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Advanced Pediatric Pharmacology Exam 1 > Cardiology 2 > Flashcards

Cardiology 2 Flashcards

1
Q

Phases of the Action Potential

A

Phase 0: Depolarization

  • Rapid Na entry
  • Slow Ca entry

Phas 1: Repolarization
- K expulsion

Phase 2: Plateau

  • Slow Ca entry
  • Slow K expulsion

Phase 3: Resting potential
- K expulsion

Phase 4: Quiescence

  • Na exits
  • K reenters
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2
Q

EKG P Wave (Length and Description)

A

Length: <0.1

Description: Atrial Depolarization

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3
Q

QRS Complex (Length and Description)

A

Length: 0.05-0.1

Description: Ventricular Depolarization

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4
Q

T Wave (Description)

A

Ventricular repolarization

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5
Q

ST Segment (Description)

A

Ventricular repolarization

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6
Q

QT Interval (Length and Description)

A

Length: <0.5

Description: Ventricular depolarization and repolarization

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7
Q

Most common pediatric asymptomatic arrhythmias (3)

A
  1. Sinus arrhythmia
  2. Ventricular premature beats (VPBs)
  3. Atrial premature beats (APBs)
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8
Q

Sinus Arrhythmias (4)

A
  1. Normal physiologic variant characterized by increased heart rate during inspiration and a decreased heart rate during expiration
  2. Caused by changes in parasympathetic input to the heart
  3. Usually a benign condition
  4. Diagnosis confirmed by electrocardiogram
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9
Q

Ventricular Premature beats (6)

A
  1. Also known as ‘Premature Ventricular Contractions (PVCs)’
  2. Premature depolarizations of the ventricles leading to early systolic contractions
  3. Usually followed by a pause resulting in irregular heart rates and irregular patterns
  4. Occur in isolation and are generally benign
  5. MAY cause hemodynamic compromise
  6. May present as bigemonys or trigemonys
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10
Q

Atrial Premature Beats

A
  1. Also known as ‘Premature Atrial Contractions (PACs)’
  2. Early depolarizations of atrial myocardium leading to propagation of electrical impulses through the atrium
  3. Results in early systolic ventricular contractions
  4. Usually benign and rarely associated with sustained tachyarrhythmias
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11
Q

Symptomatic Arrhythmias (3)

A
  1. Underlying etiology may be due to a sustained tachyarrhythmia
  2. Clinical symptoms often present as
    – Palpitations
    – Syncope
    – Chest pain
  3. Supraventricular Arrhythmias
    – Atrial Fibrillation (AFib)
    – Paroxysmal Supraventricular Tachycardia
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12
Q

Different Classifications of Atrial Fibrillation (5)

A
  1. Acute: Onset within 48 hours
  2. Paroxysmal: Abrupt start, converts spontaneously within 7 days
  3. Persistent: Does not convert spontaneously, lasts longer than 7 days
    4: Permanent: Does not terminate with pharmacological conversion or electrical conversion
  4. Recurrent: > 2 episodes
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13
Q

Goal of therapy for atrial fibrillation

A

normalize ventricular rate

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14
Q

Rate Control Therapies (4)

A

Everyone should receive rate control!!!

  1. Beta Blockers
  2. Non-DHP calcium channel blockers
  3. Digoxin
  4. Amiodarone*
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15
Q

Rhythm Control Therapies (7)

A

Not everyone receives rhythm control!; incidence of rhythm control comes with more series side effects such as stroke/embolism and death

  1. Amiodarone*
  2. Sotalol (a rhythm control beta blocker)
  3. Propafenone
  4. Procainamide
  5. Quinidine
  6. Flecainide
  7. Dofetilide
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16
Q

Inotropes

A

Soft vs. Hard; strengthens or weakens the heartbeat

Ex: Digoxin is a positive inotrope

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17
Q

Chronotope

A

Fast versus slow; alters the heart rate

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18
Q

Dromotrope (2)

A
  1. Speed of electrical conduction from either nerve or cardiac muscle
  2. Usually has both inotropic and chronotropic effects as well (i.e. chronotrope)
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19
Q

Beta blockers mechanism of action (5)

A
  1. Blocks effect of sympathetic neurotransmitters (norepinephrine) on the heart and vasculature
  2. Decreased ventricular arrhythmias
  3. Decreased ventricular response rate
  4. Decreased AV nodal conduction
  5. Decreased impulse transmission
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20
Q

Zabeta (Generic Name, Mechanism, Route)

A

Generic Name: Bisorolol

Mechanism: b1 selective

Route: PO

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21
Q

Brevibloc (Generic Name, Mechanism, Route)

A

Generic Name: Esmolol

Mechanism: B1 selective

Route: IV

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22
Q

Tenormin (Generic Name, Mechanism, Route)

A

Generic Name: Atenolol

Mechanism: B1 Selective

Route: PO

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23
Q

Lopressor (Generic Name, Mechanism, Route)

A

Generic Name: Metoprolol IR

Mechanism: B1 Selective

Route: IV and PO

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24
Q

Bystolic (Generic Name, Mechanism, Route)

A

Generic Name: Nebivolol

Mechanism: B1 selective

Route: PO

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25
Q

Inderal (Generic Name, Mechanism, Route)

A

Generic Name: Propranolol

Mechanism: Non-selective

Route: IV and PO

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26
Q

Cautions with Beta Blockers (4)

A
  1. Severe bronchospastic disease (Asthma)
  2. Bradycardia
  3. Symptomatic hypotension
  4. 2nd or 3rd degree heart block
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27
Q

Beta Blocker Clinical Pearls (4)

A
  1. Acute rate control in patients with normal left ventricular function
  2. Chronic rate control in patients with normal or impaired left ventricular function
  3. Higher doses needed for acute rate control compared to heart failure
  4. IV route is preferred for acute rate control
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28
Q

Non-Dihydropyridine CCBs Mechanism of Action (5)

A
  1. Decreases influx of calcium on vascular smooth muscle and myocardium; slows conduction and automaticity through AV node
  2. Decreased ventricular arrhythmias
  3. Decrease ventricular response rate
  4. Decrease AV nodal conduction
  5. Decrease impulse transmission
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29
Q

Types of CCBs (6)

A
  1. Diltiazem
  2. Cardizem
  3. Tiazac
  4. Verapamil
  5. Calan
  6. Verelan
30
Q

CCB Clinical Pearls (6)

A
  1. Major CYP3A4 substrate
  2. More constipation w. verapamil
  3. With IV formulation have more pronounced side effects (Caution with IV use)
  4. Agent of choice for acute rate control (but always use BB first with pediatric patients)
  5. Avoid as chronic therapy for patients with impaired left ventricular function
  6. IV CCBs should be used for LESS than 48 hours.
31
Q

CCB ADEs (6)

A
  1. Hypotension
  2. Decreased HR
  3. Fluid retention
  4. Dizziness
  5. Flushing
  6. Constipation (specifically verapamil)
32
Q

CCB Cautions (3)

A
  1. Sick Sinus Syndrome
  2. Wolff-Parkinson White Syndrome
  3. 2nd or 3rd degree AV block
33
Q

Digoxin Mechanism of Action (2)

A
  1. Direct inhibition of Na/K ATPase –> inhibition of Na/K ATP dependent pump
    - Indirect activation Na/Ca transport pump increased intracellular Ca = increased efficiency of excitationcontraction of cardiac muscle; “Positive Inotrope”
  2. Indirect effect @ AV & SA nodes through vagal stimulation; “Negative chronotrope”
34
Q

Digoxin Dosing (2)

A

mcg/kg/day

  1. Loading dose is based on: Age, Formulation, indication
    - May not be necessary
  2. Maintenance dose: 2.5 – 10 mcg/kg q24
    – Requires renal dose adjustments***
35
Q

Digoxin Dose Monitoring

A

HF: 0.5-0.9

Toxicity: Over 2

36
Q

Digoxin ADEs (9)

A

MUST KNOW ALL

  1. 3rd degree block, cardiac changes (PVC, VT/Vfib, etc)
  2. Rash
  3. N/V/D
  4. Abdominal pain
  5. anorexia
  6. Visual disturbances
  7. HA
  8. dizziness
  9. delerium
37
Q

Risk for Digoxin Toxicity (6)

A

MUST KNOW ALL

  1. Hypokalemia
  2. Hypomagneseia
  3. Hypercalcemia
  4. Decreased clearance
  5. Low body weight (children)
  6. *Digoxin has a very long half life
38
Q

Digibind (4)

A
  1. Immune antigen-binding fragments for digoxin
  2. Binds to digoxin to then be eliminated through kidneys
  3. Onset: 20 – 90 min to resolution of symptoms
  4. **Once administered lab values become irrelevant
39
Q

Normal Sinus Rhythm Conversion Therapies (5)

A
  1. Dofetilide
  2. Flecainide
  3. Propafenone
  4. Sotalol
  5. Amiodarone*
40
Q

Vaughan Williams Classifications: Classification 1 (3 and what they block)

A

*Classifies different anti-arrhythmic drugs

1A: Quinidine, Procainamide, Disopyramide
Blocks - Na channel

1B: Lidocaine, Mexilitine
Blocks - Na channel

1C: Flecainide, Propafenone
Blocks - Na channel

41
Q

Vaughan Williams Classifications: Classification 2 (3 and what it blocks)

A

*Classifies different anti-arrhythmic drugs

  1. Propranolol
  2. Esmolol
  3. Sotalol

Blocks beta adrenergics

42
Q

Vaughan Williams Classifications: Classification 3 (3 and what it blocks)

A

*Classifies different anti-arrhythmic drugs

  1. Dofetilide
  2. Sotalol
  3. Amiodarone

Blocks potassium channels

43
Q

Vaughan Williams Classifications: Classification 4 (2 and what it blocks)

A

*Classifies different anti-arrhythmic drugs

  1. Verapamil
  2. Diltiazem

Blocks Ca channel

44
Q

Dofetilide Mechanism of action (3)

A
  1. Classification: Class III antiarrhythmic
  2. Blocks potassium channels to increase action potential due to delayed repolarization
  3. NO effect on:
    - Sodium channels
    - Adrenergic alpha-receptors
    - Adrenergic beta-receptors
45
Q

Dofetilide ADEs (5)

A
  1. Hypotension
  2. Decreased HR
  3. QTc prolongation
  4. Syncope
  5. Dizziness
46
Q

Dofetilide Cautions (3)

A
  1. QTc > 440 msec
  2. CrCl < 20 mL/minute
  3. Concurrent use of verapamil
47
Q

Dofetilide Monitoring (6)

A
  1. Vitals
  2. BP
  3. HR
  4. EKG: Rhythm and QTc (delays action potential)
  5. Basic metabolic panel (look at potassium; can affect rhythmic state)
  6. Adverse effects
48
Q

Dofetilide Clinical Pearls (3)

A
  1. Safe and effective in heart failure patients
  2. Prolonged QTc requires 50% dose reduction
    * The starting dose should be reduced due to the baseline QTc prolongation.
  3. Potential for proarrhythmic effects
49
Q

Sotalol Mechanism of Action (3)

A
  1. Classification: Class II and III antiarrhythmic
  2. Beta-Blocker (class II) effects
    - beta-adrenoreceptor-blocking properties
    - Cardiac action potential prolongation
  3. Class III effects: Blocks K+ channels at higher doses
50
Q

Sotalol ADEs (7)

A
  1. Hypotension
  2. Decreased HR
  3. AV block
  4. QTc prolongation (dose reduce if > 450 QTc)
  5. Bradyarrhythmia
  6. Dizziness, headache
  7. Fatigue
51
Q

Sotalol Cautions (4)

A
  1. Severe bronchial asthma
  2. 2nd or 3rd degree AV block
  3. Uncontrolled heart failure
  4. Renal failure
52
Q

Sotalol Clinical Pearls (4)

A
  1. Potential for proarrhythmic effects
  2. Titrate doses ONLY after 5-6 doses have been administered (titrate dose only after reaching steady state)
  3. Decrease or discontinue if QTc exceeds 25% of baseline
  4. May mask signs of hyperthyroidism (due to beta blocker effects)
53
Q

Flecainide Mechanism of Action (4)

A
  1. Classification: Class Ic antiarrhythmic
  2. Blocks sodium channels to prolong refractory periods and increases electrical thresholds
  3. Moderate negative inotropic effects
  4. Increases both anterograde & retrograde
54
Q

Flecainide Indications of Use (5)

A
  1. Atrial flutter
  2. Ectopic atrial and junctional tachycardia
  3. Re-enterant atrial tachycardia
  4. Wolf Parkinson White sundrome
  5. Neonatal & Fetal tachycardia
55
Q

Flecainide ADEs (5)

A
  1. Dizziness
  2. Visual disturbances
  3. Dyspnea
  4. Ventricular arrhythmias
  5. Worsening heart failure
56
Q

Flecainide Cautions and Contraindications (2,2)

A

Cautions:
1. 1st or 2nd degree
heart block
2. Renal disease

Contraindications:

  1. Congestive heart failure
  2. Post-myocardial infarction
57
Q

Flecainide Clinical Pearls (4)

A
  1. Drug of choice for non-heart disease patients
  2. Titrate dose by lowest effective dose not more often than once every week
  3. Unique place in therapy – Used in neonates
  4. Decrease dose by 50% in impaired renal function
    - Severely impaired renal function may require larger dose decreases
58
Q

Propafenone Mechanism of Action (3)

A
  1. Classification: Class Ic antiarrhythmic
  2. Blocks sodium channels to prolong refractory periods and increases electrical thresholds
  3. Exhibits some beta-blockade activity
59
Q

Propafenone ADEs (7)

A
  1. Decreased HR
  2. QTc prolongation
  3. Bronchospasms
  4. Worsening heart failure, edema
  5. Arrhythmias
  6. Impaired taste sensations
  7. Dizziness
60
Q

Propafenone Cautions (4)

A
  1. Severe bronchial asthma
  2. Congestive heart failure
  3. Liver disease
  4. Elevated ANA titers
61
Q

Propafenone monitoring (7)

A
  1. BP
  2. HR
  3. EKG
  4. LFTs
  5. CBC
  6. Lupus panel
  7. Adverse effects
62
Q

Propafenone Clinical Pearls (3)

A
  1. Titrate not more often than every 4-5 days
  2. Reduce dose by 25-50% in patients with:
    – Liver disease
    – QRS widening
    – Heart block
  3. Immediate release recommended for acute control, sustained release recommended for chronic control
63
Q

Amiodarone (4)

A
  1. Fits in ALL Vaughan Williams Classifications
  2. Has Most Class III effects
3. Place in therapy:
– Multiple arrhythmias
– Also helpful in retrograde eletrical disorders (i.e. WPW sundrome)
– Angina (due to vasodilatory effects)
– HF
64
Q

Amiodarone Mechanism of Action

A

Main effect works at the potassium channels to increase

the action potential (Class III)

65
Q

Amiodarone ADEs (14)

A
  1. Decreased BP and HR; QTc prolongation; AV block
  2. N/V
  3. decreased appetite
  4. constipation
  5. Phlebitis
  6. Optic neuropathy/neuritis (visual disturbances)
  7. Dizziness
  8. peripheral neuropathy
  9. coordination
    disorders
  10. Hepatitis
  11. Hypo/hyperthyroidism
  12. Blue-gray skin discolorations
  13. photosensitivity
  14. Pulmonary fibrosis (rare)
66
Q

Amiodarone Cautions (5)

A
  1. Iodine allergies
  2. 2nd or 3rd degree heart block
  3. Hepatic disease
  4. Drug interactions
  5. QTc prolongation
67
Q

Amiodarone Monitoring (6)

A
  1. Vitals (BP and HR)
  2. EKG
  3. Pulmonary testing
  4. Thyroid testing
  5. Ophthalmic testing
  6. Adverse effects
68
Q

Amiodarone Pearls (

A
  1. Intravenous route preferred in symptomatic patients
    – Quicker onset of action in correlation with long half-life
  2. Safe and effective in patients with AFib and heart failure
  3. The FDA REQUIRES that patients receive a drug information patient education leaflet
69
Q

QT Interval (3)

A
  1. Duration from early ventricular depolarization to latest repolarization
  2. QTc = corrected QT interval accounting for heart rate
    * Correction to take into account for HR
If greater than 450-470 be concerned 
Greater than 500 = definite prolongation; particularly concerning for medications
  3. Standard values
    – Normal: < 430 (men) & < 450 (women)
    – Borderline: > 450 (men); > 470 (women)
    – Prolonged: > 450 (men) & > 470 (women)
70
Q

QTc Calculation

A

QTc= corrected QT interval

QTc = (QT Interval) / (RR interval in seconds)

*QT interval is from beginning of QRS complex (Q) to end of T wave; entire ventricular depolarization
and repolarization phase 
the longer it goes, the longer the ventricle is in limbo; higher risk for inducing a cardiac arrythmia

71
Q

Torsades De Pointes (3)

A
  1. Life threatening; a specific form of polymorphic VT in patients with A PROLONGED QT INTERVAL. It is characterized by rapid, irregular QRS complexes, which appear to be twisting around the ECG baseline. This arrhythmia may cease spontaneously or degenerate into ventricular fibrillation.
  2. Requires cardioversion
3. Use Class III anti-arrhythymic drugs
– Ondansetron (Zofran), Granisetron (Kytril)
– Methadone
– Fluoroquinolones
– Haloperidol

*Prolonged QT that turns into torsades de pointes is life threatening and requires cardioversion

72
Q

Prolonged QT Interval (3)

A
  1. Congenital or Acquired
  2. Risk factors for prolonged QT:
    – Multiple prolonging agents OR high doses of 1x agent; higher dose of any agent that prolonges QT can induce porsades
    – HypoK, hypoCa, HypoNa
  3. So anything that can affect electrolyte balance can potentiate the risk (ie diuretics)
    - Lasix + QT prolonging agent + dehydration = higher risk of porsades
    – Female
    – Congenital prolonged QT

Advanced Pediatric Pharmacology Exam 1 (8 decks)

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