Objective 1: Differentials and risk factors for palpitations

Objective 2: Link impulse transmission in the heart with the

molecular events of cardiac action potential.
Objective 3: Cardiac impulse pathway in both normal and
abnormal conditions.
Objective 4: Discuss different types/classification of arrhythmias
Objective 5: Discuss different types of heart.
Objective 6: Pacemakers and the indications for temporary and
permanent pacemaker
Objective 7: Atrial Fibrillation
a. Causes
b. Pathogenesis
c. Diagnosis
d. Presentation
e. Investigations
f. Complications

Objective 8: Compare normal and abnormal findings on the

electrocardiogram in the case of atrial fibrillation.
Objective 9: CHA2DS2-VASc score
Objective 10: Atrial fibrillation: principles of management of atrial
fibrillation.
Objective 11: Why did they continue the amiodarone after
pacemaker insertion? How long do you need to continue
management for that case?
Objective 12: Pharmacology of drugs; metoprolol and amiodarone
and their toxic effects.
Objective 13: Relate the presenting signs and symptoms of
syncope to its pathophysiological basis.
 Part I
Mr. Arshad Khan, a retired government officer, enjoyed his early morning stroll in a
nearby park. However, for the last month, he had been feeling extremely tired and was
having difficulty in carrying out his daily activities. In addition, he was also experiencing
occasional episodes of palpitation lasting for two to three minutes. One morning he
experienced similar symptoms of palpitation and as these symptoms did not resolve he
was taken to a nearby hospital.

Part II
On examination, Mr. Khan was found to have a pulse of 160 beats per minute,
irregularly irregular and blood pressure of 110/60 mm of Hg. On auscultation of the
precordium, there was varying intensity of the first heart sound and examination of the
chest revealed clear lung fields.
The electrocardiogram revealed atrial fibrillation with a rapid ventricular response.

Part III
Investigations show:
CBC: Hb: 13.2 g/dl, HCT: 40 %, MCV 81 fl, MCH: 28 pg
WBC 6.2 x 109/l, Platelets: 340 x106/
Serum Creatinine 1.2 mg/dl
K+ 4.8 mEq/L, Na+ 138 mEq/L, Cl- 104 mEq/L, HCO3- 24 mEq/L
Troponin T: 0.01 ng/ml
B-type natriuretic peptide (BNP): 57 pg/ml
TSH: 1.4 mIU/L
Normal echocardiogram.
Initial administration of intravenous metoprolol did not result in a significant slowing of
the ventricular rate. Therefore, after appropriate anticoagulation, the patient was started
on an infusion of amiodarone. Following initiation of IV amiodarone, he reverted to sinus
rhythm. He was kept under observation for 24 hours during which he had no further
episode of palpitation and was subsequently discharged on oral amiodarone and
rivaroxaban.

Part IV

Two weeks later, when his son went to wake him up in the morning, he found Mr. Khan
lying on the floor unresponsive. He was rushed to a nearby hospital where he was
found to be drowsy with a pulse of 36 beats per minute and blood pressure of 70/40 mm
of Hg. JVP was 7 cm with occasional rise to 12 cm. ECG revealed sinus arrest with a
junctional escape rhythm. A temporary pacemaker was applied.

The next morning, the cardiologist told Mr. Khan that he would require a permanent
pacemaker as the natural pacemaker within his heart was not functioning properly. In
addition, he would also require oral amiodarone (for his symptoms of palpitation) and
rivaroxaban. “How does an artificial pacemaker work?” asked one of the medical
students. The doctor explained that the cardiac pacemaker replicates the depolarization
that occurs at the cellular level in the sinus node thereby mimicking its actions. The
following day a permanent pacemaker was inserted, and Mr. Khan was subsequently
discharged from the hospital.
 Gender: Male.
 Occupation: Retired government officer.
 Main complaint: In the morning, he had palpitations that didn`t resolve.
 Previously: For the last month, he felt hardly tired and had episodes of
palpitation for 2-3 min.
 Examination:
o Pulse 160 beats/min, irregularly irregular. (Tachycardia).
o Bp 110/60 mm of Hg (normal).
o Auscultation of the precordium: varying intensity of the first heart sound.
o Examination of the chest: clear lung fields.
 The electrocardiogram revealed atrial fibrillation with a rapid ventricular
response.

(Interpretation: the rate is Tachycardic, the rhythm is irregularly irregular, no

obvious P-wave, narrow QRS).
  Investigations:
o CBC: Hb, HCT, MCV, MCH, WBC, and platelets (we can consider them
around the normal, so exclude anemia).
o Serum Creatinine is normal.
o K+, Na+, Cl-, HCO3- are normal.
o Troponin T is normal (We can exclude MI).
o B-type natriuretic peptide (BNP) is normal (We can exclude Congestive
heart failure).
o TSH: normal (We can exclude hyperthyroidism).
o Normal echocardiogram.

 Management:
o IV Metoprolol didn`t slow ventricular rate significantly.
o After the anticoagulation was given, an IV Amiodarone was started and
followed by a reverted sinus rhythm.
o After 24 hours of observation, the patient was discharged on oral
amiodarone and rivaroxaban.

 After two weeks, he was found unresponsive lying on the floor.

 He was drowsy.
 lower pulse (36 beats/min) and BP (70/40 mm Hg).
 At first, JVP was 7cm (normal), but then it rose to 12cm.
 Sinus arrest with a junctional escape rhythm was revealed by the ECG.
 They applied a temporary pacemaker.
 The cardiologist informed him that he needs
 A permanent pacemaker because his natural one isn't working well.
 Require oral amiodarone (For the palpitation) and rivaroxaban.
 After the insertion of the permanent pacemaker, the patient was discharged.

(Interpretation: There are P-waves, QRS less than three small boxes (narrow) and
sometimes the QRS disappears for some P-waves. It seems like the P-waves are there
but alone with no relation to QRS, so it is most likely a third-degree heart block).
01. Differentials and risk factors for palpitations.
Differentials

 Atrial Fibrillation:
o A common arrhythmia characterized by rapid and irregular electrical
signals in the atria, causing them to fibrillate (quiver) instead of contracting
effectively.
o Patients may experience palpitations as their heart rhythm becomes
erratic.
 Supraventricular Tachycardia (SVT):
o A group of heart rhythm problems (arrhythmias) that originate above the
ventricles, usually in the atria or the atrioventricular (AV) node.
o These arrhythmias are characterized by an abnormally fast heart rate,
often exceeding 100 beats per minute.
o Palpitations in SVT are typically sudden in onset and can be felt as a
rapid, regular pounding in the chest.
o SVT can be triggered by stress, caffeine, alcohol, or thyroid dysfunction.
 Premature Ventricular Contractions (PVCs):
o early heartbeats originating from the ventricles. These extra beats disrupt
the regular heart rhythm often causing a sensation of the heart skipping a
beat or fluttering.
o They can cause palpitations, often described as a skipped beat or a strong
beat.
o PVCs can be idiopathic or associated with electrolyte imbalances, heart
disease, or stimulants.
 Panic Attack or Anxiety Disorder:
o Palpitations are a common symptom of panic attacks and anxiety
disorders.
o During a panic attack, the release of adrenaline leads to increased heart
rate and palpitations.
o Anxiety can also cause hyperawareness of one's heartbeat, making
normal variations feel like palpitations.
 Hyperthyroidism:
o In hyperthyroidism, excess thyroid hormone increases the metabolic rate,
leading to symptoms such as palpitations, increased heart rate
(tachycardia), and sometimes atrial fibrillation.
o Common causes include Graves' disease and toxic multinodular goiter.
 Mitral Valve Prolapse (MVP):
 o MVP is a condition where the mitral valve does not close properly,
allowing blood to leak backward into the left atrium.
o It is associated with palpitations, often due to the accompanying
arrhythmias or autonomic dysfunction.

Anemia:

o Anemia, particularly severe cases, can lead to palpitations as the heart

compensates for reduced oxygen-carrying capacity by pumping more
frequently and forcefully.
o Common causes include iron deficiency, chronic disease, or hemolysis.
Palpitations may be accompanied by fatigue, weakness, and shortness of
breath.

Risk Factors

 Caffeine Intake
 Stress and Anxiety
 Hyperthyroidism
 Electrolyte Imbalances
 Alcohol Consumption
 Cardiovascular Disease
 Smoking
 Recreational Drug Use

Resource: NIH

02. Link impulse transmission in the heart with the molecular events
of cardiac action potential.
Myocardial Action Potential (Myocardium, Bundle of His, Purkinje Fibres)

Phase 0: Upstroke and Depolarization

Upstroke: An action potential from a pacemaker cell or adjacent cardiomyocyte

causes the transmembrane potential (TMP) to rise above -90 mV.

Depolarization: Fast voltage-gated Na⁺ channels open at -65 mV, leading to a

rapid influx of Na⁺ into the cell. This raises the TMP further, eventually reaching
just above 0 mV.

Phase 1: Early Repolarization

Na⁺ Channel Inactivation: Voltage-gated Na⁺ channels inactivate.

 K⁺ Efflux: Transient K⁺ channels open, allowing K⁺ to flow out, which returns the
TMP to around 0 mV.

Phase 2: Plateau Phase

Ion Balance: K⁺ efflux continues through delayed rectifier K⁺ channels, while

Ca²⁺ influx occurs through voltage-gated L-type Ca²⁺ channels. This Ca²⁺ influx
triggers additional Ca²⁺ release from the sarcoplasmic reticulum (Ca²⁺-induced
Ca²⁺ release), leading to myocyte contraction.

Plateau Maintenance: Unlike skeletal muscle, cardiac myocytes require

extracellular Ca²⁺ for this process. The TMP remains stable just below 0 mV
during this phase.

Phase 3: Rapid Repolarization

Ca²⁺ Channel Inactivation: Voltage-gated Ca²⁺ channels close.

K⁺ Efflux: K⁺ efflux continues through delayed rectifier K⁺ channels. The

persistent K⁺ outflow surpasses Ca²⁺ inflow, bringing the TMP back down to -90
mV.

Restoration of Ionic Gradients: The Na⁺/Ca²⁺ exchanger, Ca²⁺-ATPase, and

Na⁺/K⁺-ATPase restore normal ionic concentrations, with Na⁺ and Ca²⁺ returning
to the extracellular space and K⁺ to the intracellular space.

Phase 4: Resting Phase

Resting Membrane Potential: The resting membrane potential is stable at -90
mV,
maintained by the continuous outward flow of K⁺ through inward rectifier
channels.

Channel Status: Na⁺ and Ca²⁺ channels remain closed.

2. Pacemaker Action Potential (SA Node and AV Node)

Phase 0: Upstroke

Depolarization: When the transmembrane potential (TMP) reaches -40 mV (the

threshold potential for pacemaker cells), L-type Ca²⁺ channels open, leading to
an influx of Ca²⁺ ions and increasing the TMP to approximately +40 mV.

Slower Conduction: There is no rapid depolarization because fast voltage-

gated Na⁺ channels are inactivated in pacemaker cells. This results in a slower
conduction velocity between the atria and ventricles.
 Phase 1 and Phase 2: Absent

Pacemaker cells do not exhibit distinct Phase 1 or Phase 2 as seen in other

cardiac cells.

Phase 3: Repolarization

Ion Movement: Voltage-gated Ca²⁺ channels close, and delayed rectifier K⁺

channels open, allowing K⁺ to exit the cell. This K⁺ efflux brings the TMP back
down to around -60 mV.

Phase 4: Spontaneous Depolarization

Unstable Membrane Potential: There is no true resting phase; instead, the

membrane potential is unstable.

Funny Current: Slow, spontaneous depolarization occurs due to the gradual

entry of Na⁺ and K⁺ through funny channels (I\(_f\) channels), raising the TMP
above -60 mV without the need for an external action potential. This reflects the
automaticity of the SA and AV nodes.

T-type Ca²⁺ Channels: At TMP around -50 mV, T-type Ca²⁺ channels open,
further contributing to depolarization.

Sympathetic Stimulation: Increases the conductance of I\(_f\) channels,

which steepens the slope of Phase 4, thereby increasing the heart rate.

Resource: Amboss

03. Describe the cardiac impulse pathway from its generation to its
spread in both normal and abnormal conditions.

 Normal:
o The SA node starts the sequence by causing the atrial muscles to
contract.
o The signal travels to the AV node, where it’s delayed for a fraction of a
second
o Then it goes through the bundle of HIS, down the bundle branches, and
through the Purkinje fibres, causing the ventricles to contract.

 Abnormal:
o Sick sinus syndrome (SSS):
  group of heart rhythm disorders caused by the malfunction of the
sinus node, the heart's natural pacemaker.
 The sinus node is responsible for initiating the electrical impulses
that regulate the heart's rhythm.
 When this node fails to function properly, it can lead to various
arrhythmias.
 Sinus Bradycardia → The heart rate is slower than normal,
typically less than 60 beats per minute, due to reduced
impulse generation by the sinus node.
 Sinus Arrest or Pause → There are prolonged periods
without any sinus node activity, leading to missed
heartbeats.
 Sinoatrial Block → The impulse generated by the sinus
node is blocked or delayed from reaching the atria.
 Tachy-Brady Syndrome → A combination of fast
(tachycardia) and slow (bradycardia) heart rhythms. This is
often seen with atrial fibrillation or flutter alternating with
periods of slow heart rate.

 Chronotropic Incompetence → The heart's inability to

increase its rate appropriately in response to physical activity
or stress.

o Atrioventricular block:
 First-Degree Heart Block → Characterized by a prolonged PR
interval (>200 ms) without dropped beats. The impulse is delayed
at the AV node but eventually reaches the ventricles.
 Second-Degree Heart Block:
 Mobitz Type I (Wenckebach) →The PR interval
progressively lengthens until a ventricular beat is dropped.
 Mobitz Type II → Random dropped beats without a
preceding PR interval change. This type is more serious and
often progresses to a complete block.
 Third-Degree (Complete) Heart Block → No atrial impulses reach
the ventricles. The atria and ventricles beat independently, often
with the ventricles relying on a slower, less reliable escape rhythm
originating below the block.

o Bundle branch blocks:

 Impulses are delayed or blocked in the right or left bundle
branches.
 Right Bundle Branch Block (RBBB): Delay in depolarization of the
right ventricle.
  Left Bundle Branch Block (LBBB): Delay in depolarization of the left
ventricle, which is more concerning as it can indicate underlying
heart disease.

o Fibrillation:
 Atrial Fibrillation (AFib): Rapid, irregular electrical impulses in the
atria cause them to quiver instead of contracting effectively.
 The irregular impulses reaching the AV node result in an
irregular ventricular rate, leading to inefficient blood flow and
increased risk of thromboembolic events, such as stroke.
 Ventricular Fibrillation (VFib): Chaotic electrical activity in the
ventricles leads to quivering rather than coordinated contraction,
resulting in a complete loss of effective cardiac output.
 VFib is a medical emergency requiring immediate
defibrillation to restore normal rhythm.

Resource: NIH website + Amboss

04. Discuss different types/classification of arrhythmias (including

Rapid Ventricular Response).
Supraventricular tachycardias: These are usually narrow complex tachycardias with
QRS width being less than 3 mm or 120 milliseconds on the EKG strip.

1. Atrioventricular reciprocating tachycardia (AVRT): As found in Wolff-

Parkinson-White syndrome
o Mechanism: Accessory pathway present outside of the AV node-Bundle
of Kent (an abnormal extra or accessory conduction pathway between the
atria and ventricles)
o Signs & Symptoms: Palpitation, shortness of breath, or syncope.
o EKG Findings: Slurred upstroke of the QRS, delta wave, may give an
impression of the wide QRS complex.

2. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

o Mechanism: Slow & fast fibers present in AV node & peri-nodal tissue
leading to re-entry.
o Signs & Symptoms: Sudden tachycardia, palpitation, shortness of
breath, chest tightness, or syncope.
o EKG Findings: Narrow complex tachycardia with P waves hidden in T
waves. Heart rate is in the range of 150-160 bpm.\
3. Atrial fibrillation:
o Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle
fibers near the proximal part of the pulmonary vein.
o Signs & Symptoms: Can be asymptomatic or can cause symptoms like
palpitation, shortness of breath, irregularly irregular pulse, or even
hypotension
o EKG Findings: Irregularly irregular narrow complex tachycardia with no
discernable P-waves
o Types, based on duration:
 New-onset
 Paroxysmal: Self-terminating or intermittent
 Persistent: Fails to self-terminate within 7 days and requires
treatments (medical or electrical cardioversion)
 Long-standing Persistent: Lasts for ≥ 1 year
 Permanent: Persistent for ≥ 1 year despite treatment
o Rapid ventricular response: a ventricular rate > 100–110/minute
occurring in response to a supraventricular tachyarrhythmia.

4. Atrial Flutter:
o Mechanism: Reentrant circuit usually around the tricuspid annulus in the
right atrium
o Signs & Symptoms: Can be asymptomatic, or it can cause palpitation,
shortness of breath, or hypotension
o EKG Findings: Regular tachycardia with Saw-tooth appearance of p-
wave with a variable degree of AV block

5. Ventricular Tachycardias: Origin is below the AV node

1. Non-Sustained Ventricular Tachycardia: When the rapid ventricular rhythm

terminates on its own within 30 seconds.
o Mechanism: Channelopathies secondary to structural abnormality,
electrolyte disturbances, metabolic imbalance, and the effect of pro-
arrhythmic drugs
o Risk Factors: Structural or ischemic heart disease
o Signs & Symptoms: Asymptomatic or palpitations
o EKG Findings: Monomorphic wide complex with more than three beats in
a row but lasts less than three seconds
2. Sustained Ventricular Tachycardia:
o Mechanism: Presence of damaged fibers in ischemic heart disease → re-
entry of current
o Risk Factors: Structural heart disease and post-myocardial infarction
o Signs & Symptoms: Palpitation,
hypotension, or syncope
o EKG Findings: Monomorphic wide
complex tachycardia

3. Ventricular Fibrillation
o Mechanism: Presence of damaged fibers
in ischemic heart disease → re-entry of
current → disorganized high-frequency
excitation. Patients with cardiomyopathies
can have ventricular fibrillation due to an
increase in end-diastolic pressure, wall
tension, or the presence of abnormal
channels in ventricular fibers.
o Signs & Symptoms: Syncope and death if
not treated immediately
o EKG Findings: Polymorphic fibrillatory
waves

4. Torsades De Pointes:
o Mechanism: It is usually precipitated by
premature ventricular contraction leading to
the “R on T phenomenon”, where a
ventricular depolarization is superimposed
on the previous beat’s repolarization.
o EKG Findings: Polymorphic wide-complex
tachycardia with a heart rate > 300 bpm.

Resource: MedBullets and NIH

05. Discuss different types of heart block (including sinus arrest) and
their management.
Heart blocks: types of arrhythmias that occur due to conduction problems in the
conduction system of the heart ( SAN, AVN, bundles and purkinje fibers)

Types of heart block include:

 1st degree AV-block:
o Prolonged PR-interval (>200ms), but everything else is normal:
 Normal rate and regular rhythm
 Normal upright P-wave
 Narrow QRS
 Every P-wave followed by QRS
o Treatment: usually asymptomatic and doesn’t require treatment

 2nd degree AV-block: 2 subtypes→ Mobitz 1 and Mobitz2

1. Mobitz type 1 (Wenckebach)
 Progressive prolongation of PR-interval, it continues on
prolonging until the beat is dropped
o beat is dropped → non-conducted P-wave: P-wave NOT
followed by QRS complex
 Treatment:
o Asymptomatic: no treatment required
o Symptomtic: pacemaker considered
 
1. Mobitz type 2
 PR-interval is constant (no prolongation or progressive
prolongation) but p-waves are not followed by a QRS (lots of
dropped beats)
 P-wave - no QRS, another p-wave - QRS → 2 p-waves before QRS
can be seen
 More severe than type 1 because it can progress into 3rd
degree/complete heart block
 Treatment: pacemaker to prevent the progression to 3rd degree

2. 3rd degree AV-block or Complete heart block

 Complete dissociation of signals between atria and ventricles
 Function independently of each other, as opposed to the normal
synchronized activity
 No relation between p-waves and QRS, not every p-wave has a
QRS and rhythm is irregular
  Treatment: pacemaker is required

Sinus arrest:
 SAN loses its automaticity and fails to generate an impulse down the normal
conduction system of the heart → temporary cessation of heart beats
 SAN normally causes atrial depolarization which gives us the p-wave, no SAN
activity→ no atrial depolarization→ no p-wave
 ECG will have absent p-waves.
 Treatment: Medications like BB and CCB, if severe then pacemaker

Summary picture
Resource: Pictures from Google , Osmosis + Lecture notes

06. Explain the pacemakers and the indications for temporary and
permanent pacemakers.

 Pacemakers are medical devices used to regulate the heartbeat in individuals

with abnormal heart rhythms.
 They work by sending electrical impulses to the heart to maintain a normal heart
rate and rhythm.
 They are composed of three parts: pulse generator, leads, and electrodes.
 There are two types: Permanent and Temporary
o Permanent pacemakers: involve creating a subcutaneous pocket for the
pulse generator. They do this by making a small incision just under the
collarbone. They provide continuous monitoring and pacing as needed to
ensure the heart maintains a normal rhythm and rate.
 Indictations:
 Bradycardia: This can be due to various types of heart
block or sick sinus syndrome.
 Atrial Fibrillation with Slow Ventricular Response: When
the heart’s upper chambers atria beat irregularly, and the
lower chambers ventricles do not respond adequately.
 Tachy-Brady Syndrome: A condition where the heart
alternates between very fast and very slow rhythms,
requiring a pacemaker to prevent bradycardia episodes.
 Heart Failure: In cases of heart failure, a pacemaker may be
used in conjunction with other treatments to improve the
heart's ability to pump blood
o Temporary pacemakers: use external generators connected to leads that
are inserted into veins and provide pacing temporarily and are monitored
closely.
 Indications:
 Acute Bradycardia: Temporary pacing may be needed in
emergency situations where the heart rate drops suddenly
due to conditions like heart attack, drug overdose, or severe
electrolyte imbalances.
 Post-Surgical: After certain cardiac surgeries or
procedures, temporary pacing might be used to ensure
proper heart function during recovery.
 Drug-Induced: Some medications can cause bradycardia or
heart block, and a temporary pacemaker may be used until
the effects of the drug are resolved.
  Diagnostic: Sometimes used temporarily to assess heart
function or the need for a permanent pacemaker.

Resource: American Heart Association + Mayo Clinic

07. Atrial Fibrillation:

A. Causes
The exact cause of atrial fibrillation is unknown, but it’s more common with old age ,and
it affects certain groups of people more than others. Some contributing factors include:

 Hemodynamic stress
o Increased intra-atrial pressure → atrial electrical and structural remodeling
→ predisposition to AF
 Causes of increased intra-atrial pressure: mitral or tricuspid valve
disease, left ventricular dysfunction, systemic or pulmonary
hypertension.
 Atrial ischemia
 Inflammation
o Myocarditis and pericarditis.
 Noncardiovascular respiratory causes
o PE, pneumonia, lung cancer, and hypothermia
 Alcohol and drug use
 Catecholamine excess
 Endocrine disorders
o Hyperthyroidism, diabetes, pheochromocytoma
 Neurologic disorders
o SAH or stroke
 Genetic factors
 Advancing age
o 4% of individuals older than 60 and 8% of individuals older than 80

Resource: MedScape

A. Pathogenesis
 In AF, the heart's atria (upper chambers) experience abnormal electrical
impulses that cause them to contract rapidly and irregularly.
 These impulses override the heart’s natural pacemaker, which normally
regulates a steady rhythm, causing a highly irregular pulse rate.
 The irregular and rapid contractions prevent the heart muscle from relaxing
properly between beats.
  This reduces the heart’s efficiency in pumping blood, leading to a decrease in
overall cardiac performance.
 The cause is not fully understood, but it tends to affect certain groups of people,
such as older people and people living with chronic conditions such as heart
disease, hypertension or obesity. It may also be triggered by certain situations
such as drinking too much alcohol or smoking.
 However, it’s important to note that AF can also occur in individuals without any
identifiable underlying conditions.

Resource: NHS.uk

A. Diagnosis
If an AF is suspected during auscultation of the patient→ obtain 12-lead ECG. Findings
from the ECG would usually confirm the diagnosis ,and it would include the following:
 Because AF is due to irregular atrial activation at the rate of 350-600 bpm with
irregular conduction through the atrioventricular node, it will appear on ECG as
irregularly irregular narrow complex tachycardia with an absent p wave.
 The F waves may be seen as fibrillatory waves or may be absent.
 Unless the heart is under excess sympathetic or parasympathetic stimulation, the
ventricular rate is usually between 80 and 180 bpm.
 With an abnormality in the intraventricular conduction system, the QRS
complexes may become wide.

Resource: MedScape

B. Presentation

 Patients can be in Asymptomatic (Stable) or Unstable states.

 Stable patients may present with less severe symptoms including:
o Palpitations
o Fatigue or poor exercise tolerance
o Presyncope or syncope
o Generalised weakness, dizziness, fatigue
 Unstable patients who require immediate DC cardioversion (defibrillation)
present with:
o Decompensated congestive heart failure (CHF)
o Hypotension
o Uncontrolled angina/ischemia

Resource: Medscape
 C. Investigations

 12 Lead ECG to confirm atrial fibrillation

 Serum cardiac biomarkers: To exclude ischemia
 B type natriuretic peptide
 Might need cardiac catheterization
 Thyroid function test
 Chest radiography: To exclude heart failure

Resource: Medscape

D. Complications

 Stroke: When the upper chambers of the heart (atria) do not pump efficiently, as
in atrial fibrillation, there's a risk of blood clots forming.These blood clots may
move into the lower chambers of the heart (ventricles) and get pumped into the
blood supply of the lungs or the general blood circulation. Clots in the general
circulation can block arteries in the brain, causing a stroke.

 Heart failure: If the atrial fibrillation is persistent, it may start to weaken the heart.
In extreme cases, it can lead to heart failure, as your heart is unable to pump
blood around your body efficiently.
 Those with hypertensive heart disease and valvular heart diseases are
particularly at high risk for developing heart failure when AF occurs.

Resource: NHS website , Medscape

08. Compare normal and abnormal findings on the electrocardiogram

in the case of atrial fibrillation.

Normal ECG Findings:

 Rhythm: Regular rhythm with consistent intervals between beats.

 P Waves:
o Present before each QRS complex.
o Smooth, rounded, and uniform in appearance.
o Occur at regular intervals, indicating regular atrial depolarization.
 QRS Complex:
o Follow each P wave consistently.
o Indicates synchronized atrial and ventricular activity.
 T Wave: Follows each QRS complex, indicating ventricular repolarization.
  Heart Rate: Typically 60-100 beats per minute in a resting adult.

Abnormal ECG Findings in Atrial Fibrillation (AF):

 Rhythm: Irregularly irregular rhythm (the heartbeats occur at random

intervals with no predictable pattern); intervals between QRS complexes are
variable.
 P Waves:
o Absent due to lack of coordinated atrial depolarization.
o Replaced by small, erratic fibrillatory waves (F waves).
 Fibrillatory Waves (F waves):
o Irregular, chaotic waves varying in size, shape, and timing.
o Best seen in leads V1, V2, or the inferior leads (II, III, aVF).
 QRS Complex:
o Normal in shape but occur at irregular intervals.
o Reflects inconsistent transmission of impulses through the AV node.

 Ventricular Rate:
o Variable; can be slow (bradycardia), normal, or fast (tachycardia)
depending on impulse transmission.
 R-R Intervals: The intervals between successive R waves (which correspond to
the ventricular contractions) are variable and irregular due to the irregular atrial
impulses reaching the AV
node.
 Resource: ECG in arrhythmias Lecture + American Heart Association (AHA)
Guidelines

09. Explain CHA2DS2-VASc score and its indications.

 CHA2DS2-VASc is a point-based scoring system for assessing the risk of

stroke in Afib patients. The acronym CHA2DS2-VASc stands for congestive heart
failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular
disease, age 65 to 74 and sex category (female).

 Although it’s beneficial, it’s not used in conditions including:

 Moderate to severe mitral stenosis
 Mechanical heart valves
 HCM (Hypertrophic Cardiomyopathy)

Why?

1. Mitral stenosis (increased stroke risk): Patients with moderate to severe mitral
stenosis have significantly elevated risk of stroke due to

A. Turbulent blood flow

B. Thrombus formation in the left atrium

Therefore, The CHA2DS2-VASc score may underestimate this risk by focusing on other
factors.

1. Mechanical heart valves (anticoagulation requirement): Patients with

mechanical heart valves are typically on anticoagulation therapy regardless of
their CHA2DS2-VASc score, so they are at high risk for thromboembolic events,
and the score does not capture the inherent stroke risk.
2. HCM (complex risk factors): Patients with HCM (hypertrophic cardiomyopathy)
have their own risk factors for stroke which includes
A. The potential for arrhythmias
B. Left atrial enlargement

Therefore, The CHA2DS2-VASc score may not fully account for these additional risks,
leading to potential under-treatment or over-treatment decisions.
 CHA2DS2-VASc scoring system:

 Risk of stroke (interpretation of the score):

 0 points (male) or 0–1 point (female) > low risk
 1 point (male) or 2 points (female) > intermediate risk
 ≥ 2 points (male) or ≥ 3 points (female) > high risk

Resource: AMBOSS

10. Atrial fibrillation: principles of management of atrial fibrillation

(rate control, anticoagulation, & rhythm control).

 Rate control + Rhythm control

o Anti-arrhythmic drugs
 Beta blockers
 selective to B-1 receptors
 Non-dihydropyridine calcium channel blockers
 such as: verapamil, diltiazem
 they slow the conduction of AV node and has negative
inotropic & chronotropic effects
 Digoxin
 reduces ventricular rate by slowing AV nodal conduction
  Rhythm control (specific)
o Cardio-version:
 Electrical cardio-version: a treatment that uses quick, low-energy
shocks to restore a regular heart rhythm
 Drug cardio-version: medicine is given through an IV or orally to
reset heart rhythm
o AV node ablation: helps block faulty signals that causes A fib using heat
(radiofrequency) or cold (cyroblation) energy to create tiny scars in an
area of the heart

 Anticoagulants
o Used to prevent blood clots and reduce risk of stroke
o Direct thrombin inhibitors: dabigatran
o Factor Xa inhibitors: rivaroxaban & apixaban

Resource: NCBI + Mayo Clinic

11. Management with amiodarone for atrial fibrillation patients.

(duration and significance with pacemaker)

1. Duration of management with amiodarone for atrial fibrillation patients

o Initially, amiodarone is used for 1-3 weeks to restore sinus rhythm. Once
sinus rhythm is restored, the maintenance dose of amiodarone is typically
lower and can be continued for several months or even years.
o For patients with persistent or permanent AF, long-term management
with amiodarone or other antiarrhythmic drugs may be necessary.

o Continuous monitoring and evaluation of the patient's response to

treatment are essential.

o Regular follow-ups are essential to assess treatment effectiveness,

monitor side effects (especially with amiodarone), and adjust as needed.
Treatment duration may be indefinite for some, while others may require
reassessment based on clinical changes.

1. Why was amiodarone continued after the pacemaker insertion?

  It's important to note that amiodarone has a long half-life, meaning it can remain
in the body for a significant amount of time.
 This can make it difficult to discontinue the medication if necessary.

a. Management of Atrial Fibrillation:

 Amiodarone is effective in controlling and maintaining sinus rhythm in
patients with AF.
 Even after a pacemaker is inserted, continuing amiodarone may be
necessary to prevent recurrence of atrial fibrillation.
 Patients with AF are at risk of recurrent episodes, and amiodarone is one
of the most effective antiarrhythmic agents for this purpose.
 Continuing the medication helps reduce the risk.

b. Bradyarrhythmia Management:
 Amiodarone can slow heart rate, but a pacemaker can manage this,
allowing continued use of amiodarone for arrhythmia control without
affecting heart function.

Resource: Pubmed, NIH

12. Pharmacology of drugs: roles of Metoprolol and Amiodarone as

antiarrhythmics and their toxic effects.

 Antiarrhythmic change the shape of the cardiac action potential by altering the
channels that control the flow of ions across the cardiac cell membrane.

Amiodarone: K+ channel blockade

 Prolong repolarization in phase 3 of the myocyte (Phase three is repolarization,

involving the closing of Ca2+ channels and opening of Voltage-gated K+
channels open)
 Amiodarone prevents and treats a fast or irregular heartbeat by slowing down
overactive electric signals in the heart, which stabilises your heart rhythm.
 Toxic effects:

 Pulmonary toxicity (5-15%)

 Thyroid dysfunction (3-4%)
 Cardiac toxicity; bradycardia, AV blocks, QT prolongation
 Hepatitis (<3%)
 Skin reactions (2.3%) : photosensitivity or blue-man syndrome
 Corneal micro-deposits (1.5%)

Before administering the drug , you need to check the patient thyroid hormone, cardiac and
liver enzymes

Metoprolol: Beta Blocker

 Blocks sympathetic stimulation of ß1 adrenergic receptors which slows the firing

of SA node and the conduction through AV node.
 Slows phase 4 depolarization (spontaneous depolarization (pacemaker potential)
that triggers the action potential once the membrane potential reaches a
threshold)
 Toxic effects:

 Bronchospasm (concern in asthmatic patients)

 Bradycardia / heart block
 Mask & prolong the symptoms of hypoglycemia (contraindicated in
diabetes)Abrupt withdrawal can precipitate ischemic heart events
 Decreased exercise tolerance, fatigue
 Impotence

Resource: Anti-hypertensive drugs II lecture, Anti-arrhythmics lecture, NIH

13. Relate the presenting signs and symptoms of syncope to its

pathophysiological basis.
Signs and Symptoms of Syncope

Loss of Consciousness: A sudden and brief blackout.

Dizziness or Lightheadedness: Feeling faint before passing out.
Weakness or Fatigue: Often feeling tired or weak leading up to the event.
Palpitations: Noticing a racing or irregular heartbeat.
Pallor or Sweating: Skin may look pale, and sweating can occur.
Confusion Afterward: Feeling disoriented right after waking up.

What Causes Syncope?

The pathophysiology of syncope involves several mechanisms that lead to

reduced cerebral perfusion and subsequent loss of consciousness:

Decreased Blood Flow to the Brain:

 Cardiac Causes: Conditions like bradycardia (slow heart rate) or arrhythmias

can lead to inadequate cardiac output. In Mr. Khan's case, a pulse of 36 beats
per minute indicates severe bradycardia, resulting in insufficient blood flow to the
brain.
 Vasodilation and Hypotension: Situations that cause vasodilation, such as
emotional stress or dehydration, can lead to a drop in blood pressure, further
reducing cerebral perfusion.

Neurological Response:
  The brain requires a certain level of blood flow to maintain consciousness. When
perfusion drops below this threshold, syncope occurs. This can happen rapidly in
cases of arrhythmias or severe hypotension.

Autonomic Nervous System Dysfunction:

 Dysregulation of the autonomic nervous system can lead to inappropriate heart
rate and blood pressure responses, contributing to syncope. For instance, the
lack of sympathetic tone can cause a sudden drop in blood pressure.

How Symptoms Relate to Causes

 Loss of Consciousness & Bradycardia: A slow heart rate can mean the brain
isn’t getting enough blood, leading to fainting.
 Dizziness and Weakness: These feelings often happen because the brain isn’t
getting enough oxygen.
 Palpitations: A racing heart can signal that something is wrong, which might lead
to fainting.
 Pallor and Sweating: These are signs that the body is reacting to low blood flow.

Resource: PUBMED AND LECTURES