Pathophysiology and Treatment of Arrhythmias Flashcards

(110 cards)

1
Q

Relationship Between ECG and Action Potential

A

P: atrial depolarization
QRS: firing of the AV node + ventricular depolarization
ST: plateau in myocardial AP
QT: ventricular repolarization
PR interval used as AV node conduction time
Lengthening of QT interval causes an arrhythmia, QT interval is an indicator for risk of arrhythmias

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2
Q

Torsades de Pointes

A
  • When the QTc interval is >/= 500 ms, there is increased risk of the drug-induced arrhythmia known as torsades de pointes
  • Torsades de pointes can cause sudden cardiac death
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3
Q

Antiarrhtyhmic agents that may cause Torsades de Pointes

A

procainamide, flecainide, ibutilide, dofetilide, sotalol, amiodarone, dronedarone

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4
Q

SUPRAVENTRICULAR ARRHYTHMIAS

A
  • Sinus bradycardia
  • Atrioventricular (AV) block
  • Sinus tachycardia
  • Atrial fibrillation
  • Supraventricular tachycardia
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5
Q

VENTRICULAR ARRHYTHMIAS

A
  • Premature ventricular complexes (PVCs)
  • Ventricular tachycardia
  • Ventricular fibrillation
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6
Q

Sinus Bradycardia

A
  • Heart rate < 60 beats per minute
  • Impulses originating in sinoatrial (SA) node (just too slow)
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7
Q

Sinus Bradycardia MOA

A
  • Decreased automaticity of the SA node
    no reentry present
    problem in sinus node - depolarizing too slowly
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8
Q

Sinus Bradycardia Etiologies/Risk Factors

A
  • Myocardial infarction or ischemia
  • Abnormal sympathetic or parasympathetic tone
  • Electrolyte abnormalities * Hyperkalemia
  • Hypermagnesemia
  • Drugs
  • Digoxin
  • ß-blockers
  • CCBs (Diltiazem, verapamil)
  • Amiodarone
  • Dronedarone
  • Ivabradine
  • Idiopathic
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9
Q

Sinus Bradycardia Symptoms

A
  • Hypotension
  • Dizziness
  • Syncope
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10
Q

Sinus Bradycardia Treatment

A
  • Only necessary if patient is symptomatic
  • Atropine 0.5 -1 mg IV, repeat every 5 minutes
  • Maximum dose 3 mg
  • If unresponsive to atropine:
  • Transcutaneous pacing
  • Dopamine 5-20 mcg/kg/minute
  • Epinephrine 2-10 mcg/min or 0.1-0.5 mcg/kg/min
  • Isoproterenol 20-60 mcg IV bolus followed by doses of 10- 20 mcg or infusion of 1-20 mcg/min
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11
Q

Atropine AEs

A
  • Tachycardia
  • Urinary retention
  • Blurred vision
  • Dry mouth
  • Mydriasis
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12
Q

Treatment of Sinus Bradycardia After Heart Transplant or Spinal Cord Injury

A
  • Aminophylline 6 mg/kg IV over 20-30 minutes OR
  • Theophylline:
    o Heart transplant: 300 mg IV followed by oral dose of 5-10 mg/kg/day titrated to effect
    o Spinal cord injury: Oral dose of 5-10 mg/kg/day titrated to effect
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13
Q

Sinus Bradycardia Long Term Treatment

A

*Some patients require a permanent pacemaker (doesn’t regulate QT interval)
* For patients unwilling to undergo implantation of a permanent pacemaker:
* Theophylline oral 5-10 mg/kg/day titrated to effect

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14
Q

Atrial Fibrillation Epidemiology

A
  • 2.7-6.1 million people in the US have atrial fibrillation
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15
Q

Atrial Fibrillation Features

A

Atrial activity: Chaotic and disorganized – no atrial depolarizations
Ventricular rate: 120-180 bpm
Rhythm: Irregularly irregular
P waves: Absent

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16
Q

Atrial Fibrillation Stages 1 + 2

A

Stages
* Stage 1
o Presence of modifiable and nonmodifiable risk
factors associated with AF
* Stage 2
o Pre-atrial fibrillation: Evidence of structural or electrical findings that further predispose patients to AF -
§ Atrial enlargement
§ Frequent atrial premature beats
§ Atrial flutter

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17
Q

Atrial Fibrillation Stage 3

A
  • Stage 3
    o Atrial fibrillation
    3A – Paroxysmal AF: AF that is intermittent and terminates within </= 7 days of onset; 3B – Persistent AF: AF that is continuous and sustains for > 7 days and requires
    intervention; 3C – Long-standing persistent AF: AF that is continuous for > 12 months in duration; 3D – Successful AF ablation: Freedom from AF after percutaneous or surgical intervention to eliminate AF
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18
Q

Atrial Fibrillation Stage 4

A
  • Stage 4
    o Permanent trial fibrillation: No further attempts at rhythm control after discussion between the patient and clinician
    never again in sinus rhythm
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19
Q

Atrial Fibrillation Mechanisms

A
  • Abnormal atrial/pulmonary vein automaticity
  • Atrial reentry
    abnormal/premature impulse generated in the pulmonary veins that causes reentry –> AF
    no fully formed atrial depolarizations
    multiple, simultaneously active reentry circuits –> electrical chaos
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20
Q

Atrial Fibrillation Etiologies and Risk Factors

A
  • Advancing age
  • Cigarette smoking
  • Sedentary lifestyle
  • Alcohol
  • Obesity
  • Hypertension
  • Diabetes mellitus
  • Coronary artery disease
  • Heart failure
  • Obstructive sleep apnea
  • Valvular heart disease
  • Chronic kidney disease
  • Familial (genetic)
  • Idiopathic
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21
Q

Atrial Fibrillation Social Determinants of Health

A

socioeconomic status

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22
Q

Atrial Fibrillation Etiologies of Reversible Atrial Fibrillation

A
  • Hyperthyroidism
  • Thoracic surgery:
    o Coronary artery bypass graft (CABG)
    o Lung resection
    o Esophagectomy
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23
Q

Atrial Fibrillation Symptoms

A
  • Maybeasymptomatic
  • Palpitations
  • Dizziness
  • Fatigue
  • Lightheadedness
  • Shortnessofbreath
  • Hypotension
  • Syncope
  • Angina (in patients with coronary artery disease)
  • Exacerbation of heart failure symptoms
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24
Q

Atrial Fibrillation Morbidity/Mortality

A
  • Stroke/systemic embolism– risk increased 5x
  • Heart failure–risk increased 3x
  • Dementia–risk increased 2x
  • Mortality–risk increased 2x
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25
Prevention of Atrial Fibrillation
* Lifestyle and risk factor modification: Weight loss in individuals who are overweight or obese (BMI > 27 kg/m2) * Physical fitness: Target 210 minutes vigorous exercise each week * Smoking cessation * Minimize or eliminate alcohol consumption * Blood pressure control in patients with hypertension * Optimal glucose and A1C management in patients with diabetes
26
Atrial Fibrillation Goals of Therapy
* Prevent stroke/systemic embolism * Slow ventricular response by inhibiting conductionof impulses to ventricles o AKA ventricular rate control * Convert atrial fibrillation to normal sinus rhythm * Maintain sinus rhythm (reduce frequency of episodes)
27
Atrial Fibrillation - Prevention of Stroke/Systemic Embolism
CHAsDS2-VASc score * Oral anticoagulants are recommended for patients with atrial fibrillation and the following CHAsDS2-VASc scores: >/= 2 in men >/= 3 in women * Oral anticoagulants is reasonable for patients with atrial fibrillation and the following CHAsDS2-VASc scores: 1 in men, 2 in women * Oral anticoagulants may be omitted for patients with atrial fibrillation and the following CHAsDS2-VASc scores: 0 in men, 0-1 in women
28
Prevention of Stroke/Systemic Embolism
* DOACs are preferred over warfarin for most patients with atrial fibrillation
29
Warfarin is preferred over DOACs in the following patients with atrial fibrillation:
o Mechanical heart valves - Target INR 2.5-3.5 o Atrial fibrillation associated with heart valve disease (moderate-to-severe mitral valve stenosis) - Target INR 2.0-3.0
30
Warfarin or apixaban are preferred in the following patients with atrial fibrillation:
End-stage chronic kidney disease (creatinine clearance < 15 mL/min); Hemodialysis
31
Warfarin monitoring
* Measure INR at weekly intervals during initiation of therapy * Measure INR at least monthly in all patients after INR is stable
32
Comparison of DOACs
apixaban only one used in end-stage kidney disease (CrCl < 15 mL/min) all p-glycoprotein substrates
33
Atrial Fibrillation Drugs for Ventricular Rate Control
goal is to inhibit conduction of impulse to AV node (b/c this is where the misfiring occurs) diltiazem, verapamil - direct AV node inhibition beta-blockers - direct AV node inhibition digoxin - vagal stimulation, direct AV node inhibition amiodarone - beta blocker, CCB
34
Diltiazem AEs
Hypotension Bradycardia Heart failure exacerbation AV block
35
Verapamil AEs
Hypotension Bradycardia Heart failure exacerbation AV block
36
Beta-blockers AEs
Hypotension Bradycardia Heart failure exacerbation (if dose too high or dose increased too aggressively) AV block
37
Digoxin AEs
Nausea, vomiting, anorexia, ventricular arrhythmias
38
Amiodarone AEs
Hypotension (IV) Bradycardia Blue-grey skin discoloration Photosensitivity Corneal microdeposits Pulmonary fibrosis Hepatotoxicity Hypothyroidism Hyperthyroidism
39
Hemodynamically unstable
anyone of the 4: SBP < 90 mmHg, HR > 150 bpm, lost conciousness, ischemic chest pain
40
Atrial Fibrillation Algorithm for Acute Ventricular Rate Control (IV drugs)
hemodynamically stable? - no --> DCC; yes - decompensated HF? - yes --> amiodarone; no --> b-blocker, diltiazem, verapamil --> digoxin --> amiodarone HR goal: < 100-110bpm and asymptomatic
41
Do not administer diltiazem or verapamil to patients with
decompensated heart failure (LVEF < 40%)
42
Atrial fibrillation Algorithm for Long-Term Ventricular Rate Control (Oral drugs)
long-term ventricular rate control --> LVEF > 40% --> b-blockers, diltiazem, verapamil --> digoxin; LVEF b-blockers --> digoxin
43
Conversion to Sinus Rhythm
* If AF has been present 48 hours, conversion to sinus rhythm should not be performed until patient has been anticoagulated for 3 weeks, or unless a transesophageal echocardiogram (TEE) has been performed to rule out a clot in the atrium don't try in pts with permanent AF
44
Drugs for Conversion to Sinus Rhythm
DC cardioversion (may be elective or emergent) - simultaneously depolarizes all myocardial cells, allowing sinus node to take over as pacemaker amiodarone ibutilide procainamide flecainide propafenone
45
DC cardioversion AEs
Risks of general anesthesia – aspiration, allergy
46
Amiodarone AEs
Hypotension Bradycardia QT prolongation
47
Ibutilide AEs
torsades de pointes
48
Procainamide AEs
QT prolongation Torsades de pointes Hypotension HFrEF exacerbation Agranulocytosis Neutropenia
49
Flecainide AEs
Dizziness Blurred vision HFrEF exacerbation
50
Propafenone
Dizziness Blurred vision HFrEF exacerbation
51
Artial Fibrillation Algorithm for Conversion of Hemodynamically Stable AF to Sinus Rhythm
normal LV function --> IV amiodarone, ibutilide --> procainamide HFrEF (LVEF IV amiodarone AF occurring outside the hospital in patients with normal LV function --> flecainide, propafenone
52
Do not administer procainamide if patient has already received
amiodarone or ibutilide due to the risk of excessive QT prolongation and torsades de pointes
53
Drugs for Maintenance of Sinus Rhythm
amiodarone, dofetilide, dronedarone, sotalol, propafenone, flecainide
54
Dofetilide dose
CrCl > 60 - 500 mcg BID CrCl 40-60 - 250 mcg BID CrCl 20-39 - 125 mcg BID CrCl < 20 - contraindicated
55
Dofetilide AEs
torsades de pointes
56
Dronedarone AEs
Bradycardia Diarrhea Nausea Asthenia Rash
57
Sotalol AEs
ß-blockade, torsades de pointes
58
Dofetilide dose
CrCl > 60: 500 mcg orally twice daily 40-60: 250 mcg orally twice daily 20-39: 125 mcg orally twice daily < 20: Contraindicated
59
Amiodarone – Recommended Monitoring
AE: hypo- or hyperthyroidism, hepatotoxicity, QT interval prolongation, pulmonary fibrosis, corneal microdeposits, dermatologic (blue-grey skin discoloration, photosensitivity)
60
Hypo- hyperthyroidism
baseling testing: TSH (T3 and T4 if TSH abnormal initial follow-up testin: 3-6 mo additional follow-up testin: every 6 mo
61
Hepatotoxicity
baseline testing: liver function tests (ALT, AST) initial follow-up testing: 3-6 mo additional follow-up testing: every 6 mo
62
QT interval prolongation
baseline testing: ECG initial follow-up testing: annually
63
Pulmonary fibrosis
baseline testing: chest x-ray initial follow-up testing: If patient develops unexplained cough or dyspnea or other symptoms suggestive of lung disease
64
Corneal microdeposists
baseline testing: not recommended initial follow-up testing: Ophthalmologic exam recommended if patient develops visual abnormalities
65
Dermatologic
baseline testing: not recommended initial follow-up testing: physical exam annually additional follow-up testing: development of skin discoloration, photosensitivity
66
Atrial fibrillation Algorithm for Maintenance of Sinus Rhythm Following Conversion to SR or for Paroxysmal AF
normal LV function, nor prior MI or significant structural heart disease --> dofetilide, dronedarone, flecainide, propafenone --> amiodarone --> sotalol prior MI or significant structural heart disease, including HFrEF (LVEF amiodarone, sotalol; NYHA class III or IV or recent decompensated HF --> no - dronedarone, yes - dronaderone contraindicated
67
Neither flecainide nor propafenone should be administered to patients with
prior MI, significant structural heart disease and/or HFrEF
68
Algorithm for Inpatient Initiation of Dofetilide
Place patient on continuous ECG monitoring, proceed only if QTc CrCl > 60 - 500 mcg BID, CrCl 40-60 - 250 mcg BID, CrCl 20-39 - 125 mcg BID --> Post-dose adjustment 2-3 hrs after 1st dose – check QTc interval --> If QTc increases 15% or to > 500 ms, decrease dose: 500 mcg to 250 mcg twice daily, 250 mcg to 125 mcg twice daily, 125 mcg twice daily to once daily --> If at any time after 2nd dose QTc is > 500 ms, discontinue dofetilide
69
Algorithm for Inpatient Initiation of Sotalol
Place patient on continuous ECG monitoring, proceed only if QTc CrCl > 60 - 80 mg BID, CrCl 40-60 - 80 mg once daily --> Check QTc interval 2-4 hours after each dose --> If QTc < 500 ms after 3 days (or after 5th or 6th dose if once daily dosing) patient can de discharged OR dose can be increased to 120 mg twice daily and patient can be followed for 3 days on this dose; If QTc increases >/= 500 ms, discontinue sotalol
70
Catheter Ablation
* Catheter ablation for rhythm control is useful to improve symptoms in patients in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated, or not preferred. * In selected patients (generally younger and with fewer comorbidities) with symptomatic paroxysmal atrial fibrillation, catheter ablation can be used as first-line therapy to improve symptoms and reduce progression to persistent atrial fibrillation
71
Supraventricular Tachycardia
* Regular rhythm * Narrow QRS complexes * Heart rate110 --> 250 beats per minute * Spontaneous initiation and termination * Prevalence: 225 per 100,000 * Incidence: 35 cases per 100,000 persons per year
72
Supraventricular Tachycardia: Paroxysmal SVT (PSVT)
o A subset of SVT o Intermittent episodes (paroxysms) of SVT o Episodes start suddenly and spontaneously, last for minutes to hours, and terminate suddenly and spontaneously
73
Supraventricular Tachycardia: Mechanisms
* Reentry within: o AV node (60%) o Accessory pathway (Wolff-Parkinson-White syndrome (30%) o Atria (4-8%) o SA node (4%) Afib has mutltiple simultaneous active reentry circuits across both atrium; supraventricular tachycardia has single reentry circuit inside the AV node
74
Supraventricular Tachycardia: Etiologies/Risk Factors
* Women have 2x higher risk than men * Age > 65 years: 5x greater risk than younger people * Often occurs in individuals with no underlying CVD
75
Supraventricular Tachycardia: Symptoms
* “Neck-pounding” * Palpitations * Dizziness * Weakness * Lightheadedness * Near-syncope * Syncope * Polyuria
76
Supraventricular Tachycardia: Goals of Therapy
* Terminate SVT, restore sinus rhythm * Prevent recurrences if you give drugs that inhibit conduction through the AV node, you can terminate supraventricular tachycardia
77
Supraventricular Tachycardia Drugs for Termination of SVT
adenosine, b-blockers, diltiazem, verapamil inhibit AV node conduction, terminates reentrant pathway
78
Adenosine AEs
Chest pain, flushing, shortness of breath, sinus pauses, bronchospasm
79
Supraventricular Tachycardia Algorithm for Termination of Hemodynamically Stable SVT
SVT --> vagal maneuvers and/or IV adenosine --> if ineffective or not feasible --> IV b-blocker or IV diltiazem or IV verapamil --> if not effective or not feasible --> synchronized DCC
80
Supraventricular Tachycardia Algorithm for Prevention of Recurrence of SVT
SVT --> symptomatic --> catheter ablation candidate, pt prefers catheter ablation --> yes - catheter ablation; no - HFrEF --> amiodarone, digoxin, dofetilide, sotalol, no HFrEF --> b-blockers, diltiazem, verapamil --> flecainide, propafenone (contradindicated in CAD) SVT --> asymptomatic.minimally symptomatic --> clinical follow-up without treatment
81
VENTRICULAR ARRHYTHMIAS
* Premature ventricular complexes (PVCs) * Ventricular tachycardia * Ventricular fibrillation
82
Premature Ventricular Complexes
* Wide QRS complexes * Prevalence in a healthy population: 0.8% * Prevalence increases with advancing age: < 20 years of age: 0.6%; > 50 years of age: 2.7% abnormal automaticity in ventricles; premature abnormal ectopic beats in the ventricles, depolarizations occurring outside the HIS purkinje system
83
Premature Ventricular Complexes: Types
* Simple – isolated single PVCs * Frequent/repetitive forms: o Pairs (couplets) o Every 2nd beat (bigeminy) o Every 3rd beat (trigeminy) o Every 4th beat (quadrigeminy) o Frequent: At least one PVC on a 12-lead ECG; > 30 PVCs per hour
84
Premature Ventricular Complexes: Mechanism
* Increased automaticity of ventricular muscle cells/Purkinje fibers no reentry present
85
Premature Ventricular Complexes: Etiologies/Risk Factors
* Ischemic heart disease * Myocardial infarction * Anemia * Hypoxia * Cardiac surgery HFrEF
86
Premature Ventricular Complexes: Symptoms
* Usually asymptomatic * Frequent/repetitive PVCs can result in: o Palpitations o Dizziness o Lightheadedness
87
Premature Ventricular Complexes: Prognostic Implications
* <= 30 years of age: no prognostic significance * > 30 years of age: PVCs influence long-term risk * Frequent PVCs are associated with increased long-term risk of CVD and mortality * Very frequent PVCs (> 10,000-20,000 per day) are associated with cardiomyopathy * In patients with established CAD, PVCs are associated with increased mortality * In survivors of MI, frequent/repetitive PVCs are associated with increased risk of SCD, which is further enhanced in patients with HF
88
Premature Ventricular Complexes: Asymptomatic Treatment
* Asymptomatic PVCs should not be treated * Treatment of symptomatic PVCs in patients who do not have CAD or HF: ß-blockers, diltiazem or verapamil; If unresponsive – antiarrhythmic medication * Treatment of frequent symptomatic PVCs(> 15% of beats) unresponsive to ß-blockers, CCBs or antiarrhythmic drugs: Catheter ablation
89
Premature Ventricular Complexes: Sypmtomatic Treatment
* Treatment of symptomatic PVCs in patients who have CAD: ß-blockers, diltiazem or verapamil; If unresponsive – antiarrhythmic medication * Treatment of symptomatic PVCs in patients who have HF: ß-blockers
90
Ventricular Tachycardia
* Regular rhythm * Wide QRS complexes - depolarizations slower b/c outside purkinje * Defined as a series of >/= 3 consecutive VPDs at a rate of > 100 bpm
91
Ventricular Tachycardia: Types
* Nonsustained: >/= 3 consecutive VPDs, terminates spontaneously * Sustained: VT lasting > 30 seconds, or Requires termination because of hemodynamic instability in < 30 seconds * Sustained monomorphic VT in patients with no structural heart disease is known as: Idiopathic VT; Idiopathic VT is sometimes responsive to verapamil – known as “verapamil-sensitive VT”; Idiopathic VT may also occur in the right or left ventricular outflow tract, and is known as “outflow tract VT”
92
Ventricular Tachycardia: Mechanisms
* Increased ventricular automaticity * Reentry
93
Ventricular Tachycardia: Etiologies/Risk Factors
* Coronary artery disease * Myocardial infarction * HFrEF * Electrolyte abnormalities (hypokalemia, hypomagnesemia) * Drugs: Flecainide, Propafenone, Digoxin
94
Ventricular Tachycardia: Symptoms
* May be asymptomatic (nonsustained VT) * Palpitations * Hypotension * Dizziness * Lighteadedness * Syncope * Angina
95
Ventricular Tachycardia: Prognostic Significance
* Sustained VT may progress to ventricular fibrillation, a life-threatening arrhythmia * Patients with sustained VT are at risk for the syndrome of sudden cardiac death
96
Ventricular Tachycardia: Goals of Therapy
* Terminate VT, restore sinus rhythm * Prevent recurrence of VT * Reduce the risk of sudden cardiac death
97
Drugs for Termination of Ventricular Tachycardia
procainamide, amiodarone, sotalol, verapamil, b-blockers
98
Ventricular Tachycardia Algorithm for Termination of Hemodynamically Stable VT
VT --> structural heart disease: DCC, IV amiodarone or IV sotalol, IV procainamide --> VT terminated? --> yes - therapy to prevent recurrence guided by underlying heart disease, no - DCC VT --> no structural heart disease --> idopathic VT diagnosed based on ECG morphology --> verapamil-sensitive VT --> verapamil; outflow tract VT --> b-blocker --> VT terminated? --> yes - therapy to prevent recurrence, no - DCC
99
Ventricular Tachycardia: Prevention of Recurrence and Sudden Cardiac Death
implantable cardioverter-defibrillator, amiodarone (Recommended for patients with ICDs who have significant symptoms or frequent ICD shocks, to suppress recurrent VT and reduce frequency of shocks), sotalol (Recommended for patients with ICDs who have significant symptoms or frequent ICD shocks, to suppress recurrent VT and reduce frequency of shocks), catheter ablation (Recommended for patients with prior MI and recurrent episodes of VT, who present with VT and who have failed or are intolerant of amiodarone or other antiarrhythmic drugs)
100
Ventricular Fibrillation
* Irregular, disorganized, chaotic electrical activity * No recognizable QRS complexes no ventricular depolarizations/contractions, no BP or pulse, no CO - asystole
101
Ventricular Fibrillation: Etiologies/Risk Factors
* Myocardial infarction * HFrEF * Coronary artery disease
102
Ventricular Fibrillation: Symptoms
* Syndrome of sudden cardiac death
103
Ventricular Fibrillation: Treatment
* Goal: o Terminate ventricular fibrillation, restore sinus rhythm and spontaneous circulation * Important: o The only effective treatment is defibrillation o Drugs are used to facilitate defibrillation o Drugs alone will not terminate ventricular fibrillation
104
Treatment of Ventricular Fibrillation
defibrillation: Simultaneously depolarizes all myocardial cells, allowing sinus node to resume as pacemaker; ephinephrine: vasopressor; amiodarone; lidocaine
105
Epinephrine AEs
Post-resuscitation tachycardia
106
Amiodarone AEs for ventricular fibrillation tx
Post-resuscitation hypotension
107
Lidocaine AEs
Post-resuscitation confusion, seizures
108
Ventricular Fibrillation Algorithm for Termination of VF (or VT without a pulse)
VF --> CPR x 2 min, obtain IV/IO access --> defibrillation shock --> CPR x 2 min --> epinephrine 1 mg IV/IO --> defibrillation shock --> CPR x 2 min --> amiodarone 300 mg IV/IO or lidocaine 1-1.5 mg/kg IV/IO --> defibrillation shock --> CPR x 2 min --> epinephrine 1 mg IV/IO --> defibrillation shock --> CPR x 2 min --> amiodarone 150 mg IV/IO or lidocaine 0.5-0.7 mg/kg IV/IO --> defibrillation shock --> CPR x 2 min --> epinephrine 1 mg IV/IO
109
Ventricular Fibrillation Algorithm for Termination of VF (or VT without a pulse) cont.
* Continue pattern of defibrillation, shock, then CPR x 2 min, then epinephrine 1 mg i.v. every 3-5 min until patient is resuscitated or resuscitation attempt is terminated
110
Automatic External Defibrillator
* Available in airports, shopping malls, fitness centers, on airplanes * Easy to use – machine “talks” user through the procedure * Potential to save thousands of lives * Cost - $250 - $1,700 per machine