Etiology

Sinus Tachycardia

Inadequate anesthesia and light plane, anxiety, pain, fever, hypovolemia, hypoxia, hypercarbia,drug effect, heart failure.

ECG Criteria Rate > 100/ min Rhythm regular P wave upright in I,II, aVF P:QRS 1:1 QRS complex normal ST depression can occur due to ischaemia

Treatment

Treat underlying cause Beta blockers Esmolol, Metaprolol

A.Fibrillation

Rate:Wide ranging ventricular response to Atrial rate of 300 to 400bpm. Impulse takes multiple, chaotic, random Rhythm:Irregularly irregular. P wave:Chaotic atrial fibrillatory waves pathways through atria. only. P/QRS - Cannot be measured

A.Flutter

Impulse takes a circular course around atria.

Rate:Atrial rate 220 to 350bpm Ventricular response rarely >150bpm. Rhythm:Regular.Set ratio to atrial rhythm e.g, 2 to1 P wave:No true P waves P/QRS Cannot be measured

Normal Heart Diltiazem or another calcium channel blocker Metaprolol or another beta blocker DC cardioversion or Amiodarone Provide anticoagulation Impaired Heart Digoxin or Diltiazem or Amiodarone DC cardioversion or Amiodarone Provide anticoagulation

Junctional Tachy

Pathophysio:Area of automaticity develops in AV node. Both retrograde and ante grade transmission occurs. Etio:Digoxin toxicity Acute sequence of acute coronary syndrome.

Rate 100 180/min Rhythm- regular atrial and ventricular firing PR- not measurable or will be short P wave - obscured, may arise before, after or with QRS QRS complex - narrow

Diagnosis Unknown Vagal stimulation/Adenosine Preserved heart function Beta blockers Calcium channel blockers Amiodarone NO DC CONVERSION Impaired heart function Amiodarone NO DC CONVERSION

Multifocal Atrial Tachy

Areas of automaticity originate irregularly and rapidly at different points in atria. Most common cause is COPD (corpulmonale). Impaired and hypertrophied atrium. Digoxin toxicity. Acute coronary syndromes. RHD.

Rate- >100bpm Rhythm- irregular atrial firing PR- variable P wave- 3 or more that differ in polarity QRS complex- narrow Key- 3 or more P wave that differ in polarity, shape, size

Preserved heart function Beta blockers Calcium channel blockers Amiodarone Impaired heart function Amiodarone Diltiazem NO DC cardioversion

PSVT

Re entry phenomenon impulse arise and recycle repeatedly in AV node because of unidirectional block in Purkinje fibers. Accessory conduction pathway. Factors like caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, medications in healthy individuals Unhealthy individuals with CAD, COPD, CHF.

Diagnosis Unknown Vagal stimulation/Adenosine Preserved heart function AV nodal blockade - blocker, Calcium channel blocker, Digoxin DC Cardio version Parenteral antiarrhythmics Procainamide, Amiodarone, Sotalol Impaired heart function DC cardioversion Digoxin Key Regular, Narrow complex tachycardia without P waves and sudden, Amiodarone Diltiazem paroxysmal onset or cessation or both Rate exceeds upper limit of sinus tachycardia (>120bpm ); seldom<150 bpm up to 250bpm Rhythm regular P waves seldom seen, rapid rate cause P wave loss in T wave or low origin in atrium QRS complex- narrow

Results from ectopic pacemaker activity from either ventricle. PVC Electrolyte abnormalities, Blood gas abnormalities, Drug inter actions, Brainstem stimulation.

Wide, bizarre QRS complex Unifocal- PVCs from same focus; coupling interval is normal Multifocal- coupling interval and QRS morphology vary Ventricular bigeminy- every other beat is a PVC Ventricular trigeminy- 2 normal beats and a PVC or 1 normal beat and 2 PVCs

Lidocaine Esmolol Bretylium Verapamil Atropine

PAC

Impulses arise in atria, outside SA node. Rate- variable Occurs before next expected sinus beat. Rhythm- irregular Sympathomimetics, P wave- abnormal with different Hypoxia, morphology High atrial pressures, PR interval shorter or longer Digitalis toxicity. QRS- normal

Usually not needed If hemodynamically unstable Digitalis Beta blockers Verapamil

Occurs due to decrease in rate of discharge of impulses from S.A node. Not pathological, not an abnormal arrhythmia, more a physical sign. Sinus Bradycardia Etiology Drug effects, acute inferior wall MI, Hypoxia, vagal stimulation, sympathetic blockade, parasympathetic stimulation, sick sinus syndrome.

Rarely indicated, treat only if significant Oxygen is always appropriate Intervention sequence Atropine 0.5 to 1mg i.v Key Regular P waves followed by Transcutaneous pacing if available regular QRS complexes at rate < 60/min Catecholamine infusion in severe cases Dopamine 5 to 20 g/kg/min Epinephrine 2 to 10 g/min Isoproterenol 2 to 10 g/min

Ist AV block

Impulse conduction is slowed (partial block) at AV node by a fixed amount. Closer to being a physical sign than an abnormal arrhythmia. Etiology Drugs Usually AV node blockers, parasympathetic stimulation, inferior AMIs .

Rate bradycardia or tachycardia Rhythm sinus, regular PR prolonged, > 0.20 sec, fixed P wave size & shape normal, each P wave have 1 QRS complex QRS complex narrow: 0.10 sec in absence of intraventricular conduction defect Key- PR interval > 0.20 sec

Iind AV type I block

Pathophysio :Site of pathology is AV node. Impulse conduction is increasingly slowed at AV node causing increasing PR interval. Occurs till one sinus impulse is completely blocked and a QRS complex Key- Progressive lengthening of PR fails to follow. interval until one P wave is not followed Etiology : AV nodal blocking agentsby QRS complex Beta blockers, Calcium channel blockers, Digoxin Stimulation of Para sympathetic system Acute coronary syndrome- right coronary

Intervention sequence Atropine 0.5 to 1mg i.v Transcutaneous pacing if available If signs and symptoms are severe Dopamine 5 to 20 g/kg/min Epinephrine 2 to 10 g/min Isoproterenol 2 to 10 g/min

Iind AV Type II block

Atrial rate- usually 60 to 100 bpm Ventricular rate- slower than atrial rate Rhythm- Atrial- regular; Ventricularirregular Pathophysio:Infra nodal block site of PR- constant, no progressive block most often below AV node. prolongation Impulse conduction is normal through P wave- some P waves will not be the node. followed by QRS complex Etiology :Acute coronary syndrome left QRS complex- narrow implies high coronary. block; wide implies low block Key - No progressive prolongation of P wave

Prepare for Tran venous pacer Atropine is seldom effective Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 g/kg/min Epinephrine 2 to 10 g/min Isoproterenol 2 to 10 g/min

3 rd degree AV block

Atrial rate- usually 60 to 100 bpm, Impulses completely independent from ventricular rate Ventricular rate- depends on rate of escape beats; slower than atrial rateInjury to cardiac conduction system third degree block; faster- AV producing complete block of impulses. dissociation Block can occur at AV node or Bundle of Rhythm- Atrial&Ventricular- regular, His or Bundle branches. independent Etiology :Acute coronary syndrome- LAD PR- no relationship between P and R wave P wave- typical in size and shape QRS complex- narrow implies high block; wide implies low block

Prepare for Tran venous pacer Transcutaneous pacing If signs and symptoms are severe, unresponsive Dopamine 5 to 20 g/kg/min Epinephrine 2 to 10 g/min Isoproterenol 2 to 10 g/min Never treat third degree block plus ventricular escape beats with Lidocaine