1️⃣ GOOD AFTERNOON EVERYONE! SO yung atrial impulses..
may nauunang
WE WILL NOW PROCEED TO ATRIAL beat.
ARRHYTHMIAS. BUT BEFORE THAT, FOR EXAMPLE:Imagine you’re
LETS HAVE A QUICK RECALL KUNG clapping to a song with your friends.
TANDA PA BA NATIN. The leader (SA node) starts the
beat:
2️⃣HERES THE ONE NORMAL CYCLE OF Clap… clap… clap…
CARDIAC RATE
depo? Suddenly, one friend (the ectopic
repo? focus) claps too early:
atrial depo? Clap… clap… CLAP!.. clap… clap…
ventricular repo?
ventricular depo? That early clap is the premature
atrial complex.
3️⃣ WHAT IS ATRIAL ARRHYTHMIA?
- irregular heartbeats that cause poor The rest of the clapping goes back
circulation. to normal after it..nakaabang na si
- Yung upper chambers (atrium) of our SA node para normal na yong next.
heart are out of rhythm with the naka antabay na sya.
lower chamber (ventricles)
- may abnormal electrical activity na - A-fib Naman is yung most common
nanggagaling sa ectopic foci..etong type ng arrhythmia..
ectopic na ito is location (Ectopic foci - Normally, nakaka receive si AV node
can occur in any cardiac tissue NG one clear impulse pero dito sa
capable of generating or A-fib..madami since merong multiple
conducting electrical impulses: ectopic foci..eh di ba si AV node
but in this case is nasa atrial ang? Gatekeeper or pacemaker?
myocardium) and ito Yung nati Gatekeeper..(even may signal na si
trigger kaya naga result ng atrial SA node, si AV mode will be the one
arrhythmias. (irregular atrial na magapatuloy..so since there's
contractions) chaotic impulses (madami na,
- this can cause your heart to beat magulo na) si AV node yung
either too fast or slow. bombarded. kaya ang result Yung
ventricular rhythm ay irregularly
So merong abberancies or 3 types irregular
here:
PAC atrial fibrillation, the atria can fire
A-fib 300–600 impulses per minute from
A-flutter many ectopic foci.
If every one of those reached the
4️⃣ Here's the table para Makita nation Yung ventricles, the heart would beat so
comparison between those 3. fast it couldn’t pump blood effectively
- so sa PAC: from the word itself — or at all.
PREMATURE..meaning early..early
AV node (atrioventricular node) is can sometimes set off A-fib or A-flutter in
like the traffic controller of the vulnerable hearts.
heart’s electrical system.
● How:
Imagine the AV node as a narrow doorway ○ Caffeine, nicotine, stress
with a guard. → stimulate the sympathetic
nervous system → atrial cells
● People (impulses) keep running become more excitable →
toward the door at random. ectopic focus fires early →
PAC.
● The guard can only let someone
through after taking a short break ○ Alcohol → can directly
(refractory period). irritate atrial cells and disrupt
conduction (“holiday heart
● Some people make it through, syndrome”).
others bounce off and have to wait
— but there’s no predictable pattern. ○ Electrolyte imbalance (low
potassium, magnesium,
calcium) → disrupts electrical
stability → increases risk of
- Atrial Flutter
early or erratic firing.
problem with how electricity moves through
the atrial tissue.
○ Ischemia (reduced blood
flow) → damages atrial
Normally, an impulse from the SA node
tissue → changes conduction
spreads through the atria once, then dies
speed → promotes reentry or
out when it reaches tissue that’s already
ectopic firing.
been activated.
● Example: A healthy person drinks
In reentry, the impulse circles back and
too much coffee → gets a few PACs
re-excites the same tissue over and over,
but recovers. Someone with an
creating a loop of continuous depolarization.
enlarged atrium gets a PAC →
triggers a reentrant loop → leads to
atrial flutter or AFib.
5️⃣
Caffeine, alcohol, nicotine,
stress, electrolyte Hypertension (HTN),
imbalance, ischemia Coronary Artery Disease
(CAD), Valvular Disease,
Common outcome: These can trigger
PACs (Premature Atrial Complexes), which Heart Failure (HF),
● How:
Obstructive Sleep Apnea
(OSA), Hyperthyroidism ○ CAD → scars interrupt
normal conduction, creating
Common outcome: Chronic structural and “one-way blocks” → sets up
electrical changes in the atria → higher risk reentrant circuits (flutter) or
of A-fib and A-flutter. multiple foci (AFib).
● How: ○ Valvular disease → chronic
pressure/volume overload →
○ HTN & HF → cause atrial atrial stretch → conduction
enlargement/stretching → slowing + reentry risk.
slows conduction in some
areas → easier for reentrant ○ Heart Failure → combination
loops to form. of stretch, fibrosis, and poor
blood supply → major
○ CAD → causes ischemic arrhythmia risk.
scars → creates conduction
blocks that allow reentry. ○ Post–Cardiac Surgery →
surgical incisions in the atria
○ Valvular disease (esp. act as artificial barriers →
mitral) → increases left atrial perfect for forming reentrant
pressure & size → disturbs loops (often causing flutter).
conduction pathways.
If you want, I can make a one-page table
○ OSA → repeated drops in that links each cause → exact mechanism
oxygen + pressure changes → which arrhythmia it’s most likely to cause.
→ strain & inflammation in That would make it super quick to
atria. memorize.
○ Hyperthyroidism →
increases heart’s metabolic
and electrical activity →
makes atrial cells more
excitable. 6️⃣
PATHOPHYSIOLOGY
CAD, Valvular Disease, HF, PAC
Post–Cardiac Surgery Structural / electrical atrial changes
(HTN, CAD, valvular disease, HF)
Common outcome: Can directly cause ↓
atrial flutter or AFib, sometimes Atrial dilation, fibrosis, ischemia → altered
permanently. conduction
↓
Multiple ectopic foci & reentry circuits ● The atria quiver instead of
↓ contracting effectively.
Chaotic atrial depolarization (300–600 bpm)
→ quivering atria, no organized contraction ● No distinct P waves on ECG, only
↓ irregular fibrillatory waves.
Loss of atrial kick (↓ preload)
↓
↓ Ventricular filling → ↓ Stroke Volume → ↓ 4. Loss of atrial kick
Cardiac Output
↓ ● Normally, atrial contraction
Blood stasis in atria (esp. LAA) contributes ~20–30% of ventricular
↓ filling (“atrial kick”).
Thrombus formation
↓ ● In AF, this is lost → reduced
↑ Stroke risk (embolus to cerebral arteries preload.
→ ischemic stroke)
5. ↓ Ventricular filling → ↓ Stroke Volume
ATRIAL FIBRILLATION
→ ↓ Cardiac Output
1. Structural/electrical atrial changes
● Without atrial kick and with irregular
● Common causes: HTN, CAD, ventricular response, less blood
valvular disease, heart failure. leaves the heart per beat.
● These lead to atrial dilation, ● Symptoms: fatigue, hypotension,
fibrosis, or ischemia, altering dyspnea, exercise intolerance.
conduction pathways.
6. Blood stasis in atria (esp. Left Atrial
2. Multiple ectopic foci & reentry circuits Appendage)
in atria
● The quivering atria don’t move blood
● Instead of one orderly SA node efficiently → blood pools in the LAA.
impulse, many abnormal
pacemaker sites (ectopic foci) fire
7. Thrombus formation
simultaneously.
● Stagnant blood is prone to clot
● Multiple reentry loops cause rapid, formation.
irregular activation of atrial muscle.
8. ↑ Stroke Risk
3. Chaotic atrial depolarization (300–600
bpm) ● A clot can dislodge → embolus →
commonly lodge in cerebral arteries
→ ischemic stroke.
4. ↓ Ventricular filling
ATRIAL FLUTTER
● Because the atria are contracting so
1. Reentrant conduction loop in atrium rapidly and rhythmically, there’s less
time for ventricles to fill between
● In atrial flutter, an abnormal beats.
electrical circuit forms—most often
in the right atrium.
5. ↓ Cardiac Output
● Instead of impulses starting at the
SA node and traveling normally, the ● Lower filling = lower stroke volume,
current keeps circulating in a loop and combined with rapid ventricular
(reentry), repeatedly activating atrial rate → overall decreased cardiac
tissue. output.
● This can cause fatigue,
2. Rapid, regular atrial depolarization hypotension, syncope, or heart
(250–350 bpm) failure symptoms.
● This reentry causes the atria to
depolarize very fast but in a 6. Risk of thrombus formation
regular rhythm—much faster than
the ventricles can handle. ● The rapid, uncoordinated atrial
contractions reduce effective atrial
● On ECG, this produces the classic emptying, especially in the left
“sawtooth” flutter waves. atrial appendage.
● This stagnant blood increases the
3. AV node conducts in fixed ratio (2:1, risk of clot formation.
3:1 block)
● The AV node acts as a gatekeeper, 7. Stroke risk
not letting every atrial impulse
through (otherwise the ventricles ● If a clot dislodges, it can travel
would be overwhelmed). through the arterial system →
embolism (often to the brain) →
● Commonly, for every 2 atrial beats, 1 ischemic stroke.
impulse gets through (2:1
conduction) → ventricular rate ≈
150 bpm.
● Sometimes, it’s 3:1 or 4:1,
depending on AV node
refractoriness.
3. Restore sinus rhythm – Antiarrhythmic
7️⃣ drugs or cardioversion
● Antiarrhythmics (flecainide,
1. Prevent embolic events – amiodarone, dofetilide, propafenone,
Anticoagulants/antiplatelets based on ibutilide) can restore and maintain
CHA₂DS₂-VASc score normal sinus rhythm.
● AF increases stroke risk due to ● Electrical cardioversion is used
thrombus formation in the atria when the patient is unstable (e.g.,
(especially LAA). hypotension, shock) or when
medications fail.
● CHA₂DS₂-VASc score is used to
determine stroke risk and decide on
anticoagulation: 4. Lifestyle / risk factor management
○ Anticoagulants (e.g., ● Avoid triggers (caffeine, alcohol,
warfarin, DOACs) reduce clot nicotine).
formation.
● Treat underlying causes like
○ Antiplatelets (e.g., aspirin) hypertension and sleep apnea to
are less effective but may be prevent recurrence.
used in low-risk or
contraindication cases.
2. Control ventricular rate – Beta-blockers Surgical Management
(Class II) or calcium channel blockers
1. Catheter ablation
(Class IV)
● A minimally invasive procedure
● Even if the atria are fibrillating,
where a catheter delivers
controlling the ventricular rate
radiofrequency or cryoenergy to
helps improve filling time and
destroy the small areas of atrial
cardiac output.
tissue causing abnormal impulses.
● Beta-blockers slow conduction
through AV node and reduce heart
2. Maze or mini-maze procedure
rate.
● Surgical incisions or ablations in the
● Non-DHP Calcium channel atria form a “maze” pattern to direct
blockers (diltiazem, verapamil) do electrical impulses in a normal path.
the same.
3. Convergent procedure
● A hybrid approach combining ● Emphasize compliance to prevent
surgical and catheter techniques, stroke or bleeding.
used for refractory AF (not
responsive to drugs or ablation
alone). 4. Prepare for cardioversion or ablation
● Ensure the patient is adequately
4. Left Atrial Appendage Occlusion anticoagulated before elective
(LAAO) cardioversion to prevent embolism.
● Closes off the LAA, the main site of
clot formation in AF, for patients who 5. Post-procedure care
cannot take long-term
anticoagulants. ● Monitor puncture sites after catheter
procedures.
● Watch for complications: bleeding,
pericardial effusion, arrhythmia
recurrence
Nursing Management
1. Monitor heart rate, rhythm, and vital
signs 8️⃣
PATHO IN IM
● Early detection of worsening AF or
hemodynamic instability. 1. Loss of coordinated atrial contraction
(loss of atrial kick)
● In normal sinus rhythm, the atria
2. Assess for decreased cardiac output contract in a coordinated way just
and thromboembolism before the ventricles, pushing extra
blood into them (“atrial kick”).
● Watch for symptoms like
hypotension, dizziness, chest pain,
● In AF, the atria quiver chaotically
shortness of breath, stroke signs
instead of contracting effectively →
(weakness, speech difficulty).
that extra push of blood is lost.
3. Educate on medication adherence &
2. Reduced ventricular filling time
INR monitoring
● Without the atrial kick, the ventricles
● Warfarin requires regular INR
rely only on passive filling.
checks (goal: 2.0–3.0).
● If the ventricular rate is also fast and
irregular, diastolic filling time is
further shortened. ● If a clot breaks free, it can travel
through the arterial system.
3. ↓ Stroke volume & ↓ Cardiac output ● The brain is a common target →
ischemic stroke is the most feared
● Stroke volume = amount of blood complication of AF.
pumped per beat.
● Less filling → less blood pumped →
cardiac output (CO = SV × HR) 9️⃣
decreases, especially if HR is very
irregular or too fast. CLINICAL MANIFESTATIONS
1. May be asymptomatic
4. Potential hemodynamic instability
(hypotension, fatigue, dyspnea) ● Some patients discover AF
incidentally during a check-up or
● Lower CO can cause low blood ECG for another reason.
pressure (hypotension), reduced
oxygen delivery to tissues (fatigue), ● This often happens if the ventricular
and fluid backup in the lungs rate is controlled and there’s no
(dyspnea). significant drop in cardiac output.
5. Blood stasis in atria (especially left 2. Palpitations
atrial appendage)
● The sensation of rapid, irregular, or
● Because the atria are not “fluttering” heartbeat.
contracting, blood can pool —
especially in the LAA, a pouch-like ● Caused by irregular ventricular
structure in the left atrium where flow contractions from chaotic atrial
is sluggish. impulses.
6. ↑ Risk of thrombus formation 3. Irregular pulse
● Stagnant blood is more likely to clot. ● On palpation, the pulse has an
irregularly irregular rhythm — no
● A thrombus in the LAA can form predictable pattern.
silently and grow over time.
● This reflects the unpredictable
conduction through the AV node.
7. Embolic events (e.g., stroke)
4. Shortness of breath
● Due to reduced cardiac output and ● In atrial fibrillation, anticoagulants
possible pulmonary congestion from like warfarin are often prescribed to
poor ventricular filling. prevent clot formation and stroke.
● Warfarin works by interfering with
5. Fatigue vitamin K–dependent clotting
factors, but its effect can vary greatly
● Caused by decreased tissue between people and can be
perfusion from lower cardiac output. influenced by diet, other
medications, and illness.
6. Dizziness
● Because of this variability, patients
● Related to reduced cerebral blood need regular blood tests to check
flow from irregular ventricular the INR (International Normalized
contractions. Ratio) — a standardized measure of
how long it takes blood to clot.
7. Signs of heart failure
Why monitor INR?
● Dyspnea on exertion: lungs can’t
handle fluid shift due to backup in ● Goal INR: 2.0–3.0 for most AF
pulmonary circulation. patients.
● Hypotension: low cardiac output ○ < 2.0 → blood is not thin
reduces arterial pressure. enough → higher risk of clot
and stroke.
● Edema: fluid retention from
right-sided heart strain. ○ > 3.0 → blood is too thin →
higher risk of bleeding.
8. Pulse deficit ● Regular monitoring helps keep the
INR in the safe range and allows
● When apical pulse (heard at the timely dose adjustments.
heart) is faster than radial pulse (felt
at the wrist).
Why stress adherence?
● This happens because some
ventricular beats are too weak to ● Missing doses can drop INR quickly
generate a palpable pulse wave. → clot risk.
● Taking extra doses or interacting
drugs can spike INR → bleeding
risk.
🔟Educate on medication adherence &
INR monitoring
● Consistent medication use and
follow-up checks are essential for
safety and stroke prevention.
Class IC – Strong
___________________________ Depolarization Blockers
Summary: Greatly slow conduction, little
Class IA – Moderate effect on repolarization → powerful rhythm
control.
Depolarization Blockers Use: Atrial & ventricular arrhythmias (but
not in damaged hearts).
Summary: Slow conduction and lengthen Examples: Flecainide, Propafenone.
repolarization → helps prevent abnormal Key Side Effects: Can trigger dangerous
rhythms. rhythms, worsen HF, cause dizziness,
Use: Atrial & ventricular arrhythmias. blurred vision, and shortness of breath.
Examples: Quinidine, Procainamide, Nursing Notes: Avoid in CAD or HF,
Disopyramide. reduce dose in kidney disease, and be
Key Side Effects: Weak heart pumping, cautious in patients with certain diets (e.g.,
prolonged QRS/QT (can cause dangerous vegetarian low-protein diets can affect drug
rhythms), BP drop (IV), metabolism).
diarrhea/constipation, lupus-like syndrome,
anticholinergic effects.
Nursing Notes: Monitor for heart failure
signs, BP, ECG changes (especially
QRS/QT), drug levels (procainamide), and Class II – Beta Blockers
pretreat AF with AV nodal blocker to avoid
Summary: Slow the heart’s natural
rapid ventricular rate.
pacemaker (SA node) and AV node
conduction.
Use: Both atrial and ventricular
arrhythmias; also useful for rate control in
Class IB – Minimal AF.
Examples: Metoprolol, Propranolol,
Depolarization Blockers
Esmolol, Atenolol, Sotalol (also Class III).
Summary: Slightly slow conduction but Key Side Effects: Slow heart rate, AV
shorten repolarization → best for ventricular block, low BP, HF worsening,
rhythm problems. bronchospasm, masks low blood sugar
Use: Ventricular arrhythmias. signs, dizziness, depression.
Examples: Lidocaine, Mexiletine. Nursing Notes: Monitor HR, PR interval,
Key Side Effects: Confusion, lethargy, BP, watch for HF, check blood sugar in
tremors, slow heart rate, GI upset. diabetics, and avoid sudden withdrawal.
Nursing Notes: Watch for CNS changes,
tremors, and adjust dose in elderly or with
heart/liver disease.
Class III – Repolarization Class IA – Moderate
Prolongers Depolarization Blockers
Summary: Delay repolarization so the heart Flow of Action:
cells take longer before they can beat again
→ prevents reentry arrhythmias. 1. Drug binds to sodium (Na⁺)
Use: AF and ventricular arrhythmias (esp. channels during depolarization in
with poor heart function). cardiac cells.
Examples: Amiodarone, Dofetilide,
Ibutilide, Dronedarone, Sotalol. 2. Slows Phase 0 (initial
Key Side Effects: Lung damage depolarization) → conduction
(amiodarone), corneal deposits, skin through atria, ventricles, and
sensitivity to sunlight, slow heart rate, low His-Purkinje slows.
BP (IV), nausea/vomiting, rare dangerous
VT. 3. Also blocks potassium (K⁺)
Nursing Notes: Get baseline lung tests channels → prolongs Phase 3
(PFTs) with amiodarone, monitor QT (repolarization).
interval, use continuous ECG for
dofetilide/ibutilide start, monitor kidneys, 4. Effect: Slower conduction + longer
watch for digoxin interaction. refractory period → prevents reentry
circuits and ectopic beats.
Class IV – Calcium
Channel Blockers Class IB – Minimal
(Non-DHP) Depolarization Blockers
Summary: Slow conduction through AV Flow of Action:
node and decrease heart contractility.
Use: Paroxysmal atrial arrhythmias; rate 1. Binds to Na⁺ channels but more
control in AF. selectively in ischemic/damaged
Examples: Verapamil, Diltiazem. ventricular tissue.
Key Side Effects: Slow heart rate, AV
block, low BP (IV), HF worsening, swelling, 2. Shortens Phase 3 repolarization
constipation, dizziness, headache. → cells reset faster.
Nursing Notes: Monitor HR, PR interval,
BP, watch for HF signs, and do not crush 3. Effect: Suppresses ventricular
sustained-release tablets. arrhythmias, especially post-MI,
without much effect on atrial tissue.
Class IC – Strong Class III – Repolarization
Depolarization Blockers Prolongers
Flow of Action: Flow of Action:
1. Potent Na⁺ channel blockade → 1. Block K⁺ channels → prolong
markedly slows Phase 0 Phase 3 repolarization.
depolarization.
2. This increases the effective
2. Little to no effect on repolarization refractory period (ERP).
(Phase 3).
3. Effect: Cells take longer before they
3. Effect: Very strong suppression of can depolarize again → reduces
conduction through atria and reentry arrhythmias and stabilizes
ventricles → stops reentry rhythm.
arrhythmias, but can be
proarrhythmic in diseased hearts.
Class IV – Calcium
Class II – Beta Blockers Channel Blockers
(Non-DHP)
Flow of Action:
Flow of Action:
1. Block β₁-adrenergic receptors in the
heart. 1. Block L-type Ca²⁺ channels in SA
and AV nodes.
2. ↓ cAMP → ↓ calcium influx in SA
and AV node cells. 2. Slows Phase 0 depolarization in
nodal cells (Ca²⁺-dependent).
3. Slows Phase 4 depolarization in
nodal tissue → reduces automaticity 3. Prolongs AV node conduction and
(SA node) and conduction velocity decreases contractility.
(AV node).
4. Effect: Controls ventricular rate in
4. Effect: Slower heart rate, longer AV AF/flutter and prevents AV
node conduction → prevents rapid node–dependent tachycardias.
ventricular rates in AF/flutter and
decreases ectopic beats.