Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHRM 845 Module #1 > Pathophysiology and Treatment of Arrhythmias > Flashcards

Pathophysiology and Treatment of Arrhythmias Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antiarrhtyhmic agents that may cause Torsades de Pointes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SUPRAVENTRICULAR ARRHYTHMIAS

A
  • Sinus bradycardia
  • Atrioventricular (AV) block
  • Sinus tachycardia
  • Atrial fibrillation
  • Supraventricular tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

VENTRICULAR ARRHYTHMIAS

A
  • Premature ventricular complexes (PVCs)
  • Ventricular tachycardia
  • Ventricular fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sinus Bradycardia

A
  • Heart rate < 60 beats per minute
  • Impulses originating in sinoatrial (SA) node (just too slow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sinus Bradycardia MOA

A
  • Decreased automaticity of the SA node
    no reentry present
    problem in sinus node - depolarizing too slowly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sinus Bradycardia Symptoms

A
  • Hypotension
  • Dizziness
  • Syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Atropine AEs

A
  • Tachycardia
  • Urinary retention
  • Blurred vision
  • Dry mouth
  • Mydriasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Atrial Fibrillation Epidemiology

A
  • 2.7-6.1 million people in the US have atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Atrial Fibrillation Social Determinants of Health

A

socioeconomic status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atrial Fibrillation Etiologies of Reversible Atrial Fibrillation

A
  • Hyperthyroidism
  • Thoracic surgery:
    o Coronary artery bypass graft (CABG)
    o Lung resection
    o Esophagectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Prevention of Atrial Fibrillation

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Atrial Fibrillation Goals of Therapy

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Atrial Fibrillation - Prevention of Stroke/Systemic Embolism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Prevention of Stroke/Systemic Embolism

A
  • DOACs are preferred over warfarin for most patients with atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Warfarin is preferred over DOACs in the following patients with atrial fibrillation:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Warfarin or apixaban are preferred in the following patients with atrial fibrillation:

A

End-stage chronic kidney disease (creatinine clearance < 15 mL/min); Hemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Warfarin monitoring

A
  • Measure INR at weekly intervals during initiation of therapy
  • Measure INR at least monthly in all patients after INR is stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Comparison of DOACs

A

apixaban only one used in end-stage kidney disease (CrCl < 15 mL/min)
all p-glycoprotein substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Atrial Fibrillation Drugs for Ventricular Rate Control

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diltiazem AEs

A

Hypotension
Bradycardia
Heart failure exacerbation AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Verapamil AEs

A

Hypotension
Bradycardia
Heart failure exacerbation AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Beta-blockers AEs

A

Hypotension
Bradycardia
Heart failure exacerbation (if dose too high or dose increased too aggressively) AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Digoxin AEs

A

Nausea, vomiting, anorexia, ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Amiodarone AEs

A

Hypotension (IV) Bradycardia
Blue-grey skin discoloration Photosensitivity
Corneal microdeposits
Pulmonary fibrosis Hepatotoxicity Hypothyroidism Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hemodynamically unstable

A

anyone of the 4: SBP < 90 mmHg, HR > 150 bpm, lost conciousness, ischemic chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Atrial Fibrillation Algorithm for Acute Ventricular Rate Control (IV drugs)

A

hemodynamically stable? - no –> DCC; yes - decompensated HF? - yes –> amiodarone; no –> b-blocker, diltiazem, verapamil –> digoxin –> amiodarone
HR goal: < 100-110bpm and asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Do not administer diltiazem or verapamil to patients with

A

decompensated heart failure (LVEF < 40%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Atrial fibrillation Algorithm for Long-Term Ventricular Rate Control (Oral drugs)

A

long-term ventricular rate control –> LVEF > 40% –> b-blockers, diltiazem, verapamil –> digoxin; LVEF </= 40% –> b-blockers –> digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Conversion to Sinus Rhythm

A
  • If AF has been present </= 48 hours, conversion to sinus rhythm is safe
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Drugs for Conversion to Sinus Rhythm

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

DC cardioversion AEs

A

Risks of general anesthesia – aspiration, allergy

46
Q

Amiodarone AEs

A

Hypotension
Bradycardia
QT prolongation

47
Q

Ibutilide AEs

A

torsades de pointes

48
Q

Procainamide AEs

A

QT prolongation
Torsades de pointes
Hypotension
HFrEF exacerbation
Agranulocytosis
Neutropenia

49
Q

Flecainide AEs

A

Dizziness
Blurred vision
HFrEF exacerbation

50
Q

Propafenone

A

Dizziness
Blurred vision
HFrEF exacerbation

51
Q

Artial Fibrillation Algorithm for Conversion of Hemodynamically Stable AF to Sinus Rhythm

A

normal LV function –> IV amiodarone, ibutilide –> procainamide
HFrEF (LVEF </= 40%) –> IV amiodarone
AF occurring outside the hospital in patients with normal LV function –> flecainide, propafenone

52
Q

Do not administer procainamide if patient has already received

A

amiodarone or ibutilide due to the risk of excessive QT prolongation and torsades de pointes

53
Q

Drugs for Maintenance of Sinus Rhythm

A

amiodarone, dofetilide, dronedarone, sotalol, propafenone, flecainide

54
Q

Dofetilide dose

A

CrCl > 60 - 500 mcg BID
CrCl 40-60 - 250 mcg BID
CrCl 20-39 - 125 mcg BID
CrCl < 20 - contraindicated

55
Q

Dofetilide AEs

A

torsades de pointes

56
Q

Dronedarone AEs

A

Bradycardia
Diarrhea
Nausea
Asthenia
Rash

57
Q

Sotalol AEs

A

ß-blockade, torsades de pointes

58
Q

Dofetilide dose

A

CrCl > 60: 500 mcg orally twice daily
40-60: 250 mcg orally twice daily
20-39: 125 mcg orally twice daily
< 20: Contraindicated

59
Q

Amiodarone – Recommended Monitoring

A

AE: hypo- or hyperthyroidism, hepatotoxicity, QT interval prolongation, pulmonary fibrosis, corneal microdeposits, dermatologic (blue-grey skin discoloration, photosensitivity)

60
Q

Hypo- hyperthyroidism

A

baseling testing: TSH (T3 and T4 if TSH abnormal
initial follow-up testin: 3-6 mo
additional follow-up testin: every 6 mo

61
Q

Hepatotoxicity

A

baseline testing: liver function tests (ALT, AST)
initial follow-up testing: 3-6 mo
additional follow-up testing: every 6 mo

62
Q

QT interval prolongation

A

baseline testing: ECG
initial follow-up testing: annually

63
Q

Pulmonary fibrosis

A

baseline testing: chest x-ray
initial follow-up testing: If patient develops unexplained cough or dyspnea or other symptoms suggestive of lung disease

64
Q

Corneal microdeposists

A

baseline testing: not recommended
initial follow-up testing: Ophthalmologic exam recommended if patient develops visual abnormalities

65
Q

Dermatologic

A

baseline testing: not recommended
initial follow-up testing: physical exam annually
additional follow-up testing: development of skin discoloration, photosensitivity

66
Q

Atrial fibrillation Algorithm for Maintenance of Sinus Rhythm Following Conversion to SR or for Paroxysmal AF

A

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 <//= 40%) –> amiodarone, sotalol; NYHA class III or IV or recent decompensated HF –> no - dronedarone, yes - dronaderone contraindicated

67
Q

Neither flecainide nor propafenone should be administered to patients with

A

prior MI, significant structural heart disease and/or HFrEF

68
Q

Algorithm for Inpatient Initiation of Dofetilide

A

Place patient on continuous ECG monitoring, proceed only if QTc </= 440 ms –> 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% - continue current dose; 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
Q

Algorithm for Inpatient Initiation of Sotalol

A

Place patient on continuous ECG monitoring, proceed only if QTc </= 450 ms –> 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
Q

Catheter Ablation

A
  • 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
Q

Supraventricular Tachycardia

A
  • 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
Q

Supraventricular Tachycardia: Paroxysmal SVT (PSVT)

A

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
Q

Supraventricular Tachycardia: Mechanisms

A
  • 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
Q

Supraventricular Tachycardia: Etiologies/Risk Factors

A
  • 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
Q

Supraventricular Tachycardia: Symptoms

A
  • “Neck-pounding”
  • Palpitations
  • Dizziness
  • Weakness
  • Lightheadedness
  • Near-syncope
  • Syncope
  • Polyuria
76
Q

Supraventricular Tachycardia: Goals of Therapy

A
  • Terminate SVT, restore sinus rhythm
  • Prevent recurrences
    if you give drugs that inhibit conduction through the AV node, you can terminate supraventricular tachycardia
77
Q

Supraventricular Tachycardia Drugs for Termination of SVT

A

adenosine, b-blockers, diltiazem, verapamil
inhibit AV node conduction, terminates reentrant pathway

78
Q

Adenosine AEs

A

Chest pain, flushing, shortness of breath, sinus pauses, bronchospasm

79
Q

Supraventricular Tachycardia Algorithm for Termination of Hemodynamically Stable SVT

A

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
Q

Supraventricular Tachycardia Algorithm for Prevention of Recurrence of SVT

A

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
Q

VENTRICULAR ARRHYTHMIAS

A
  • Premature ventricular complexes (PVCs)
  • Ventricular tachycardia
  • Ventricular fibrillation
82
Q

Premature Ventricular Complexes

A
  • 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
Q

Premature Ventricular Complexes: Types

A
  • 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
Q

Premature Ventricular Complexes: Mechanism

A
  • Increased automaticity of ventricular muscle cells/Purkinje fibers
    no reentry present
85
Q

Premature Ventricular Complexes: Etiologies/Risk Factors

A
  • Ischemic heart disease
  • Myocardial infarction
  • Anemia
  • Hypoxia
  • Cardiac surgery
    HFrEF
86
Q

Premature Ventricular Complexes: Symptoms

A
  • Usually asymptomatic
  • Frequent/repetitive PVCs can result in:
    o Palpitations
    o Dizziness
    o Lightheadedness
87
Q

Premature Ventricular Complexes: Prognostic Implications

A
  • <= 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
Q

Premature Ventricular Complexes: Asymptomatic Treatment

A
  • 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
Q

Premature Ventricular Complexes: Sypmtomatic Treatment

A
  • 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
Q

Ventricular Tachycardia

A
  • 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
Q

Ventricular Tachycardia:
Types

A
  • 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
Q

Ventricular Tachycardia: Mechanisms

A
  • Increased ventricular automaticity
  • Reentry
93
Q

Ventricular Tachycardia: Etiologies/Risk Factors

A
  • Coronary artery disease
  • Myocardial infarction
  • HFrEF
  • Electrolyte abnormalities (hypokalemia, hypomagnesemia)
  • Drugs: Flecainide, Propafenone, Digoxin
94
Q

Ventricular Tachycardia: Symptoms

A
  • May be asymptomatic (nonsustained VT)
  • Palpitations
  • Hypotension
  • Dizziness
  • Lighteadedness
  • Syncope
  • Angina
95
Q

Ventricular Tachycardia: Prognostic Significance

A
  • 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
Q

Ventricular Tachycardia: Goals of Therapy

A
  • Terminate VT, restore sinus rhythm
  • Prevent recurrence of VT
  • Reduce the risk of sudden cardiac death
97
Q

Drugs for Termination of Ventricular Tachycardia

A

procainamide, amiodarone, sotalol, verapamil, b-blockers

98
Q

Ventricular Tachycardia
Algorithm for Termination of Hemodynamically Stable VT

A

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
Q

Ventricular Tachycardia: Prevention of Recurrence and Sudden Cardiac Death

A

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
Q

Ventricular Fibrillation

A
  • Irregular, disorganized, chaotic electrical activity
  • No recognizable QRS complexes
    no ventricular depolarizations/contractions, no BP or pulse, no CO - asystole
101
Q

Ventricular Fibrillation: Etiologies/Risk Factors

A
  • Myocardial infarction
  • HFrEF
  • Coronary artery disease
102
Q

Ventricular Fibrillation: Symptoms

A
  • Syndrome of sudden cardiac death
103
Q

Ventricular Fibrillation: Treatment

A
  • 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
Q

Treatment of Ventricular Fibrillation

A

defibrillation: Simultaneously depolarizes all myocardial cells, allowing sinus node to resume as pacemaker; ephinephrine: vasopressor; amiodarone; lidocaine

105
Q

Epinephrine AEs

A

Post-resuscitation tachycardia

106
Q

Amiodarone AEs for ventricular fibrillation tx

A

Post-resuscitation hypotension

107
Q

Lidocaine AEs

A

Post-resuscitation confusion, seizures

108
Q

Ventricular Fibrillation
Algorithm for Termination of VF (or VT without a pulse)

A

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
Q

Ventricular Fibrillation
Algorithm for Termination of VF (or VT without a pulse) cont.

A
  • 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
Q

Automatic External Defibrillator

A
  • 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

PHRM 845 Module #1 (50 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions