after
corrective surgery. The cause of SND in these children is likely related to the underlying
structural heart disease and surgical trauma to the SN and/or SN artery..
In addition, sinus venosus atrial septal defect (ASD), Ebstein anomaly, and heterotaxy
syndromes, particularly left atrial isomerism, can lead to SND.

Mechanisms in tachy-brady syndrome

Tachycardia-mediated remodeling of the SN is present in patients with atrial
fibrillation/flutter and it may contribute to SND in these patients. In patients with tachy-brady
syndrome, atrial fibrillation ablation can reverse SND, as evidenced by a reduction in SN
recovery time, an increase in mean and maximal heart rates, and a lack of symptoms related to
sinus bradycardia or pause. The mechanism of SND in tachy-brady syndrome may involve the
abnormal function of voltage and calcium clocks in the SN.
Other heart diseases
Other structural heart diseases are uncommon causes of SND. These include, but are not limited
to, the following:

Various cardiomyopathies

Infiltrative heart diseases - Amyloidosis, hemochromatosis, neoplasm

Collagen vascular diseases - Systemic lupus, scleroderma
Neuromuscular diseases - Myotonic dystrophy, Friedreich ataxia
Extrinsic SND
Beta blockers, calcium channel blockers, digoxin, and various anti-arrhythmic drugs suppress SN
function. Antiarrhythmic drugs that can lead to SND include the following:

Digitalis - Because of SN exit block

Autonomic dysfunction
SND can be secondary to autonomic nervous system dysfunction in patients with
neurocardiogenic syncope, and carotid sinus hypersensitivity. Conditions associated with marked
hypervagotonia, as in well-trained athletes, can also result in SND. However, evidence suggests
that there may be some intrinsic factor as well in well-trained athletes who develop SND.
Surgical causes, especially from operations involving the right atrium
Gradual loss of sinus rhythm occurs after the Mustard, Senning, and all varieties of the
Fontan operation. This is thought to be secondary to direct injury to the SN during surgery and
also due to later, chronic hemodynamic abnormalities. Paroxysmal atrial tachycardias are
frequently associated with SND, and loss of sinus rhythm appears to increase the risk of sudden
death. Patients with transposition of the great arteries now undergo the arterial switch operation,
which avoids the extensive atrial suture lines that lead to SN damage.
SND was described in 15% of patients who had undergone the Ross operation for aortic valve
disease or complex left-sided heart disease, 2.6-11 years earlier. Other arrhythmias, such as
complete AV block and ventricular tachycardia, were present as well after the Ross operation.
When repairing ASDs, especially sinus venosus ASDs, SND frequently occurs because of the
proximity of the defect with SN tissue.
Other surgically related causes of SND include the following:

Patients who have undergone surgery for endocardial cushion defects (ECDs) may later
develop SND
SND may be caused by a Blalock-Hanlon atrial septectomy

SND may occur after repair of partial anomalous pulmonary venous return
(PAPVR) or total anomalous pulmonary venous return (TAPVR)
Cannulation of the superior vena cava (SVC), usually performed for cardiopulmonary
bypass or extracorporeal membrane oxygenation (ECMO), may damage SN tissue.
Ischemic cardiac arrest may cause SND.
Rheumatic fever is another cause of SND. Such dysfunction may also result from CNS
disease, which is usually secondary to increased intracranial pressure with subsequent increase in
the parasympathetic tone.
Endocrine-metabolic diseases (hypothyroidism and hypothermia) and electrolyte imbalances
(hypokalemia and hypocalcemia) are other conditions that can contribute to SND.
A study by Sunaga et al of 202 subjects indicated that in patients with persistent atrial
fibrillation, those with low-amplitude fibrillatory waves and a large left atrial volume index are at
increased risk for the appearance of concealed SND after catheter ablation has restored sinus
For my patient septal abnormality was present but he was not undergone any corrective


Etiological factors

Degenerative changes in the S.A node

Normal cells in the S.A node is replaced by fibrouos tissue

Abnormal impulse generation from S.A node( increased or





With mild sinus node dysfunction (SND), patients are usually asymptomatic. As SND
progresses, patients often develop symptoms due to pulse irregularity and organ hypoperfusion.
The severity of organ hypoperfusion symptoms depends on the severity of the SND and on the
functional reserve state of an organ.

Specific symptoms of SND include the following:

Cerebral symptoms - Irritability, labile mood swings, forgetfulness, dizziness, slurred

speech, blanking periods, falls, and syncope
Cardiac symptoms - Palpitations, angina, CHF symptoms, and sudden cardiac death
Vague gastrointestinal symptoms and oliguria
Patients with tachy-brady syndrome may have symptoms of stroke or transient ischemia
attack (TIA)
Exercise intolerance
Shortness of breath with or without palpitations
Infants may present with poor feeding or easy fatigability, which may also be evident in toddlers
and older children.
Physical Examination
Patients may demonstrate an inappropriately slow heart rate. Carotid sinus massage may
reveal sinus pause of more than 3 seconds and/or hypotension symptoms in patients with carotid
sinus hypersensitivity.
Patients with SND and no structural congenital heart defects may be asymptomatic in general,
despite being bradycardic for their age. Conversely, they may present with signs and symptoms
of CHF, especially those who have undergone a Mustard operation for transposition of the great
arteries or a Fontan operation for a single ventricle.
Infants with CHF secondary to SND may be tachypneic and may have signs of pulmonary
congestion on auscultation (ie, wheezing and rales), as well as hepatomegaly. In addition, they
may show evidence of failure to thrive, with weight below the fifth percentile.

Approach Considerations
The current recommendation is that the diagnosis of sinus node dysfunction (SND) should rely
on noninvasive methods rather than on measuring SN recovery time (SNRT) or sinoatrial
conduction time (SACT) in the electrophysiology laboratory, because results can be normal
despite the patient having symptoms of SND or vice versa. The most reliable noninvasive
methods for diagnosing SND are 24-hour Holter monitoring (which may show 1 or more of the
ECG criteria for SND) and exercise testing (which may reveal chronotropic incompetence).
Laboratory studies
Because hypothyroidism and electrolyte imbalances can contribute to SND, thyroid function
testing and serum electrolyte testing (Na+, K+, Ca2+) can be useful. Infiltrative cardiomyopathies
(eg, amyloid, sarcoid) can present with evidence of diffuse conduction system disease, but

screening is typically reserved for patients in whom specific clinical factors suggest the
No specific imaging studies are required in the initial workup of SND. However, an
echocardiogram should be considered because it can document the presence of underlying
valvular or ischemic heart disease and may suggest the diagnosis of amyloid when diffuse
conduction system findings are present.
In addition, this study is suitable for the evaluation of ventricular function and is also useful in
patients with coexistent CHD for the assessment of associated anatomic and hemodynamic
Transesophageal atrial pacing
Esophageal EP study constitutes a relatively safe and inexpensive method to detect SND by
determining SN recovery time in patients who present with dizziness or syncope and
Electrocardiographic criteria for SND include the presence of 1 or more of the following (see the
images below):

Sinus bradycardia below the heart rate expected for age - Ie, under 100 beats per minute
(bpm) in an infant, under 80 bpm in a preschool child, under 60 bpm in a school child, and
under 50 bpm in an adolescent
Sinus pause or absence of an expected P wave for more than 3 seconds - May be due to
sinus arrest (failure of the SN pacemaker cells to depolarize) or be the result of sinoatrial exit
block (depolarization of the SN but failure to conduct to the atria)
Slow escape rhythms that originate within the atria, His bundle, or ventricles
Marked sinus arrhythmia with constant variation in the P-P interval, which is likely to be
accompanied by sinus bradycardia
Presence of both bradyarrhythmias and tachyarrhythmias - Ie, SN reentry tachycardia,
atrial tachycardias from an ectopic focus, atrial flutter, and atrial fibrillation
Inappropriate sinus bradycardia
The arbitrary cutoff for a low sinus rate in a person who is at rest but awake is usually defined as
under 55-60 bpm. However, a study in 500 healthy subjects suggested that the low afternoon
sinus rate for men and women should be around 46 and 51 bpm, respectively. Pacemaker therapy
is a class IIb indication for patients with minimal symptoms and a chronic heart rate of less than
40 bpm while awake, according to the 2008 guidelines from the American College of Cardiology
(ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS). A focused update of
these guidelines was published in 2013.]
Sinus pause or arrest
Sinus pause or arrest is defined as absence of sinus P waves on the electrocardiogram (ECG) for
more than 2 seconds due to a lack of sinus nodal pacemaker activity. The duration of the pauses
should have no arithmetical relationship to the baseline sinus rate (ie, the P-P interval should not

be an interval of the pause); otherwise, the diagnosis of sinoatrial exit block should be
considered. Symptomatic long sinus pauses or arrests in patients with SND often occur after the
termination of atrial fibrillation or atrial flutter.
A sinus pause of 2 seconds is not unusual in a healthy person. However, a sinus pause of more
than 3 seconds is very uncommon except under certain conditions, such as sleep apnea,
hypervagotonia state, or seizure activity
Sinoatrial exit block
First degree
First-degree sinoatrial (SA) exit block reflects a conduction delay between the SN and the atrium
that cannot be recognized on regular electrocardiographic recordings.
Second degree
Second-degree SA exit block reflects intermittent conduction block between the SN and the
atrium. It has 2 classic types and likely some atypical types. Only the classic types can be
recognized on regular electrocardiographic recordings. They are as follows:

Type I (Wenckebach type) - Manifested as group beating, which is progressive shortening

of the P-P intervals, and then a pause that is less than twice the shortest P-P interval

Type II - Manifested as a pause that is a multiple of the baseline sinus P-P interval
Type I SA exit block occurs when prolonged conduction of the SN impulse through the atrial
tissue is present without actual block in the AV node (all QRS complexes are preceded by P
waves). The P-P intervals shorten until block occurs (ie, while the SN-to-SN interval is constant,
the SNtohigh right atrium [HRA] interval lengthens until an SN impulse is not followed by a P
wave). The surface ECG shows progressively shortening P-P intervals until the SN impulse is
dropped; it also shows P-P intervals that are less than twice the preceding (normal) P-P intervals.
Long pauses follow PACs. Sinoatrial conduction time can be directly measured with
electrophysiologic (EP) testing when PACs are present. In SND, the prolonged P-P interval is not
a multiple of the sinus (normal) P-P interval. Pauses in SND occur at the end of lengthening P-P
intervals rather than at the end of shortening P-P intervals (which is observed in type 1 SA exit
Third degree
Third-degree SA exit block reflects complete conduction block from the SN to the atrium. It
cannot be definitely distinguished from sinus arrest on regular electrocardiographic recordings.
An atrial, junctional, or ventricular escape rhythm is present.
Escape rhythms
Escape rhythms occur at slow rates occurs after prolonged sinus arrest. The escape rhythm may
originate in the atria, such as an ectopic right or left atrial rhythm, or it may originate from
multiple foci in the atria, as is observed in wandering atrial pacemaker (in which the P-wave axis
changes on the same electrocardiographic recording).

An escape rhythm may also originate below the atria at the His-Purkinje junction (ie, junctional
escape rhythm, with a rate of 60-80 min in infants and 50-70 min in children) or lower if
originating in the ventricles (ie, ventricular escape rhythm). The further below the atria the
escape rhythm originates, the slower the rate.
Escape rhythms, which are those that occur by default, should be distinguished from usurpation
rhythms, which are those that occur because of increased automaticity from pacemakers that fire
at a faster rate than the SN.
Chronotropic incompetence
Because the SN usually responds to autonomic nervous system input, exercise increases the heart
rate in response to increased sympathetic tone. Patients with SND usually have a blunted
response. Therefore, an exercise stress test can determine whether chronotropic incompetence is
Chronotropic incompetence is defined as failure to achieve 70-80% of maximal predicted heart
rate (maximal predicted heart rate = 220 - age) at peak exercise. The clinical value of this
definition, however, has not been well validated.[25] The peak exercise heart rate can be
influenced by multiple factors.
Tachy-brady syndrome
Bradyarrhythmias-tachyarrhythmias occur when bradycardia and tachycardia alternate. The
bradycardia may originate in the sinus, atria, AV junction, or ventricle; the tachycardia is usually
caused by atrial flutter or fibrillation, although it can also be caused, albeit less commonly, by
reentrant supraventricular tachycardia in the SN or atrial muscle.
Holter Monitoring
Recording the ECG for 24-48 hours is useful in the assessment of SND related to the previously
explained ECG findings that may be present.
The specificity of a direct observation of spontaneous (ie, not provoked by EP study) SND is
100%, and an EP study is not required. Therefore, cardiac monitoring, rather than EP study, is the
method of choice to assess SND.
A 24-hour Holter study also has the advantage of revealing whether SND produces symptoms
such as dizziness, presyncope, or syncope; these cannot be determined during an EP study,
because the patient is heavily sedated. Therefore, a 24-hour Holter study can help decide if
pacemaker therapy is required.
Pharmacologic Stimulation Tests
Due to their moderate sensitivity and specificity for SND diagnosis, intrinsic heart rate and
atropine stimulation tests are occasionally used as accessory tests in selected patients (such as
those with suspected hypervagotonia). The value of isoproterenol, propranolol, and adenosine
stimulation tests in SND diagnosis is more controversial.
Intrinsic heart rate

Atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) have been used to pharmacologically
denervate the SN, which is then followed 5-20 minutes later by an evaluation of its intrinsic heart
rate (IHR). The IHR in a healthy person is approximately equal to 117.2 (0.53 x Age).
Intrinsic SND is presumed to be present if the sinus rate after medications is below the calculated
IHR. Patients with mild SND may have a normal or exacerbated response. This test is probably
helpful in patients with sinus bradycardia due to suspected hypervagotonia, [26] in whom the IHR
is expected to be normal.
Atropine test
Atropine alone (up to 0.04 mg/kg) may provide as much information as the combination of
atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). [27] Atropine (1-3 mg) is the most commonly
used agent to assess the parasympathetic tone. A normal response is an increase in the sinus rate
above 90 bpm or an increase of more than 25% above the baseline sinus rate. [25] Patients with
symptomatic SND usually demonstrate a decrease in IHR. However, patients with only mild
SND may have a normal or exacerbated response to atropine
Electrophysiologic Studies
EP studies are indicated in patients with signs of bradyarrhythmias (mainly syncope) in whom
bradycardia could not be documented during Holter monitoring. Classic EP criteria for SND
include the presence of 1 or more of the following:

Corrected SN recovery time (CSNRT) greater than 275 milliseconds

SA conduction time greater than 200 milliseconds
SA node arrest
SA exit block
SN reentry tachycardia
SN recovery time
EP studies can document SND when studying SN automaticity by directly recording electrical
activity. One EP catheter, which has 2 proximal electrodes that record the HRA electrogram and
2 distal electrodes to pace the HRA near the SN, is positioned in the RA.
A second EP catheter, which is used to record low RA (LRA) electrical activity, is positioned
across the tricuspid valve.
Measurement of SNRT is achieved by pacing the atrium. Pacing should be performed in the
HRA near the SN at the junction of the superior vena cava (SVC) and the RA for 4-6 trials of 30
seconds each. Each trial should use successively shorter pacing cycle lengths (eg, 600 ms, 550
ms, 500 ms), beginning with a cycle length just shorter than the resting sinus cycle length. SNRT
is the time interval between the last paced captured beat to the first spontaneous sinus beat.
Gradual return of the SN to its baseline rate occurs over 5-6 beats. Prolonged pauses (ie,
secondary pauses) can occur after the initial recovery interval in SND.
If the longest interval for the recovery interval or secondary pause exceeds 1500 ms, the SNRT is

To adjust for heart rate and before each pacing increase, the resting sinus cycle length (SCL) is
measured. When the resting SCL is subtracted from SNRT, the CSNRT is obtained. Its upper
reference range limit is 525 ms; if the SNRT exceeds the SCL by more than 525 ms, the SNRT is
abnormal. The same occurs if the ratio of SNRT to SCL (ie, SNRT/SCL x 100) is more than
Sinoatrial conduction time
SACT is another parameter to use in assessing SN function. It is the time interval in milliseconds
for an impulse that originates in the SN to conduct through the perinodal tissue to the adjacent
right atrial tissue. (The tissue that surrounds the SN or perinodal tissue has characteristics that are
similar to those of the AV node.)
Eight premature atrial contractions (PACs) are fired in the HRA at 5-10 bpm faster than the SN
rate before they are stopped abruptly.
SACT represents the time in milliseconds that it takes for the PAC fired in the HRA to enter and
reset the SN. It also represents the time for the new spontaneous SN impulse (ie, SCL) to reach
the HRA. SACT is measured as the time in milliseconds from the last PAC to the first
spontaneous sinus beat.
When the time interval between the last spontaneous SN depolarization (ie, before the PAC) and
the one that occurred after a PAC is less than twice the value of the 2 previous spontaneous SN
depolarizations, reset of the SN by the PAC has occurred.
SACT can be calculated as the interval from the PAC to the next spontaneous SN beat, which
includes conduction through the perinodal tissue into the SN, resetting the SN, and conduction
through the same perinodal tissue back into the HRA (ie, [return interval - SCL]/2). The
reference range is 50-125 ms in children and 200-250 ms in adults.
If the SN cannot produce a spontaneous impulse following PACs (ie, these have not reset the SN,
and, therefore, SACT cannot be calculated), SA entrance block is present.
This block could be caused by markedly prolonged SA conduction and/or increased refractory
period of peri-SN or SN fibers, both of which indicate SND. SN entrance block alternating with
reset responses also denotes SND.
SN reentry tachycardia occurs when activation of the atrium during the supraventricular
tachycardia is the same as sinus beats (ie, P-wave axis and morphology are the same as those in
the sinus rhythm). It is usually indicative of SND.
Complications from a diagnostic EP study are rare but may include the following:

Hematoma at the puncture site in the groin and or neck

Infection caused by manipulation of catheters inside the heart (theoretical risk)
Perforation upon catheter manipulation inside the heart of small patients (most commonly
involving the right atrial appendage and the right ventricular (RV) outflow tract)

The complications of SND include the following:

Sudden cardiac death (rare)

Thromboembolic events, including stroke - Especially in patients with tachy-brady
Exercise intolerance
Cardiac dysfunction due to bradycardia and loss of AV synchrony
Atrial tachyarrhythmias - Such as atrial flutter or fibrillation
Symptoms of SN dysfunction almost invariably progress over time. The most dramatic symptom
in patients with SND is syncope.
About 50% of patients with SND develop tachy-brady syndrome over a lifetime; such patients
have a higher risk of stroke and death. However, the incidence of sudden death owing directly to
SND is extremely low.[18]
The treatment of symptoms is achieved with the implant of an atrial pacemaker to provide atrial
rate support. This prevents symptoms related to bradycardia from occurring. In patients with
atrial tachyarrhythmias, it is a useful adjunct to antiarrhythmic therapy.
Approach Considerations
The only effective medical care in patients with sinus node dysfunction (SND) is correction of
extrinsic causes.
No treatment is required for asymptomatic patients, even if they have abnormal SNRTs or
SACTs. If the patient is receiving medications that can provoke sinus bradyarrhythmias (eg, betablockers, angiotensin-converting enzyme [ACE] inhibitors), the medications should be stopped if
Acute treatment consists of atropine (0.04 mg/kg intravenously every 2-4 h) and/or isoproterenol
(0.05-0.5 mcg/kg/min intravenously). A transvenous temporary pacemaker sometimes is required
despite medical therapy.
In patients with bradyarrhythmias-tachyarrhythmias, the tachyarrhythmias may be controlled
with digoxin, propranolol, or quinidine. However, these patients should be monitored closely
with frequent Holter monitoring to ensure that the bradyarrhythmias are not exacerbated or
causing symptoms (eg, dizziness, syncope, CHF); if this is the case, permanent pacemaker
therapy is also required.
Inpatient care
Admit patients for testing and pacemaker placement when indicated.

Patients with vasovagal syncope may require increased dietary salt intake.
Patients with symptomatic SND who are not on pacemaker therapy should titrate their level of
activity to minimize symptoms.
These include cardiac electrophysiology consultation.
Transfer patients for complicated dysrhythmias and pacemaker implant.
Pacemaker Therapy
Pacemaker therapy is the only effective surgical care for patients with chronic, symptomatic
Because the incidence of sudden death in patients with SND is extremely low and pacemaker
therapy does not appear to affect survival, the major goal of pacemaker therapy in patients with
SND is to relieve symptoms.
Pacemaker indications
According to the 2008 ACC/AHA/HRS guidelines (updated in 2013), pacemaker therapy has the
following indications[2, 3] :

Class I indication - For patients with documented symptomatic sinus bradycardia, sinus
pause, and chronotropic incompetence; this includes patients who have iatrogenic SND
secondary to essential medications for which no acceptable alternatives exist
Class IIa indication - For patients with SND and a sinus rate below 40 bpm when a clear
association between symptoms (ie, symptoms consistent with bradycardia) and bradycardia has
not been documented
Class IIa indication - For patients with syncope of unexplained origin when clinically
significant abnormalities of SN are discovered or provoked in EP studies
Class IIb indication - For patients with minimal symptoms and a chronic heart rate of less
than 40 bpm while awake
Class III indication - Pacemaker therapy is contraindicated in patients with asymptomatic
SND or symptomatic bradycardia due to medications that are not essential.
In 2013, the European Society of Cardiology (ESC) published clinical practice guidelines on
cardiac pacing and cardiac resynchronization therapy.[28]
Single- versus dual-chamber pacemakers
In patients with SND, the annual incidence of complete heart block is about 0.6%. [29] In the
United States, the implantation of dual-chamber pacemakers is preferred in practice because their
use anticipates the possible subsequent development of conducting system dysfunction.

This practice is supported by data from the Danish Multicenter Randomized Trial on Single Lead
Atrial Pacing versus Dual Chamber Pacing in Sick Sinus Syndrome (DANPACE) trial, in which
9.3% of patients with single-lead atrial pacing (AAIR) required upgrade to a dual-chamber
pacemaker (DDDR) over 5.4 years follow-up due to new development of significant AV
conduction abnormalities. This was necessary despite the fact that these patients had no
significant intraventricular conduction abnormality, PR intervals below 260ms, and no
Wenckebach AV block with atrial pacing at 100 bpm at baseline.[30]
In addition, patients in AAIR mode had more atrial fibrillation than did patients in DDDR mode.
Importantly, however, no significant mortality difference between AAIR and DDDR mode was
Arguably, a single-chamber atrial pacemaker with AAI mode is an acceptable alternative in
patients with SND and normal AV and intraventricular conduction because of the added expense
of and the potential for more lead extraction with a dual-chamber pacemaker.
In patients with SND and known AV conduction abnormality (including bundle branch block and
bifascicular block), a dual-chamber pacemaker should be used due to the high risk of AV block
(about 36% in a 5-year follow-up study).
Pacemaker programming features
Chronic right ventricular pacing has been shown to be associated with an increased incidence of
atrial fibrillation, stroke, heart failure, and probably death.[18, 31, 32] A study suggested that RV
pacing is detrimental to left ventricular (LV) function even in patients with a normal LV ejection
fraction (LVEF).[33] Therefore, avoiding RV pacing is advantageous in patients with SND treated
with pacemaker therapy.
However, using the intrinsic AV conduction in patients with a very long intrinsic PR interval may
not be beneficial clinically, as suggested by a trial in patients with an intracardiac defibrillator
(ICD).[30] Theoretically, a very long PR interval may result in pacemaker syndrome during sinus
tachycardia or fast atrial pacing rhythm.
In the DANPACE trial, about 65% of patients with a moderate AV delay setting in DDDR mode
with mean RV pacing had less atrial fibrillation and no increased rate of heart failure, as
compared with patients in AAIR mode. Clearly, the optimal AV delay settings in patients with
SND are still unknown, although various programming algorithms from different pacemaker
companies are very effective in reducing RV pacing.
Mode switch is an important feature to monitor atrial flutter and fibrillation events. Because
more than 50% of patients with SND may over time develop tachy-brady syndrome, [18] it is very
important to identify these patients through pacemaker monitoring and anticoagulate them to
reduce their risk of stroke. However, the most appropriate anticoagulant therapy is still uncertain
for patients in whom atrial fibrillation is detected only as an incidental finding on pacemaker or
ICD diagnostics.
Pacemakers with a rate drop response program may benefit some patients with neurocardiogenic
syncope. Studies have suggested that closed-loop stimulation technique in the Biotronik
pacemaker may be quite helpful in reducing syncope in patients with neurocardiogenic syncope.
[34, 35]

Rate response features have been used in patients with SND, especially in the presence of
chronotropic incompetence. However, the clinical benefits of this program feature are still
Long-Term Monitoring
Asymptomatic patients with SND should be observed for symptoms. In patients with a
pacemaker, carry out the following on routine pacemaker interrogations:

Monitor leads and battery status

Ensure adequate heart rate support at rest, during daily activities, and during exercise
Monitor for pacemaker malfunction, such as pacemaker-mediated tachycardia
Ensure minimal RV pacing.
Monitor for atrial fibrillation and atrial flutter events
Patients with SND who become pregnant and take antiarrhythmic medications should have their
levels measured because they frequently require adjustment. In addition, medication with
teratogenic effects (eg, amiodarone, which is associated with fetal thyroid dysfunction) should be
replaced, if possible.
Patients with SND who become pregnant and have a pacemaker are advised to perform frequent
pacemaker checks and make the appropriate adjustments (especially when an increase in the
lead's threshold is noted).
Patients with SND who become pregnant and have ventricular dysfunction due to
cardiomyopathy or a Mustard or Fontan procedure should have regular and close medical followups with the obstetrician and cardiologist. This permits appropriate adjustment and
implementation of anti-CHF medication. If the CHF progresses despite medical management and
becomes intractable, the mother and fetus are at risk and early delivery may be schedule
Anticholinergic Agents
Class Summary
Atropine depresses the vagus, thereby increasing the heart rate. This agent is used in various
disorders or circumstances in which bradyarrhythmias occur and is frequently used in suddenonset bradyarrhythmias. Although it may also be used for the initial treatment of chronic
arrhythmias, cardiac pacing is preferred for long-term control.
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Atropine increases the heart rate through vagolytic effects, causing an increase in cardiac output.
0.4 mg PO q4-6hr PRN
Beta1/Beta2 Adrenergic Agonists
Class Summary
When given systemically, isoproterenol stimulates beta receptors in the heart, which produces
positive inotropic and chronotropic effects. This results in increased cardiac output.

Dosage Forms & Strengths

Adams-Stokes Attacks, Cardiac Arrest, or Heart Block
IV bolus: 0.02-0.06 mg (1-3 mL of a 1:50,000 dilution), initially, THEN doses of 0.01-0.2 mg
IV infusion: 5 mcg/min (1.25 mL of a 1:250,000 dilution), initially, THEN doses of 2-20
mcg/min based on patient's response
Isoproterenol (Isuprel)
Class Summary
These agents are used to treat syncopal episodes caused by fluid or electrolyte imbalances. They
restore fluid and electrolyte balance by enhancing sodium reabsorption in the kidney, which
results in expanded extracellular fluid volume. Mineralocorticoids also increase renal excretion
of potassium and hydrogen ions.
Isoproterenol has sympathomimetic effects; specifically, beta1- and beta2-adrenergic receptor
agonist activity.
Cardiovascular, Other
Class Summary
These agents alter the EP mechanisms responsible for arrhythmia. In SND, they may be used
when tachyarrhythmias occur. Patients must be carefully monitored to ascertain if
bradyarrhythmia is exacerbated.
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Digoxin (Lanoxin)
Digoxin is a cardiac glycoside with direct inotropic effects, as well as indirect effects, on the
cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic
contractions. Digoxin's indirect actions result in increased carotid sinus nerve activity and
enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
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Quinidine maintains normal heart rhythm following cardioversion of atrial fibrillation or flutter.
It depresses myocardial excitability and conduction velocity. Control the ventricular rate and
CHF (if present) with digoxin or calcium channel blockers before the administration of
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Propranolol (Inderal LA, InnoPran XL)
Propranolol is a class II antiarrhythmic, nonselective beta-adrenergic receptor blocker; it has
membrane-stabilizing activity that decreases the automaticity of contractions.
Atrial Fibrillation

Rapid digitalizing (loading-dose) regimen

IV: 8-12 mcg/kg (0.008-0.012 mg/kg) total loading dose; administer 50% initially; then
may cautiously give 1/4 the loading dose q6-8hr twice; perform careful assessment of clinical
response and toxicity before each dose

PO: 10-15 mcg/kg total loading dose; administer 50% initially; then may cautiously give
1/4 the loading dose q6-8hr twice; peform careful assessment of clinical response and toxicity
before each dose

PO: 3.4-5.1 mcg/kg/day or 0.125-0.5 mg/day PO; may increase dose every 2 weeks based
on clinical response, serum drug levels, and toxicity
IV/IM: 0.1-0.4 mg qDay; IM route not preferred due to severe injection site reaction
Dosage Forms & Strengths
Quinidine Sulfate

Test Dose: 200 mg PO quinidine sulfate several hr before full dosage

AFib: 300-400 mg PO q6hr
PSVT: 400-600 mg PO q2-3hr until paroxysm terminated
Atrial/Ventr Premature Contractions: 200-300 mg PO TID/QID
Maint: 200-400 mg PO TID/QID or 600 mg of SR PO q8-12hr
No more than 3-4 g/d
Quinidine Gluconate
324-660 mg PO q8-12hr
Maint: 648 mg PO q12hr OR 324-660 mg PO q8hr
PSVT:400 - 600 mg PO q2-3hr until paroxysm is terminated
IV: usu <5 mg/kg (but may need up to 10 mg/kg) at 0.25 mg/kg/min

Supraventricular Arrhythmia
PO: 10-30 mg q6-8hr
IV: 1-3 mg at 1 mg/min initially; repeat q2-5min to total of 5 mg
Once response or maximum dose achieved, do not give additional dose for at least 4 hours