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Cardiac Arrhythmias
Atrial Depolarization and the Inscription of the P-wave
Ventricular Depolarization and the Inscription of the QRS complex
1. The septum depolarizes from the
inside out and the resulting
depolarization wave moves
away from the electrode
recording Lead II
2. The rest of the left ventricle
depolarizes counter-clockwise
from the inside out and creates
the main cardiac vector (large arrow)
which is essentially, the algebraic
sum of all of the small depolarization
vectors (including the small
contribution from the right ventricle)
. In a normal heart, this vector
is always moving directly
toward Lead II, generating a
mostly positive QRS complex
Note: compared to
the left ventricle, the
right ventricle is much
smaller and contributes
little to the overall main
vector of depolarization
o
60
Lead
II electrode
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60 downward
rotation angle
o
from the horizontal 0
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”
Summary of the
“Limb Leads”
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.
LEAD AVR
LEAD AVL
-150o
-30o
0o
LEAD I
60o
120o
LEAD III
90o
LEAD AVF
LEAD II
The “Precordial Leads”
4th
intercostal
V1
V2
Each of the 6
V3
precordial leads is space
V4 V5 V6
unipolar (1 electrode
constitutes a lead)
and is designed to
view the electrical
activity of the heart
in the horizontal or V1 - 4th intercostal space - right margin of sternum
V2 - 4th intercostal space - left margin of sternum
transverse plane
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
Precise Axis Calculation
• Diagnosis and treatment of arrhythmias can be
simplified by using the following checklist when
looking at an electrocardiographic display:
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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
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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
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
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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
• Hypotension and shock
• Pulmonary embolism
• Acute coronary ischemia
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depletion
Anxiety
Pheochromocytoma
Sepsis
Anemia
Exposure to stimulants
(nicotine, caffeine) or
illicit drugs
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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
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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)
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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
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Irregular rhythm
Absence of definite p waves
Narrow QRS
Can be accompanied by rapid ventricular response
Atrial Fibrillation—causes and
associations
• Hypertension
• Hyperthyroidism and
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subclinical
hyperthyroidism
CHF (10-30%), CAD
Uncommon presentation
of ACS
Mitral and tricuspid valve
disease
• Hypertrophic
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cardiomyopathy
COPD
OSA
ETOH
Caffeine
Digitalis
Familial
Congenital (ASD)
Atrial fibrillation--assessment
• H & P—assess heart rate, sxs of SOB, chest
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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
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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 2448 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
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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
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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
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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
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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
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Rate?
Regularity?
P waves?
PR interval?
QRS duration?
30 bpm
regular
normal
0.12 s
0.10 s
Interpretation? Supraventricular
Bradycardia
Supraventricular Bradyarrhythmia
• sinus or junctional in origin
• second-degree (types I and II) or third-degree atrioventricular (AV)
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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