5. • The baseline heart rate in an individual patient is determined by the balance between the
parasympathetic and the sympathetic nervous systems.
• The ‘normal’ heart rate has been defined arbitrarily as 60–100 beats per minute (b.p.m.) at rest,
although a range of 50–90 b.p.m. has also been suggested.
• Interestingly, the ‘intrinsic’ rate of the sinus node, after sympathetic and vagal blockade, is
around 110 b.p.m.
• The heart rate may vary from patient to patient depending on age, training status and time-point
of the observation
• In a healthy asymptomatic population, the ‘normal’ range of heart rates in the afternoon was
found to be 46–93 b.p.m. in men and 51–95 b.p.m. in women, nocturnal rates being lower.
• At rest or during sleep, heart rates as low as 40 b.p.m. may be normal, even in healthy subjects.
• In contrast, sinus or atrial bradycardia below 30 b.p.m. may be of concern in patients with sinus
node dysfunction, especially if symptomatic .
• Bradycardia is a frequent finding in trained athletes and heart rates below 40 b.p.m. are often
observed at rest
6. • Sinus pauses of up to 2.5 s were found in 10% of normal healthy individuals, pauses of
more than 2 s in 20% of athletes] and pauses of 2–3 s in 37% of athletes during sleep
However, even in athletes, pauses of more than 3 s require further medical attention,
especially if associated with a history of syncope
• Another important component of the definition of bradycardia is the chronotropic
response to exercise, which reflects the ability of the heart to accelerate according to the
degree of exertion.
• An inadequate chronotropic response, together with inability to reach the maximum
predicted heart rate (defined as 220 minus age in years) at peak exercise, strongly
suggest that a relative bradycardia may require further attention
• During atrial fibrillation, the ventricular rate is determined by atrioventricular nodal
refractoriness.
• Affected patients warrant special consideration, as they exhibit greater beat-to-beat
variability than patients in sinus rhythm
• During atrial fibrillation, daytime pauses of up to 2.8 s and night-time pauses of up to 4.0
s may be considered as within acceptable limits, if well tolerated by the patient
• Reflecting the above, at the individual patient level, bradycardia may be defined as an
inappropriately low heart rate in relation to age, gender, activity level and physical
training status. Clinical attention is required only if bradycardia is associated with
symptoms, at rest or during exercise, that may put the patient at risk.
8. Signs and symptoms
• The clinical challenge is to separate those patients who are symptomatic, at risk of complications
(low cardiac output, dizziness, heart failure) and in need of further investigation from those who
are healthy, in whom the bradycardia is physiological.
• Eventual symptoms depend on cardiac output, defined as the product of left ventricular stroke
volume and heart rate. As long as changes in stroke volume compensate for the decrease in heart
rate, even patients with profound bradycardia may remain asymptomatic, the disorder only being
detected as an incidental finding on clinical examination or on ECG performed for other reasons.
• At the other end of the clinical spectrum, the patient with bradycardia may present with a variety
of signs and symptoms.
• Amongst these, syncope is the most dramatic, although cardiac standstill of more than 6 s is
generally required before loss of consciousness will occur.
• Symptoms are often non-specific and chronic, for example transient dizziness, light-headedness
or confusional states, reflecting cerebral hypo perfusion due to decreased cardiac output, or
episodes of fatigue or muscular weakness with exercise intolerance.
• Bradyarrhythmia may also present with palpitation, which simply means a perception of the
beating heart. The patient may describe ‘pauses’ or ‘strong beats’, which are often manifestations
of premature beats or just increased awareness of the action of the heart during a period of
emotional sensitivity
9. Sinus node dysfunction
• Sinus node dysfunction, also known as sick sinus syndrome, is a common cause of
bradycardia, which encompasses a variety of sinoatrial disorders, ranging from
the usually benign sinus bradycardia to the more severe and often symptomatic
bradycardia–tachycardia syndrome, characterized by paroxysmal, rapid, regular or
irregular atrial tachyarrhythmias, alternating with periods of slow atrial and
ventricular rates
• Other manifestations of sinus node dysfunction include serious, persistent and
otherwise inexplicable sinus bradycardia and bradyarrhythmia, sinus arrest with
ectopic atrial or nodal escape rhythms, paroxysmal or chronic atrial fibrillation
secondary to sinus arrest, sinoatrial exit block and inadequate chronotropic
response to exercise.
10. Sinus bradycardia
• Sinus bradycardia is defined by sinus node depolarizations at a rate below
60 b.p.m., with normal P waves before each QRS complex.
• Sinus bradycardia is a common and usually benign finding.
• Transient sinus bradycardia may be observed in patients after myocardial
infarction and also following resuscitation from cardiac arrest, in which
context it is associated with a poor prognosis [
11.
12. Sinus pauses
• Sinus pauses may be due to failure of impulse formation in the sinus node (sinus arrest)
or a failure of conduction out of the nodal region to the surrounding atrium (sinoatrial
exit block).
• In pauses due to sinoatrial exit block, the P–P interval during the pause is typically a
multiple of the basic P–P interval, whereas in sinus arrest no such relationship is seen .
• Although sinus pauses or arrest may have no intrinsic clinical significance, the emergence
of surrogate atrial or nodal pacemaker escape rhythms to prevent ventricular asystole
increases the risk of atrial fibrillation or flutter, thromboembolic events and bradycardia–
tachycardia syndrome.
• The latter, a combination of alternating atrial tachyarrhythmia and sinus bradycardia
episodes, is usually symptomatic, since the overdrive suppression of sinus automaticity
during the tachycardic phase may result in long pauses due to increased sinus node
recovery time and syncope when tachycardia terminates. In addition, attempts to
decrease the rapid heart rate (e.g. with beta-blockers or digitalis) may further depress
the sinus node or atrioventricular conduction and accentuate the abnormality.
13. Tacy-brady syndrome
• Is identified by bradycardia alternating with paroxysmal
supraventricular arrhythmia, most frequently atrial fibrillation.
• This results from abnormal automaticity and conduction within atrial
tissue.
• It affects about 50% of patient with sinus node dysfunction
14. Chronotropic incompetence
• Defined as inappropriate bradycardia resulting in an ability to meet
the metabolic demands.
• It is estimated to occur in 20% to 60% of patiens.
16. • Atrioventricular conduction disturbance may occur at any level, from the
atrioventricular junction down to the intraventricular conduction system.
• It includes varying degrees of block in the atrioventricular node, the His bundle or
the right or left bundle branches and/or in the anterior and posterior divisions of
the left bundle branch (left anterior or left posterior fascicular blocks).
• Block may either occur at a single site or affect two or more components of the
conduction system
• The atrioventricular node and the His bundle are particularly sensitive to
ischaemia and to traumatic injury, as they constitute a narrow preferential cond
17. First degree AV block
• Benign, does not require treatment
• PR interval > 200ms ( 5 small squares)
• During 1st degree AV block, every atrial conducts to ventricle and a
regular ventricular rate is produced, but PR intervals exceeds 0.20s in
adults.
• PR interval prolongation can be caused by
Conduction delay in AV node, in His Purkinje system or at both sites.
Delayed conduction over both bundle branches
Intra arterial conduction delay
18.
19. Second degree heart block
Mobitz type I (Wenckebach)
• is often a normal variant and seen in individuals with a high vagal tone without evidence
of structural heart disease.
• this rhythm can result from inferior myocardial ischemia, medication toxicity (AV nodal
blocking agents), hyperkalemia, cardiomyopathy (Lyme disease), or following cardiac
surgery.
• Common drugs that are known to cause AV block include beta-blockers, digoxin, calcium
channel blockers, and many antiarrhythmic agents. Recently the immunosuppressant
agent, fingolimod, used to treat relapsing multiple sclerosis was also found to cause AV
block.
20. • Characterized by progressively increasing PR interval, until a P wave s not
conducted. During the following cycle, the PR interval resumes its original value
and progressively increases again until next P wave is blocked
• Observation of the jugular venous pressure may reveal repetitive sudden loss of
the v wave, corresponding to the ventricular pause, despite the persistence of an
a wave.
• Rarely manifest with syncope.
21. Treatment & Management
Mobitz type I (Wenckebach)
• is often not necessary. Occasionally type I blocks may result in bradycardia
leading to hypotension. If hypotension and bradycardia occur, type I blocks
respond well to atropine. If unresponsive to atropine, pacing (transcutaneous or
transvenous) should be initiated for stabilization.
• If the patient is on any beta blockers, calcium channel blockers or digoxin, the
dose of these medications should be reduced or the medication discontinued.
• All patients with Mobitz 1 block should be admitted and monitored.
22. Mobitz type II
• is rarely seen in patients without structural heart disease.
• It is often associated with myocardial ischemia and fibrosis or sclerosis of the
myocardium. This rhythm often progresses to third-degree atrioventricular block.
Other causes of AV block include the following:
• Infiltrative heart disease- amyloidosis, hemochromatosis
• Acute rheumatic fever
• Malignancies- lymphoma
• Hyperthyroidism, myxedema
• Collagen vascular disorders
• Cardiac tumors
• Following transcatheter placement of valves
• Ethanol injection for hypertrophic cardiomyopathy
23. • Is characterized by abrupt conduction failure.
• Generally originated from an infra-Hisian lesion, may be associated
with wide QRS complex, often progress abruptly to complete AV block
• Manifests with syncope
24. Treatment & Management
Mobitz type II
• involves initiating pacing as soon as this rhythm is identified. Type II blocks imply
structural damage to the AV conduction system. This rhythm often deteriorates
into complete heart block.
• These patients require transvenous pacing until a permanent pacemaker is
placed.
• Unlike Mobitz type I (Wenckebach), patients that are bradycardic and
hypotensive with a Mobitz type II rhythm often do not respond to
25. Third degree heart block ( complete heart block)
• Is characterized by the complete dissociation of atrial and ventricular activity,
each following has its own rhythm.
• Usually symptomatic, patient may presents with sign related to reduced cardiac
output such as syncope or dyspnoea.
• The escape rhythm may provide indication of the location of block : sustained
rhythm between 40 and 60 bpm with narrow QRS complex , suggests junctional
rhythm associated with supra- Hisian block, whereas wide QRS complexes at a
slower heart rate indicated block at a lower level in His- Purkinje system and
more urgent need for theraupeutic intervention.
26.
27.
28. Intraventricular block
• Intraventricular conduction delay (bundle branch block) at any level of the His–
Purkinje system leads to the loss of synchronous ventricular activation and
contraction.
• Intraventricular block may be fascicular (left anterior or left posterior hemiblock)
leading to left intraventricular dyssynchrony, or it may affect the bundle branch
itself (left or right bundle branch block) leading to interventricular dyssynchrony.
• These different types of block may be isolated or combined, rate dependent or
not, and may indicate an increased risk of development of high-degree
atrioventricular block.
30. 1. Patient evaluation begins with a detailed history, including an attempt to
identify potentially reversible causes of bradycardia (with a specific focus on
drug treatments, including non-cardiovascular drugs).
2. Physical examination, including careful cardiac auscultation.
3. Commonly reported symptoms include palpitation, presyncope or syncope,
and dyspnoea or fatigue. These symptoms may be paroxysmal or chronic, may
be triggered or aggravated by physical exercise, or may occur only in specific
situations (e.g. during the night).
31. • Long-term ECG recording
1. Holter recording
• Ambulatory ECG monitoring over 24–48 h is appropriate for patients with suspected
intermittent symptomatic bradycardia in order to correlate the symptoms with the
bradycardic episodes
2. Transient-event recorders
• may be kept for a month or more, allowing digital recording of the ECG for up to 30 s
initiated by the patient at the time he or she experiences symptoms. This presupposes
that the patient remains conscious at the onset of the symptoms but most modern
recorders have permanent monitoring for arrhythmic events.
3. Implantable loop recorders
• may be particularly useful in the investigation of infrequently recurring symptoms,
especially if Holter and transient-event recorders have failed to establish the diagnosis.
• Implantable loop recorders allow patients to be monitored over a prolonged period,
increasing the diagnostic yield to as much as 85% in syncope that is difficult to diagnose
32. Electrophysiological testing
• may be used for the elucidation of atrioventricular or intraventricular conduction disturbance
when the level of the block cannot be established from the ECG.
• Electrophysiological studies may help to identify patients at high risk of progression to complete
atrioventricular block, in whom implantation of a pac
• Unexplained syncope may be due to sinus node dysfunction or atrioventricular block and is an
indication for electrophysiological testing if non-invasive assessment fails to identify the aetiology.
