Atrial Fibrillation and
Ventricular Arrhythmias
Ibrahim Sales, Pharm.D.
Assistant Professor of Clinical Pharmacy
King Saud University
isales@ksu.edu.sa
Supraventricular Arrhythmias
• Supraventricular arrhythmia
•
•
•
•
Sinus Bradycardia
AV Nodal Block
Atrial fibrillation
Paroxysmal Supraventricular Tachycardia (PSVT)
• Ventricular arrhythmia
•
•
•
•
Ventricular Premature depolarization
Ventricular tachycardia
Ventricular fibrillation
Torsades de Pointes
2
Atrial Fibrillation
• The most common sustained arrhythmia
encountered in clinical practice
• Rapid & disorganized conduction in atria leading
to loss of mechanical contraction
• "irregularly irregular" appearance on ECG
• HR of 120–180 usually observed because AV
node unable to block all atrial impulses
3
Classification of AF
• Paroxysmal (self-terminating) :
• episodes terminate spontaneously in less than
seven days,
• usually less than 48 hours.
• Persistent AF :
• fails to self-terminate within 7 days.
• Episodes may eventually terminate spontaneously,
or they can be terminated by cardioversion.
4
ACC/AHA/European Society of Cardiology
Classification of AF
• Permanent AF
• arrhythmia lasts for more than one year and
cardioversion either has not been attempted
or has failed.
• "Lone" AF:
• describes paroxysmal, persistent, or
permanent AF in individuals without structural
heart disease (usually young patients, <60 yrs)
5
Classification of AF
• Nonvalvular AF:
• Not caused by valvular disease, prosthetic heart
valves, or valve repair
• Recurrent atrial fibrillation:
• ≥ 2 episodes of atrial fibrillation
6
Causes of AF
•
•
•
•
•
•
•
•
•
•
•
Hypertensive heart disease
Coronary disease
Valvular heart disease
Heart failure
Hypertrophic cardiomyopathy
Congenital heart disease
pulmonary embolism
COPD
Obstructive sleep apnea
Hyperthyroidism
Alcoholism (Holiday Heart
Syndrome)
• Surgery: CABG 30-40%
• Inflammation and infection
• Medications: theophylline,
bisphosphonate
7
Clinical implications of AF
Loss of coordinated atrial Contraction
Rapid Ventricular
response
Tachycardia: Shorter diastolic fill
time. Reduced coronary
circulation and possible ischemia.
Tachycardia medicated
cardiomyopathy
Am Fam Physician.
2011 Jan 1;83(1):61-68
Decreased diastolic
filling
Blood stasis and atrial
clot formation
Decreased
cardiac
output
Thromboe
mbolism
Increased Morbidity & Mortality
Increased
risk of
stroke
Goals of Therapy
• Disease specific goals of therapy
•
•
•
•
Control ventricular rate
Preventing thromboembolic events
Restore sinus rhythm
Maintain sinus rhythm
• Global goals:
•
•
•
•
Reduce mortality
Improve QOL
Decrease hospitalization and ER visits
Optimize the cost effectiveness of treatment
10
Approach to therapy of AFib
1. Evaluate the need for acute treatment
By starting a rate control drug
2. Contemplate restoration of SR taking into
consideration the risks
restoring and maintaining SR may not be a
desirable goal for all patients
3. Consider thromboembolic prophylaxis
with appropriate antithrombotic drug
based on stroke risk
11
Rate control vs. rhythm
Control
• Overall Conclusion:
No significant difference in overall mortality
between rate-control and rhythm-control
strategies
Anticoaugulant
(AC) need is similar in both
groups
12
Rate control Strategy
• At least as effective as rhythm control strategy for preventing stroke
and death in atrial fibrillation
• Fewer adverse events than rhythm control strategy
• Rhythm control with AAD maybe considered if patient remained
symptomatic despite adequate ventricular rate control
• Target HR:
• Lenient resting HR< 110 bpm vs. strict rate control, resting
HR< 80 BPM, have similar cardiovascular outcomes
• Therefore, target a resting heart rate of < 110 bpm
13
AAD: anti-Arrhythmic Drugs
Rate control Strategy
• Drugs for long-term rate control
• Beta blocker (oral)
• metoprolol 50-200 mg/day, propranolol 80-240 mg/day)
• Non-dihydropyridine (oral)
• diltiazem 120-360 mg/day, verapamil 120-360 mg/day)
• Digoxin (oral)
• AF with HF, LVD (LVEF < 40%) or for sedentary individuals
• not recommended as monotherapy to control ventricular
rate in patients with paroxysmal atrial fibrillation
14
Rate control Strategy
• Amiodarone (oral)
• when other medical therapy has failed to control
heart rate adequately
• AF with pre-excitation
• preferred drugs for rate control are oral
propafenone or amiodarone
• combination therapy with any of digoxin, beta blocker, or
non-DHP-CCB may be used to control heart rate at rest
and with exercise
15
Rhythm control strategy
• Recommended in patients with symptomatic AF
despite rate control
• Pharmacologic rhythm control strategy
associated with more hospitalizations and
adverse events without apparent benefit
compared to rate control strategy in AF
• Rate control should be continued throughout
rhythm control approach
16
Rhythm control strategy
• Cardioversion with DCC
• DCC is useful to start rhythm control strategy for atrial fibrillation
• Pretreatment with amiodarone, flecainide, ibutilide, propafenone
or sotalol before DC cardioversion may increase success rate and
prevent recurrent atrial fibrillation
• Pharmacological cardioversion:
• Success rate lower than DC
• Selection of agent:
• If the AF is ≤7 days duration:
• Dofetilide, flecainide, ibutilide, propafenone or, to a lesser
degree, amiodarone (preferred if structural heart dz)
• If the AF is >7 days duration
• dofetilide or, to a lesser degree, amiodarone or ibutilide
17
Rhythm control strategy
• Thromboembolic prophylaxis during cardioversion:
• for AF of known duration < 48 hours
• immediate cardioversion indicated without delay
for anticoagulation if hemodynamic instability
• starting anticoagulation (with LMWH or IV UFH at
full venous thromboembolism treatment doses)
before cardioversion suggested if possible
18
Rhythm control strategy
• for atrial fibrillation of ≥ 48 hours or of
unknown duration
• initial therapeutic anticoagulation recommended
with either:
• Option 1: Therapeutic anticoagulation (adjusteddose vitamin K antagonist [VKA] therapy to target
INR range 2-3, LMWH at full venous
thromboembolism treatment doses, or dabigatran)
for at least 3 weeks before cardioversion
19
Rhythm control strategy
• Option 2: Transesophageal echocardiography
(TEE)-guided approach with initial
anticoagulation (LMWH or IV heparin) then
cardioversion within 24 hours of confirmation
of no thrombus
• less hemorrhagic complications, but trend
toward increased mortality
• Post-cardioversion anticoagulation
recommended for ≥ 4 weeks
20
Rhythm control strategy
• Maintenance of NSR
• Intermittent antiarrhythmic drug therapy
• “Pill in the Pocket”
• AAD:
• Also increase the risk of arrhythmia
• torsades de pointes (TdP): a potential adverse effect with
dofetilide and sotalol
• ventricular tachycardia or conversion to atrial flutter with
tachyarrhythmia is a potential adverse effect with flecainide and
propafenone
• The AAD associated with increased mortality include sotalol,
quinidine, and possibly disopyramide
21
Rhythm control strategy
• “Pill in the Pocket”
• A transient outpatient therapy for reversion of NSR in
paroxysmal AF
• single oral high dose taken only when an episode of AF
is recognized by the patient
• Agents: propafenone 600 mg, or flecainide 300 mg
• Very strict patient criteria
• Absence of: structural heart disease, sinus and AV
node dysfunction, QT interval prolongation, Brugada
syndrome
• Presence of AV nodal blockade with a BB or CCB to
prevent rapid AV conduction if atrial flutter occurs.
22
Recommended Antiarrhythmic Therapy in Patients with
Recurrent Paroxysmal or Persistent Atrial Fibrillation:
Clinical Scenario
No or minimal heart disease, or
hypertension without left
ventricular hypertrophy
Hypertension with substantial
left ventricular hypertrophy
Coronary artery disease
Heart failure
First-line
Therapies
Dronedarone
Flecainide
Propafenone
Sotalol
Amiodarone
Dofetilide
Dronedarone
Sotalol
Amiodarone
Dofetilide
Second-line
Therapies
Amiodarone
Dofetilide
Catheter ablation
Catheter ablation
Amiodarone
Catheter ablation
23
Catheter ablation
Ablation Therapy
• ablation of AV node or accessory pathway (and
pacemaker implantation)
• indicated when medical therapy fails to control heart rate or
produces intolerable side effects
• Catheter ablation, or surgical ablation in patients having
cardiac surgery for other reasons
• recommended for patients with symptomatic
paroxysmal atrial fibrillation after failure of
antiarrhythmic drugs
• may improve quality of life and reduce hospital
readmission rates
24
Antithrombotic
Therapy
25
Thromboembolic Prophylaxis
• Guidelines consistently agree that most patients with
AF should receive antithrombotic therapy.
• AT is recommended to patients with permanent,
persistent, or paroxysmal atrial fibrillation, atrial
flutter, and patients managed with rate or rhythm
control strategy
26
Antithrombotic in Atrial
Fibrillation
• Return of SR restores effective contraction
in the atria >> dislodge poorly adherent
thrombi
Selection of the antithrombotic
agent depend on the level of risk:
• CHADS2 or CHA2DS2-VASc
score for risk stratification
27
Stroke Risk Stratification
High Risk Patients:
• Have ONE of the following factors:
• Prior ischemic stroke, TIA
• Mitral valve stenosis
• Prosthetic heart valve
Have > 2 of the
• Age > 75 y
OR
• HTN
• DM
• Moderately or severely
Intermediate Risk Patients:
impaired LVSD and/or HF
• Have ONLY one of the following factors:
• Age > 75 y Or HTN Or DM Or moderately or severely
impaired LV systolic function and/or HF
Low-Risk Patients:
• Age > 75 y With none of the conditions listed above in the highor intermediate-risk categories
28
29
Recommendations About
Antithrombotic Therapy
Stroke Risk Stratification
• CHADS2 risk score predicts stroke risk
• Helps predict stroke risk in AF patients and determine which
antithrombotic (AT) is appropriate
CHADS2 Risk Factors
Recent Congestive HF exacerbation
Points
1
History of Hypertension
Age > 75 y
Diabetes Mellitus
1
1
1
Prior history of stroke or TIA
2
ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF
30
Recommendation for AT in AF
CHADS2
Score
0
Annual stroke Recommended Antithrombotic
rate (range)
therapy
1. No RX (preferred)
1.9 (1.2-3)
2. ASA (for those electing Rx)
1
2.8 (2-3.8)
2-6
4-18
1. Warfarin, Dabigatran,
rivaroxaban (AC preferred)
2. ASA + Clopidogrel
3. ASA
1. Warfarin, dabigatran,
rivaroxaban
31
AC: Anticoagulation
ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF
CHA2DS2-VASc
CHA2DS2-VASc Risk Factors
Points
Congestive Heart Failure
1
Hypertension
1
Age > 75
2
Diabetes
1
Previous stroke, TIA, systemic embolism
2
Vascular disease (MI, CAD, aortic plaque)
1
Age 65-74
1
Sex (Female)
1
Recommended Antithrombotic Therapy
Score of 0
No anticoagulation (Preferred) Or ASA 75-325 mg/d
Score of =1
Either anticoagulation (Preferred) or ASA 75-325 mg/d
Score of > 1
Anticoagulation with Warfarin, Dabigatran or rivaroxaban
ACCP 9th edition, 2012 Guidelines for the Management of Patients With AF
32
Overview on Antithrombotic
Therapies
33
Vitamin K antagonist:
Warfarin
• The most commonly used AC
• Target INR of 2-3 in patients without
mechanical heart valves
• lower target INR of 2 (range 1.6-2.5) may
be considered for patients ≥ 75 y/o or if at
 risk of bleeding but without
contraindications to oral anticoagulant
therapy
34
Vitamin K antagonist:
Warfarin
• Starting dose 5-10 mg adjusted based on
INR
• No need to bridge patient with heparin
when initiating warfarin in AF patients
• Determine INR at least weekly during
initiation and monthly when INR is stable.
• suggests monitoring INR at least every 12
weeks rather than every 4 weeks when INR
consistently stable
35
Vitamin K antagonist:
Warfarin
Limitation:
Narrow therapeutic index
Require frequent dose adjustments and
monitoring
Significant drug-drug and drug-food interaction
time required to achieve its pharmacologic effect
is dependant on the T½ of the coagulation
proteins.
full antithrombotic effect achieved in 5 to 7 days
after
Pregnancy Category X
36
Dabigatran (Pradaxa®)
• Dabigatran etexilate is a selective,
competitive, reversible direct thrombin
inhibitor
• Approved by FDA in 2010 for stroke
prevention in atrial fibrillation
• Approved in Canada & Europe for VTE
prevention after hip and knee replacement
surgery
37
Dabigatran (Pradaxa®)
• Oral capsule
• Rapid onset of action
• Half-life 12-17 hours, dosed TWICE Daily
• No routine monitoring required
• No reversal antidote
• dialyzable
• No dietary/food interactions
• SE: Bleeding, Dyspepsia (common, likely due to
tartaric acid)
• Cost: $$$ compared to warfarin
Dabigatran (Pradaxa®)
• Renal elimination
• CrCl >30 ml/min:
• 150 mg orally twice daily
• Outside US: 110 mg twice daily for age >75 or
propensity for GI bleeding
• CrCl 15-30 ml/min:
• 75 mg orally, twice daily*
• Metabolism: P-gp substrate
• use with caution when administered
concomitantly with P-gp inhibitors or inducers
39
Dabigatran (Pradaxa®)
Drug
Dronedarone
Ketoconazole
Interaction
Comments
Consider dosage
 dabigatran
bioavailability (70–140%) reduction to 75 mg twice
daily in patients with Clcr
30–50 mL/minute
Consider dosage
 dabigatran
concentrations and AUC reduction to 75 mg twice
daily in patients with Clcr
30–50 mL/minute
40
Dabigatran (Pradaxa®)
Drug
Rifampin
Interaction
Potentially dabigatran
concentrations and AUC
Amiodarone  dabigatran
concentrations
Verapamil
Comments
Avoid concurrent use
Dosage adjustment not
necessary.
Potentially  dabigatran Dosage adjustment not
concentrations and AUC necessary.
41
Converting to and from
Dabigatran
• Warfarin to Dabiatran
• D/c warfarin and start dabigatran when INR <2.0
• Dabigatran to Warfarin
• CrCl >50 ml/min: start warfarin 3 days before d/c
Dabi CrCl 31-50 ml/min: start warfarin 2 days before
D/c dabigatran
• CrCl 15-30 ml/min: start warfarin 1 day before
stopping dabigatran
42
• CrCl <15 ml/min: no recommendation
Dabigatran (Pradaxa®)
• Product Stability:
• Once bottle is opened, manufacturer
recommends that drug be used within 30 days.
Keep bottle tightly closed
• Manufacturer package insert indicates potency
is maintained for 120 days after first opening
bottle.
43
Dabigatran (Pradaxa®)
• Contraindications:
• Active pathologic bleeding
• History of serious hypersensitivity
reaction to dabigatran (e.g., anaphylaxis,
anaphylactic shock)
• Patients with mechanical prosthetic
heart valves
• Pregnancy Category C
44
Rivaroxaban (Xarelto®)
• Direct factor Xa inhibitor
• Approved by FDA in 2011 for prevention of
stroke in non-valvular AF.
• Also in treatment and prophylactic in DVT/PE and
following knee- or hip-replacement surgery
• No laboratory monitoring required
• No dosage adjustment for gender, age, extreme
body weight
• No reversal
• Half life 5-9 hours
Rivaroxaban (Xarelto®)
• Dosing:
• Oral tablet, once daily (cost $231.60 USA)
• Primarily renal elimination
• If CrCl> 50 ml/min: give 20 mg once daily with
evening meal
• If Crcl 15-50 ml/min give 15 mg once daily with
evening meal
• Contraindicated for creatinine clearance < 15
mL/minute
46
Rivaroxaban (Xarelto®)
• Contraindications:
• Active pathologic bleeding
• Severe hypersensitivity reaction to rivaroxaban
• Pregnancy Category C
• Lactation: Discontinue nursing or the drug
• DI: Drugs Affecting and/or P-glycoprotein and
CYP3A4
• Avoid using with itraconazole, ketoconazole,
Antiretrovirals, HIV protease inhibitors,
Carbamezapine, rifampin, phenytoin, St. John's
wort
47
Apixaban (Eliquis®)
• Direct factor Xa inhibitor
• Approved by FDA in 2012 for risk reduction of
stroke and systemic embolism in nonvalvular AF
• No routine lab testing
• No reversal
• Half life 8-15 hours
• Metabolized in liver via CYP3A4 and CYP
independent mechanisms
• Eliminated via multiple pathways
Apixaban (Eliquis®)
• Dose: 5 mg tablet Twice daily
• To switch from warfarin, stop warfarin, then start
apixaban when INR <2
• Cost: (5 mg BID): $250.37 (USA)
• Pregnancy Category B
• Lactation: Discontinue nursing or the drug
• May prolong PTT and INR in a concentrationdependent fashion
49
Stopping Pradaxa (dabigatran), Xarelto
(rivaroxaban), or Eliquis (apixaban) in AF patients
• Discontinuing new oral AC places patients at an
increased risk of thrombotic events. An
increased rate of stroke was observed following
discontinuation in clinical trials in patients with
nonvalvular atrial fibrillation.
• If anticoagulation must be discontinued for a
reason other than pathological bleeding,
coverage with another anticoagulant should be
strongly considered.
50
Limitations of Novel AC
• Irreversibility
• Cost
• Renal function
• Not studied where CrCL<30mL/min
• Lack of monitoring
• No readily available test
• No therapeutic interval
• Long term safety not known
• No data on use in pediatric population
51
Summary of Major Results of Phase 3
Trials of New Anticoagulants vs Warfarin
in AF
Drug/Trial
Efficacy:
Stroke/TE
Hemorrhagic
stroke
Major
bleeding
Dabigatran in RELY
34% 
74% 
SIMILAR
Rivaraoxaban in
ROCKET
Noninferior
to warfarin
40% 
SIMILAR
Apixaban in
ARISTILE
20% 
50% 
30% 
Ventricular
Arrhythmias
53
Types of Ventricular
Arrhythmias
• Premature Ventricular Contractions (PVCs)
• Ectopic ventricular beat
• non-life-threatening and usually asymptomatic.
• Sx: palpitations or uncomfortable heartbeats.
• Ventricular Tachycardia (VT)
• a life-threatening situation associated with hemodynamic
collapse or may be totally asymptomatic.
• >3 consecutive PVCs occurring at a rate >100 beats/min
• Could be monomorphic or polymorphic
• Ventricular Fibrillation (VF)
• results in hemodynamic collapse, syncope, and cardiac arrest.
Cardiac output and blood pressure are not recordable.
54
PVCs Treatment
• No drug therapy indicated for asymptomatic
patients without structural heart disease
• BB is drug of choice for symptomatic patients
• after myocardial infarction BB improve survival
• no evidence that prolonged suppression with
drugs AAD improves survival
• CAST I and II studies demonstrated higher
mortality in the AAD group
55
Treat Guidel Med Lett 2007 Jun;5(58):51
Ventricular Tachycardia (VT)
• Non-sustained VT: last < 30 sec
• Self terminate
• May consider primary prevention in high risk
groups to prevent conversion to sustained VT
• Sustained VT last > 30 sec
• Requires intervention to prevent VF or SCD
56
Ventricular Tachycardia (VT)
• Causes:
• Ischemia: MI (very common)
• Stimulant use:
• Caffeine, cocaine abuse
• Metabolic abnormalities:
• Acidosis, hypoxemia, hyperkalemia,
hypokalemia, hypomagnesemia
• Drugs:
• Digoxin, theophylline, antipsychotics, TCA, AAD:
flecainide, dofetilide, sotalol, quinidine
57
Ventricular Tachycardia (VT)
• Treatment:
• correction of the underlying precipitating factors
• acute episode of VT (with a pulse)
• Severe symptoms:
• DCC
• Long term AAD is not needed if there was
precipitating factors
• Mild symptoms:
• AAD: procainamide, amiodarone, sotalol
and lidocaine
• Assess patient’s risk for recurrence
58
Ventricular Tachycardia (VT)
• Treatment of chronic, recurrent, sustained VT :
• Empiric amiodarone
• Catheter ablation: if idiopathic
• Implantable cardioverter-defibrillator (ICD)
• +/- amiodarone or sotalol
•  frequency of VT/VF episodes >>  frequency of
shocks
•  rate of VT >> can be terminated with BB
•  episodes of concomitant supraventricular
arrhythmias
• minimize patient discomfort
• prolong the battery life of the ICD
59
Ventricular Tachycardia (VT)
• Primary prevention of SCD in VT/VF
• High risk: CAD, LV dysfunction, and nonsustained VT
• Undergo electrophysiologic testing to guide
subsequent therapy
• No inducible sustained VT/VF, chronic AAD
therapy is unnecessary
• If inducible sustained VT/VF, implantation of an
ICD is warranted.
• Secondary prevention of SCD in VT/VF:
• ICD is the first-line treatment
60
Torsade de Pointes (TdP)
• TdP is a rapid form of polymorphic VT
• ECG:
• long QT interval or prominent U waves
(Delayed ventricular repolarization)
• Etiology of TdP:
• Genetic, electrolyte disturbances ( K,  Mg),
subarachnoid hemorrhage, myocarditis,
arsenic poisoning, severe hypothyroidism, or
drug therapy (most common)
61
Torsade de Pointes (TdP)
• Drugs that can cause TdP:
• AAD: Quinidine, Procainamide, Disopyramide, Amiodarone,
Dofetilide, Dronedarone, Sotalol and Ibutilide
• Psychotropics
• Phenothiazines (e.g., thioridazine, chlorpromazine)
TCA (Haloperidol, Pimozide) Atypical antipsychotics
(e.g., quetiapine, ziprasidone)
• Organophosphate insecticides
• Arsenic Antibiotics
• Pentamidine, Macrolides (erythromycin and
clarithromycin), Trimethoprim-sulfamethoxazole,
Fluoroquinolones (levofloxacin, moxifloxacin,
gemifloxacin) and Voriconazole
62
Torsade de Pointes (TdP)
• Risk factors for drug-induced TdP:
•
•
•
•
•
High dose (quinidine, TdP at low doses)
concurrent structural heart disease
Evidence of mild QT prolongation at baseline
Evidence of mild QT prolongation after initiation of drug
Female gender
• QT interval prolongation has been used as a measurement of
risk of TdP
• If baseline QTc interval > 450 msec AVOID drugs that can prolong
QT
• If QTc interval is 560 msec after the initiation of the drug >>
discontinue or reduce dose of the drug
63
Torsade de Pointes (TdP)
• Treatment of Acute TdP
• DCC
• Followed by IV magnesium sulfate to
prevent recurrence
• Discontinue all drugs that prolong the QT
interval
• Correct exacerbating factors (e.g.,
hypokalemia or hypomagnesemia)
64
Ventricular Fibrillation (VF)
•
•
•
•
•
•
A Tachyarrhythmia
The most common underlying rhythm of cardiac arrest
If not treated: pulseless electrical activity, asystole
no cardiac output leads to rapid fatality
Causes:
frequently associated with CAD (only 20% patients rescued
from VF have evidence of evolving MI)
65
Treatment of pulseless VT or
VF
• ABCs
• CPR until defibrillator attached
• Check pulse between every intervention (except sequential
shocks with persistent VF
• defibrillate up to 3 times as needed for V fib or pulseless VT
(200 joules, 300 J, 360 J)
• if no pulse and persistent or recurrent VF/VT –
• CPR, intubation, establish IV access
• epinephrine, defib 360, lidocaine, defib 360, bretylium, repeat
epi/defib, consider bicarbonate, defib 360, bretylium, defib 360,
repeat lidocaine or bretylium, defib 360, magnesium,
procainamide
66
VF Treatment
• Prevention of recurrence:
• long-term therapy implantable cardioverterdefibrillator (ICD)
• Amiodarone or beta blockers often added
• if ICD shocks are frequent, consider adding
sotalol, amiodarone or mexiletine; if shocks
recur, radiofrequency catheter ablation
67
Sinus Bradycardia
• Heart rate <60 beats/min
• Not always pathologic
• Symptoms:
• fatigue, dizziness, inability to concentrate, forgetfulness, syncope
• Causes:
• sinus node dysfunction: aging, accompanying a conduction
disease (e.g. AV block, AF), CHD
• Treatment:
 treat the underlying cause,
 atropine
 Pacemaker if patient is hemodynamically compromised
69
AV Nodal Block
• A type of bradyarrhythmia
• Types
• 1st-degree heart block—PR interval >0.1ms; AV conduction remains
1:1
• 2nd-degree heart block-- progressive prolongation of PR interval AV
conduction <1:1
• 3rd-degree heart block—no AV conduction, atria & ventricles
contract independently from 1 another
• Causes:
• Use of AV nodal blocking agents (digoxin, -blockers,
nondihydropyridine CCBs, amiodarone, dronedarone), hyperkalemia
• Treatment
• treat underlying cause;
• symptomatic patients: atropine 0.5mg IV Q3–5min up to total 3mg,
• transcutaneous pacing; permanent pacemaker needed in patients
without underlying treatable cause
70
Paroxysmal Supraventricular Tachycardia
(PSVT)
• HR >100bpm,
• ECG: narrow QRS complexes
• Symptoms: chest pressure or discomfort, dyspnea, fatigue,
lightheadedness, dizziness, palpitations;
• Treatment:
• hemodynamically stable patients: vagal maneuvers to
sympathetic tone are 1st line;
• Adenosine
71
Wolff-Parkinson-White (WPW)
Syndrome
• A type of SVT
• Etiology:
• accessory pathway that bypasses
AV node & causes tachycardia; HR
>200bpm,
• life-threatening, may lead to VF
• Symptoms:
• chest pain or tightness, dizziness,
lightheadedness, fainting, palpitations,
SOB
72
Wolff-Parkinson-White (WPW)
Syndrome
• Treatment:
• Avoid AV nodal blocking agents (b-blockers,
non-DHP CCBs, adenosine, lidocaine, &
digoxin)
• short term electrical cardioversion:
• amiodarone 150mg IV over 10min;
• procainamide LD 20mg/min IV until arrhythmia
resolves, hypotension, or QRS widens by >50% or
total of 17mg/kg; continuous infusion 1–4mg/min
• long term catheter ablation
73