tonystep1's version from 2017-08-26 08:23

Arrhythmias - CAUSES

Question Answer
Premature Atrial ComplexesCauses include adrenergic excess, drugs, alcohol, tobacco, electrolyte imbalances, ischemia, and infection.
Premature Ventricular ComplexesCauses include hypoxia, electrolyte abnormalities, stimulants, caffeine, and medications.
Atrial Fibrillation IAFib)Causes include Heart disease , Pericarditis and pericardial trauma , Pulmonary disease including PE, Hyper/Hypothyroidism , Systemic illnesses, Stress, Excessive alcohol intake , Sick Sinus Syndrome, and Pheochromocytoma
Atrial Flutter COPD-most common association // Heart disease: rheumatic heart disease, CAD, CHF // Atrial septal defect (ASD)
Multifocal Atrial TachycardiaUsually occurs in patients with severe pulmonary disease (e.g., COPD)
Paroxysmal Supraventricular Tachycardia (PSVT)Ischemic heart disease // Digoxin toxicity // AV node reentry // Atrial flutter with rapid ventricular response // AV reciprocating tachycardia (accessory pathway) // Excessive caffeine or alcohol consumption
Wolff-Parkinson-White SyndromeAn accessory conduction pathway from atria to ventricles causes premature ventricular excitation because it lacks the delay seen in the AV node
Ventricular Tachycardia (VT)CAD with prior MI is most common cause // Active ischemia, hypotension // Cardiomyopathies // Congenital defects // Prolonged QT syndrome // Drug toxicity
Ventricular Fibrillation 􀂍VFib)Ischemic heart disease is the most common cause // Antiarrhythmic drugs, especially those that cause torsades de pointes (prolonged QT intervals)
Sinus BradycardiaCauses include ischemia, increased vagal tone, antiarrhythmic drugs; may be a normal finding in trained athletes
Sick Sinus SyndromeSinus node dysfunction characterized by a persistent spontaneous sinus bradycardia
AV BlockDelay is usually in the AV node
Second-degree AV block Mobitz type I (Wenckebach)Benign condition
Second-degree AV block Mobitz type IISite of block is within the His-Purkinje system
Third-degree (complete) AV blockAbsence of conduction of atrial impulses to the ventricles

Arrythmias - ECG FINDINGS

Question Answer
Premature Atrial ComplexesOn ECG, look for early P waves that differ in morphology from the normal
sinus P wave (because these P waves originate within the atria and not the
sinus node) . // QRS complex is normal because conduction below the atria is normal. There is
usually a pause before the next sinus P wave. //
Premature Ventricular ComplexesBecause conduction is not through normal conduction pathways, but rather
through ventricular muscle, it is slower than normal, causing a wide QRS. // Wide, bizarre QRS complexes followed by a compensatory pause are seen; a P wave
is not usually seen because it is "buried" within the wide QRS complex
Atrial Fibrillation IAFib)ECG findings: Irregularly irregular rhythm (irregular RR intervals and excessively rapid
series of tiny, erratic spikes on ECG with a wavy baseline and no identifiable P waves)
Atrial FlutterECG provides a saw-tooth baseline, with a QRS complex appearing after every
second or third "tooth" (P wave). Saw-tooth flutter waves are best seen in the inferior
leads (II, III, aVF ) .
Multifocal Atrial TachycardiaECG findings: variable P-wave morphology and variable PR and RR intervals. At least
three different P-wave morphologies are required to make an accurate diagnosis
Paroxysmal Supraventricular Tachycardia IPSVT)AV nodal reentrant type (Initiated or terminated by PACs
• ECG: narrow QRS complexes with no discernible P waves (P waves are buried
within the QRS complex). This is because the circuit is short and conduction is
rapid, so impulses exit to activate atria and ventricles simultaneously) //
Othrodomic reentrant type (Initiated or terminated by PACs or PVCs
• ECG: narrow QRS complexes with P waves which may or may not be discernible,
depending on the rate. This is because the accessory pathway is
some distance from the AV node (reentrant circuit is longer), and there is a
difference in the timing of activation of the atria and ventricles.)
Wolff-Parkinson-White SyndromeECG: narrow complex tachycardia, a short P-R interval, and a delta wave (upward
deflection seen before the QRS complex)
Ventricular Tachycardia (VT)ECG: Wide and bizarre QRS complexes // QRS complexes may be monomorphic or polymorphic //
Ventricular Fibrillation 􀂍VFib)ECG: No atrial P waves can be identified. // No QRS complexes can be identified // In sum, no waves can be identified; there is a very irregular rhythm.
Sinus BradycardiaSinus rate <60 bpm: clinically significant when rate is persistently <45 bpm
Sick Sinus SyndromeSinus node dysfunction characterized by a persistent spontaneous sinus bradycardia
AV BlockPR interval is prolonged (>0.20 sec). // A QRS complex follows each P wave //
Second-degree AV block Mobitz type I (Wenckebach)Characterized by progressive prolongation of PR interval until a P wave fails to
Second-degree AV block Mobitz type IIP wave fails to conduct suddenly, without a preceding PR interval prolongation;
therefore, the QRS drops suddenly.
Third-degree (complete) AV blockAbsence of conduction of atrial impulses to the ventricles; no correspondence
between P waves and QRS complexes


Question Answer
Premature Atrial ComplexesUsually asymptomatic and do not require treatment. Monitor for increased frequency
If symptomatic (e.g., palpitations) , {3-blockers may be helpful
Premature Ventricular ComplexesMost patients are asymptomatic. lf symptomatic, ,8-blockers may be used
Acute AFib in a hemodynamically unstable patientimmediate electrical cardioversion to sinus rhythm
Acute AFib in a hemodynamically stable patientRate control - Calcium channel blockers are preferred. /3-blockers are an alternative // Cardioversion to sinus rhythm (after rate control is achieved) // Anticoagulation to prevent embolic cerebrovascular accident (CVA) // If AFib present >48 hours (or unknown period of time) , risk of embolization
during cardioversion is significant (2% to 5%) . Anticoagulate patients for 3 weeks before and 4 weeks after cardioversion. - An INR of 2 to 3 is the anticoagulation goal range
Chronic AFibRate control with a {3-blocker or calcium channel blocker // chronic anticoagulation (warfarin)
Patients with "lone" AFib (i.e., AFib in the absence of underlying heart disease or other cardiovascular risk factors) under age 60do not require anticoagulation because they are at low risk for embolization (aspirin may be appropriate) .
Atrial FlutterTreatment is identical to Afib
Multifocal Atrial TachycardiaTreatment involves improving oxygenation and ventilation. If left ventricular function
is preserved, acceptable treatments include calcium channel blockers, ,beta-blockers, digoxin,
amiodarone, IV flecainide, and IV propafenone. If LV function is not preserved, use digoxin,
diltiazem, or amiodarone. Electrical cardioversion is ineffective and should not be used
Paroxysmal Supraventricular Tachycardia IPSVT) Acute treatmentIV adenosine-agent of choice due to short duration of action and effectiveness in terminating SVTs; works by decreasing sinoatrial and AV nodal activity
Paroxysmal Supraventricular Tachycardia IPSVT) PreventionDigoxin is usually the drug of choice. // Verapamil or /3-blockers are alternatives
PSVT with episodes that are recurrent and symptomatic.Radiofrequency catheter ablation of either the AV node or the accessory tract (depending on which is the accessory pathway
Wolff-Parkinson-White SyndromeRadiofrequency catheter ablation of one arm of the reentrant loop (i.e., of the
accessory pathway) is an effective treatment
Sustained VT Hemodynamically stable patients with mild symptoms and systolic BP >90New advanced cardiac life support (ACLS) guidelines recommend IV amiodarone,
IV procainamide, or IV sotalol over IV lidocaine or IV bretylium.
Hemodynamically unstable patients or patients with severe symptomsImmediate synchronous DC cardioversion // Follow with IV amiodarone to maintain sinus rhythm
Nonsustained VTIf no underlying heart disease and asymptomatic, do not treat. These patients are not at increased risk of sudden death
Ventricular Fibrillation 􀂍VFib)Initiate unsynchronized DC cardioversion immediately. If the equipment is not ready, start CPR until it is. // Give up to three sequential shocks to establish another rhythm; assess the rhythm between each.
Sinus BradycardiaAtropine can elevate the sinus rate by blocking vagal stimulation to the sinoatrial // A cardiac pacemaker maybe needed if bradycardia persists.
Sick Sinus SyndromePacemaker implantation may be required
First- degree AV BlockBenign condition that does not require treatment
Second-degree AV block Mobitz type I (Wenckebach)Benign condition that does not require treatment
Second-degree AV block Mobitz type IIPacemaker implantation is necessary
Third-degree (complete) AV blockPacemaker implantation is necessary.