Dysrhythmias Flashcards
What is a sinus arrhythmia?
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
What is a sinus paues/sinus arrest?
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
What medications can cause bradycardia?
beta blockers, digoxin
What are treatment options for bradycardia?
Symptomatic and hemodynamically unstable: Atropine 1mg IV (anticholinergic). Temporary Pacer
What is pharmacologic treatment of sinus tachycardia?
calcium channel blockers (diltiazem, verapamil) or beta blockers (symptomatic tach)
Where are supraventricular tachycardias likely to originate from?
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
What drugs may cause supraventricular tachycardia as a side effect?
digitalis, asthma medications, or cold remedies. Caffeine, ephedra. Cocaine, meth
What does a EKG in PSVT look like?
HR 140-240, regular rate, P wave different from sinus wave and buried in narrow QRS
What are symptoms of tachycardic rhythms?
Palpitations , Dizziness, or light-headedness, or syncope (rare), SOB, Anxiety, Chest pain or tightness
What is nonpharmacologic treatment for SVT?
Vagal maneuvers (hold breath, dip face in cold water, cough, tense stomach muscles
What is pharmacologic treatment for SVT?
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
What therapy is used to prevent recurrence of SVT?
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
What is wolff-parkinson-white syndrome?
Form of supraventriuclar tachycardia but involves an accessory pathway that bypasses the AV node and conduct impulses faster than normal.
What is the greatest concern for people with WPW?
the possibility of having atrial fibrillation with a fast ventricular response that worsens to ventricular fibrillation, a life-threatening arrhythmia.
What are EKG characteristics for WPW?
HR >200, PR interval is short <.12ms, and the upstroke of the QRS wave is slurred; this is known as a delta wave.
What are treatment options for WPW?
Radiofrequency ablation-Ablation of accessory pathway(s). Beta blockers, Calcium Channel Blockers, Flecainide
How is an acute episode of WPW terminated?
Vagal maneuvers, IV Adenosine or IV diltiazem, Have defib ready as meds may turn the rhythm from SVT into afib. cardiovert if unstable
What is paroxysmal atrial tachycardia (PAT)?
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.
What are treatment options for PAT?
vagal manuevers, adenosine, cardioverions. digoxin, beta blockers, calcium channel blockers to prevent recurrence
What is a premature atrial contraction?
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
What causes an increased incidence of PACs?
Mitral valve disease, MI, Cardiomyopathy, Smoking, Alcohol, Caffeine
What is treatment for PACs?
Asymptomatic-No special treatment or Avoid the precipitants. Symptomatic-Controlled with beta blockers
What is a wandering atrial pacemaker?
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
What are characteristics of a wandering atrial pacemaker on EKG?
rate is variable depending on the site of the pacemaker; usually 45-100/ bpm. Needs to have 3 distinctly different P wave morphologies.
What is multifocal atrial tachycardia?
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
What is multifocal atrial tachycardia common with?
lung disease, COPD, acute MI, sepsis, hypokalemia, theophylline toxicity, low magnesium
What are treatment options for mutlifocal atrial tachycardia?
Treatment is directed at the underlying medical problems.May suppress the rate with AV nodal blocking agents-Calcium Channel Blockers or Beta-blockers
What is atrial fibrillation?
Multiple reentrant loops generate chaotic atrial depolarization. Most common encountered arrhythmia in clinical practice
What are EKG characteristics of atrial fib?
AV node is bombarded with rates greater than 400 bpm for atrial foci. Ventricular rate is irregularly irregular. No distinguishable P waves on EKG
What are common underlying causes of atrial fib?
Valvular disease, Heart failure, Ischemic Heart Disease
What is the pharmacologic treatment of a. fib?
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
What can be used to estimate embolic risk?
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
When do you use cardioversion to treat a. fib?
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
What type of esophageal echo should be used to check for thrombus in a. fib?
transesophageal echo prior to cardioversion
Why should you evaluate new onset afib or a.flutter?
presence of valvular heart disease (echo), presence of ischemic heart disease (nuclear stress test), and Rule out sleep apnea (sleep study), or thyroid studies
What is atrial flutter?
almost always occurs in diseased heart and precipitates CHF. Caused by macro reentrant circuit.
What are EKG characteristics of atrial flutter?
atrial rate 250-350, ventricular rate 150. AV node blocks at 2:1, 3:1, 4:1 rate. Irregularly irregular. sawtooth pattern
What can cause atrial flutter?
thyrotoxicosis, pericarditis, alcohol ingestion
What is treatment of atrial flutter?
ASA. Class IA antirrhythmics (Pronestyl/Procainmide). Beta blockers, calcium channel blockers, or digoxin. ablation if failed cardioversion and medical therapy.
In what patients is an accelerate junctional rhythm common?
patients with inferior MI or digoxin toxicity
What are EKG findings of a junctional escape or accelerated junctional rhythm?
Narrow complex QRS. Retrograde P wave: Inverted P with very short PR interval, P wave immediately after QRS, sometimes no P wave
Describe junctional tachycardia
150 – 250 bpm. Occurs more commonly in women. May occur in absence of heart disease. Usually initiated by a PAC
What is treatment for junctional tachycardia?
acute: vagal manuevers, adenosine. long term: beta blockers, calcium channel blockers, class IA, 1C, or III antiarrhythmics
What is a 2nd degree AV block (Mobitz Type I, Wenckebach)?
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
What characteristics describe a 2nd degree AV block (Mobitz Type I, Wenckebach) on EKG?
Rate may be variable. PR interval gets progressively longer until a QRS is dropped (or blocked)
What characteristics are expected from a 2nd degree AV block (Mobitz type II)?
variable rate, normal P wave, wide QRS, with normal P-R until dropped QRS
What is treatment for a 2nd degree AV block (Mobitz type II)?
artificial pacing, via external pacer or temporary pacer wire insertion. Usually requires permanent pacemaker
What is a 3rd degree heart block?
Block of the atrial impulses occurs at the A-V junction, common bundle or bilateral bundle branches. Atrial and ventricular activities are unrelated
What can cause a 3rd degree heart block?
Digitalis toxicity, Acute infection, MI, Degeneration of the conductive tissue
What characteristics describe a 3rd degree heart block on EKG?
normal atrial rate, ventricular rate < 70. normal P waves w/constant P-P interval but don’t match QRS which may be wide
What is treatment for a 3rd degree heart block?
external pacing and atropine for acute, symptomatic episodes. permanent pacing for chronic complete heart block
What can cause PVCs?
Increasing circulating catecholamines, Coronary ischemia, Hypokalemia, Low magnesium level, Drug (such as digitalis) toxicities. also can occur in healthy hearts
What characterizes PVCs on EKG?
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
What is treatment for many PVCs?
Lidocaine, Procainamide (Pronestyl), or
Amiodarone (Cordorone). Replace Magnesium, potassium if appropriate
What is the most important arrhythmic trigger clinically of ventricular tachycardia?
Hypokalemia followed by hypomagnesemia. Hyperkalemia also may predispose to VT and VF, particularly in patients with structural heart disease
What other conditions that can trigger Vtach?
MI, congenital heart defects, dilated cardimyopathy, hypertrophic cardiomyopathy
What does Vtach look like on EKG?
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
What is treatment for vtach?
Pulse: Cardioversion and antiarrhythmics to prevent recurrence-Amiodarone. Pulseless – Defibrillation and Antiarrhythmics
What is Torsades de Pointes?
upward and downward deflection of the QRS complexes around the baseline. caused by QT lengthening drugs, hypokalemia/magnesemia, MI
What is treatment for Torsades de Pointes?
cardioversion when patient is unstable. IV magnesium or IV potassium to correct an electrolyte imbalance. Overdrive pacing
What is ventricular fibrillation?
dysrhythmia results in the absence of cardiac output. Almost always occurs with serious heart disease, especially acute MI.
What is treatment for vfib?
Immediate defibrillation and ACLS protocols.
Identification and treatment of the underlying cause. Will require implantation of an ICD
What causes an idioventricular rhythm?
MI, pacemaker failure, metabolic imbalance
What should you be cautious of when treating idioventricular rhythms?
Suppressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill
What is asystole?
Asystole in the presence of acute MI and CAD is almost always fatal. Complete cessation of any electrical or mechanical activity.
How is asystole treated?
CPR, 100% oxygen, IV intubation, transcutaneous pacing, epinephrine 1.0 mg., IV push, q3-5 minutes
atropine
What is pulseless electrical activity?
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
What is treatment for pulseless electrical activity (electromechanical dissociation)?
Correct underlying cause, Epinephrine – 1:10,000, Atropine, CPR
What are the class 1A antiarrhythmics (only used with ACLS protocol)?
Pronestyl (Procainimide) and Quinidine (Cardioquin)
What are the class III antiarrhythmics?
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.
What are the class IC antiarrhythmics?
Propafenone (Rythmol) and Flecainide (Tambocor). Used only in patients with structurally normal hearts (ie, absence of coronary artery disease or cardiomyopathy)
