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Cardiology > Dysrhythmias > Flashcards

Dysrhythmias Flashcards

1
Q

What is a sinus arrhythmia?

A

Common in younger patients. Synchronizes with respiratory cycle. Inspiratory reflex inhibition of vagal tone. Benign and requires no treatment. Rhythm sometimes appears irregular, but originates from the sinus node

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2
Q

What is a sinus paues/sinus arrest?

A

can occur in healthy hearts, increased vagal tone, mycarditis, MI, digitalis toxicity. duration of pause has no relationship to sinus rate. if symptomatic treat w/pacemaker or atropine 1mg IV if unstable

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3
Q

What medications can cause bradycardia?

A

beta blockers, digoxin

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4
Q

What are treatment options for bradycardia?

A

Symptomatic and hemodynamically unstable: Atropine 1mg IV (anticholinergic). Temporary Pacer

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5
Q

What is pharmacologic treatment of sinus tachycardia?

A

calcium channel blockers (diltiazem, verapamil) or beta blockers (symptomatic tach)

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6
Q

Where are supraventricular tachycardias likely to originate from?

A

above the His bundle. commonly caused by a reentrant circuit in the AV node and likely to begin or end with a premature atrial or ventricular contraction

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7
Q

What drugs may cause supraventricular tachycardia as a side effect?

A

digitalis, asthma medications, or cold remedies. Caffeine, ephedra. Cocaine, meth

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8
Q

What does a EKG in PSVT look like?

A

HR 140-240, regular rate, P wave different from sinus wave and buried in narrow QRS

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9
Q

What are symptoms of tachycardic rhythms?

A

Palpitations , Dizziness, or light-headedness, or syncope (rare), SOB, Anxiety, Chest pain or tightness

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10
Q

What is nonpharmacologic treatment for SVT?

A

Vagal maneuvers (hold breath, dip face in cold water, cough, tense stomach muscles

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11
Q

What is pharmacologic treatment for SVT?

A

Adenosine (Adenocard) 6mg IV followed by NS flush. Blocks conduction at the AV node. If unsuccessful, cardioversion if unstable or IV beta/calcium channel blocker

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12
Q

What therapy is used to prevent recurrence of SVT?

A

Beta Blockers (Metoprolol) 25-100mg po BID. Calcium channel blockers (Diltiazem) 180-360mg po qday. Digoxin - 0.125 -.25mg po qday. Permanent treatment is an SVT ablation

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13
Q

What is wolff-parkinson-white syndrome?

A

Form of supraventriuclar tachycardia but involves an accessory pathway that bypasses the AV node and conduct impulses faster than normal.

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14
Q

What is the greatest concern for people with WPW?

A

the possibility of having atrial fibrillation with a fast ventricular response that worsens to ventricular fibrillation, a life-threatening arrhythmia.

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15
Q

What are EKG characteristics for WPW?

A

HR >200, PR interval is short <.12ms, and the upstroke of the QRS wave is slurred; this is known as a delta wave.

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16
Q

What are treatment options for WPW?

A

Radiofrequency ablation-Ablation of accessory pathway(s). Beta blockers, Calcium Channel Blockers, Flecainide

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17
Q

How is an acute episode of WPW terminated?

A

Vagal maneuvers, IV Adenosine or IV diltiazem, Have defib ready as meds may turn the rhythm from SVT into afib. cardiovert if unstable

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18
Q

What is paroxysmal atrial tachycardia (PAT)?

A

can occur in healthy or diseased heart. atrial rate 150-250. AV node will try to block impulses. P wave morphology varies from sinus, narrow QRS. Transient.

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19
Q

What are treatment options for PAT?

A

vagal manuevers, adenosine, cardioverions. digoxin, beta blockers, calcium channel blockers to prevent recurrence

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20
Q

What is a premature atrial contraction?

A

Discharge from non-sinus atrial pacemakers. P-wave preceding may not look like the sinus P waves. May be a precursor to the development of atrial fibrillation

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21
Q

What causes an increased incidence of PACs?

A

Mitral valve disease, MI, Cardiomyopathy, Smoking, Alcohol, Caffeine

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22
Q

What is treatment for PACs?

A

Asymptomatic-No special treatment or Avoid the precipitants. Symptomatic-Controlled with beta blockers

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23
Q

What is a wandering atrial pacemaker?

A

Seen in patients with heart disease and COPD. may also be precursor to Multifocal Atrial Tachycardia. May occur in normal hearts as a result in fluctuations in vagal tone. Usually no treatment required

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24
Q

What are characteristics of a wandering atrial pacemaker on EKG?

A

rate is variable depending on the site of the pacemaker; usually 45-100/ bpm. Needs to have 3 distinctly different P wave morphologies.

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25
Q

What is multifocal atrial tachycardia?

A

Irregular cardiac rhythm caused by at least 3 different sites of competing atrial activity. Presence of 3 or more P wave morphologies on a given lead. It usually does not cause hemodynamic instability. HR > 100

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26
Q

What is multifocal atrial tachycardia common with?

A

lung disease, COPD, acute MI, sepsis, hypokalemia, theophylline toxicity, low magnesium

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27
Q

What are treatment options for mutlifocal atrial tachycardia?

A

Treatment is directed at the underlying medical problems.May suppress the rate with AV nodal blocking agents-Calcium Channel Blockers or Beta-blockers

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28
Q

What is atrial fibrillation?

A

Multiple reentrant loops generate chaotic atrial depolarization. Most common encountered arrhythmia in clinical practice

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29
Q

What are EKG characteristics of atrial fib?

A

AV node is bombarded with rates greater than 400 bpm for atrial foci. Ventricular rate is irregularly irregular. No distinguishable P waves on EKG

30
Q

What are common underlying causes of atrial fib?

A

Valvular disease, Heart failure, Ischemic Heart Disease

31
Q

What is the pharmacologic treatment of a. fib?

A

warfarin (coumadin), pradaxa, or xalreto to get INR btw 2-3. ventricular rate btw 60-100 with diltiazem, beta blockers, or digoxin. Antiarrhythmics (amiodarone) to restore sinus rhythm

32
Q

What can be used to estimate embolic risk?

A

CHADS calculator. 1 pt for each except stroke gets 2 points in the setting of a.fib. if they have 2 points or more they need anticoagulation

33
Q

When do you use cardioversion to treat a. fib?

A

Less than 48-72hours of a-fib: Safe to cardiovert without anticoagulation. If duration unknown: try to restore sinus rhythm, Anticoagulate x 4-6 weeks then cardiovert. Anticoagulants x 6 weeks after successful cardioversion or indefinitely if patient was unaware that they were in atrial fibrillation

34
Q

What type of esophageal echo should be used to check for thrombus in a. fib?

A

transesophageal echo prior to cardioversion

35
Q

Why should you evaluate new onset afib or a.flutter?

A

presence of valvular heart disease (echo), presence of ischemic heart disease (nuclear stress test), and Rule out sleep apnea (sleep study), or thyroid studies

36
Q

What is atrial flutter?

A

almost always occurs in diseased heart and precipitates CHF. Caused by macro reentrant circuit.

37
Q

What are EKG characteristics of atrial flutter?

A

atrial rate 250-350, ventricular rate 150. AV node blocks at 2:1, 3:1, 4:1 rate. Irregularly irregular. sawtooth pattern

38
Q

What can cause atrial flutter?

A

thyrotoxicosis, pericarditis, alcohol ingestion

39
Q

What is treatment of atrial flutter?

A

ASA. Class IA antirrhythmics (Pronestyl/Procainmide). Beta blockers, calcium channel blockers, or digoxin. ablation if failed cardioversion and medical therapy.

40
Q

In what patients is an accelerate junctional rhythm common?

A

patients with inferior MI or digoxin toxicity

41
Q

What are EKG findings of a junctional escape or accelerated junctional rhythm?

A

Narrow complex QRS. Retrograde P wave: Inverted P with very short PR interval, P wave immediately after QRS, sometimes no P wave

42
Q

Describe junctional tachycardia

A

150 – 250 bpm. Occurs more commonly in women. May occur in absence of heart disease. Usually initiated by a PAC

43
Q

What is treatment for junctional tachycardia?

A

acute: vagal manuevers, adenosine. long term: beta blockers, calcium channel blockers, class IA, 1C, or III antiarrhythmics

44
Q

What is a 2nd degree AV block (Mobitz Type I, Wenckebach)?

A

occurs in the AV node above the Bundle of His. often transient and may be due to acute inferior MI or digitalis toxicity. treatment not indicated unless sx

45
Q

What characteristics describe a 2nd degree AV block (Mobitz Type I, Wenckebach) on EKG?

A

Rate may be variable. PR interval gets progressively longer until a QRS is dropped (or blocked)

46
Q

What characteristics are expected from a 2nd degree AV block (Mobitz type II)?

A

variable rate, normal P wave, wide QRS, with normal P-R until dropped QRS

47
Q

What is treatment for a 2nd degree AV block (Mobitz type II)?

A

artificial pacing, via external pacer or temporary pacer wire insertion. Usually requires permanent pacemaker

48
Q

What is a 3rd degree heart block?

A

Block of the atrial impulses occurs at the A-V junction, common bundle or bilateral bundle branches. Atrial and ventricular activities are unrelated

49
Q

What can cause a 3rd degree heart block?

A

Digitalis toxicity, Acute infection, MI, Degeneration of the conductive tissue

50
Q

What characteristics describe a 3rd degree heart block on EKG?

A

normal atrial rate, ventricular rate < 70. normal P waves w/constant P-P interval but don’t match QRS which may be wide

51
Q

What is treatment for a 3rd degree heart block?

A

external pacing and atropine for acute, symptomatic episodes. permanent pacing for chronic complete heart block

52
Q

What can cause PVCs?

A

Increasing circulating catecholamines, Coronary ischemia, Hypokalemia, Low magnesium level, Drug (such as digitalis) toxicities. also can occur in healthy hearts

53
Q

What characterizes PVCs on EKG?

A

variable rate, P wave usually obscured by the QRS w/PVC. Wide QRS with full compensatory pause. may occur in singles, couplets or triplets; or in bigeminy, trigeminy or quadrigeminy

54
Q

What is treatment for many PVCs?

A

Lidocaine, Procainamide (Pronestyl), or

Amiodarone (Cordorone). Replace Magnesium, potassium if appropriate

55
Q

What is the most important arrhythmic trigger clinically of ventricular tachycardia?

A

Hypokalemia followed by hypomagnesemia. Hyperkalemia also may predispose to VT and VF, particularly in patients with structural heart disease

56
Q

What other conditions that can trigger Vtach?

A

MI, congenital heart defects, dilated cardimyopathy, hypertrophic cardiomyopathy

57
Q

What does Vtach look like on EKG?

A

Absent P waves. QRS >.12. Regular rate and morphology. Classified as sustained >30 seconds or nonsustained (NSVT) < 30 seconds. life threatening rhythm can degenerate to v.fib

58
Q

What is treatment for vtach?

A

Pulse: Cardioversion and antiarrhythmics to prevent recurrence-Amiodarone. Pulseless – Defibrillation and Antiarrhythmics

59
Q

What is Torsades de Pointes?

A

upward and downward deflection of the QRS complexes around the baseline. caused by QT lengthening drugs, hypokalemia/magnesemia, MI

60
Q

What is treatment for Torsades de Pointes?

A

cardioversion when patient is unstable. IV magnesium or IV potassium to correct an electrolyte imbalance. Overdrive pacing

61
Q

What is ventricular fibrillation?

A

dysrhythmia results in the absence of cardiac output. Almost always occurs with serious heart disease, especially acute MI.

62
Q

What is treatment for vfib?

A

Immediate defibrillation and ACLS protocols.

Identification and treatment of the underlying cause. Will require implantation of an ICD

63
Q

What causes an idioventricular rhythm?

A

MI, pacemaker failure, metabolic imbalance

64
Q

What should you be cautious of when treating idioventricular rhythms?

A

Suppressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill

65
Q

What is asystole?

A

Asystole in the presence of acute MI and CAD is almost always fatal. Complete cessation of any electrical or mechanical activity.

66
Q

How is asystole treated?

A

CPR, 100% oxygen, IV intubation, transcutaneous pacing, epinephrine 1.0 mg., IV push, q3-5 minutes
atropine

67
Q

What is pulseless electrical activity?

A

There is electrical activity, but no mechanical response. What is seen on the EKG is electrical activity appearing as normal sinus rhythm. There will be NO pulse

68
Q

What is treatment for pulseless electrical activity (electromechanical dissociation)?

A

Correct underlying cause, Epinephrine – 1:10,000, Atropine, CPR

69
Q

What are the class 1A antiarrhythmics (only used with ACLS protocol)?

A

Pronestyl (Procainimide) and Quinidine (Cardioquin)

70
Q

What are the class III antiarrhythmics?

A

Sotalol (Betapace)120-160mg po BID. Ibutilide (Corvert) IV only. Amiodarone – titrated up to 400mg po qday. **Long-term toxicity issues, lungs, thyroid, liver and eyes need monitoring.

71
Q

What are the class IC antiarrhythmics?

A

Propafenone (Rythmol) and Flecainide (Tambocor). Used only in patients with structurally normal hearts (ie, absence of coronary artery disease or cardiomyopathy)

Cardiology (19 decks)

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