3. Conductive system of the heart
It consists of the following structures:
-Sino-atrial node (SA node).
-Atrio-ventricular node (AV node).
-Internodal atrial pathways.
-Bundle of His.
-2 Bundle branches (BB): Right bundle branch (RBB) – left bundle branch (LBB).
-Purkinje fibers.
4.
5. SA Node
- Pacemaker of the heart under normal circumstances.
- It can discharge AP spontaneously.
- It is supplied by symp. Neurons (increases rate of discharge), and by parasymp.
Neurons (decreases rate of discharge)
- Without innervation, its rate of discharge =100/min, with innervation = 70/min
(parasymp. Effect is more dominant).
- It’s AP is characterized by the prepotential ( symp. Makes the prepotential more
vertical >> Increase HR, Parasymp. Makes it more horizontal >> decrease HR).
- P wave: atrial depolarization.
6.
7. AV node
- Electrical connection between atrium and ventricles
- Slows conduction (this allows atrial contraction to precede
ventricular contraction >> completes ventricular filling with blood).
- Protects against very rapid ventricular rates.
- PR interval –slowing in the AVN and bundle of His.
8. Bundles
- Narrow QRS complex – Normal ventricular depolarization.
- Diseases of Purkinje system produce bundle branch block (BBB).
- Diseases of AVN cause heart blocks.
9. Standard ECG
The normal waves
- P wave > Atrial depolarization
- QRS complex > Ventricular
depolarization
- T wave > ventricular
repolarization
- U wave > papillary muscle
repolarization (may be absent
from ECG)
11. Cardiac arrhythmias
●An abnormality of the cardiac rhythm is called a cardiac arrhythmia.
● Arrhythmias may cause sudden death, syncope, heart failure, dizziness,
palpitations or no symptoms at all.
● There are two main types of arrhythmia:
- Bradycardia: the heart rate is slow (< 60 b.p.m).
- Tachycardia: the heart rate is fast (> 100 b.p.m).
12. Mechanisms of Cardiac Arrhythmias
Mechanisms generating tachycardias include:
Accelerated automaticity.
Triggered activity
Re-entry (or circus movements)
Mechanisms of bradicardias:
Sinus bradycardia is a result of abnormally slow automaticity while bradycardia
due to AV block is caused by abnormal conduction within the AV node or the
distal AV conduction system.
13. ACCELERATED AUTOMATICITY
- It occurs due to increasing the rate of diastolic depolarization or changing the
threshold potential.
- Abnormal automaticity can occur in virtually all cardiac tissues and may initiate
arrhythmias.
- Such changes are thought to produce sinus tachycardia, escape rhythms and
accelerated AV nodal (junctional) rhythms.
14. AUTOMATICITY CAN BE FROM INCREASED SNS TONE:
- Anxiety
- Fever
- Thyrotoxicosis
- MI
- Overdose –Drug abuse
TREATMENT:
1- Treat underlying problem
2- Treat with drugs to reduce automaticity
3-Overdrive pacing
15. TRIGGERED ACTIVITY
-Myocardial damage can result in oscillations of the transmembrane potential at
the end of the action potential. These oscillations, which are called 'after
depolarizations', may reach threshold potential and produce an arrhythmia.
-The abnormal oscillations can be exaggerated by pacing, catecholamines,
electrolyte disturbances, and some medications.
- Examples as atrial tachycardias produced by digoxin toxicity and the initiation of
ventricular arrhythmia in the long QT syndrome.
16. Re-entry (or circus movement)
When a cardiac impulse travels in a path such as
to return to and reactivate its original site and
self perpetuate rapid reactivation independent of
normal sinus node conduction.
Requires:
-- Available circuit
- Unequal responsiveness of the 2 segments of
the circuits
- Slow conduction in one limb
- Re-excitation of the initial blocked pathway
17. Arrhythmia Approach
1- Prepare IV, O2, monitor, airway equipment and defibrillator.
2- Is the patient stable or unstable?
3- Is the rate regular or irregular?
4- Narrow complex narrow or wide?
5- Are there P waves?
6- Are the P waves of the same morphology?
7- Are they related to the QRS?
8- Are there flutter waves?
18. IS THE PATIENT STABLE OR UNSTABLE?
Unstable Patient:
•Ischemic Chest pain
•Hypotension
•Altered LOC
•Poor perfusion
•CHF
70% of patient with tachyarrhythmias
complain of chest pain most not
having MI
Unstable usually means cardioversion or
defibrillation but may sometimes try
medications.
19. Is the rate regular or irregular
Irregular rhythms usually generated about the AV
node and treatment consist of blocking AV Node
20. Are the QRS Wide or Narrow
> 0.12 seconds (or 3 small squares) = wide. Most
much greater than 0.12
Wide rhythms
•Block of normal conduction
pathway (BBB)
•Rhythm start in ventricle
Safest to assume wide rhythms are
ventricular
21. ARE THERE P WAVES
Are they related to the QRS?
•Check the different leads
•? From sinus node (P upright in
II, negative in aVR)
Are there flutter waves?
•Saw tooth
•Regular at 150
Are the P waves of the same morphology?
•MAT at least 3 different P waves
25. Background
It is characterized by an irregular and often rapid heartbeat.
This classification schema pertains to cases that are not related to a reversible cause of AF (eg,
thyrotoxicosis, electrolyte abnormalities, acute ethanol intoxication).
Classification of AF:
1- Paroxysmal AF – Episodes of AF that terminate spontaneously within 7days (most
episodes last less than 24 hours).
2- Persistent AF - Episodes of AF that last more than 7 days and may require either
pharmacologic or electrical intervention to terminate.
3- Permanent AF - AF that has persisted for more than 1 year, either because
cardioversion has failed or because cardioversion has not been attempted.
26. Etiology
Atrial fibrillation (AF) is strongly associated with the following risk factors:
- Hemodynamic stress.
- Atrial Ischemia.
- Inflammation: Myocarditis and Pericarditis (idiopathic or associated with
infections, collagen vascular disease or surgeries).
- Noncardiovascular respiratory causes – PE, pneumonia, lung cancers.
- Alcohol and drugs use.
- Endocrine disorders e.g. hyperthyroidism, DM, Pheochromocytoma
- Neurologic disorders e.g. SAH, stroke
- Advancing age - strongly age-dependent, affecting 4% of individuals older
than 60 years and 8% of persons older than 80 year
27. History
- Initial evaluation – hemodynamic stability .
- While up to 90% of AF episodes may not cause symptoms, many patients
experience a wide variety of symptoms, including palpitations, dyspnea,
fatigue, dizziness, angina, and decompensated heart failure.
- Any precipitating factors, history of heart disease, previous episode and how
was it terminated.
28. Physical Examination
- Heart rate, blood pressure, respiratory rate, and oxygen saturation are
particularly important in evaluating hemodynamic stability and adequacy of rate
control in AF.
- Patients will have an irregularly irregular pulse and will commonly be
tachycardic, with heart rates typically in the 110- to 140-range, but rarely over
160-170. Patients who are hypothermic or who have cardiac drug toxicity may
present with bradycardic atrial fibrillation.
- The physical examination also provides information on underlying causes and
sequelae of atrial fibrillation.
29. Diagnosis
• The diagnosis of atrial fibrillation is based on the physical finding of an
irregular heart rhythm and is confirmed with an ECG or rhythm strip.
• It appears on ECG as irregularly irregular narrow complex tachycardia
• Discrete P waves are absent, replaced by irregular, chaotic F waves, in the
setting of irregular QRS complexes
• The ventricular rate is usually between 80 and 180 bpm.
• It is important to pay attention to the electrocardiographic signs of associated
cardiac diseases, such as left ventricular hypertrophy and preexcitation.
30.
31.
32. Treatment and Management
• The cornerstones of atrial fibrillation management are rate control and
anticoagulation and rhythm control for those symptomatically limited by
AF.
• One of the major management decisions in AF is determining the risk of
stroke and appropriate anticoagulation regimen for low-, intermediate-,
and high-risk patients. For each anticoagulant, the benefit in terms of
stroke reduction must be weighed against the risk of serious bleeding.
• Several risk factor assessment algorithms have been developed to aid
the clinician on decisions on anticoagulation for patients with AF. The
CHADS2 index (Cardiac failure, Diabetes, Stroke [or S2 = transient ischemic
attack]) is the most widely used of these algorithms. The CHADS2 index
uses a point system to determine yearly thromboembolic risk.
36. The updated guidelines also state the following :
• Evidence indicates that aspirin’s use as a means of lowering stroke risk in
patients with AF should be reduced or eliminated
• In addition to warfarin, 3 new anticoagulants are recommended for patients
with nonvalvular AF who have previously suffered a stroke or TIA or whose CHA2
DS2 –VASc score is 2 or above: dabigatran etexilate, rivaroxaban, and apixaban
• Radiofrequency catheter ablation can be used as initial treatment in recurrent
symptomatic paroxysmal AF.
37.
38. Rate Control
• Control of ventricular rate is a critical component of management of new
onset AF
• Beta-blockers and calcium channel blockers are first-line agents for rate
control in AF. These drugs can be administered either intravenously or orally.
Commonly used are IV metoprolol or diltiazem in AF with RVR.
• Amiodarone can be used as a rate-controlling agent for patients who are
intolerant of or unresponsive to other agents, such as patients with CHF who
may otherwise not tolerate diltiazem or metoprolol.
• In patients with inadequate ventricular rate control despite drug therapy,
atrioventricular (AV) nodal ablation and pacemaker implantation may be
considered
39. Anticoagulation
• Acute cardioversion for AF carries a risk of thromboembolism unless
anticoagulation therapy is initiated prior to the procedure and continued post
procedure. Risk of thromboembolism is similar in patients undergoing either
pharmacologic or electrical cardioversion. The risk of thromboembolic events is
greatest when AF has been present for longer than 48 hours.
• Patients with newly diagnosed AF and patients awaiting electrical
cardioversion can be started on intravenous heparin (activated partial
thromboplastin time [aPTT] of 45-60 seconds) or low-molecularweight heparin
(1 mg/kg bid).
• Patients can be started concomitantly on warfarin in an inpatient setting while
awaiting a therapeutic INR value (2-3).
• New anticoagulants: dabigatran, rivaroxaban, apixaban
40.
41. Long-Term Management
• Long-term management of atrial fibrillation is focused on reducing the likelihood of AF
recurrence, reducing AF-related symptoms, control of ventricular rate, and reducing stroke risk.
• Anticoagulation with either aspirin or warfarin should be initiated for all individuals with AF,
except those with contraindications. Selection of the appropriate antithrombotic regimen for a
given patient should be balanced between the risk of stroke and the risk of bleeding.
• Antiarrhythmic therapy can aid in maintenance of sinus rhythm in certain patients but requires
close monitoring
• As a rule, younger patients with more severe symptoms and fewer comorbidities tend to derive
greater benefit from a long-term focus on rhythm control. Older patients with structural heart
disease (e.g., left ventricular hypertrophy, prior MI, depressed ejection fraction, atrial dilation) are
less likely to remain in sinus rhythm and are more likely to have serious side effects from
antiarrhythmic drugs, most clinicians focus on long-term rate control.
42. New anticoagulant regimens
• Compared with warfarin, low-dose new anticoagulant regimens showed similar overall
reductions in stroke or systemic embolic events and a more favorable bleeding profile, but
significantly more ischemic strokes
• Guidelines from the American College of Cardiology Foundation (ACCF)/American Heart
Association (AHA)/Heart Rhythm Society (HRS) on atrial fibrillation have been updated to
include the use of oral direct thrombin inhibitors (ie, dabigatran)
• The guidelines recommend dabigatran may be used as an alternative to warfarin for the
prevention of stroke and systemic thromboembolism in patients with paroxysmal-to-permanent
atrial fibrillation and risk factors for stroke or systemic embolization. Patients with atrial
fibrillation who are not candidates include those with prosthetic heart valves or
hemodynamically significant valve disease, severe renal failure (creatinine clearance ≤15
mL/min), or advanced liver disease.
43. Rate Control
• AV nodal blocking medications are the cornerstone of rate control in
longstanding AF, oral beta-blockers, nondihydropyridine calcium channel
blockers, and digoxin are effective. Generally, co administration of beta blockers
and calcium channel blockers is reserved for patients in whom adequate rate
control cannot be achieved with a single agent.
• Digoxin can be effective in sedentary patients (especially in those with heart
failure) but requires close monitoring of drug levels and renal function.
44.
45. Supraventricular Tachycardia (SVT)
- Supraventricular tachycardias (SVTs) arise from the atrium or the
atrioventricular junction.
- Conduction is via the His-Purkinje system; therefore the QRS shape during
tachycardia is usually similar to that seen in the same patient during baseline
rhythm.
- In the absence of a bundle branch block, there is intact conduction to the
ventricles via the right and left bundles leading to a narrow and normal-
appearing QRS. Therefore, these arrhythmias are also often called narrow
complex tachycardias
53. Sinus Tachycardia
• Essentials of Diagnosis:
- Onset and termination: gradual
- Heart rate: 100 to (220 – age) bpm.
- P wave: identical to normal sinus rhythm P wave.
- R-P relationship: long
Symptoms may occur with rapid heart rates including; weakness, fatigue, dizziness, or
palpitations.
• Sinus tachycardia is often temporary, occurring under stresses from exercise, strong
emotions, fever, dehydration, thyrotoxicosis, anemia and heart failure.
• If necessary, beta-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism
54.
55. Atrial Arrhythmias
Atrial Flutter (HR 200-350/min)
- A condition in which the electrical signals come from the atria at a fast but
even rate, often causing the ventricles to contract faster and increase the heart
rate.
- When the signals from the atria are coming at a faster rate than the ventricles
can respond to, the ECG pattern develops a signature "sawtooth" pattern,
showing two or more flutter waves between each QRS complex.
56.
57.
58.
59. Treatment of Atrial Flutter:
- Treatment of the symptomatic acute paroxysm is electrical cardioversion.
- Patients who have been in atrial flutter more than 1-2 days should be treated in a
similar manner to patients with atrial fibrillation and anticoagulated for 4 weeks
prior to cardioversion.
- The treatment of choice for patients with recurrent atrial flutter is radiofrequency
catheter ablation
- Several antiarrhythmic agents can prevent recurrences of atrial flutter. It appears
that both class Ia and Ic agents are effective. Class III agents, such as sotalol and
amiodarone, can also work very well.
- It should be emphasized that an AV nodal blocking agent should be started before
initiating a class I drug. If the AV node is unblocked, a type I agent could facilitate
conduction of atrial flutter by improving nodal conduction or by slowing the flutter
rate and paradoxically increasing the ventricular response.
60. Paroxysmal Supraventricular tachycardia [HR 160-250/min]
Atrioventricular nodal re-entry tachycardia (AVNRT)
- It usually begins and ends rapidly, occurring in repeated periods. This condition can cause
symptoms such as weakness, fatigue, dizziness, fainting, or palpitations if the heart rate
becomes too fast.
- In AVNRT, there are two functionally and anatomically different pathways within the AV
node: one is characterized by a short effective refractory period and slow conduction, and the
other has a longer effective refractory period and conducts faster.
- In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the
fast pathway.
- If the atrial impulse (e.g. an atrial premature beat) occurs early when the fast pathway is still
refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles. It
then travels back through the fast pathway which has already recovered its excitability, thus
initiating the most common 'slow-fast', or typical, AVNRT.
61.
62. AVNRT
The rhythm is recognized on
ECG by normal regular QRS
complexes, usually at a rate
of 140-240 per minute.
Sometimes the QRS
complexes will show typical
bundle branch block. P
waves are either not visible
or are seen immediately
before or after the QRS
complex because of
simultaneous atrial and
ventricular activation
63.
64.
65. SVT
Atrioventricular reciprocating tachycardia (AVRT)
- In AVRT there is a large circuit comprising the AV node, the His bundle, the
ventricle and an abnormal connection from the ventricle back to the atrium.
This abnormal connection is called an accessory pathway or bypass tract.
- Bypass tracts result from incomplete separation of the atria and the ventricles
during fetal development.
- Atrial activation occurs after ventricular activation and the P wave is usually
clearly seen between the QRS and T complexes
66.
67.
68. PSVT
Acute Management
- Patients presenting with SVTs and haemodynamic instability require
emergency cardioversion.
- If the patient is haemodynamically stable, vagal manoeuvres, including right
carotid massage, Valsalva manoeuvre and facial immersion in cold water can be
successfully employed.
- If not successful, intravenous adenosine (up to 0.25 mg/kg) , verapamil 5-10
mg i.v. over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried.
Long-term management
- It includes ablation of an accessory pathway. Also, verapamil, diltiazem & β-
blockers; are effective in 60-80% of patients.
69. Multifocal Atrial Tachycardia (MAT)
- It is related to pulmonary disease in 60–85% of cases, with chronic obstructive
pulmonary disease (COPD) exacerbation being the most common.
-In addition, MAT is precipitated by respiratory failure, acute decompensated
cardiac function, and infection.
-Distention of the right atrium from elevated pulmonary pressures causes
multiple ectopic foci to fire, with ventricular rates not usually exceeding 150
bpm.
- Whether this rhythm is due to abnormal automaticity or triggered activity is
uncertain, but the ability of verapamil to suppress the ectopic atrial activity by
virtue of its calcium channel blocking properties supports the latter assumption.
70. - Three ECG criteria must be met to diagnose MAT:
(1) the presence of at least 3 distinct P-wave morphologies recorded in the same lead;
(2) the absence of one dominant atrial pacemaker;
(3) varying P-P, P-R, and R-R intervals.
- Treatment:
- The primary treatment for MAT should be directed at the underlying disease state.
- Oral and intravenous verapamil and several formulations of intravenous β-blockers have been
effective to varying degrees in either slowing the heart rate (without terminating the rhythm) or
in converting the arrhythmia to sinus rhythm.
71.
72.
73.
74. Atrial Arrythmias
Premature supraventricular contractions or premature atrial
contractions (PAC):
- A condition in which an atrial pacemaker site above the ventricles sends out an
electrical signal early. The ventricles are usually able to respond to this signal,
but the result is an irregular heart rhythm.
- PACs are common and may occur as the result of stimulants such as coffee, tea,
alcohol, cigarettes, or medications.
- Treatment is rarely necessary.
75.
76.
77. The Wolff Parkinson White Syndrome
(WPW)
►An abnormal band of atrial tissue connects the atria and ventricles and
can electrically bypass the normal pathways of conduction; a re-entry
circuit can develop causing paroxysms of tachycardia. Kent bundle act as
direct link between atria and ventricles -bypass AV Node
►ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
►Drug treatment includes flecainamide, amiodarone or disopyramide.
►Digoxin and verapamil are contraindicated.
►Transvenous catheter radiofrequency ablation is the treatment of
choice.
78.
79. TREATMENT FOR STABLE PT.
- WPW A-FIB:
•Caridoversion or
Procainanamide
- ATRILA FIB WITH BBB:
•Same as for narrow complex
irregular tachycardia
TREATMENT FOR UNSTABLE PT.
•Cardioversion
80.
81.
82.
83. Ventricular Tachyarrhythmias
Ventricular tachyarrhythmias can be considered under the following headings:
- Life-threatening ventricular tachyarrhythmias (Sustained ventricular
tachycardia and ventricular fibrillation)
- Torsades de pointes
- Normal heart ventricular tachycardia
- Non-sustained ventricular tachycardia
- Ventricular premature beats
84. Ventricular Arrhythmias
Ventricular Tachycardia (VT)
- A condition in which an electrical signal is sent from the ventricles at a very fast
but often regular rate.
- The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more),
abnormal QRS complexes. AV dissociation may result in visible P waves
- Treatment: in haemodynamically compromised patients, emergency DC
cardioversion may be required. If the blood pressure and cardiac output are well
maintained, intravenous therapy with class I drugs or amiodarone is usually
used. First-line drug treatment consists of lidocaine (50-100 mg i.v. over 5
minutes) followed by a lidocaine infusion (2-4 mg i.v. per minute). DC
cardioversion is necessary if medical therapy is unsuccessful.
85.
86. Ventricular Tachyarrhythmias
Ventricular Fibrillation (VF)
- A condition in which many electrical signals are sent from the ventricles at a very fast and
erratic rate. As a result, the ventricles are unable to fill with blood and pump.
- This rhythm is life-threatening because there is no pulse and complete loss of consciousness.
- The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes
- A person in VF requires prompt defibrillation to restore the normal rhythm and function of the
heart. It may cause sudden cardiac death. Basic and advanced cardiac life support is needed
- Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable reversible
cause (e.g. acute myocardial infarction, severe metabolic disturbance), at high risk of sudden
death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management
of these patients
87.
88.
89. Ventricular Tachyarrhythmias
Torsades de Pointes
- This is a type of short duration tachycardia that reverts to sinus rhythm spontaneously.
- It may be due to:
- Congenital
- Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia.
- Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics.
- It may present with syncopal attacks and occasionally ventricular fibrillation.
- QRS complexes are irregular and rapid that twist around the baseline. In between the
spells of tachycardia the ECG show prolonged QT interval.
90.
91.
92. Torsades de Pointes (Treatment):
- Treatment includes; correction of any electrolyte disturbances, stopping of
causative drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol (mg2+)
over 10-15 min for acquired long QT, IV isoprenaline in acquired cases and B
blockers in congenital types
- Long-term management of acquired long QT syndrome involves avoidance of
all drugs known to prolong the QT interval. Congenital long QT syndrome is
generally treated by beta-blockade, left cardiac sympathetic denervation, and
pacemaker therapy. Patients who remain symptomatic despite conventional
therapy and those with a strong family history of sudden death usually need ICD
therapy.
93. Ventricular Arrhythmias
Premature Ventricular Contractions (PVCs):
- A condition in which an electrical signal originates in the ventricles and causes
the ventricles to contract before receiving the electrical signal from the atria.
- ECG shows wide and bizarre QRS complex
- Early 'R-on-T' ventricular premature beats may induce ventricular fibrillation
- PVCs are not uncommon and often do not cause symptoms or problems.
- Treated only if symptomatic with beta-blockers.
