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Spring 2024 Therapeutics 3 > Exam 2 Arrhythmias > Flashcards

Exam 2 Arrhythmias Flashcards

1
Q

Which ventricle has a larger muscle mass and why?

A

Left ventricle

-has to squeeze blood out against higher pressure

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2
Q

What does the P wave represent?

A

Atrial depolarization

*not atrial contraction, immediately followed by it

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3
Q

What is the PR interval a measure of?

A

AV nodal conduction time

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4
Q

What drugs slow AV node conduction and can lengthen the PR interval?

A

Beta blockers

CCB (diltiazem, verapamil)

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5
Q

What does the QT interval represent?

A

Ventricular repolarization

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6
Q

What does the early part of the QRS wave represent?

A

Ventricular depolarization

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7
Q

What is an electrocardiogram?

A

Non-invasive representation of electrical activity of the heart

*12 lead often used
*3 lead good enough to diagnose arrythmias

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8
Q

How can we determine heart rate by looking at an ECG?

A

Multiple the number of R waves present by 10

(if 8 present, x10=80bpm)

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9
Q

What are the 4 questions to ask to determine if a rhythm is normal?

A
  1. Is there a P wave in front of every QRS complex?
  2. Is there a QRS complex after every P wave?
  3. Is the rhythm regular (interval between R waves all the same)?
  4. What is the heart rate (too slow/fast)?
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10
Q

What is QTc?

A

The corrected QT interval for heart rate

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11
Q

If the PR interval is longer than what it is too long?

A

0.2 seconds

(if P wave falls in one box and R wave is greater than a box away it is too long!)

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12
Q

What causes lengthening of the QRS interval?

A

Sodium blocking

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13
Q

Drugs that make what change to the ECG are the most concerning?

A

Lengthen the QT interval

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14
Q

AT what lengthening of the QT interval do we start to get concerned?

A

0.5 seconds or greater
(> or = 500 ms)

*increases Torsades de Pointes risk

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15
Q

When the QTc interval is > or = 500 ms, what does this increase the risk of?

A

Torsades de Pointes

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16
Q

What is a big risk with development of Torsades de Pointes?

A

Sudden cardiac death

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17
Q

What are the risk factors for developing Torsades de Pointes?

A

65 or older
Electrolyte imbalance (hypokalemia)
Heart failure

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18
Q

What are the 5 Supraventricular Arrhythmias?
(occur above the ventricles)

A

-Sinus Bradycardia
-Atrioventricular (AV) Block
-Sinus Tachycardia
-Atrial Fibrillation
-Supraventricular Tachycardia

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19
Q

What are the 3 Ventricular Arrhythmias?

A

-Premature Ventricular Complexes (PVCs)
-Ventricular Tachycardia
-Ventricular Fibrillation

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20
Q

What is considered “tachycardia”?

A

HR => 100

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21
Q

What is considered “bradycardia”?

A

HR => 60

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22
Q

What is sinus bradycardia?

A

HR < 60 BPM

Impulses originate in SA node

*Note: everything on ECG is normal, just too slow (Not enough R waves)

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23
Q

What is a common cause of sinus bradycardia?

A

Drug-induced

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24
Q

What is the mechanism behind sinus bradycardia?

A

Decreased automaticity of SA node

*depolarizes too slowly

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25
Q

What are some risk factors for sinus bradycardia?

A

MI or ischemia

Abnormal sympathetic or parasympathetic tone

Electrolyte abnormalities

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26
Q

What drugs can cause sinus bradycardia?

A

Digoxin
Beta blockers
CCBs (diltiazem, verapamil)
Amiodarone, Dronedarone
Ivabradine

*stop the drug unless patient needs it
*patients who need beta blockers may receive a pacemaker

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27
Q

What is idiopathic sinus bradycardia?

A

We do not know what is causing it

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28
Q

What are the symptoms of sinus bradycardia?

A

Hypotension (CO low)
Dizziness, Syncope (not enough brain perfusion)

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29
Q

When do we treat sinus bradycardia?

A

Only if symptomatic!

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30
Q

What is the treatment for sinus bradycardia?

A

Atropine 0.5-1mg IV, repeat every 5 min

Max dose: 3mg

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31
Q

If a patient with sinus bradycardia does not respond to atropine what do we do?

A

Start one of the following:
-Transcutaneous pacemaker (on skin)

-Dopamine 5-20 mcg/kg/mim

-Epinephrine 2-10 mcg/min or 0.1-0.5mcg/min

-Isoproterenol 20-60 mcg IV bolus then doses of 10-20 mcg or IV infusion of 1-20 mcg/min

*note: only start on one drug but can have on pacemaker and drug at same time

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32
Q

What are the adverse effects of atropine?

A

-Tachycardia
-Urinary retention
-Blurred vision
-Dry mouth
-Mydriasis (dilated pupils)

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33
Q

What patients experiencing sinus bradycardia require a different treatment regimen?

A

Heart Transplant patients

Spinal Cord Injury patients

**atropine will not work

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34
Q

What treatment should patients experiencing sinus bradycardia who have had a heart transplant or spinal cord injury receive?

A

Aminophylline 6 mg/kg IV over 20-30min

Theophylline
Heart Trans: 300 mg IV followed by po 5-10 mg/kg/day
Spinal CI: PO 5-10 mg/kg/day

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35
Q

What is the long-term treatment for sinus bradycardia?

A

Permanent pacemaker

OR

Theophylline po 5-10 mg/kg/day

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36
Q

What is the most common arrythmia?

A

Atrial Fibrillation

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37
Q

What is the mechanism of Afib?

A

Atria does not have enough time to fill with blood before constricting and passing into the ventricle

*Abnormal atrial/pulmonary vein automaticity
*Atrial reentry

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38
Q

What are the ECG features of Afib?

A

Activity: Chaotic, disorganized
HR: 120-180bpm
Rhythm: Irregularly Irregular
NO P WAVE (no atrial depolarization)

-ungulated (uneven) baseline
-interval between R waves are all different (irregularly irregular)

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39
Q

What feature of Afib causes the chaos seen on the ECG?

A

There is no single reentry circuit

-each reentry circuit tries to create a wave of depolarization and they interact with each other
-bombards the AV node with signals

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40
Q

What is Stage 1 Afib?

A

Presence of risk factors associated with Afib
(modifiable and nonmodifiable)

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41
Q

What is Stage 2 Afib?

A

Pre-Afib (not present yet)

-evidence of structural or electrical findings further predisposing the patient to afib

ex:
-atrial enlargement
-frequent atrial premature beats
-atrial flutter

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42
Q

What is Stage 3 Afib?

A

AFIB PRESENT

*Comes in 4 stages: A,B,C,D

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43
Q

What is Stage 3A Afib?

A

Paroxysmal Afib

-Intermittent
-Terminates within <= 7 days of onset

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44
Q

What is Stage 3B Afib?

A

Persistent Afib

-Continuous
-Sustains for > 7 days and requires intervention

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45
Q

What is Stage 3C Afib?

A

Long-Standing Persistent Afib

-Continuous for > 12 months in duration (year)

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46
Q

What is Stage 3D Afib?

A

Successful Afib Ablation

-No more Afib after percutaneous or surgical intervention to eliminate it

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47
Q

What is Stage 4 Afib?

A

Permanent Trial Fibrillation

-no further attempts at rhythm control made
-discontinue medications

*Left atrium can no longer contract blood into left ventricle, completely reliant on pressure changes

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48
Q

What are two causes of reversible Afib?

A

*Hyperthyroidism

Thoracic surgery
(CABG, Lung resection, Esophagectomy, Valve replacement surgery)

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49
Q

True or False: if a patient has Afib caused by hyperthyroidism and you manage the hyperthyroidism, the Afib is often also managed as well and does not require medication

A

True

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50
Q

What is a major reason why we need to treat Afib and why it is a concern?

A

Does not just cause symptoms, also causes morbidity and mortality!

**Undiagnosed Afib is a huge problem right now since it can present asymptomatically

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51
Q

What disease states associated with morbidity/mortality are more likely to occur with Afib?

A

Stroke/ Systemic Embolism (5x more)
Heart Failure (3x more)
Dementia (2x more)
Mortality (2x more)

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52
Q

What kind of strokes does Afib cause?

A

Large and devastating strokes

**the clots that are formed from Afib are big which makes the strokes more devastating

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53
Q

Where does a clot travel with Afib?

A

Forms in left atrium

Sucked into left ventricle even though the atria are nut pumping

Ends up in coronary artery

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54
Q

What are 3 lifestyle modifications that can be made to prevent Afib?

A

Weight loss (for patients with BMI > 27)

210 minutes vigorous exercise weekly

Smoking cessation

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55
Q

True or False: No amount of alcohol is safe with Afib

A

TRUE
-eliminate consumption

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56
Q

What are the goals of Afib therapy?

A

-Prevent stroke/ Systemic embolism

-Slow ventricular response (inhibit conduction of impulses to ventricle) (**ventricular rate control)

-Convert Afib to normal sinus rhythm

-Maintain sinus rhythm

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57
Q

What are the components of a CHADS-VASc Score?

A

Congestive heart failure
Hypertension
Age => 75 years
Diabetes
Stroke/ TIA

Vascular disease (MI, PAD, aortic plaque)
Age 65-74 years
Sex (female)

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58
Q

What components of the CHADS-VASc score are worth 2 points?

A

Age => 75 years

Stroke/ TIA history

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59
Q

Patients with what CHADS-VASc scores should receive anticoagulation?

A

Men: 1

Women: 2

*with afib

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60
Q

What is the preferred anticoagulation therapy for most patients with afib?

A

DOACs

*preferred over warfarin for most patients

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61
Q

In which patients with afib would warfarin anticoagulation be preferred over DOACs?

A

Mechanical heart valves

Afib associated with heart valve disease (moderate-to-severe mitral valve stenosis)

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62
Q

What is the typical INR target in patients?

A

2-3

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63
Q

What is the INR target in patients with a mechanical heart valve?

A

2.5-3.5

*slightly more aggressive

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64
Q

What is the INR target in patients with moderate-to-severe mitral valve stenosis?

A

2-3

*same as normal

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65
Q

In what patients with afib are Warfarin or Apixaban the preferred anticoagulation treatment options?

A

End-stage chronic kidney disease

Hemodialysis

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66
Q

What value indicates that a patient has end-stage chronic kidney disease?

A

CrCl < 15 mL/min

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67
Q

When should we measure INR of patients on anticoagulants?

A

During initiation: Weekly

After stable: Monthly

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68
Q

What is the antidote of Dabigatran?

A

Idarucizumab

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69
Q

What is the antidote of Rivaroxaban?

A

Andexanet alfa

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70
Q

What is the antidote of Apixaban?

A

Andexanet alfa

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71
Q

What is the antidote of Edoxaban?

A

Andexanet alfa

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72
Q

What drug (s) is Andexanet Alfa the antidote for?

A

Rivaroxaban, Apixaban, Edoxaban

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73
Q

What drug (s) is Idarucizumab the antidote for?

A

Dabigatran

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74
Q

What drugs can be used for ventricular rate control in patients with Afib?

A

Diltiazem (IV)
Verapamil (IV)
Beta Blockers
Digoxin
Amiodarone

75
Q

What is the MOA of diltiazem, verapamil, and beta blockers regarding afib ventricular rate control?

A

Direct AV node inhibition

*reduces rapid heart rate but does not eliminate the Afib

76
Q

What are the 3 beta blockers that can be used for rate control in Afib?

A

Esmolol
Propranolol
Metoprolol

77
Q

What is the MOA of digoxin in rate control of Afib?

A

Vagal stimulation

Direct AV node inhibition

78
Q

What is the MOA of Amiodarone in ventricular rate control of Afib?

A

Beta-blocker

Calcium channel blocker

79
Q

What are some concerns regarding use of Amiodarone?

A

Many adverse effects

-Hypotension
Bradycardia
-Blue-grey skin
-Photosensitivity
-Corneal deposits
-Pulmonary fibrosis
-Hepatotoxicity
Hypothyroidism
-Hyperthyroidism

80
Q

What are the 4 criteria for determining if a patient is hemodynamically unstable?

A

Systolic BP < 90

HR > 150 bpm

Loss of consciousness

Experiencing ischemic chest pain (possibly an MI)

81
Q

If a patient with Afib is hemodynamically unstable what treatment should they receive?

A

Direct Current Cardioversion
(shock them)

82
Q

If a patient with Afib is hemodynamically stable, and does not have decompensated HF what treatment should they receive?

A

Beta blocker, Diltiazem, or Verapamil IV

83
Q

If the first line option for treatment of stable Afib without decompensated HF does not work (BB, Diltiazem, Verapamil), what are the other treatment options?

A

Digoxin

*if this also does not work, give Amiodarone

84
Q

If a patient with Afib is hemodynamically stable, but has Decompensated HF, what treatment should they receive?

A

Amiodarone

**skip all other drugs (BB, Non-DHP CCB take too long to work)

85
Q

What are the goals with Afib treatment?

A

HR <100-110 bpm

Asymptomatic

*increase medications until this occurs or shock

86
Q

What medications should patients with HFrEF never receive?

A

Diltiazem + Verapamil

87
Q

For patients with Afib and HFrEF, what medications should they receive for long-term ventricular rate control?

A

Beta Blockers (likely already on, make sure target dose achieved)

*If this does not reach goal, use Digoxin (combo)

88
Q

For patients with Afib and HFpEF, what medications should they receive for long-tern ventricular rate control?

A

Beta blockers, Diltiazem, or Verapamil

*If this does not reach goal, use Digoxin

*note: Interaction with Dig and Verapamil, have to decrease Dig dose, better to switch to other option

89
Q

What drug does Digoxin interact with that can affect Afib treatment?

A

Verapamil

*have to decrease the dose of Digoxin if using these concomitantly
*better to switch to BB or Diltiazem and avoid this

90
Q

When is it safe to convert Afib patients to sinus rhythm?

A

If Afib present for <= 48 hours

91
Q

If Afib has been present for > 48 hours (unsafe), and we want to convert the patient to sinus rhythm, what must be done?

A

Anticoagulate patient for 3 weeks
OR
Perform a Transesophageal Echocardiogram (TEE) to rule out a clot in the atrium

92
Q

Why is it unsafe to convert an Afib patient to sinus rhythm if the Afib has been present > 48 hours?

A

Could dislodge a clot and cause a stroke

93
Q

If a clot is found in an Afib patient’s atrium after performing a Transesophageal Echocardiogram (TEE), what should be done?

A

Do not convert to sinus rhythm

-Send patient home on anticoagulants and recheck TEE in 2 weeks

94
Q

What treatments can be used to convert Afib patients to sinus rhythm?

A

DC cardioversion (elective or emergent)

Amiodarone

Ibutilide

Procainamide

Flecainide

Propafenone

95
Q

Which two drugs are considered “Pill in the Pocket” drugs for converting Afib to sinus rhythm?

A

Flecainide

Propafenone

**paroxismal Afib patients will carry around a pill with them and if they feel symptoms they will take a single oral dose which will return them to sinus rhythm in a few hours

96
Q

Which medication used to convert Afib patients tp sinus rhythm has a large risk of Torsades de Pointes?

A

Ibutilide

*po with lots of side effects
*Need to monitor QT interval

97
Q

Why do we need to synchronize direct current cardioversion shocks?

A

So that they do not occur during a vulnerable period
-If the shock occurred on a T wave it could trigger ventricular fibrillation which is life threatening

98
Q

In a patient with Afib who has normal LV function and is able to be converted to sinus rhythm, what treatment would we use?

A

IV Amiodarone or Ibutilide
first choice
(Amiodarone better, less Torsades de Pointes)

OR: Procainamide
**not first recommended, cannot start other two and switch, would have to use this from beginning

99
Q

Can we initiate procainamide if patient has already received Amiodarone or Ibutilide?

A

NO
-increased risk of excessive QT prolongation and Torsades de Pointes

100
Q

If a patient with Afib has HFrEF and is able to be converted to sinus rhythm, what treatment would you use?

A

IV Amiodarone

**only medication option, if it does not work we sedate and shock
**higher risk of Torsades de Pointes

101
Q

In patients with Afib that occurs outside of the hospital and normal LV function, what treatment would we use?

A

“Pill-in-Pocket”

-Flecainide
-Propafenone

*single po dose
*DO NOT GIVE TO HF PATIENTS, WILL WORSEN

102
Q

What two drugs used in Afib are associated with causing HFrEF exacerbations?

A

Flecainide
Propafenone

103
Q

What drugs can be used to maintain sinus rhythm in Afib patients?

A

-Amiodarone
-Dofetilide
-Dronedarone
-Sotalol
-Propafenone
-Flecainide

104
Q

When drugs are dosed for maintenance of sinus rhythm, how are they administered?

A

PO

105
Q

What are the adverse effects of Amiodarone to be aware of?

A

Blue-grey skin discoloration
-Photosensitivity
-Pulmonary fibrosis
-Bradycardia
-Hypo/Hyperthyroidism

*skin discoloration is asymptomatic
*need to wear sunscreen
*pulmonary fibrosis is scar tissue in lungs
*may need pacemaker to stay on drug
*drug contains iodine which messes with thyroid

106
Q

What is the scariest symptom of Amiodarone?

A

Pulmonary Fibrosis
(scar tissue in lungs)

107
Q

What drugs interact with amiodarone?

A

Warfarin
Digoxin
Statins

108
Q

What adjustment needs to be made if a patient is on warfarin and amiodarone at the same time?

A

Reduce warfarin dose by 1/3

109
Q

What adjustments need to be made if a patient is on digoxin and amiodarone at the same time?

A

Reduce digoxin dose by 1/2

110
Q

What is a concerning side effect of dofetilide?

A

Torsades de Pointes

111
Q

What drug is contraindicated with dofetilide?

A

Verapamil

112
Q

Why was dronedarone developed?

A

To be similar to amiodarone but with less side effects

**Important to note that this drug is less effective than amiodarone

113
Q

What are important things to note about dronedarone side effects/ drug interactions?

A

*Does not contain iodine like amiodarone, will not affect thyroid

*Pulmonary fibrosis is rarer than with amiodarone

*Does not interact with warfarin

*Still interact with digoxin

114
Q

What are the effects of sotalol?

A

Beta blocker but also has K channel blocking activity

115
Q

How do we dose Dofetilide based on CrCl?

A

> 60: 500 mcg po BID

40-60: 250 mg po BID

20-39: 125 mg po BID

<20: Contraindicated

116
Q

What does the QTc need to be at in order to initiate Dofetilide?

A

<= 440 ms

117
Q

How do we initiate dofetilide in the hospital?

A

Initiate dosing based on CrCl

Adjust dose 2-3 hours after 1st dose (Check QTc interval)

If QTc increases <= 15%, continue current dose

If QTc interval increases > 15% or to > 500 ms, decrease dose by half!

If QTc is > 500 ms after second dose, discontinue

118
Q

When dosing dofetilide, the QTc interval can increase by how much before we have to adjust the dose?

A

<= 15%

119
Q

When dosing dofetilide, how much does the QTc interval have to increase before adjusting the dose?

A

> 15%
or
500 ms

*decrease dose by 1/2

120
Q

When would we have to discontinue a dofetilide dose?

A

If QTc > 500 ms after 2nd dose check

121
Q

What does the QTc have to be at before we can initiate Sotalol in the hospital?

A

<= 450 ms

122
Q

How do we dose sotalol based on CrCl?

A

> 60: 80 mg BID

40-60: 80 mg once daily

<40: CONTRAINDICATED

123
Q

How do we initiate sotalol in the hospital?

A

Only proceed it QTc <= 450ms

Dose based on CrCl

Check QTc interval 2-4 hours after dose

If QTc< 500ms after 3 days: discharge patient or increase dose to120 mg BID

If QTc>= 500: Discontinue

124
Q

Which two drugs used for maintenance of sinus rhythm in Afib need to be started in the hospital?

A

Dofetilide

Sotalol

125
Q

What monitoring needs to be done with Amiodarone?

A

TSH, Liver Function Test:
Init: 3-6 months
Follow-up: q 6 months

ECG: Annually

Chest X-ray: Upon symptoms of cough, dyspnea, or other lung symptoms

Corneal Microdeposits: If visual abnormalities occur

Dermatological: Physical exam annually

126
Q

In a patient with Afib and normal LV function, and no prior MI or heart disease (HF), for maintenance of sinus rhythm what would be the recommended treatment?

A

Start one of these:
Dofetilide
Dronedarone
Flecainide
Propafenone

If it does not work (try multiple first-line first):
Amiodarone

Last Line:
Sotalol

127
Q

In a patient with Afib with prior MI or heart disease (HFrEF), for maintenance of sinus rhythm what would be the recommended treatment?

A

MI:
Start Amiodarone or Dofetilide
Last line: Sotalol

HF:
USE ANYTHING EXCEPT DRONEDARONE

128
Q

What drugs should patients with prior MI or Heart Disease/HFrEF never receive?

A

Flecainide

Propafenone

129
Q

When can we use catheter ablation in Afib treatment?

A

-Improve symptoms in patients where antiarrhythmic drugs have been ineffective

-First line in: young patients with few comorbidities who have symptomatic paroxysmal Afib (intermittent)

130
Q

What is catheter ablation?

A

Catheter inserted through vein into heart using fluoroscopy

-put into all 4 pulmonary veins
-delivers burn of energy and creates circular burn to electrically isolate and block faulty electrical impulses

*used for rhythm control

131
Q

What are the characteristics of supraventricular tachycardia (SVT)?

A

Rhythm: regular
Narrow QRS complex
HR: Very fast, 110-250 bpm

Spontaneously initiates and terminates (paroxysms)

*All waves are present

132
Q

What is paroxysmal SVT? (PSVT)

A

Subset of supraventricular tachycardia

-Intermittent episodes (paroxysms) of SVT

-Start suddenly and spontaneously, last mins to hours, terminate suddenly and spontaneously

133
Q

What is the mechanism of Supraventricular Tachycardia (SVT)?

A

Reentry within:
AV node
-Accessory pathway
-Atria
-SA node

Has a single reentry circuit
**different than afib which has many

134
Q

What side of the AV node do ablations occur on? (Slow or Fast)

A

Slow
-moves down AV node to depolarize ventricles, repolarizes atria

135
Q

Who has a greater risk of developing Supraventricular Tachycardia?

A

-Women
-Age > 65 years
-Can occur with no underlying CVD

136
Q

What is the defining symptom of Supraventricular Tachycardia?

A

Neck pounding

(force of blood going up coronary arteries)

137
Q

True or False: SVT does not cause stroke

A

TRUE

138
Q

Why do patients with SVT not need anticoagulation?

A

The atria are still contracting so blood is not able to pool and clot

139
Q

What are the goals of therapy with SVT?

A

-Terminate SVT
-Restore sinus rhythm
-Prevent recurrences

140
Q

What 4 drugs can be used to terminate SVT?

A

*Adenosine
Beta-Blockers
Diltiazem
Verapamil

141
Q

By what mechanism do drugs that terminate SVT work?

A

Inhibit AV node conduction

142
Q

How do we dose Adenosine in SVT?

A

6 mg IV bolus

no response in 1-2 mins:
12 mg IV bolus
*Can repeat 12 mg IV bolus once

**Remember: 6-12-12
*bolus done rapidly

143
Q

What are the notable adverse effects of adenosine?

A

Chest Pain

Sinus Pauses (ECG flatline 2-3 secs)

144
Q

What is the treatment options for termination hemodynamically stable SVT?

A

Vagal Maneuvers and/or IV Adenosine

if ineffective:
-IV Beta Blockers
-IV Diltiazem
-IV Verapamil

if ineffective or hemodynamically unstable:
-Shock (Synchronized DCC)

145
Q

How can vagal maneuvers help with SVT?

A

-Stimulate vagus nerve to increase parasympathetic nervous system
-This causes HR to slow down and acetylcholine release
-Conduction to AV node inhibited

146
Q

What is the treatment used to prevent recurrence of SVT?

A

No symptoms:
-follow-up, do not treat

Symptomatic:
Catheter ablation preferred

If no catheter ablation:
No HFrEF:
BB, Diltiazem, Verapamil
Then: Flecainide, Propafenone *not in CAD

HFrEF:
Digoxin
Amiodarone
Dofetilide
Sotalol

*at any point can opt into catheter ablation

147
Q

What are the characteristics of Premature Ventricular Complexes (PVCs)?

A

Wide QRS complex
(all waves present though)

Occasional abnormal beats occurring randomly

148
Q

What is Simple PVC?

A

Isolates single PVCs (irregular beats)

149
Q

What are the frequent/repetitive forms of PVC?

A

Pairs of 2 beats: (Couplets)

Every 2nd Beat: (Bigeminy)
Every 3rd Beat: (Trigeminy)
Every 4th Beat: (Quadrigeminy)

Frequent: (At least 1 PVC on ECG, > 30 per hour)

150
Q

What is considered Frequent PVC?

A

At least one PVC on 12-lead ECG

> 30 PVCs per hour

151
Q

What is the mechanism of Premature Ventricular Complexes?

A

Increased automaticity of ventricular muscle cells/ Purkinje Fibers

*no reentry

152
Q

What are the symptoms of PVC’s?

A

*Usually asymptomatic

Can have:
-palpitations, dizziness, lightheadedness

153
Q

What risks are PVCs associated with?

A

Frequent PVCs:
-CVD
-Morbidity/Mortality

Very Frequent PVCs:
-Cardiomyopathy (can cause HF)

With CAD:
-Mortality

Survivors of MI:
Increased risk of sudden cardiac death (SCD)

154
Q

How do we treat asymptomatic PVCs?

A

DO NOT TREAT

**know this

155
Q

How do we treat symptomatic PVC in patients WHO DO NOT HAVE HF?

A

Beta Blockers
Diltiazem
Verapamil

If unresponsive:
Antiarrhythmic

156
Q

If patient with PVC is unresponsive to BB, CCB, or Antiarrhythmic, what do we do?

A

Catheter ablation
**difficult for this arrythmia

157
Q

How do we treat symptomatic PVC in patients with HF?

A

Beta Blocker
*only option

158
Q

What are the characteristics of Ventricular Tachycardia?

A

Regular Rhythm

Wide QRS complex

*Series of consecutive PVCs, but all point upward
*Series of >=3 Ventricular Premature Depolarizations (VPD)

HR > 100 BPM

159
Q

What is nonsustained ventricular tachycardia?

A

> = 3 consecutive Ventricular Premature Depolarizations (VPDs) that terminate spontaneously

160
Q

What is sustained ventricular tachycardia?

A

VT lasting > 30 seconds

OR

Requires termination because of hemodynamic instability < 30 secs

161
Q

What is Sustained Monomorphic Ventricular Tachycardia?

A

-Idiopathic VT (do not know cause)
-QRS complexes all the same

162
Q

What are the 2 Types of Sustained Monomorphic Ventricular Tachycardia?

A

Verapamil Sensitive

Outflow Tract VT
(occurs in right or left ventricular outflow tract)

163
Q

What are the mechanisms of Ventricular Tachycardia?

A

-Increased ventricular automaticity

-Reentry **Different from PVCs

164
Q

What conditions can cause Ventricular Tachycardia?

A

-Coronary Artery Disease
-Myocardial Infarction
-HFrEF
-Electrolyte Abnormality

165
Q

What drugs can cause Ventricular Tachycardia?

A

-Flecainide
-Propafenone
-Digoxin

166
Q

If ventricular tachycardia is sustained, what may it progress to?

A

Ventricular Fibrillation
(bad, no pulse, no HR)
*risk for sudden cardiac death

167
Q

What are the drugs used for termination of Ventricular Tachycardia?

A

Procainamide
Amiodarone
Sotalol
Verapamil
Beta Blockers

168
Q

How do we terminate hemodynamically Stable VT in patients with Structural Heart Disease?

A

DCC (electric shock)
IV Procainamide
IV Amiodarone
IV Sotalol

If this does not work: DCC

169
Q

How do we terminate hemodynamically Stable VT in patients who do not have structural heart disease?

A

Verapamil Sensitive: Verapamil

Outflow Tract: Beta Blocker

If this does not work: DCC

170
Q

What treatments can be used to prevent recurrence of VT and Sudden Cardiac Death?

A

Implantable Cardioverter-Defibrillator (ICD)
Amiodarone
Sotalol
Catheter Ablation

171
Q

Which treatment to prevent VT recurrence is best at mortality reduction?

A

ICD

172
Q

How do ICDs work?

A

Detects VT or Vfib and delivers a shock

*does not prevent the episode but prevents patient from dying from it

**Can use drugs in combo with this if patient is receiving too many shocks

173
Q

What VT patients are recommended to receive a catheter ablation?

A

Patients with prior MI and recurrent VT

-who present with VT and have failed or are intolerant to amiodarone or other antiarrhythmics

174
Q

What does “fibrillation” mean?

A

Atria are quivering

175
Q

What are the characteristics of Ventricular Fibrillation on an ECG?

A

Irregular, disorganized, chaotic electrical activity

**No recognizable QRS complexes or any waves at all

**No pulse, no BP, no CO, no blood pumped to body

176
Q

What is asystole?

A

ECG flatline

177
Q

What role does Vfib play in Myocardial Infarction?

A

Vfib is what these patients die of

178
Q

What is a symptom of Vfib?

A

Sudden cardiac death

179
Q

What is the only effective treatment for Vfib?

A

Defibrillation

*not the same as cardioversion

180
Q

What is the difference between direct cardioversion and defibrillation?

A

Cardioversion is synchronized (avoids end of T wave)

Defibrillation is not synchronized (nothing to synchronize it to)

181
Q

True or False: Drugs used alone will not terminate Vfib

A

TRUE
-only used to facilitate defibrillation

182
Q

What are the 3 drugs we can give to facilitate defibrillation in Vfib?

A

Epinephrine

Amiodarone

Lidocaine

183
Q

What is the algorithm for termination of Vfib?

A

CPR x 2min
Obtain IV/IO access

Defibrillate

CPR x 2 min

*Epinephrine 1 mg IV/IO

Defibrillate

CPR x 2 min

*Amiodarone 300 mg IV/IO OR Lidocaine 1-1.5 mg/kg IV/IO

**continue pattern, next dose of Amiodarone is 150 mg IV/IO or Lidocaine 0.5-0.75 mg/kg IV/IO

Spring 2024 Therapeutics 3 (24 decks)

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