MEDICAL SURGICAL
CARDIOVASCULAR DISORDERS PART 2
Cardiac Arrhythmias
Cardiac Dysrhythmias
★ A disturbance, irregularity or abnormal in the
electrical system of the heart. Dysrhythmias may
initially be evidenced by the hemodynamic effect
they cause (e.g., a change in conduction may
change the pumping action of the heart and
cause decreased blood pressure), and are
diagnosed by analyzing the electrocardiographic
(ECG) waveform
★ Also known as arrhythmia
​Heartbeat may be too fast or too slow, regular or
irregular
★ Primary disorder or secondary response to a
systemic problem or complications of drug toxicity
or electrolytes imbalance.
★ Heart rate influenced by the ANS which consists
of SNS and PNS
Major Classification of Dysrhythmias
❏ Cardiac Rhythm is identified according to the site
of origin like SA node, AV node, conjunction, or
ventricles
❏ It could be identified as a mechanism of
conductions like normal rhythm, bradycardia,
tachycardia, dysrhythmia, flutters, fibrillation,
premature complexes or conduction block.
1. Rate​ ​– ​very slow or very rapid
➔ Such as a patient who has hypoxia,
metabolic alkalosis, electrolytes
imbalance. Imbalances like hypokalemia,
hypocalcemia which cause prolonged
duty ​can lead to electrical instability.
2. ​Mechanisms ​– ​based on the electrophysiologic
mechanism
a. re-entrant
➔ electrical impulse travels in a
tight circle within the heart
instead of moving from one end
to another
● Several conditions that may cause re-entry to
occur:
1. At a point where there are two conduction
pathways for an impulse to follow.
2. Because of the slow conduction through one
portion ​of that pathway.
3. There is a newly directional block at some
point along the conduction pathway.
b) ​abnormal enhanced automaticity
➔ Normally the SA node has a higher automaticity
than the rest of the heart, so any part of the heart
that initiates an impulse with outweighing the SA
node is called ectopic focus. For a node open
than the SA node it can produce abnormal
rhythm therefore every heartbeat that did not
originate from SA node is considered an ectopic
beat. When the ectopic beat is early it is called
extrasystole while if it is too late it is called
escape.
➔ Factors the contribute to reduce resting
membrane potential:
★ Ischemia, Hypokalemia, Hypoxia or
Effect of Drugs
c)​ conduction disturbances
➔ It ​accounts​ for bradyarrhythmia
Classification of Arrhythmias by Site
1.SA node (60 ​– ​100 bpm) ​– ​normal looking PQRST
complex
• Sinus bradycardia - Slow heartbeat, distant
• Sinus tachycardia - Fast heartbeat, close
• Sinus arrhythmia - Distance depends on respiration
> 1-3 they have a normal looking or normal PQRST the
difference is the rate.
2. Atria ​– ​abnormal looking P wave, normal QRS complex
• Premature atrial contraction
• Atrial flutter
• Atrial fibrillation
3. AV junction (40 ​– ​60 bpm) ​– ​prolong
PR interval > 0.20 seconds
• AV blocks
4. Ventricles (30 ​– ​40 bpm) ​– ​abnormal wide QRS
complex
> 0.20 seconds; serious life threatening
● Premature ventricular contractions (PVC)
● Ventricular tachycardia
● Ventricular fibrillation
Causes of Cardiac Dysrhythmias
1. Myocardial Infarction (MI)
❖ because of the conduction problem on the
damage tissue
2. Rheumatic Heart Disease (RHD)
3. Heart failure
4. Electrolyte Imbalances
5. Drug toxicity – esp. those taking digitalis, quinidine
6. Hypothermia
7. Trauma
8. Coronary Artery Disease (COD)
Sign and Symptoms of Dysrhythmias
1. Palpitations – most common
● pt. had a feeling of a skip heart beat
● some palpitations may be harmless but many of
them predispose to adverse outcomes like a
higher risk of blood clotting or insufficient transfer
of the blood because of the weak heartbeat
● others are embolisation, stroke or sudden cardiac
death
2. Lightheadedness or dizziness
3. Syncope – fainting
4. Chest discomfort
5. Pounding chest
6. Weakness or Fatigue
DIAGNOSTIC STUDIES
1. 12 lead ECG
2. 24-hour ambulatory ECG or Holter monitoring
3. Electrophysiologic studies (EPS)
➔ This is to assess the electrical activity
and conduction pathway of the heart.
➔ need to investigate the location of origin
are best treatment for various abnormal
heart rhythm
➔ Stress Test - considered as one of the
diagnostic studies for patients who have
cardiac arrhythmia or dysrhythmia.
4.​ Laboratory test
● Electrolytes – K, calcium, Mg and FBS
★ Fasting Blood Sugar - bc hypoglycemia can lead
to prolong heartbeat that may sidtubed blood flow
to the heart which results in a lethal cardiac
event.
★ Test for digitalis and quinidine levels in order to
assess its toxicity level to the patient.
General Management for Cardiac Dysrhythmias
1. Diet – SVT (Supraventricular Tachycardia) avoid
overuse of stimulants such as caffeine.
2. Cessation of smoking – effects on ventricular
threshold which may be a basis for arrhythmias
3. ​Oxygen therapy – low-flow oxygen may benefit pt
who has dysrhythmic or chest pain.
4.​Cardiac monitoring - in order to provide most efficient
and reliable method for detections of arrhythmia
5. Antiarrhythmic drugs – lidocaine, β-adrenergic
blockers, calcium channel blockers, digitalis preparation
Antiarrhythmic Drugs:
Class 1 – depress upstroke of action potential (lidocaine,
quinidine, pronestyl)
➢ It interferes with the sodium channel that
depresses the​ fasting wipe off of​ sodium
● Quinidine - to treat fever, malaria and contain
antiarrhythmic properties at the same time it
could also suppress the supraventricular
tachycardia and ventricular arrhythmia.
● Lidocaine - it is not widely used because of the
effect on ischemic tissue. It suppresses the
conduction more on ischemia tissue than on
normal that why lidocaine is no longer routinely
used for the treatment of acute ventricular
arrhythmia.
Class II ​– beta-adrenergic receptor blockers (effect on
BP, HR and myocardial contractility) metoprolol
❖ anti sympathetic nervous system agent that
allows the SA node to fight ​spontaneously,
therefore, it may decrease the blood pressure,
heart rate or myocardial contractility.
❖ Ex. atenolol, metoprolol, propranolol or even
carvedilol
➔ These drugs have the ability to inhibit
sympathetic activation of ​cardiac ​automaticity
and conduction.
➔ Beta Blockers also have an effect of decreased
MI mortality, preventing recurrence of
tachyarrhythmia.
➔ Propranolol - has a sodium channel blocking
effect
Class III – prolong duration of action potential (S/E:
hypotension and bradycardia)
● it prolongs the repolarization and prevents
re-entrance arrhythmia.
● It does not allow the permeability of this ion bc it
may cause stimulation on the contraction.
● Amiodarone - most common, it prevents the
repentance of arrhythmia, increases the PR
interval and the QT interval.
● it causes a slight prolongation of QRS duration
● It is also a powerful inhibitor of ectopic
pacemaker automaticity.
➔ Side effects are hypotension and
bradycardia.
➔ Usually treat ventricular tachycardia and
ventricular fibrillation
 ➔ It should not be used for AV block or any
allergies to iodine.
➔ Contraindicated to patients who have
bradycardia and avoid eating grapefruits
because it may increase the side effects
of the drugs ​by increasing the amount of
this medicine in your body​.
➔ It also causes photosensitivity to
ultralights and should instruct patients to
avoid sun exposure and should use
sunscreen.
Class IV​ – calcium channel blockers
❖ it may decrease the conduction into the AV node
and shorten the phase two of the cardiac action
potential therefore it prevents the calcium from
entering the cell of the heart and blood vessels.
At the same time it also relaxes and widens the
blood vessels of the atrial node.
❖ Verapamil and Diltiazem​ - most common
➔ It is not appropriately used for those who
had heart failure because it reduces the
contractility of the heart.
➔ Side effects: Reduce BP, headache
(common), nausea and constipation.
Unknown Mechanism Drugs:
❏ Digoxin ​- which decreases conduction of
electrical impulse to the AV node and increases
fatal activity and increases in acetyl production
which may decrease speed of conduction.
❏ Adenosine - which is used intravenously for
supraventricular tachycardia.
❏ Magnesium Sulfate - decrease the calcium
influx that prevents early depolarization.Widely
used for patient who have di ko maintindihan
sinabi ni Maam hehe
6. Electrical countershock ​– terminate ventricular
fibrillation.
7. Adjunctive therapy
a. Cardiac pacemakers ​– are battery-operated
generators that initiate and control the heart rate
by delivering an electrical impulse via an
electrode to the myocardium.
● Burrowed within subcutaneous tissue below right
clavicle
● Bed rest for 24 hours and gradual increase of
activity to prevent dislodging of the lid
● Lifespan of battery from 6 to 12 years
Indications of Pacemaker Therapy
*The primary indications for symptomatic bradyarrhythmia
and those who have a long ​(di ko maintindihan slide #14)
syndrome.
1. Maintenance of adequate HR and rhythm during
surgery and postoperative recovery.
2. Irreversible bradycardia
➔ which is not responsive to medication
3. Sinus node dysfunction.
4. Tachyarrhythmias
5. Symptomatic AV Heart Block
➔ esp. the second type on the third degree
AV block
➔ patients who have fibrosis or sclerotic
changes of the cardiac conduction
system.
Forms of Pacemaker Implantation
• Temporary cardiac pacing ​– ​used for hemodynamic
or life-support purposes.
INDICATION:
1. Complete heart block
2. Symptomatic Bradyarrhythmia
3. Acute MI
4. Emergency measure for for malfunction of
implanted permanent pacemaker
NOTE: This temporary cardiac pacing is not only for
controlling heart rate but also used in
electrophysiological laboratories to evaluate cardiac
dysrhythmia and interact with tachycardia.
• ​Permanent cardiac pacing ​– ​indicated in the
continuous presence of symptomatic bradyarrhythmias.
INDICATION:
1. Chronic Atrial fibrillation because of low
ventricular response.
Complications of Pacemaker Use:
1. Dislodgment of the pacing electrode ​– ​common
2. Local infection
➔ because it is being inserted on the
subcutaneous
3. Pneumothorax
4. Bleeding and hematoma
5. Hiccups ​– ​sign of phrenic nerve, diaphragmatic
stimulation
➔ because of irritation on the phrenic
nerves
6. Hemothorax ​– ​puncture of the subclavian vein or
internal mammary artery.
Measures to Prevent Complications * this is one type of adjunctive
therapy
1. Prophylaxis antibiotics *very common for patient who has
➔ To prevent infection tachyarrhythmia and not
2. CXR ​– ​to check for placement and r/o responsive to medication
pneumothorax ➢ RFA ​– ​radiofrequency ablation
3. Continuous ECG monitoring ➔ Used in patient who has
4. Bed rest for 12 hours with minimal arm and atrial flutter, atrial
shoulder activity to prevent dislodgement of fibrillation and
implanted pacemaker lid. unresponsive to
medication therapy
NOTES: ➢ Cryoablation
1.If the patient is taking antiplatelets or antithrombotic ➔ Applied cold temperature
medications, it needs to be discontinued in order to to destroy the the selected
prevent the risk of bleeding or hematoma. cardiac cells
2. Use of plastic sheets in order to reduce the risk of ❖ Maze procedure
pneumothorax. ➔ A doctor creates a pattern
of scar tissue (the ​maze​) in
Health Teachings (for patient with pacemaker) the upper chambers of the
1. Wound care heart by applying heat or
2. Discuss activity allowances and limitations - NO cold. Or, the doctor uses a
strenuous exercise or lifting heavy objects, avoid scalpel to make several
contact sports; avoid arm and shoulder activity precise incisions.
● To avoid dislodgement of the lid ➔ To prevent reentry
3. Avoid near high voltage wires, power plants, conduction of the electrical
radio transmitters, microwave ovens, theft impulse
detectors
● Avoid those that contain magnets, stereo
speakers and jewelry should not be near
Sinus Rhythms
to the generator for longer than a few
seconds.
● The use of cellular phones is at least
6-12 inches away from the pacemaker
generator or opposite side, so the patient
needs to move from the area if they are
experiencing palpitation or dizziness.
4. Move away from the area if dizziness or
palpitations occur
5. Describe signs and symptoms of pacemaker
failure
● Dizziness
● Weakness
● Lightheadedness
● A drop in pacemaker set rate Disorders of Atria
6. Avoid traveling and driving for 1​st 4 weeks
following insertion 1. Sinus bradycardia
7. Explain the need for continuous medical follow-up
2. Sinus tachycardia
and for periodic battery check-up.
8. Avoid constricting clothing 3. Premature atrial contraction (PAC)
4. Supraventricular Tachycardia (SVT)
B. ​Cardiac Conduction surgery
5. Atrial flutter
★ Electrode catheter ablation ​–
radiofrequency energy “burn” the 6. Atrial fibrillation (AF)
areas or pathways of the abnormal
rhythm and promote normal
conduction of impulses or electrical
pathways between the atria and
the ventricle.
Sinus Bradycardia

❖ The conduction pathway is similar to normal Bradycardia & Hypotension Medical Management “IDEA”

sinus rhythm which has a normal PQRST but the

★ ISOPROTERENOL
SA node is discharging at a rate of less than 60
➔ Action: acts on beta 2 ​– ​adrenergic
bpm
receptors, causing relaxation on
❖ Rate: < 60 bpm
bronchial smooth muscles; acts on beta 1
❖ Causes of sinus bradycardia are:
– ​adrenergic receptors in heart, causing
a) low metabolic needs (athletes, sleeping,
positive inotropic and chronotropic effects
hypothyroidism)
and increasing cardiac output. Also,
b) vagal stimulation ​– ​vomiting, suctioning,
lowers peripheral vascular resistance in
severe pain, fever), and Valsalva maneuver
skeletal muscle and inhibits
means straining that reduces cardiac output
antigen-induced histamine release.
because of increased intrathoracic pressure
therefore decreasing the venous return and
★ DOPAMINE
cardiac output .
➔ Action: causes norepinephrine release
c) medications ​– ​calcium channel blockers,
(mainly on dopaminergic receptors),
amiodarone, beta-blockers
leading to vasodilation of renal and
➔ NOTE: If the patient is taking this
mesenteric arteries. Also exerts
medication then the nurse should check
ionotropic effects on heart, which
the heart rate prior to administration.
increases the heart rate,blood flow,
➔ If the patient has <60 bpm do not give the
myocardial contractility, and stroke
medication because it has an effect that
volume.
may reduce the heart rate of the patient
d) carotid sinus massage
★ EPINEPHRINE
➔ Or patient who has MI
➔ Action: stimulates alpha- and
beta-adrenergic receptors, causing
❖ 0.5 mg of AtSO4 (Atropine Sulfate) every 3 ​– ​5
relaxation of cardiac and bronchial
minutes for a maximum total dose of 3 mg
smooth muscle and dilation of skeletal
➔ If this drug is not responsive then Doctor
muscles. Also decreases aqueous humor
may have transcutaneous pacing or the
production, increases aqueous outflow,
use of dopamine or epinephrine.
and dilates pupil by contracting dilator
➔ Atropine may increase the heart rate and
muscle.
SA is charging so it blocks the vagus
nerve
★ ATROPINE
❖ Theophylline ​100 ​– ​200 mg SIVP (Slow IV Push)
➔ Action: inhibits acetylcholine at
who had a cardiac transplantation and acute
parasympathetic neuroeffector junction of
inferior MI or spinal cord injury
smooth muscle and cardiac muscle,
❖ It may increase the heart rate and contractility
blocking sinoatrial (SA) and
therefore it also relax bronchial smooth muscle
atrioventricular (AV) nodes. These
actions increase impulse conduction and
raise heart rate.
● These medications are used to increase heart
rate peripheral vaso pulsation.
 ● Another treatment is the use of a pacemaker. ➔ Serves as vasodilator
➔ Contraindicated to a patient who has
asthma because it could cause
Sinus Tachycardia bronchoconstriction due to the histamine
release and the relationship of this to
muscle.
3. Vagal maneuvers
➔ Because it may increase the
parasympathetic nervous stimulation
causing a slow conduction through the
AV node that blocks the re-entry of the
impulse.
➔ Example: Coughing, squatting, hold
breathe, carotid sinus massage, cold
● This is wherein the SA node is charging at a rate
application to the face, jogging and
of >100 bpm
straining.
● The result of inhibition of vagal reflex or
4. Beta-blockers and calcium channel blockers –
stimulation of sympathetic nervous system.
rarely used considering narrow QRS tachycardia
● If there is an increase in heart rate and reduction
➔ Class II Antiarrhythmic Agents like
in systolic filling time, it may reduce cardiac
metoprolol, atenolol
output.
➔ These agents are used to reduce heart
● If the rapid rate persists the heart cannot
rate and decrease Myocardial oxygen
compensate for the decreased ventricular filling
consumption, therefore it will decrease
therefore acute pulmonary edema may develop.
the heart rate, decrease the BP and
cardiac output. It also decrease the
Causes of Sinus Tachycardia
automaticity in the heart rate except it is
1. Physiologic and psychological stress – acute
rarely used if the patient has a narrow
blood loss, hypoglycemia (rt. to sympathetic
QRS tachycardia
nervous response that cause palpitations) ,
5. Procainamide, amiodarone ​– options for wide
hyperthyroidism, fever, anxiety, severe pain,
QRS tachycardia
hypoxia and MI)
6. Catheter ablation
2. Effects of medications – epinephrine,
norepinephrine, atropine, theophylline, nifedipine,
hydralazine
Sinus Arrhythmia
➔ These medications will increase the heart
rate of the patient
3. Autonomic dysfunction – postural orthostatic
tachycardia syndrome(POTS)
● It results from sinus tachycardia ​without
hypotension within 5-10 mins of standing
or sitting
● is an abnormal increase in heart rate that
occurs after sitting up or standing
● Treatment: Increase fluid intake, use of
compression stocking to prevent the
pulling of blood to the lower extremities.

Management of Sinus Tachycardia ● The ECG shows that there are changes in the
rhythm of the ECG depending on the respiration.
1. Synchronized cardioversion – hemodynamic
● The rhythm is irregular but it has a normal PQRS
instability
and interval is within normal.
2. Adenosine administration
➔ This would decrease the conduction of
the AV node
Sinus Arrhythmia
❖ One upright uniform p-wave for every QRS
➔ The rate is within 60-100 bpm but the
rhythm is irregular depending on the
changes so the RR interval changes are
depending on the changes on respiration.
❖ Rhythm is irregular
➔ Rate increases as the patient breathes in
➔ Rate decreases as the patient breathes
out
❖ Rate is usually 60-100 (may be slower)
❖ Variation of normal, not life threatening
➔ There is no treatment
➔ Common in children and young adult
Premature Atrial Complex (PAC)
➢ Also known as Premature Atrial Contraction or
Atrial Extrasystole or Atrial Ectopic Beat
➔ This is due abnormal electrical ​focal
➢ ​Early, extra heartbeats that originate in the atria
➢ 60 – 100 bpm and irregular
➢ P wave is abnormal
➔ It has a different​ control ​wave
➔ It may be a notched or a negative
deflection or hidden in the proceeding of
the P wave.
➢ P
​ R interval delayed or normal or shorter
➢ ​Result from emotional stress, use of caffeine,
nicotine or alcohol, low potassium level.
➔ Hypermetabolic state like pregnancy
➔ Patient who has lung diseases
➢ ​Infection, hyperthyroidism, COPD, heart disease
(CAD) and valvular disease
Premature Atrial Contraction (PAC)
● Those patients who have enlarged heart may
have premature atrial contraction although it is
not necessary for any treatment but if it is
frequent of more than 6 per minute then it will be
the sign of atrial fibrillation.
● Treatment: Withdraw from sources of stimulation
like caffeine or ​sympathomimetic ​ drugs
● Beta blockers may be used to decrease
premature atrial contractions
● PAC is not significant for a healthy person but
with those heart diseases who have frequent
premature atrial contraction or complex it
indicates enhanced automaticity of the atria or
the entry mechanism.
Supraventricular Tachycardia (SVT) or
Paroxysmal Atrial Tachycardia (PAT)
● In which the atria originating anywhere above the
Bundle of HIS or anywhere above the ventricle.
● If the P wave cannot be identified then the rhythm
may be called supraventricular tachycardia
(SVT).
● Rapid but regular heart rhythm that comes from
the atria. Prevent the gating mechanism
➔ When an impulse is conducted to an area
in the Av node that causes the impulse
re-acted back into the same area over
and over again at a very fast rate.
➔ Each time that the impulse is conducted
thru this area it is also conducted down
into the ventricle cause extra ventricular
rate of 150-250 bpm.
➔ Normally, the ventricle is protected
against excessive heart rate arising from
supraventricular areas by making
mechanism at the AV node which
prevents high rates, slowing the
proportion of the fast impulse to pass.
● HR regular rhythm, rate 150 – 250 bpm
● Abnormal P wave present but may be hidden on
ST segment or T wave
● PAC are common in normal hearts.
● No treatment is necessary. BUT if they are
frequent of more than 6 per minute this may be
signs of atrial fibrillation
● Associated with overexertion, emotional stress,
RHD, digitalis toxicity, CAD, or cor pulmonale
➔ Symptoms can arise suddenly and
resolve without treatment such as stress,
exercise and emotion can precipitate
SVT.
➔ Stimulants like alcohol, caffeine or
nicotine.
➔ Cor pulmonale - pulmonary heart
disease. An enlargement of the right
ventricle of the heart as response to
increased vascular resistance or high
pressure in the lungs.
 ● SVP is commonly seen in patient who have a
Wolff-Parkinson-White, a syndrome wherein it
bypass the gating mechanism, so that means it
avoid the north and its protection on passway
directly transmitted to the ventricle
● Tachycardia usually is a short duration resulting
in palpitation therefore a fast rate.
● That means Supraventricular tachycardia has a
fast rate or increase in heart rate that may cause
reduce in cardiac output resulting in significant
sign and symptoms.
● SX/ SY: Shortness of Breath, Restlessness,
Chest Pain, Pallor, Dizziness, Hypotension,
Rapid Breathing, and loss of consciousness
● HR: 150 - 250 bpm (Decreased Cardiac output
with hypotension and Myocardial Ischemia).
● Abnormal P wave present but may be hidden
before T wave or ST Segment and has abnormal
contour
● PR interval is shortened
● QRS complex normal or abnormal contour
TREATMENT FOR PSVT OR PAT
1. Vagal stimulation - Carotid massage to lower
heart rate. Instruct the patient to do valsalva
maneuver to increase intrathoracic pressure that
affects para receptors.
2. Drug therapy
a) Adenosine (Adenocard) – common
● Given rapid IV then add 20 mL of saline
flush to promote rapid circulation.
● This converts sinus to normal
● Allow slow conduction of AV node to
allow visualization of P wave
● Prevents Ca reflux
● Decreases SNS
● This has too short effects therefore if
drug not effective, Electrical
Cardioversion must be done.
b) Diltiazem - Can use other beta adrenergic
blockers.
c) Digitalis - Increase contractility to enhance
cardiac output.
d) Amiodarone - Increase contractility to enhance
cardiac output
3. Radiofrequency Ablation therapy
4. If the patient becomes hemodynamically unstable
– DC cardioversion (synchronized).
ATRIAL FLUTTER
● Conduction defect in the atrium and causes rapid,
regular atrial impulse at a rate between 250 - 400
bpm.
● More than one P-wave for every QRS complex
● Atrial rate: 250 - 400 bpm; Ventricular rate: 75
and 150 bpm;
● PR Interval: Multiple F waves make the PR
interval unidentifiable
● P wave: “​sawtooth​” appearance (F waves)
● Atrial rhythm is regular. Ventricular rhythm will be
regular if the AV node conducts consistently. If
the pattern varies, the ventricular rate will be
irregular
● Not all atrial conduction conducted in the ventricle
● 250-300bpm
● CAD, hypertension, mitral valve disorders,
pulmonary embolism, cor pulmonale,
hyperthyroidism
● If atria cannot pump effectively, blood supply is
reduced
● Signs and symptoms: Fatigue, palpitations, chest
pain, light-headedness, syncope, SOB, low BP
● Treatment:
○ Warfarin ​(risk of thrombus formation
which then may lead to stroke)
○ antiarrhythmic agents (converts atrial
flutter to sinus rhythm).
○ Coumadin ​- 48 hours duration/ prevents
stroke.
○ diltiazem, digoxin, β-adrenergic blockers
○ Adenosine can be rendered (blocks
SNS/ slows conduction therefore allows
visualization). Give Intravenously by rapid
administration followed by 20mL saline
flush and elevation of the arm with the IV
line for rapid circulation.
 ○ RFA (Radiofrequency Catheter
Ablation) – curative therapy; delivers
energy in the area heart muscles;
promotes normal conduction in the atria.
○ Electrical cardioversion - successful;
used only in emergency situations.
ATRIAL FIBRILLATION
ATRIAL FIBRILLATION CLASSIFICATION
Type Description
Paroxysmal Sudden onset with termination that
occurs spontaneously or after an
intervention lasts more than or equal to
7 days, but may recur.

Persistent Continuous, lasting more than 7 days

Long -
Standing Continuous, lasting more than 12 days
Persistent

Permanent Persistent, but decision has been made

not to restore or maintain sinus rhythm

Nonvalvular Absence of mitral Stenosis, valve

replacement or repair

CLINICAL MANIFESTATIONS OF AF:

● Characterized by a total disorganization of atrial
electrical activity without effective atrial contraction 1. Palpitations
(Affects atrium/ ventricle) 2. Shortness of breath
● Causes are unknown. 3. Hypotension
● This causes electrophysiologic changes in the atrial 4. Dyspnea on exertion
myocardium (remodeling of the atrial electrical circuit) 5. Fatigue
and structural remodeling (fibrosis), which provides 6. Pulse deficit (the difference between radial and
the basis for continuance of the dysrhythmia
apical pulse)
● Results from abnormal impulse formation that occurs
7. Anginal symptoms due to myocardial ischemia
when structural or electrophysiological abnormalities
alter the atrial tissue causing a rapid, disorganized
DIAGNOSTIC FINDINGS:
and uncoordinated twitching of the atrial musculature.
● Most common sustained dysrhythmia 1. 12-lead ECG - verify atrial fibrillation rhythm and
● Shaking chaotic electrical impulses identify the presence or absence of left ventricular
● Prevalent in advance age (aged/ older people) hypertrophy, bundle branch block, prior myocardial
● Affects upper heart chambers ischemia.
● Not typically an emergency because ventricular 2. Transthoracic echocardiogram (TEE) - identify
fibrillation is much more dangerous. presence of valvular heart disease and check LV
● It does not completely empty the blood and RV size, function, and pressures
● Risk to: HF, myocardial ischemia, embolic events 3. Thyroid screening
such as stroke, cardiomyopathy; pericarditis, caffeine, 4. ​Renal clearance test
stress, alcohol use disturbances 5. ​Hepatic function test
● Blood pooling may result to thromboembolism (may 6. Chest X-rays – evaluate pulmonary vasculature
cause stroke) suspected for pulmonary hypertension
● Too fast - may cause low cardiac output 7. Exercise stress test – to exclude myocardial
● Without P wave ischemia
● PR interval not measurable 8. Holter monitoring
9. EP study – prior to catheter ablation
 ATRIAL FIBRILLATION MANAGEMENT ○ Oxygen Support
○ Antidote: Digibind (Immunoglobulin fragment
● ANTICOAGULANTS ​– prevent embolization (Class that binds with digoxin)
II)
● BETA BLOCKERS – Antiarrhythmic drug, to block PREMATURE JUNCTIONAL CONTRACTION (PJC)
the effects of certain hormones on the heart to slow
down heart rate.
● CALCIUM CHANNEL BLOCKERS ​– Helps slow the
heart rate by blocking the number of electrical
impulses that pass through the AV node into the
lower heart chambers (ventricles). This increases
myocardial O2 supply and decreases afterload. This
has an acute alteration in the mental status.
Heart Rhythm P Wave PR QRS
● DIGOXIN ​– Helps slow heart rate by blocking the
Rate Interval
number of electrical impulses that pass through the (sec.) (Sec.)
AV node into the lower heart chambers (ventricles).
● ELECTROCARDIOVERSION ​– Procedure in which
Usually Irregular Premature, Short Normal<.12
electric currents are used to reset heart’s rhythm
normal abnormal, <.12
back to regular pattern. This is for patients that are may be
Hemodynamically unstable where medication is not inverted or
effective anymore. This resets the heart rhythm, hidden
converting it to a regular pattern.
● CATHETER ABLATION THERAPY – Destroys
specific cells that are the cause of a
tachydysrhythmia ● “​Premature Junctional Complex​”
● MAZE PROCEDURE – An open-heart surgical ● An impulse that starts in the AV nodal area before
procedure for refractory atrial fibrillation. Small the next normal sinus impulse reaches the AV
transmural incisions are made throughout the atria. node.
The resulting formation of scar tissue prevents ● Causes include digitalis toxicity, heart failure, and
reentry conduction of the aberrant electrical impulse. coronary artery disease.
● P wave: may be absent
JUNCTIONAL ARRHYTHMIAS ● QRS: less than 12 seconds

● Originate from the AV node FIRST DEGREE AV HEART BLOCK

● Idionodal rhythm occurs when AV node (instead of
the sinus node) becomes the pacemaker of the
heart.
● ​Abnormal P wave - inverted
● ​HR 40 – 60 bpm
● ​PR interval is ​< 0.12 sec ​(book: less than 0.12
seconds)
● P:QRS ratio: 1:1 or 0:1
● The ECG criteria for premature junctional complex
are the same as for PAC, except for the P wave
and the PR interval. The P wave may be absent
and PR interval of less than 0.12 seconds
● Associated with AMI especially inferior MI, digitalis
toxicity, open heart surgery
● Treatment: do not give atropine for digitalis toxicity, ● The duration of AV conduction is prolonged
β-adrenergic blockers, calcium channel blockers ● Occurs when all the atrial impulses are
and amiodarone conducted through the AV node into the
● DC cardioversion is NOT be used ventricles at a rate slower than normal
● Management for digitalis toxicity includes ● Every impulse is conducted to the ventricle
○ Hydration with IV Fluids ● delayed/ complete block
○ Correct electrolytes ● HR – normal and regular rhythm
● ​Pwave is normal ■ But remained fixed/ reconducted
● ​PR interval is prolonged > 0.20 second (5 small beats with intermittent dropped
sq) - Take note that PR interval is constant beat
● QRS complex has a normal contour ○ Serious type of block, occurs in the
His-Purkinje system
SECOND DEGREE AV BLOCK ○ ​Acute anterior MI, CAD, RHD
○ May progress to 3​rd​-Degree AV block
○ Presence of constant PR interval and
presence of more P waves than QRS.
○ QRS is usually abnormal, but may be
normal.
○ Treatment:
■ Permanent Pacemaker if block
persist
■ Temp: atropine, dopamine,
1. ​Type I (Wenckebach Phenomenon)
epinephrine
○ ​PR interval lengthen progressively (AV

conduction time that is prolonged until an

atrial impulse is not conducted and QRS
conduction is dropped)
○ Gradual lengthening of the PR
○ Dropped QRS
○ Occurs when there is a repeating pattern
through the AV node into the ventricles at a
rate slower than normal.
○ Treatment: atropine and temporary THIRD DEGREE AV BLOCK
pacemaker​.
○ Warning signs of impending AV conduction
disturbances
■ Transient
■ Well tolerated

● Sinus rate is 60 – 100 bpm, ventricular rate

2. Type II second-degree AV block
○ Ventricular rhythm is irregular
○ Less common but severe
○ Occurs when only some of the atrial
impulses are conducted through the AV
node into the ventricles.
○ PR interval is prolonged (P = 2:1 or 3:1 to 1
QRS)
■ Constant unchanged prior to the
P wave
depends on the site of the block
● PR interval is variable; no relationship between P
wave and QRS complex
● Result to ↓ CO with subsequent ischemia and heart
failure (Severe bradycardia/ asystole)
● Complete heart block (no atrial impulse is
conducted through the AV node into the ventricles).
● Treatment: temporary pacemaker, for emergency
basis; drugs (atropine, epinephrine, dopamine,
isoproterenol) - Acute Myocardial infarction
 ● However nurse should know that Atropine is not
responsive to complete AV block (lowers diastole
MAP, increases systole by HR and contraction)
● Isoproterenol produce vasodilation and cardiac
stimulation
● Having two impulses stimulate the heart results in a
condition referred to as AV dissociation which may
also occur during VT
SUMMARY OF AV BLOCKS
● 1º - prolongation of PR Interval
● 2º - Mobitz I – Increasing PR Interval until
dropped beat is seen
○ Mobitz II – Constant PR Interval with
more P waves to QRS
● 3º - Complete dissociation between P waves &
QRS
DISORDERS OF THE VENTRICLE
I. Premature Ventricular Contractions / Complex
(PVCs)
● An impulse that starts in a ventricle and is
conducted through the ventricles before the
next sinus impulse
● Can occur with healthy people especially
with intake of caffeine, nicotine, or alcohol.
● P wave is rarely visible and lost in the QRS
complex of PVC
● QRS complex is wide and distorted, > 0.12
seconds
● T wave is generally a large and opposite
direction to deflections of the QRS
(premature occurrence, wide, distorted in
shape).
● In the rhythm referred to as:
○ Bigeminy - every other complex is a
PVC
○ Trigeminy - every 3rd complex is a PVC
○ Quadrigeminy - every 4th complex is a
PVC
● Mitral valve prolapse (MVP), CHF, CAD, MI,
hypokalemia, emotional stress
● Treatment: hemodynamic assessment,
correct electrolytes when there
hypokalemia,
PVC ASSOCIATED TO VT
1. PVCs are more frequent than 6 per minute
2. Multifocal or polymorphic (having different shapes
and rhythms)
3. Occur two in a row (pair) - susceptible to VT
4. Occur on the T wave - susceptible to VT
II. Ventricular tachycardia (V- tach or VT)
● Defined as 3 or more PVC in a row with a rate of 100
– 250 bpm (book: 100 - 200 bpm)
● Severe decrease in Cardiac Output result of
decreased ventricular diastolic feeding time, leads to
atrial contraction loss, develops ventricular fibrillation.
● VT is an emergency because the patient is nearly
always unresponsive or pulseless.
● P wave is absent
● PR interval is absent ( book: Very irregular if P waves
are seen)
● QRS complex distorted and > 0.12 seconds
● Pulmonary edema, shock, decreased blood flow to
the brain
● Signs and symptoms (Severe)
○ altered level of consciousness
○ Pallor
○ Diaphoresis
○ Leads to cardiac arrest
● Signs and symptoms (Common)
○ Palpitation,
○ chest pain,
○ syncope,
○ Tachypnea
○ Anxiety
○ Lightheadedness
○ Hypotension
○ Diminished perfusion
● Treatment:
is ○ Determine if monomorphic (having consistent
QRS shape and rate) or polymorphic (having
varying QRS shape and rate).
○ Determine the existence of a prolonged QT
interval before initiation.
○ Check if the patient is stable
○ Obtain 12 lead ECG
○ Amiodarone - Medication of choice for patient
with impaired cardiac function or acute MI.
 ○ Cardioversion - treatment of choice for
monophasic VT in a symptomatic patient.
○ For conscious patients - instruct patients to cough
for 1-3 seconds to prevent sinus rhythm.
○ Defibrillation is action/ treatment of choice for
unconscious patients.
TORSADES DE POINTES
● Polymorphic V-tach
● Prolonged QT interval
● PR not measurable
● Wide QRS complex
● > 0.12 seconds
● Sy/sx: Palpitations, may lead to faintness,
syncope (may lead to sudden death)
COMMON CAUSES OF TORSADES DE POINTES
1. Diarrhea
2. Hypokalemia
3. Hypomagnesemia (may lead to malnourishment,
heart failure)
4. Chronic alcoholism
5. Certain drugs – cimetidine, haldol, amiodarone,
erythromycin which blocks Ca flow
6. Certain foods - grapefruit (may cause
hypertension/ ischemia)
Magnesium helps in the movement of calcium, potassium
and sodium in and out of the cell.
Give patient ​MgSO4 (​ Magnesium Sulfate) - 2g over 1 to
2 minutes over IV push for 4 to g hours or IV infusion to
prevent recurrence. This slows SA node and prolong
conduction time.
Treatment: avoid offending odors, magnesium sulfate,
anti-arrhythmic drugs, electrical therapy (unsynchronized
defibrillation)
VENTRICULAR FIBRILLATION
● Most common dysrhythmia
● Form of cardiac arrest
● Rapid, disorganized ventricular rhythm that
causes ineffective quivering of the ventricles.
● MEDICAL EMERGENCY! GIVE CPR TO
PATIENT IF SEEN
● Rhythm is irregular and chaotic
● P wave is NOT visible
● HR not measurable ( > 300 bpm)
● PR interval and QRS complex are NOT
measurable
● Characterized by the absence of an audible
heartbeat, a palpable pulse and respirations
● Unconscious, apnea, seizures
● If not treated, patient will die
MANAGEMENT FOR VENTRICULAR FIBRILLATION
● Early defibrillation
● CPR and ACLS (as preparing defibrillator and 5
additional cycles of CPR, about 2 minutes of
continuous chest compression
● Epinephrine
● One dose of vasopressin instead of epinephrine if
the cardiac arrest persists.
● Other antiarrhythmic medications – amiodarone
and epinephrine (facilitates return of spontaneous
pulse after defibrillation) , lidocaine, magnesium
as soon as possible after the 3​rd​ defibrillation.
 ASYSTOLE

● Total absence of ventricular electrical activity.

● End-stage CHF, advanced cardiac disease
● Commonly called “Flatline”

Treatment:

● CPR, ACLS measures which include intubation,

epinephrine and atropine