ECG.pptx electrocardiogram cardiovascular system

BASICS OF ECG & ITS
ABNORMALITIES
ENCOUNTERED IN
PERIOPERATIVE PERIOD
MODERATED BY – DR. MANJULATA TANDAN ma’am
PRESENTED BY – DR. VRITIKA MANGHNANI

What’s an ECG?
• ECG = Electrocardiogram, Tracing of heart’s electrical activity .
• Recording device –ELECTROCARDIOGRAPH
• Pacemaker = sinoatrial node
• Impulse travels across atria
• Reaches AV node
• Transmitted along interventricular septum
in Bundle of His
• Bundle splits in two (right and left branches)
• Purkinje fibers
• Ventricular Myocardium

ECG Paper
VERTICALAXIS -Voltage
Electrocardiograph is generally
calibrated such that a 1-mV signal
produces a 10-mm deflection
HORIZONTALAXIS – Time
25 small squares in --------- 1 second.
1 small square ----------- 1/25
second/ 0.04 seconds/ 40 msecs

HOW DOES IT WORKS?
• Electrical impulse (wave of depolarization) picked up by placing
electrodes on patient
• The voltage change is sensed by measuring the current change across 2
electrodes – a positive electrode and a negative electrode
• If the electrical impulse travels towards the positive electrode this
results in a positive deflection
• If the impulse travels away from the positive electrode this results
negative deflection

TYPES OF LEADS
Coronal plane (6 Limb Leads)
1. Bipolar leads — l , lI , lII
2. Unipolar leads —Augmented limb leads- aVL , aVR , aVF
Transverse plane - V1 — V 6 (6 Chest Leads)
ECG
Leads
Bipolar
3 standard
Limb Leads
Unipolar
3
Augmented
Limb Leads
6 Precordial/
Chest leads

LEADS PLACEMENT
Electrode placement in 12 lead ECG
• 6 are chest electrodes - Called V1 -V6
• 4 are limb electrodes -Right arm, Left arm, Left leg, Right leg .
• Remember - The right leg electrode is a neutral or “dummy ”!
• CHEST ELECTRODE PLACEMENT-
V1 -4th intercostal space right sternal edge
V2 -4th intercostal space left sternal edge
V4- over the apex (5th ICS mid clavicular line)
V3 -halfway between V2 and V4
V5 -at the same level as V4 but on the anterior axillary line .
V6 -at the same level as V4 and V5 but on the mid -axillary line

How are the 12 leads on the ECG (I, II, III ,aVL, aVF,
aVR, V1 –6) formed using only 9 electrodes (and a
neutral)
• -Lead I is formed using the right arm electrode
(red) as the negative electrode and the left arm
(yellow) electrode as the positive
• -Lead II is formed using the right arm electrode
(red) as the negative electrode and the left leg
electrode (GREEN) as the positive
• -Lead III is formed using the left arm electrode as the
negative and the left leg electrode as the positive electrode
• -aVL, aVF, and aVR are composite leads computed using the
information from the other leads

LEADS & WHAT THEY TELL YOU
• Limb leads look at the heart in the coronal plane
aVL, I = lateral and left surface
II, III and aVF = inferior surface of heart
V2,V3 and V4-Anterior surface of the heart
V1 and V2- Septal area
V5 and V6- Apical surface
 Mirror image changes
in leads- V1-V4- Posterior surface.

WHAT DO COMPONENTS
REPRESENTS?
• P wave = atrial depolarization
• QRS = ventricular depolarization
• T = repolarization of the ventricles
• PR Interval = impulse from atria to ventricles
• ST segment = isoelectric – part of repolarisation
• QT Interval = This interval spans the onset of depolarisation to the
completion of repolarization of the ventricles.

PREPARATION FOR 12 LEAD ECG
• SKIN PREPARATION
Hair removal, clean & dry skin surface
• PATIENT POSITIONING
Preferably flat
(heart rotates position as the patient position changes.)

INTERPRETING THE ECG
Calibration ( Ht. 10mm = 1mV , Speed - 25mm/s )
 Rate (Count the number of large squares between R waves) ; Rate = 300/ RR
0r,(1500/no.of small boxes.)
 Rhythm (Every QRS must be preceded by a P wave)
 Axis
 Elements of the tracing in each lead

AXIS
• The axis can be thought of as the overall direction of the cardiac impulse or
wave of depolarisation of the heart
• An abnormal axis (axis deviation) can give a clue to possible pathology

AXIS DEVIATION CAUSES:
• Right Axis Deviation
• Right ventricular hypertrophy
• Anterolateral MI
• Left Posterior Hemiblock
Left Axis Deviation
• Ventricular tachycardia
• Inferior MI
• Left ventricular hypertrophy
• Left Anterior Hemiblock

P WAVE
• The P wave represents atrial depolarisation
• It can be thought of as being made up of two separate waves due to
right atrial depolarisation and left atrial depolarisation.
• Smooth and rounded
• No more than 2.5 mm in height
• No more than 0.12 second in duration
• Positive in leads II, negative in aVR

P WAVE
• Height -A tall P wave (over
2.5mm) can be called P
Pulmonale
• Occurs due to Rt. atrial
hypertrophy
• Causes include: - pulmonary
hypertension, pulmonary
stenosis, tricuspid stenosis
• Length - A P wave with a length
>0.08 seconds (2 small squares)
and a bifid shape is called P
Mitrale
• It is caused by left atrial
hypertrophy and delayed left atrial
depolarisation
• Causes include: Mitral valve
disease, LVH

QRS COMPLEX
• If the complexes in the chest leads look very tall, consider left
ventricular hypertrophy (LVH)
• If the depth of the S wave in V1added to the height of the R wave in
V6 comes to more than 35mm, LVH is present (the Sokolov-Lyon criteria)
–most commonly used
• The width of the QRS complex should be less than 0.12 seconds (3
small squares)
• If the QRS is wider than this, it suggests a ventricular conduction
problem usually right or left bundle branch block (RBBB or LBBB)

LBBB/RBBB (conduction disturbances at the
level of his-Purkinje system)
• If left bundle branch block is
present, the QRS complex may
look like a W. in V1and/or an M
shape in V 6. , absence of Q wave
in lead I, aVL, V5, V6
• New onset LBBB with chest pain
consider Myocardial infarction
• It is also called rSR pattern in V1 &
V2
• Deep S wave in leads I & V6
• If right bundle branch block is
present, there may be an M in V1
and/or a W in V6.
• Can occur in healthy people with
normal QRS width (partial RBBB)

• Acute treatment of RBBB or RBBB with LAHB consists of observation &
elimination of drugs known to contribute conduction disturbances.
• Appearance of LBBB on ECG often indicates serious heart disease –
hypertension, coronary artery disease, aortic valve disease,
cardiomyopathy. It has been observed during anaesthesia ,
particularly during hypertensive or tachycardiac episodes, & might be a
sign of MI

T WAVE
• Are the T waves too tall?
• No definite rule for height
• T wave generally should not be
taller than half the size of the
preceding QRS
• Causes: Hyperkalemia, Acute
myocardial infarction
• If the T wave is flat, it may
indicate hypokalemia
• If the T wave is inverted it may
indicate ischemia

QT INTERVAL
• The QT interval is measured from the start of the QRS complex to the end of the T
wave., represents time taken for full vent.depolarization & repolarisation
• The QT interval varies with heart rate.
• As the heart rate gets faster, the QT interval gets shorter
• It is possible to correct the QT interval with respect to rate by using the following
formula: QTc = QT/√RR ( QTc = corrected QT) – bazette formula
• The normal range for QTc is 0.38-0.42 sec
• A long QTc has increased risks of developing ventricular arrhythmia especially torsades
de pointes( QTc higher than 500ms)
• Cause of prolonged QTc(>440ms) - hypokalemia, hypomagnesemia, hypocalcemia,
hypothermia, MI, raised ICP, & certain drugs.

Preoperative treatment :
• A preop ECG to r/o LQTS is useful in a patient with h/o unexplained
syncope or family history of sudden death.
• Correction of electrolyte abnormalities.
• Drugs known to cause , should be discontinued or avoided intraop.
• Cardiac pacing
• A defibrillator should be available as increased risk of periop VF is
increased

ST SEGMENT
ST ELEVATION
• Is significant when it is greater
than 1 mm (1 small square) in 2
or more contiguous chest leads
(V1-V6)or greater than 2 mm in 2
or more leads
• It is usually caused by complete
full thickness myocardial
infarction
ST DEPRESSION
• ST depression > or equal
to 0.5 mm in greater than
or equal to 2 contiguous
leads, it indicates
myocardial ischemia, LV
strain(LVH)

Significant ST elevation
• ST segment elevation measurement
• starts 0.04 seconds after J point
• ST elevation
• > 1mm (1 small box) in 2 or more contiguous chest leads (V1-V6)
• >1mm (1 small box) in 2 or more anatomically contiguous leads (ie: II, III, aVF;
I, aVL, V5, V6)
• Contiguous lead
• limb leads that “look” at the same area of the heart or are numerically
consecutive chest leads (ie: V1 – V6)

Myocardial Insult
• Ischemia
• lack of oxygenation
• ST depression or T wave inversion
• permanent damage avoidable
• Injury
• prolonged ischemia
• ST elevation
• permanent damage avoidable
• Infarct
• death of myocardial tissue; damage permanent; may have Q wave

Evolution of AMI
A - pre-infarct (normal)
B - Tall T wave (first few minutes of infarct)
C - Tall T wave and ST elevation (injury)
D - Elevated ST (injury), inverted T wave (ischemia),
Q wave (tissue death)
E - Inverted T wave (ischemia), Q wave (tissue death)
F - Q wave (permanent marking)

Contiguous ECG leads
• EKG changes are
significant when they
are seen in at least two
contiguous leads
• Two leads are
contiguous if they look
at the same area of the
heart or they are
numerically consecutive
chest leads

ARRHYTHMIAS
• AHA DEFINES ARRYTHMIA AS: “ANY CHANGE FROM THE NORMAL SEQUENCE
OF ELECTRICAL IMPULSES.”
• The electrical impulses may happen too fast, too slowly or erratically.
• When the heart doesn’t beat properly, it cant pump blood effectively , leading
to shut down or damage to the vital organs.
CLINICAL MANIFESTATIONS :
• Many may go as unnoticed arrhythmias & picked up on incidental routine ecg
examination
• Most common manifestation is palpitation, others- light headedness & syncope

BASIC TYPES:
• SINUS ORIGIN ( SINUS TACHYCARDIA & SINUS BRADYCARDIA)
• ECTOPIC RHYTHMS
• PRE- EXCITATION SYNDROMES
• CONDUCTION BLOCKS
Rapid arrhythmias can increase the oxygen demands of the myocardium and
cause angina (chest pain). The sudden onset of an arrhythmia in a patient
with underlying cardiac disease can also precipitate congestive heart failure.
Sometimes, the first clinical manifestation of an arrhythmia is sudden death.

SINUS TACHYCARDIA & S.BRADYCARDIA
Normal sinus rhythm is the normal rhythm of the heart. Depolarization
originates spontaneously within the sinus node. The rate is regular and
between 60 and 100 beats per minute.
If the rhythm speeds up beyond 100, it is called sinus tachycardia; if it slows
down below 60, it is called sinus bradycardia.
Normal Variants: Strenuous exercise, for example, can accelerate the heart rate
well over 100 beats per minute, whereas resting heart rates below 60 beats per
minute are typical in well-conditioned athletes.
Pathological: Sinus tachycardia can occur in patients with fever, congestive heart
failure, severe lung disease, or hyperthyroidism. Sinus bradycardia can be caused
by medications, eg beta-blockers, calcium channel blockers, and opioids.

(A) Sinus tachycardia. Each beat is
separated by two and one-half
large squares for a rate of 120
beats per minute.
(B) Sinus bradycardia. More than seven
Large squares separate each beat,&
the rate is 40 to 45 beats per minute.

Causes Of PERIOPERATIVE SINUS
BRADYCARDIA:
Autonomic disturbance including
vasovagal stimulation.
 Hypoxia
 Hypothermia
 Hyperkalemia
 Endotracheal suctioning
 Increased intracranial pressure
 Hypothyroidism
 Drugs like B blockers, CCB’s,
Opioids, succinylcholine

Causes of PERIOPERATIVE SINUS TACHYCARDIA:
 Pain
 Anxiety / fear
 Fever or infection
 Hypercarbia
 Hypovolemia or anemia
 Hypotension
 hypoglcemia
 Inadequate anaesthetic depth
 Pathological increase in sympathetic tone in MI,CHF,
pulm embolism, hyperthyroidism, etc.
Drugs like sympathomimetics,
antimuscarinics, caffeine
CORRECTION:
of the underlying cause is the first
step
If required beta blockers may be
used after these factors have been
worked at.
Most commonly used agents are
esmolol and metoprolol.

SINUS ARREST (ASYSTOLE)
•Sinus arrest occurs when the sinus node stops firing. If nothing else were to
happen, the EKG would show a flat line without any electrical activity, and
the patient would die. Prolonged electrical inactivity is called asystole.
•Rx- ACLS protocol.

PREMATURE ATRIAL COMPLEX (PAC)
•These arise from ectopic pace making tissue within the atria.
 An abnormal (non-sinus) P wave is followed by a normal QRS complex.
 The abnormal P wave may be hidden in the preceding T wave.

Causes
1. Anxiety.
2. Sympathomimetics.
3. Beta-agonists.
4. Excess caffeine.
5. Hypokalemia.
6. Hypomagnesaemia.
7. Digoxin toxicity.
8. Myocardial ischemia
Clinical Significance :
Frequent PACs may cause palpitations and a
sense of the heart “skipping a beat”.
In patients with underlying predispositions
(e.g LA enlargement, IHD, WPW), it may
be the trigger for the onset of a re-entrant
tachyarrhythmia — e.g. AF, flutter
Usually no treatment is required. May
use Beta blockers or Calcium Channel
blockers.

PREMATURE VENTRICULAR
COMPLEX(PVC)
 Can arise from single(unifocal) or multiple(multifocal)foci located below AV node
 ECG findings- premature & wide QRS no preceding p wave, ST segment & T wave
deflections opp.QRS deflection & compensatory pause before the next sinus beat.
 The occurrence of more than 3 consecutive PVCs is considered VT
 Most common symptoms- palpitations, syncope
 D/D- normal heart(benign PVC- occur at rest & disappear with exercise) ,acidosis,
electrolyte imbalances( hypokalemia, hypomagnesemia) , hypoxemia, MI, valvular
heat disease, cardiomyopathy, mechanical irritation from central venous or
pulmonary artery catheterisation., excessive caffeine, alcohol & cocaine

When to worry about PVCs
PVCs posing an increased risk for triggering ventricular tachycardia:
 Frequent PVCs.
 Runs of consecutive PVCs, especially three or more in a row.
 Multiform PVCs, in which the PVCs vary in their site of origin and hence in
their appearance.
 PVCs falling on the T wave of the previous beat, called the “R-on-T”
phenomenon.
Treatment –
• Defibrillator- priority
• Elimination of causative factors
• Amiodarone , lidocaine if PVCs progresses to VT or i/c/o hemodynamic instability

PAC PVC
Abnormal p waves Normal p waves
Normal QRS complex Abnormal QRS complex
Problems in the atria Problems in the ventricles
No compensatory pause Compensatory pause is present
Rarely life threatening Life threatening if progresses to VT

Supraventricular Tachycardia
• Rhythm: Regular
• Rate: >100
• P: not visible
• P-R: not defined
• QRS: narrow complex
• S-T: depression
(sometimes)
• T: normal
• Q-T: prolonged
(sometimes)

ATRIAL FIBRILLATION
• Supraventricular dysrhythmia
• Rhythm: Irregular
• Rate: A: 350 ; V: varies
• P: poorly defined
• P-R: N/A
• S-T: normal
• T: normal
• Q-T: normal

 May present as asymptomatic ECG finding
 Predisposing: RHD (mitral valve ds.), IHD, COPD, acute alcohol
intoxication, ASD, pulmonary embolus, pericarditis
 S/s: fatigue, generalised weakness, palpitations, angina pectoris,
CHF, pulmonary edema, hypotension (dec C.O.)
 Pathology: multiple areas of atria depolarize continuously and
contract in disorganized manner
 Consequences: Thromboembolic event (d/t stasis)

 AF is most coomon postop tachydysrhthmia & often occurs early in post op period (first 2-4 days) in
elderly patients following cardiothoracic sx.
 Anaesthetic management: If new onset AF occurs prior to induction, postpone the elective surgery
• Management – synchronized cardioversion at 100-120 J (if hemodynamically unstable
• When chronic AF, pt should be maintained on antidysrhythmic drugs preoperatively (close attention
to Mg and K when on digoxin)
• Transition of anticoagulants

ATRIAL FLUTTER
• Rhythm: Regular / Irregular
• Rate: A: 220 – 430; V: <300 (2:1, 3:1 or
sometimes 4:1)
• P: Saw toothed appearance
• P-R: N/A
• S-T: normal
• T: normal
• Q-T: normal

Atrial flutter association seen with -
1. Hypertension
2. Obesity
3. Diabetes mellitus
4. Electrolyte imbalances
5. Alcohol intoxication
6. Drug abuse, particularly cocaine and amphetamines
7. Pulmonary disease (e.g., chronic obstructive pulmonary disease and pulmonary embolism)
8. Thyrotoxicosis
9. Various underlying cardiac conditions, both congenital (e.g., atrial septal defect) and acquired (e.g.,
rheumatic valvular disease, coronary artery disease, and congestive heart failure)

VENTRICULAR TACHYCARDIA
• A run of three or more consecutive PVCs is called ventricular tachycardia. The rate is
usually between 120 and 200 beats.
• Sustained VT — lasting more than 30 seconds—or VT associated with
hemodynamic instability are emergencies, presaging cardiac arrest and requiring
immediate treatment.
• Polymorphic ventricular tachycardia is more commonly associated with acute
coronary ischemia, infarction, profound electrolyte disturbances, and conditions
causing prolongation of the QT interval. Uniform ventricular tachycardia is more
often seen with healed infarctions.

VENTRICULAR FIBRILLATION
•Ventricular fibrillation is a preterminal event seen solely in dying hearts.
•The EKG tracing jerks about spasmodically, there are no true QRS complexes.
•In VF, the heart generates no cardiac output, and cardiopulmonary resuscitation and
•electrical defibrillation must be performed.
•Common precipitants of ventricular fibrillation include
 Myocardial ischemia/infarction
 Heart failure
 Hypoxemia or hypercapnea
 Hypotension or shock
 Electrolyte imbalances
 Overdoses of stimulants, especially when used in combination.
•In many cases, ventricular fibrillation is preceded by ventricular tachycardia

FIRST DEGREE AV BLOCK
 The depolarisation at AV node is held up for longer than the usual.
 PR interval is longer than 0.2 seconds.
 Every QRS complex is preceded by a single P wave.
 It can also be an early sign of degenerative disease of the conduction
system or a manifestation of myocarditis or drug toxicity.
 By itself, it does not require treatment.

SECOND DEGREE AV BLOCKS
Mobitz Type 1 (Wenckebach Block)
 Almost always due to a block within the AV node.
 The delay is variable increasing with each ensuing
impulse.
 Each successive atrial impulse encounters a longer
delay in the AV node until one impulse (usually
every third or fourth) fails to make it through.

Progressive lengthening of the PR interval is seen and
then a dropped beat is seen. The sequence repeats itself,
over and over, and often with impressive regularity
Mobitz Type II Block
 Usually due to a block below the AV node.
The EKG shows two or more normal beats with
normal PR intervals and a dropped beat. The cycle is
then repeated.
 The ratio of conducted beats to nonconducted
beats is may or not be constant.
Mobitz type II block is far more serious than
type1, often signifying serious heart disease and
capable of progressing suddenly to third-degree
heart block.

THIRD DEGREE AV BLOCK
No atrial impulses at all make it through to activate the ventricles. For this
reason, it is often called complete heart block / AV dissociation.
The site of the block can be either at the AV node or lower. The ventricles
generate an escape rhythm. The atria continue to contract atria at 60 to 100
bpm and ventricles at30 to 45 bpm.
May be seen in MI / degenerative diseases / Lyme’s – reversible.

MANAGEMENT OF BLOCKS
• 1st degree
–nothing unless symptomatic and other causes of symptoms excluded
• 2nd degree (Mobitz type I)
–nothing unless symptomatic and other causes of symptoms excluded
• 2nd degree (Mobitz type II)
– pacemaker
• 3rd degree –
pacemaker

ECG.pptx electrocardiogram cardiovascular system

ECG.pptx electrocardiogram cardiovascular system

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ECG.pptx electrocardiogram cardiovascular system