Term
| What is the chief complaint when a patient comes in for an arrhythmia? |
|
Definition
|
|
Term
T/F
Bradycardia presentation is usually different from other arrhythmias. |
|
Definition
|
|
Term
| How do bradycardias present? |
|
Definition
chronic fatigue
dyspnea on exertion
syncope or near syncope |
|
|
Term
| How might you discover an arrhythmia in an asymptomatic patient? |
|
Definition
checking vitals - pulses
auscultation of the heart
routine EKG |
|
|
Term
| What lab tests would you run on a patient with an arrhythmia? |
|
Definition
chem panel - electrolytes and glucose
CBC - anemia
TSH
EKG |
|
|
Term
| When should you absolutely not give amiodarone? |
|
Definition
| pregnancy and during lactation |
|
|
Term
| What anti-arrhythmic drugs should not be given during lactation? |
|
Definition
| amiodarone and acebutolol |
|
|
Term
T/F
During pregnancy there is an increase in arrhythmias. |
|
Definition
|
|
Term
T/F
Pseudophedrine or other sympathomimetic drugs may cause an arrhythmia. |
|
Definition
|
|
Term
| What are the potential cardiac causes of PACs? Other causes? |
|
Definition
cardiac: mitral stenosis, CAD, hypertrophic cardiomyopathy
other: caffeine, theophylline, tobacco, alcohol, COPD, chronic renal |
|
|
Term
| What EKG changes are there to indicate PACs (premature atrial contraction)? |
|
Definition
short or prolonged PR interval
inverted or biphasic p waves
aberrant or absent QRS |
|
|
Term
| How do you treat asymptomatic patients with PACs? |
|
Definition
| education, reassurance, possible dietary/med changes if causative agent |
|
|
Term
| How do you treat symptomatic patients with PACs? |
|
Definition
beta blockers - variable results
refer to cardiologist |
|
|
Term
| What medications should not be used to treat symptomatic patients with PACs? Why? |
|
Definition
IA, IC, or III anti-arrhythmic agents
(quinidine, procainamide, flecainide or those that inhibit ventricular repolarization or prolong refractoriness)
high risk for proarrhythmia and QT prolongation |
|
|
Term
| How are anti-arrhythmic drugs classified? |
|
Definition
Vaughn-Williams Classification
classified by effect on ventricular contraction velocity, repolarization/refractoriness, and automaticity |
|
|
Term
| What are Class I anti-arrhythmics? |
|
Definition
|
|
Term
| What are class II anti-arrhythmic agents? |
|
Definition
|
|
Term
| What are class III anti-arrythmic agents? |
|
Definition
| drugs that inhibit ventricular repolarization or prolong refractoriness |
|
|
Term
| What are class IV anti-arrhythmic agents? |
|
Definition
| non-dihydropyridine CCBs: verapamil and diltiazem |
|
|
Term
T/F
Some drugs can have multiple anti-arrhythmic classifications based on it's effects. |
|
Definition
|
|
Term
| What are the classifications of Ia, Ib, and Ic? |
|
Definition
Ia - intermediate, intermediate potency
Ib - fast on/off, lowest potency
Ic - slow on/off, highest potency |
|
|
Term
| What do class I anti-arrhythmic agents do? |
|
Definition
1. lengthen the refractory period
2. decrease excitability
3. decrease conduction
4. block K+ channels - mild
5. lengthen the action potential duration - wider QRS |
|
|
Term
T/F
The effect of class I anti-arrhythmic drugs is rate dependent. |
|
Definition
|
|
Term
| When is slowed conduction apparent for class Ib drugs? |
|
Definition
| only apparent at fast rates |
|
|
Term
| When is slowed conduction apparent for Ic drugs? |
|
Definition
|
|
Term
T/F
Normal tissues are affected by class Ib drugs. Ic drugs? |
|
Definition
False
True - Ic drugs affect all tissue |
|
|
Term
T/F
The effect of class I anti-arrhythmic drugs is pH dependent. |
|
Definition
True - original compounds are bases and become active by adding an H+
acidosis will increase effects
alkalosis will decrease effects |
|
|
Term
|
Definition
| quinidine and procainamide |
|
|
Term
| What is quinidine syndrome? |
|
Definition
| recurrent light-headed-ness, fainting, and drug-induced Torsade de pointes caused by quinidine |
|
|
Term
| What are some problems associated with procainamide? |
|
Definition
arthralgia similar to lupus in 33%
icreased ANA titer
pleuritis
pericarditis |
|
|
Term
|
Definition
|
|
Term
| What are 2 potential problems with using lidocaine? |
|
Definition
must be injected properly or it can cause cardiac effects
can cause hypotension by depressing myocardial contractility |
|
|
Term
|
Definition
|
|
Term
| Which drug would you use the lowest dose on and has the longest lasting effect - Ia, Ib, or Ic? |
|
Definition
| Ic because it is the highest potency |
|
|
Term
| What EKG changes typify PVCs? |
|
Definition
wide, bizarre QRS
QRS > .12 sec
inverted T wave
compensatory pause following QRS |
|
|
Term
| What % of middle aged people have PVCs on a 2 minute EKG? |
|
Definition
|
|
Term
T/F
Post MI, more than 10 PVCs per hour is associated with a worse prognosis. |
|
Definition
|
|
Term
| What % of HF or cardiomyopathy patients have PVCs? Are they of prognostic value? |
|
Definition
70-95%
No prognostic value |
|
|
Term
T/F
Patients with LVH have an increased incidence of PVCs and it correlates to a higher risk of sudden death. |
|
Definition
|
|
Term
| How do you treat a patient with PVCs who has no heart disease? |
|
Definition
You don't!
anti-arrhythmic therapy increases the risk of death |
|
|
Term
| How do you treat the patient with PVCs and structural heart disease (CAD, cardiomyopathy, CHF)? |
|
Definition
| radiofrequency ablation and referral for Class I anti-arrhythmic drugs and perhaps amiodarone |
|
|
Term
| How do you treat the symptomatic patients with PVCs in the outpatient setting? |
|
Definition
First line - class II - beta blockers
- sotalol - class II and III
amiodarone may be used if Beta blockers are counterindicated |
|
|
Term
|
Definition
class II and class III anti-arrhythmic drug
Do not use in asymptomatic patients due to proarrhythmia affects
treat with O2 to avoid proarrhythmic affects of beta blockers |
|
|
Term
| Who should not be treated with beta blockers? |
|
Definition
| asymptomatic patients with PVCs - possible proarrhythmia effects |
|
|
Term
| Name 4 possible causes of bradycardia. |
|
Definition
1. Sick sinus syndrome
2. exaggerated vagal activity
3. acute MI
4. obstructive sleep apnea |
|
|
Term
| How do you treat the asymptomatic patient with bradycardia? |
|
Definition
You don't!
increase O2, have pt lie supine with raised legs, increase fluids if no JVP distension |
|
|
Term
| How do you treat the symptomatic patient with bradycardia? |
|
Definition
may require pacing
adrenaline
isoprenaline |
|
|
Term
| What is the heart rate in PSVT? |
|
Definition
|
|
Term
| What is the heart rate in atrial flutter? |
|
Definition
|
|
Term
| What is the heart rate in atrial fibrillation? |
|
Definition
|
|
Term
| Describe the EKG of PSVT. |
|
Definition
| narrow complex tachycardia with a regular rate |
|
|
Term
| What % of cases of PSVT are AV nodal re-entrant? AV re-entrant? atrial tachycardia or sinoatrial tachycardia? |
|
Definition
|
|
Term
| What disorder is AV re-entrant tachycardia associated with? |
|
Definition
|
|
Term
T/F
PSVT is benign and self-limited. |
|
Definition
|
|
Term
| What are some types of non-pharmacologic treatment fro PSVT? |
|
Definition
vagal maneuvers
avoid: caffeine, alcohol, tobacco, stress, pseudophedrine
ice-cold wet cloth to the face
stimulate gag reflex
bend over and touch floor
exhale followed by deep inspiration with mouth closed and nose pinched |
|
|
Term
| What is the most common symptomatic pediatric arrhythmia? |
|
Definition
|
|
Term
T/F
PSVT that is sustained with instability requires immediate cardioversion. |
|
Definition
True
instability may be: angina, SOB, decreased level of consciousness, hyptension, or CHF |
|
|
Term
| When is adenosine cardioversion counterindicated? |
|
Definition
| wide complex tachycardia and in WPW (delta waves) |
|
|
Term
| What drug is used to cardiovert narrow complex PSVT? |
|
Definition
|
|
Term
| After cardioversion with adenosine, what is used for maintenance? |
|
Definition
|
|
Term
| What is the mechanism of action of adenosine? |
|
Definition
enhanced K conductance
suppression of calcium dependent action potentials
This inhibits AV nodal conduction and increases the AV nodal refractory period |
|
|
Term
| What are the signs and symptoms of adenosine toxicity? |
|
Definition
flushing - 20%
SOB or chest burning - 10%
headache
hypotension
nausea |
|
|
Term
| How do you treat PSVT in outpatient? |
|
Definition
cautious use of beta-blocker
verapamil |
|
|
Term
| How do you treat PSVT in ED? |
|
Definition
emolol
selective radiofrequency ablation
cardioversion - start at 50J |
|
|
Term
| Describe atrial fibrillation. |
|
Definition
Irregularly irregular
wavy baseline with no P waves
350-600 bpm
Ventricular response 120-180 bpm |
|
|
Term
| What classifies acute atrial fibrillation? |
|
Definition
|
|
Term
| What classifies paroxysmal atrial fibrillation? |
|
Definition
| terminates spontaneously in 7 days |
|
|
Term
| What classifies persistent atrial fibrillation? |
|
Definition
|
|
Term
T/F
Permanent atrial fibrillation is not pharmacologically or electrically convertible. |
|
Definition
|
|
Term
T/F
In atrial fibrillation there are multiple re-entrant pathways. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the drug of choice to treat atrial fibrillation and atrial flutter? Name 2 other drugs that may be used. |
|
Definition
Digoxin
Beta blockers and CCBs - used to control the rate; may not be beneficial; unmask heart failure |
|
|
Term
T/F
Anticoagulate with atrial fibrillation and atrial flutter. |
|
Definition
|
|
Term
| What do you use to anticoagulate a patient with atrial fib or atrial flutter? |
|
Definition
|
|
Term
| Which clotting factors are destroyed by Protein C? |
|
Definition
|
|
Term
| Which factors are inactivated by heparin? |
|
Definition
|
|
Term
| How does heparin inactivate clotting factors? |
|
Definition
| by activating anti-clotting factors such as antithrombin III which inactivates 7a, 9a, 10a, and 2a |
|
|
Term
| Which clotting factors' synthesis is inhibited by warfarin? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Where does Warfarin sodium act? |
|
Definition
|
|
Term
| How long do the effects of warfarin take to show up? Why does it take so long? |
|
Definition
1-3 days
1. some clotting factors have long half lives, so it takes time for their synthesis inhibition to be seen
2. It takes time to get to the peak drug concentration |
|
|
Term
| What is the bioavailability of Warfarin? |
|
Definition
|
|
Term
| What is the half-life of coumadin? |
|
Definition
|
|
Term
| What is a warfarin diet? Why might it be followed? |
|
Definition
avoiding green leafy veggies because they are a source of vitamin K
Vitamin K is used to make clotting factors and therefore reduces the efficacy of the warfarin |
|
|
Term
T/F
Patients on coumadin may need higher dosing in the winter. |
|
Definition
| False - they may need higher dosing in the summer |
|
|
Term
| What meds should be avoided while on coumadin therapy? |
|
Definition
| NSAIDs and aspirin (reduce to 81 mg daily at least) |
|
|
Term
| What pregnancy category is warfarin? |
|
Definition
|
|
Term
| How do you dose coumadin? |
|
Definition
Increase dose at 1 week intervals based on INR
INR of 2-3 for anticoagulation
INR of 2.5-3.5 for mechanical heart valve patients
INR of 1.5-2.0 to prevent VTE after first six months of therapy |
|
|
Term
T/F
Drug interactions with warfarin are numerous |
|
Definition
|
|
Term
| What drugs increase the INR of a patient on coumadin? |
|
Definition
amiodarone
antibiotics
antifungals
omeprazole
cimetidine |
|
|
Term
| How do you treat overcoagulation with warfarin? |
|
Definition
|
|
Term
| Why should you limit OTC remedies with a patient on coumadin therapy? |
|
Definition
| herbal interactions also exist |
|
|
Term
| What is the success rate for direct-current cardioversion in a fib and atrial flutter? |
|
Definition
|
|
Term
| What drug is given 3-4 weeks before attempting cardioversion of a fib and atrial flutter? |
|
Definition
|
|
Term
| What test should be done before conversion? |
|
Definition
| transesophageal ECHO to find atrial thrombi that would require anticoagulation before conversion |
|
|
Term
| What 2 drugs do you use to maintain rhythm after cardioversion? |
|
Definition
|
|
Term
| Which drug is used to pharmacologically convert a fib or a flutter? What is the success rate? |
|
Definition
high dose amiodarone
86% if a fib has existed less than 2 years |
|
|
Term
| What is the action of amiodarone? |
|
Definition
1. slows the sinus rate
2. slows AV conduction - prolongs QT interval and QRS complex
3. increases refractory periods |
|
|
Term
T/F
Amiodarone is prorhythmic. |
|
Definition
| True - it is unlikely that an arrhythmia will develop or worsen while on this med. |
|
|
Term
| What is the mechanism of action of amiodarone? |
|
Definition
1. Fast Na+ channel blocker
2. K+ channel blocker
3. noncompetative alpha and beta blocker
4. weak Ca2+ channel blocker |
|
|
Term
| How is amiodarone classified as an anti-arrhthmic? |
|
Definition
| could be classified as Class I, II, III, or IV |
|
|
Term
| What are the 2 effects of amiodarone? |
|
Definition
| antianginal and peripheral vascular dilation |
|
|
Term
T/F
The number and severity of toxic effects increases with the dosage of amiodarone. |
|
Definition
|
|
Term
| Name 3 cardiac side effects of amiodarone. |
|
Definition
bradycardia
heart block
heart failure |
|
|
Term
| What % of patients on amiodarone develop pulmonary fibrosis? |
|
Definition
|
|
Term
| What are some of the extra-cardiac side effects of amiodarone? |
|
Definition
| pulmonary fibrosis, skin deposits - photodermatits or blue discoloration, CNS paresthesia, tremor, ataxia, headache, thyroid dysfunction - hyper or hypo, and liver necrosis |
|
|
Term
| What % of patients on amiodarone develop photodermatitis? Smurf discoloration? thyroid dysfunction? |
|
Definition
|
|
Term
| When do the effects of interaction between amiodarone and concomittant therapy peak? |
|
Definition
|
|
Term
| How often should liver and thyroid function tests be done on amiodarone pts? |
|
Definition
|
|
Term
| At which dose of amiodarone is there a low incidence of lung or thyroid effects? |
|
Definition
|
|
Term
| What is the half life of amiodarone? |
|
Definition
| highly variable and unusually long - averaging about 58 days |
|
|
Term
| When might Torsade de pointes be seen? |
|
Definition
| When a pacemaker is past the end of its life and needs to be replaced |
|
|
Term
| What typifies a ventricular tachycardia? |
|
Definition
wide QRS compex - VT until proven otherwise
other: evidence of AV dissociation, independent p waves, capture of fusion beats, beat to beat variability in QRS morphology, QRS complexes > .14 secs |
|
|
Term
T/F
History of ischemic heart disease makes VT more likely. |
|
Definition
|
|
Term
| How high is the mortality rate for VT after 2 years? |
|
Definition
|
|
Term
| What is the best treatment for VT? |
|
Definition
| auto cardioverter-defibrillator implantation |
|
|
Term
| How do you treat hemodynamically unstable VT patients? |
|
Definition
|
|
Term
| How do you treat stable VT patients? |
|
Definition
| amiodarone until implant can be put in |
|
|
Term
T/F
Athletes tend to have low HRs. |
|
Definition
|
|
Term
| How long can an asymptomatic sinus pause be and still be benign in an athlete? |
|
Definition
|
|
Term
| What is responsible for some cardiac related deaths in athletes? |
|
Definition
| idiopathic hypertrophic cardiomyopathy |
|
|
Term
| How do you diagnose idiopathic hypertrophic cardiomyopathy? what is the treatment? |
|
Definition
aortic murmur that increases with Valsalva's maneuver
stop playing sport |
|
|
Term
| Supraventricular tachycardias in children are usually associated with what disorder? How do you treat? |
|
Definition
WPW
adenosine or radiofrequency ablation |
|
|
Term
| What drug might you consider to control the heart rate in children (when there are extra beats)? |
|
Definition
|
|
