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
2
Q
EKG P Wave (Length and Description)
A
Length: <0.1
Description: Atrial Depolarization
3
Q
QRS Complex (Length and Description)
A
Length: 0.05-0.1
Description: Ventricular Depolarization
4
Q
T Wave (Description)
A
Ventricular repolarization
5
Q
ST Segment (Description)
A
Ventricular repolarization
6
Q
QT Interval (Length and Description)
A
Length: <0.5
Description: Ventricular depolarization and repolarization
7
Q
Most common pediatric asymptomatic arrhythmias (3)
A
- Sinus arrhythmia
- Ventricular premature beats (VPBs)
- Atrial premature beats (APBs)
8
Q
Sinus Arrhythmias (4)
A
- Normal physiologic variant characterized by increased heart rate during inspiration and a decreased heart rate during expiration
- Caused by changes in parasympathetic input to the heart
- Usually a benign condition
- Diagnosis confirmed by electrocardiogram
9
Q
Ventricular Premature beats (6)
A
- Also known as ‘Premature Ventricular Contractions (PVCs)’
- Premature depolarizations of the ventricles leading to early systolic contractions
- Usually followed by a pause resulting in irregular heart rates and irregular patterns
- Occur in isolation and are generally benign
- MAY cause hemodynamic compromise
- May present as bigemonys or trigemonys
10
Q
Atrial Premature Beats
A
- Also known as ‘Premature Atrial Contractions (PACs)’
- Early depolarizations of atrial myocardium leading to propagation of electrical impulses through the atrium
- Results in early systolic ventricular contractions
- Usually benign and rarely associated with sustained tachyarrhythmias
11
Q
Symptomatic Arrhythmias (3)
A
- Underlying etiology may be due to a sustained tachyarrhythmia
- Clinical symptoms often present as
– Palpitations
– Syncope
– Chest pain - Supraventricular Arrhythmias
– Atrial Fibrillation (AFib)
– Paroxysmal Supraventricular Tachycardia
12
Q
Different Classifications of Atrial Fibrillation (5)
A
- Acute: Onset within 48 hours
- Paroxysmal: Abrupt start, converts spontaneously within 7 days
- Persistent: Does not convert spontaneously, lasts longer than 7 days
4: Permanent: Does not terminate with pharmacological conversion or electrical conversion - Recurrent: > 2 episodes
13
Q
Goal of therapy for atrial fibrillation
A
normalize ventricular rate
14
Q
Rate Control Therapies (4)
A
Everyone should receive rate control!!!
- Beta Blockers
- Non-DHP calcium channel blockers
- Digoxin
- Amiodarone*
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
- Amiodarone*
- Sotalol (a rhythm control beta blocker)
- Propafenone
- Procainamide
- Quinidine
- Flecainide
- Dofetilide
16
Q
Inotropes
A
Soft vs. Hard; strengthens or weakens the heartbeat
Ex: Digoxin is a positive inotrope
17
Q
Chronotope
A
Fast versus slow; alters the heart rate
18
Q
Dromotrope (2)
A
- Speed of electrical conduction from either nerve or cardiac muscle
- Usually has both inotropic and chronotropic effects as well (i.e. chronotrope)
19
Q
Beta blockers mechanism of action (5)
A
- Blocks effect of sympathetic neurotransmitters (norepinephrine) on the heart and vasculature
- Decreased ventricular arrhythmias
- Decreased ventricular response rate
- Decreased AV nodal conduction
- Decreased impulse transmission
20
Q
Zabeta (Generic Name, Mechanism, Route)
A
Generic Name: Bisorolol
Mechanism: b1 selective
Route: PO
21
Q
Brevibloc (Generic Name, Mechanism, Route)
A
Generic Name: Esmolol
Mechanism: B1 selective
Route: IV
22
Q
Tenormin (Generic Name, Mechanism, Route)
A
Generic Name: Atenolol
Mechanism: B1 Selective
Route: PO
23
Q
Lopressor (Generic Name, Mechanism, Route)
A
Generic Name: Metoprolol IR
Mechanism: B1 Selective
Route: IV and PO
24
Q
Bystolic (Generic Name, Mechanism, Route)
A
Generic Name: Nebivolol
Mechanism: B1 selective
Route: PO
25
Inderal (Generic Name, Mechanism, Route)
Generic Name: Propranolol
Mechanism: Non-selective
Route: IV and PO
26
Cautions with Beta Blockers (4)
1. Severe bronchospastic disease (Asthma)
2. Bradycardia
3. Symptomatic hypotension
4. 2nd or 3rd degree heart block
27
Beta Blocker Clinical Pearls (4)
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
28
Non-Dihydropyridine CCBs Mechanism of Action (5)
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
29
Types of CCBs (6)
1. Diltiazem
2. Cardizem
3. Tiazac
4. Verapamil
5. Calan
6. Verelan
30
CCB Clinical Pearls (6)
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
CCB ADEs (6)
1. Hypotension
2. Decreased HR
3. Fluid retention
4. Dizziness
5. Flushing
6. Constipation (specifically verapamil)
32
CCB Cautions (3)
1. Sick Sinus Syndrome
2. Wolff-Parkinson White Syndrome
3. 2nd or 3rd degree AV block
33
Digoxin Mechanism of Action (2)
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
Digoxin Dosing (2)
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
Digoxin Dose Monitoring
HF: 0.5-0.9
Toxicity: Over 2
36
Digoxin ADEs (9)
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
Risk for Digoxin Toxicity (6)
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
Digibind (4)
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
Normal Sinus Rhythm Conversion Therapies (5)
1. Dofetilide
2. Flecainide
3. Propafenone
4. Sotalol
5. Amiodarone*
40
Vaughan Williams Classifications: Classification 1 (3 and what they block)
*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
Vaughan Williams Classifications: Classification 2 (3 and what it blocks)
*Classifies different anti-arrhythmic drugs
1. Propranolol
2. Esmolol
3. Sotalol
Blocks beta adrenergics
42
Vaughan Williams Classifications: Classification 3 (3 and what it blocks)
*Classifies different anti-arrhythmic drugs
1. Dofetilide
2. Sotalol
3. Amiodarone
Blocks potassium channels
43
Vaughan Williams Classifications: Classification 4 (2 and what it blocks)
*Classifies different anti-arrhythmic drugs
1. Verapamil
2. Diltiazem
Blocks Ca channel
44
Dofetilide Mechanism of action (3)
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
Dofetilide ADEs (5)
1. Hypotension
2. Decreased HR
3. QTc prolongation
4. Syncope
5. Dizziness
46
Dofetilide Cautions (3)
1. QTc > 440 msec
2. CrCl < 20 mL/minute
3. Concurrent use of verapamil
47
Dofetilide Monitoring (6)
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
Dofetilide Clinical Pearls (3)
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
Sotalol Mechanism of Action (3)
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
Sotalol ADEs (7)
1. Hypotension
2. Decreased HR
3. AV block
4. QTc prolongation (dose reduce if > 450 QTc)
5. Bradyarrhythmia
6. Dizziness, headache
7. Fatigue
51
Sotalol Cautions (4)
1. Severe bronchial asthma
2. 2nd or 3rd degree AV block
3. Uncontrolled heart failure
4. Renal failure
52
Sotalol Clinical Pearls (4)
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
Flecainide Mechanism of Action (4)
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
Flecainide Indications of Use (5)
1. Atrial flutter
2. Ectopic atrial and junctional tachycardia
3. Re-enterant atrial tachycardia
4. Wolf Parkinson White sundrome
5. Neonatal & Fetal tachycardia
55
Flecainide ADEs (5)
1. Dizziness
2. Visual disturbances
3. Dyspnea
4. Ventricular arrhythmias
5. Worsening heart failure
56
Flecainide Cautions and Contraindications (2,2)
Cautions:
1. 1st or 2nd degree
heart block
2. Renal disease
Contraindications:
1. Congestive heart failure
2. Post-myocardial infarction
57
Flecainide Clinical Pearls (4)
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
Propafenone Mechanism of Action (3)
1. Classification: Class Ic antiarrhythmic
2. Blocks sodium channels to prolong refractory periods and increases electrical thresholds
3. Exhibits some beta-blockade activity
59
Propafenone ADEs (7)
1. Decreased HR
2. QTc prolongation
3. Bronchospasms
4. Worsening heart failure, edema
5. Arrhythmias
6. Impaired taste sensations
7. Dizziness
60
Propafenone Cautions (4)
1. Severe bronchial asthma
2. Congestive heart failure
3. Liver disease
4. Elevated ANA titers
61
Propafenone monitoring (7)
1. BP
2. HR
3. EKG
4. LFTs
5. CBC
6. Lupus panel
7. Adverse effects
62
Propafenone Clinical Pearls (3)
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
Amiodarone (4)
1. Fits in ALL Vaughan Williams Classifications
2. Has Most Class III effects
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3. Place in therapy:
– Multiple arrhythmias
– Also helpful in retrograde eletrical disorders (i.e. WPW sundrome)
– Angina (due to vasodilatory effects)
– HF
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64
Amiodarone Mechanism of Action
Main effect works at the potassium channels to increase
| the action potential (Class III)
65
Amiodarone ADEs (14)
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
Amiodarone Cautions (5)
1. Iodine allergies
2. 2nd or 3rd degree heart block
3. Hepatic disease
4. Drug interactions
5. QTc prolongation
67
Amiodarone Monitoring (6)
1. Vitals (BP and HR)
2. EKG
3. Pulmonary testing
4. Thyroid testing
5. Ophthalmic testing
6. Adverse effects
68
Amiodarone Pearls (
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
4. The FDA REQUIRES that patients receive a drug information patient education leaflet
69
QT Interval (3)
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
QTc Calculation
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
Torsades De Pointes (3)
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
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3. Use Class III anti-arrhythymic drugs
– Ondansetron (Zofran), Granisetron (Kytril)
– Methadone
– Fluoroquinolones
– Haloperidol
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*Prolonged QT that turns into torsades de pointes is life threatening and requires cardioversion
72
Prolonged QT Interval (3)
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
