Cardiac Arrhythmias

Atrial Depolarization and the Inscription of the P-wave

Ventricular Depolarization and the Inscription of the QRS complex

1. The depolarizes from the inside out and the resulting depolarization wave m oves away from the electrode recording Lead II

septum

2. The rest of the depolarizes counter-clockwise from the inside out and creates the (large arrow) which is essentially, the algebraic sum of all of the sm all depolarization vectors (including the small contribution from the ) . In a normal heart, this vector is always moving directly toward Lead II, generating a mostly positive QRS com plex

left ventricle

m ain cardiac vector

right ventricle

Lead II electrode60 downwardrotation angle from the horizontal 0

o

o

Note: compared tothe left ventricle, the right ventric le is muchsm aller and contributeslittle to the overall m ainvector of depolarization

60o

Ventricular Repolarization and the Inscription of the T-wave

The ECG Complex with Interval and Segment Measurements

ECG Paper and related Heart Rate & Voltage Computations

The Concept of a “Lead”

0o

LEAD AVR LEAD AVL

LEAD AVF

LEAD II

LEAD I

LEAD III

60o

90o120o

-30o-150o

Each of the limb leads (I, II, III, AVR, AVL, AVF) can be assigned an angle of clockwise or counterclockwise rotation to describe its position in the frontal plane. Downward rotation from 0 is positive and upward rotation from 0 is negative.

Summary of the “Limb Leads”

V4 V5V6

V1 - 4th intercostal space - right margin of sternum V2 - 4th intercostal space - left margin of sternum V3 - linear midpoint between V2 and V4 V4 - 5th intercostal space at the mid clavicular line V5 - horizontally adjacent to V4 at anterior axillary line V6 - horizontally adjacent to V5 at mid-axillary line

Each of the 6 precordial leads is unipolar (1 electrode constitutes a lead) and is designed to view the electrical activity of the heart in the horizontal or transverse plane

The “Precordial Leads”

4th intercostal

spaceV2V1

V3

Precise Axis Calculation

• Diagnosis and treatment of arrhythmias can be simplified by using the following checklist when looking at an electrocardiographic display:

• 1. What is the heart rate? • 2. Is the rhythm regular? • 3. Is there one P wave for each QRS

Complex? • 4. Is the QRS complex normal? • 5. Is the rhythm dangerous? • 6. Does the rhythm require treatment?

Normal Sinus Rhythm

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II & downgoing in lead aVR

www.uptodate.com

Sinus Bradycardia

• HR< 60 bpm; every QRS narrow, preceded by p wave

• Can be normal in well-conditioned athletes• HR can be<30 bpm in children, young adults

during sleep, with up to 2 sec pauses

Sinus bradycardia--etiologies• Normal aging• 15-25% Acute MI, esp. affecting inferior

wall• Hypothyroidism, infiltrative diseases (sarcoid, amyloid)• Hypothermia, hypokalemia• SLE, collagen vasc diseases• Situational: micturation, coughing• Drugs: beta-blockers, digitalis, calcium

channel blockers, amiodarone, cimetidine, lithium

Sinus bradycardia--treatment• No treatment if asymptomatic• Sxs include chest pain (from coronary

hypoperfusion), syncope, dizziness• Office: Evaluate medicine regimen—stop

all drugs that may cause• ATROPINE 0.5 mg (max dose 0.04 mg/kg)• Ephedrine 5-25 mg• Dopamine 5-20 microgram/kg/min• Epinephrine 2-10 microgram/min

Sinus tachycardia

• HR > 100 bpm, regular• Often difficult to distinguish p and t waves

Sinus tachycardia--etiologies• Fever• Hyperthyroidism • Effective volume depletion • Anxiety • Pheochromocytoma • Sepsis • Anemia • Exposure to stimulants (nicotine, caffeine) or illicit

drugs

• Hypotension and shock • Pulmonary embolism • Acute coronary ischemia and myocardial

infarction • Heart failure • Chronic pulmonary disease • Hypoxia

Sinus Tachycardia--treatment• Office: evaluate/treat potential

etiology :check TSH, CBC, optimize CHF or COPD regimen, evaluate recent OTC drugs

• Verify it is sinus rhythm• If no etiology is found and is

bothersome to patients, can treat with beta-blocker

Sinus Arrhythmia

• Variations in the cycle lengths between p waves/ QRS complexes

• Will often sound irregular on exam• Normal p waves, PR interval, normal, narrow QRS

Sinus arrhythmia

• Usually respiratory--Increase in heart rate during inspiration

• Exaggerated in children, young adults and athletes—decreases with age

• Usually asymptomatic, no treatment or referral

• Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicity

• Referral may be necessary if not clearly respiratory, history of heart disease

•SUPRA VENTRICULAR ARRHYTMIA

Paroxysmal Supraventricular Tachycardia(PSVT)

• Heart rate : 130-270• Rhythm : regular• QRS : normal• P/QRS: 1 : 1 relationship, although the P wave may often be

hidden in the QRS complex or T wave.

PSVT treatment

Vagal maneuvers such as carotid sinus massage should be applied only to one side

Adenosine, which is the drug of choice, is given by 6-mg rapid (2 seconds) intravenous bolus, preferably through an antecubital or central vein. If no response is elicited, second and third doses of 12 to 18 mg of adenosine may be administered by rapid intravenous bolus

Verapamil (2.5 to 10 mg given intravenously)Amiodarone (150-mg infusion over a 10-

minute period for the loading dose) is a recent addition.

Atrial Fibrillation

• Irregular rhythm • Absence of definite p waves• Narrow QRS• Can be accompanied by rapid ventricular response

Atrial Fibrillation—causes and associations• Hypertension• Hyperthyroidism and subclinical hyperthyroidism• CHF (10-30%), CAD• Uncommon presentation of ACS• Mitral and tricuspid valve disease

• Hypertrophic cardiomyopathy• COPD• OSA• ETOH• Caffeine• Digitalis• Familial• Congenital (ASD)

Atrial fibrillation--assessment• H & P—assess heart rate, sxs of SOB,

chest pain, edema (signs of failure)• If unstable, need to cardiovert• Echocardiogram to evaluate valvular and

overall function• Check TSH• Assess onset of sxs—in the last 24-48

hours? Sudden onset? Or no sxs?

Atrial fibrillation--management• Rhythm vs Rate control—if onset is within

last 24-48 hours, may be able to arrange cardioversion—use heparin around procedure

• Need TEE if valvular disease (high risk of thrombus)

• If unable to definitely conclude onset in last 24-48 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 weeks after

Atrial fibrillation--management• β-Blockers such as esmolol (1 mg/kg

by intravenous bolus) or propranolol• Calcium channel blockers such as

verapamil (5 to 10 mg given intravenously) or diltiazem

Atrial fibrillation--management• Goal INR of 2.5 (2.0-3.0)• Rhythm control---second line

approach, if unable to control rate or pt with persistent sxs

• Can also consider radiofrequency ablation at pulm veins

If the ventricular response is excessively rapid or hemodynamic instability is present, or both, the following guidelines should be used

• Synchronized DC cardioversion starting at a relatively high energy of 100 J and gradually increasing to 360 J is indicated

• The class III antiarrhythmic agent ibutilide (Corvert, 1 mg in 10 mL saline or [D5W] infused slowly intravenously over a 10-minute period) has been documented to convert atrial flutter to sinus rhythm in most patients

• Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no faster than 0.5 mg/kg/min) and amiodarone

PAC

• P wave from another atrial focus• Occurs earlier in cycle• Different morphology of p wave

PAC

• Benign, common cause of perceived irregular rhythm

• Can cause sxs: “skipping” beats, palpitations

• No treatment, reassurance• With sxs, may advise to stop

smoking, decrease caffeine• Can use beta-blockers to reduce

frequency

•VENTRICULAR ARRHYTMIA

PVC

• Extremely common throughout the population, both with and without heart disease

• Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction

PVC

• No treatment is necessary, risk outweighs benefit

• Reassurance• Optimize cardiac and pulmonary

disease management

PVC treatment

• treatment is generally dictated by the presence of symptoms attributable to the VPBs.

• correct any underlying abnormalities such as decreased serum potassium or low arterial oxygen tension.

• lidocaine ; initial bolus dose of 1.5 mg/kg. Recurrent VPBs can be treated with a lidocaine infusion at 1 to 4 mg/min;

• additional therapy includes esmolol, propranolol, procainamide, quinidine, disopyramide, atropine, verapamil, or overdrive pacing

Non-sustained Ventricular tachycardia

• Defined as 3 or more consecutive ventricular beats

• Rate of >120 bpm, lasting less than 30 seconds• May be discovered on Holter, or other exercise

testing

Non-sustained ventricular tachycardia

• Need to exclude heart disease with Echo and stress testing

• If normal, there is no increased risk of death

• May need anti-arrhythmia treatment if sxs• In presence of heart disease, increased

risk of sudden death• Need referral for EPS and/or prolonged

Holter monitoring

Ventricular tachycardia

Ventricular tachycardia treatment• amiodarone administered as one or

more intravenous doses of 150 mg in 100 mL saline or D5W over a period of 10 minutes, followed by an intravenous infusion of 1 mg/min for 6 hours and 0.5 mg/min

• hypotension and bradycardia are its main side effects

Ventricular fibrillation

• Cardiopulmonary resuscitation• DefibrillationAsynchronous external

defibrillation should be performed with a DC defibrillator using incremental energies in the range of 200 to 360 J.

• 1 g of magnesium sulfate may facilitate defibrillation

• Advanced Cardiac Life Support

• Assess and support ABC• Give oxygen• Monitor ECG , BP, pulse oximetry• Check unstable signs ; chest pain,

hypotension -- unstable cardioversion

• Stablish IV access• Obtain 12 lead ECG• Identify and treat reversible causes

Tachycardia with pulse

• 1-ABC – oxygen – ECG monitor• 2-is patient stable?• 3-unstable IV access , sedation ,

cardioversion• 4- stable 12 LEAD ECG , IV

access ,check QRS• 5-narrow QRS REGULAR (PSVT)

VAGAL MANEUVRE , ADENOSINE• irregular (AF) control HR beta

blocker , ca channel blocker

• 6-wide QRS regular (VT) amiodarone , cardioversion

• Irregular AF with abberancy (AF + WPW) avoid verapamil , adenosine , digoxin , diltiazem

Bradycardia

30 bpm• Rate?• Regularity? regular

normal

0.10 s

• P waves?• PR interval?

0.12 s• QRS duration?Interpretation?Supraventricular

Bradycardia

Supraventricular Bradyarrhythmia

• sinus or junctional in origin• second-degree (types I and II) or third-degree

atrioventricular (AV) block• Treatment is indicated whenever the bradycardia,

regardless of type, leads to a significant decrease in systemic arterial pressure

• Initial treatment is atropine, 0.5 to 1.0 mg intravenously and repeated as needed at 3- to 5-minute intervals up to 0.04 mg/kg.[126

• dopamine (5 to 20 µg/kg/min) or epinephrine (2 to 10 µg/min)

• External transcutaneous pacing

Ventricular fibrilation

Ventricular fibrilation

Ventricular tachycardia

Atrial fibrilation

Atrial fibrilation

Atrial flutter

PSVT