ECG Monitoring (Basic of ECG)

Nr.M.GAJENDRAN,
MBA(H.M),MSc. Nursing.

 An ECG is a simple, noninvasive procedure; used to record the electrical
activity of the heart. Abbreviated as ECG and EKG. Electrodes are placed
on the skin of the chest and that, measures electrical activity all over the
heart.

 Electrocardiogram records the electrical signals in your heart. It's a
common test used to detect heart problems and monitor the heart's
status in many situations.
 also called ECG or EKGs
 ECG is a noninvasive, painless test with quick results. During an
ECG, sensors (electrodes) that can detect the electrical activity of
heart are attached to chest and sometimes on limbs.

 P wave
 P wave should be always before QRS complex, separated by PQ
interval. P wave is a sign of normal atrial depolarization.
 Parameters:
 duration: 110 ms; >/ 0.11 sec
 amplitude: 0.25 mV;
 positivity:
 positive − always in leads I and II;
 negative − always in aVR lead.

•The QRS complex indicates ventricular depolarization. The
QRS interval is measured from the end of the PR interval to the
end of the S.
• Duration less than or equal to 0.12 seconds, amplitude greater
than 0.5 mV in at least one standard lead, and greater than 1.0
mV in at least one precordial lead.
•Upper limit of normal amplitude is 2.5 - 3.0 mV.
small septal Q waves in I, aVL, V5 and V6 (duration less than or
equal to 0.04 seconds; amplitude less than 1/3 of the amplitude
of the R wave in the same lead).

 ST Segment
 ST segment is iso electric line, period of no electrical activity of the heart.
Should be in the same level as PQ interval. Every elevation or depression of
this line is pathological.
 Physiological duration is 320 ms.
 T Wave
 T wave represents repolarization of ventricles.]
 Normally rounded and asymmetrical,
 should be upright in leads V2 - V6, inverted in aVR
 amplitude of at least 0.2 mV in leads V3 and V4 and at least 0.1 mV in leads V5
and V6
 Physiological duration 160 ms.
 U Wave
 The U wave is ordinarily small and follows T wave and usually has the same
polarity as T wave.[1]

 P-R interval = 0.12 - 0.20 sec (3 - 5 small squares)
 QRS width = 0.08 - 0.12 sec (2 - 3 small squares)
 Q-T interval 0.35 - 0.43 sec

 PQ Interval
 PQ interval is a period of atrial contraction. The depolarization is
delayed in AV node.
 Parameters: duration: 120−200 ms
 PR interval:The PR Interval indicates atrioventricular conduction time.
The interval is measured from where the P wave begins until the
beginning of the QRS complex.
 0.12 and 0.20 seconds. The P-R interval should be between 120-200
ms (3-5 small squares)

 Durations normally less than or equal to 0.40 seconds for males and 0.44
seconds for females.
 The QT interval indicates ventricular activity, both depolarization and
repolarization. Measure the QT interval from the beginning of the QRS
complex to the end of the T wave.

Einthoven’s Law explains that Lead II’s complex
is equal to the sum of the corresponding
complexes in Leads I and III and is given as II =
I + III

 Heart rate
 Count the number of large squares present within one R-R interval
 Divide 300 by this number to calculate the heart rate

 Heart rate
 Heart rhythm
 Cardiac axis
 P-waves
 P-R interval
 QRS complex
 ST segment
 T waves
 standardization

 Sinus bradycardia
 Sinus tachycardia
 Premature atrial contraction
 Paroxysmal supraventricular tachycardia
 Atrial flutter
 Atrial fibrillation
 Junctional Dysrhythmias
 First degree AV block

 Second degree AV block, type1
 Second degree AV block , type 2
 Third degree AV block
 Premature ventricular contraction
 Ventricular tachycardia
 Ventricular fibrillation
 Asystole
 Pulseless electrical activity

 In sinus bradycardia the condition pathway is the same as that in sinus
rhythm but the SA node fires at a rate less than 60b/min .
 Symptomatic bradycardia refers to an HR that is less than 60 b/min and is
inadequate for the patient’s condition , causing the patient to experience
symptoms (eg chest pain, syncope)

 Sinus bradycardia may be a normal sinus rhythm in aerobically trained
athletes and in some people during sleep.
 It also occurs in response to carotid massage, Valsalva maneuver,
hypothermia , increased intraocular pressure, vagal stimulation , and
administration of certain drugs .
 Hypothyroidism , increased intracranial pressure, hypoglycemia and
inferior myocardial infarction.

 In sinus bradycardia, HR is less than 60 beats/min and the rhythm is
regular.
 The p wave precedes each QRS complex and has a normal shape and
duration.
 The PR interval is normal, and the QRS complex has a normal shape and
duration .
CLINICAL SIGNIFICANCE:
Signs of symptomatic bradycardia include
 pale,
 cool skin,

 hypotension ,
 weakness,
 angina,
 dizziness or syncope,
 confusion,
 disorientation and
 shortness of breath

 Atropine (An anticholinergic drug)
 Transcutaneous pacing
 Dopamine or epinephrine infusion
 Permanent pacemaker therapy may be needed.

 The condition pathway is the same in sinus tachycardia as that in normal
sinus rhythm .
 The discharge rate from the sinus node increases because of vagal
inhibition or sympathetic stimulation.
 The sinus rate is 101 to 200 b/min .
 CLINICAL ASSOCIATION :
 Physiologic and psychologic stressors such as
 Exercise
 fever

 Pain
 Hypotension
 Hypovolemia
 Anemia
 Hypoxia
 Hypoglycemia
 Myocardial ischemia
 Heart failure
 hyperthyroidism

 Anxiety
 Fear
 It also be effect of drugs such as
 Epinephrine
 Norepinephrine
 Atropine
 Caffeine
 Theophylline or
 Hydralazine
 In addition , many over-the – counter cold remedies have active
ingredients ( pseudoephedrine) that cause tachycardia.

 In sinus tachycardia HR is 101 to 200 b/min and the rhythm is regular.
 The p wave is normal , precedes each QRS complex , and has a normal
shape and duration .
 The PR interval is normal, and the QRS complex has a normal shape and
duration.
 CLINICAL SIGNIFICANCE:
 Dizziness
 DYSPNEA
 Hypotension because of decreased CO.

 Increased myocardial oxygen consumption is associated with an
increased HR.
 Angina or an increase in infarction size may accompany sinus
tachycardia in patient with CAD or acute MI.
 TREATMENT:
 Vagal maneuver
 IV beta adrenergic blockers(metoprolol)
 Adenosine
 Calcium channel blockers( diltiazem)
 Synchronized cardioversion

 PAC is a contraction starting from an ectopic focus in the atrium (eg
location other than SA node ) and coming sooner than the next expected
sinus beat.
 The ectopic signal starts in the left or right atrium and travels across the
atria by an abnormal pathway.
 This creates a distorted P wave .
 At the AV node it , it may be stopped ( nonconducted PAC) , delayed
(lengthened PR interval ) or conducted normally.
 If the signal moves through the AV node , In most cases it is conducted
normally through the ventricles.

 EMOTIONAL STRESS or physical fatigue or from the use of caffeine,
tobacco , or alcohol
 Hypoxia
 Electrolyte imbalance
 Hyperthyroidism
 COPD
 CAD and
 Valvular disease

 RHYTHM is irregular
 The P wave has a different shape from that of a P wave originating in the
SA node, or it may be hidden in the preceding T wave.
 The PR interval may be shorter or longer than the PR interval coming
from the SA node , but it is within normal limits.
 The QRS complex is usually normal
 If the QRS interval is 0.12 second or more , abnormal conduction through
the ventricles occurs.

 Patient may report palpitations or a sense that their hearts “skipped a beat
.”
 In person with heart disease , frequent PACs may indicate enhanced
automaticity of the atria or a re-entry mechanism.
 Such PACs may warn of or start more serious dysrhythmias ( eg,
supraventricular tachycardia)
TREATMENT :
 Withdrawal of sources of stimulation such as caffeine or
sympathomimetic drugs may be needed.
 Beta adrenergic blockers may be used to decrease PACs.

 PSVT is a dysrhythmia starting in an ectopic focus anywhere above the
bifurcation of the bundle of His .
 Identification of the ectopic focus is often difficult even with a 12-lead ECG
,
 PSVT occurs because of a re-entrant phenomenon (reexcitation of the
atria when there is a one-way block).
 Usually a PAC triggers a run of repeated premature beats.
 Paroxysmal refers to an abrupt onset and ending .
 Termination is sometimes followed by a brief period of asystole(absence
of all cardiac electrical activity).

 some degree of AV block may be present.
 PSVT can occur in the presence of Wolff-Parkinson –white syndrome,
or “preexcitation”.
 In this syndrome , there is extra conduction or accessory pathways.
 CLINICAL ASSOCIATION:
 Overexertion
 Emotional stress
 Deep inspiration
 Stimulants such as caffeine and tobacco
 PSVT is also associated with rheumatic heart disease
 Digitalis toxicity
 CAD and corpulmonale

 In PSVT the HR is 150 to 220 b/min , and the rhythm is regular or
slightly irregular.
 The P wave is often hidden in the preceding T wave
 If seen, it may have an abnormal shape.
 The PR interval may be shortened or normal, and the QRS complex is
usually normal.
 CLINICAL SIGNIFICANCE:
 A prolonged episode and HR greater than 180 b/min will cause
decreased CO because of Reduced stroke volume
 Symptoms often include hypotension
 Palpitations
 Dyspnea
 Angina

 PSVT includes vagal stimulation and drug therapy.
 Common vagal maneuvers include Valsalva , carotid massage and
coughing.
 IV adenosine is the drug of choice to convert PSVT to a normal sinus
rhythm .
 This drug has a short half-life (10 second) and is well tolerated .
 IV beta adrenergic blockers , calcium channel blockers ,and amiodarone
can also be used.
 If vagal stimulation and drug therapy are ineffective and the patient
becomes hemodynamically unstable , synchronized cardioversion is used.

 Injection site should be as close to the heart as possible (eg antecubital
area)
 Give IV dose rapidly (over 1-2 sec) and follow with a rapid 20ml normal
saline flush .
 Monitor patient ECG continuously .
 Brief period of asystole is common.
 Observe patient for flushing ,dizziness , chest pain, or palpitations.

 AF is an atrial tachydysrhythmia identified by recurring, regular,
sawtooth –shaped flutter waves that originate from a single ectopic
focus in the right atrium or less commonly , the left atrium.
 CLINICAL ASSOCIATIONS :
 Associated with CAD
 Hypertension
 Mitral valve disorders
 Pulmonary embolus
 Chronic lung disease
 Cor pulmonale
 cardiomyopathy

 Hyperthyroidism
 The use of drug such as digoxin
 Quinidine
 Epinephrine
 ECG CHARACTERISTICS :
 Atrial rate is 200 to 350 b/min .
 The ventricular rate varies based on the conduction ratio .
 In 2:1 conduction , the ventricular rate is typically found to be
approximately 150 b/min.

 Atrial rhythm is regular , and ventricular rhythm is usually regular.
 The atrial flutter waves represent atrial depolarization followed by
repolarization.
 The PR interval is variable and not measurable .
 The QRS complex is usually normal.
 Because the AV NODE can delay signals from the atria , there is usually
some AV block in a fixed ratio of flutter waves to QRS complex

 The high ventricular rates (greater than 100 b/min) and loss of the atrial
“kick”(atrial contraction reflected by a sinus P wave) that are associated
with atrial flutter decrease CO.
 This can cause serious consequences such as HF, especially in the patient
with underlying heart disease .
 Patients with atrial flutter have an increased risk of stroke because of the
risk of thrombus formation in the atria from the stasis of blood.
 Warfarin is given to prevent stroke in patients who have atrial flutter.

 The primary goal in treatment of AF is to slow the ventricular response by
increasing AV block.
 Drugs used to control ventricular rate include calcium channel blockers
and beta adrenergic blockers .
 Electrical cardio version can be performed when the patient is clinically
unstable.
 Antidysrhythmia drugs are used to convert AF to sinus rhythm( eg
amiodarone, flecainide , dronedarone) .
 Radiofrequency catheter ablation is the treatment of choice for AF.

 AF is characterized by a total disorganization of atrial electrical activity
because of multiple ectopic foci, resulting in loss of effective atrial
contraction.
 The dysrhythmia may be paroxysmal ( eg beginning and ending
spontaneously ) or persistent ( lasting more than 7 days ).
 AF usually occurs in underlying heart disease such as CAD , valvular
heart disease , HF , cardiomyopathy , hypertensive heart disease , and
pericarditis.
 It often develop acutely with thyrotoxicosis , alcohol intoxication ,
caffeine , electrolyte imbalance , stress and cardiac surgery

 During AF , the atrial rate may be as high as 350 to 600 b/min .
 P wave are replaced by chaotic , fibrillatory waves.
 Ventricular rate varies , and the rhythm is usually irregular .
 When the ventricular rate is between 60 and 100 b/min , it is AF with a
controlled ventricular response.
 The PR interval is not measurable and the QRS complex usually has a
normal shape and duration .

 A result in a decrease in CO because of ineffective atrial contraction or
rapid ventricular response.
 Thrombi (clots ) form in the atria because of blood stasis.
 An embolized clot may develop and move to the brain , causing a stroke.
 TREATMENT :
 The goal of treatment include a decrease in ventricular response ( to less
than 100 b/min) , prevention of stroke , conversion of sinus rhythm.
 Drugs are used to control include calcium channel blockers , beta
adrenergic blockers ( eg metoprolol, digoxin)

 For some patients, pharmacologic or electrical conversion of AF to a
normal sinus rhythm may be considered (eg reduced exercise tolerance
with rate control drugs, contraindication to warfarin).
 The most common antidysrhythmia drugs used for conversion to and
maintenance of sinus rhythm include amiodarone and ibutilide.
 If a patient is in atrial fibrillation for longer than 48 hours,
anticoagulation therapy with warfarin is needed for 3 to 4 weeks before
the cardioversion and for several weeks after successful cardioversion.
 Anticoagulation therapy is necessary because the procedure can cause
the clots to dislodge, placing the patient at risk for stroke.
 A transesophageal ECG may be performed to rule out clots in the atria.
 If no clots are present , anticoagulation therapy may not be required
before the cardioversion procedure.

 If drug or cardioversion does not convert AF to normal sinus rhythm ,
long term anticoagulation therapy is required.
 Warfarin is the drug of choice , and patients are monitored for
therapeutic levels (eg INR).
 Recently , alternatives to warfarin have been approved for
anticoagulation therapy in patients with nonvalvular atrial fibrillation.
 These drugs do not require routine laboratory testing and include
dabigatran , apixaban, rivaroxaban.
 The maze procedure is a surgical intervention that stops atrial
fibrillation by interrupting the ectopic electrical signals that are
responsible for the dysrhythmia.
 Incisions are made in both atria, and cryoablation (cold therapy) is
used to stop the formation and conduction of these signals and restore
normal sinus rhythm.

 Junctional dysrhythmias refer to dysrhythmias that start in the area of the
AV node.
 They result because the SA node fails to fire or the signal is blocked.
 When this occurs , the AV node becomes the pacemaker of the heart .
 The impulse from the AV node usually move in a retrograde (backward )
fashion.
 This procedure an abnormal P wave that occurs just before or after the
QRS complex or that is hidden in the QRS complex.
 The impulse usually moves normally through the ventricles.

 Junctional premature beats may occur , and they are treated in a manner
similar to that for PACs .
 Other junctional dysrhythmias include junctional escape rhythm
accelerated junctional rhythm , and junctional tachycardia.
 Junctional dysrhythmias are often associated with CAD , HF ,
cardiomyopathy, electrolyte imbalance ,inferior MI , and rheumatic heart
disease.
 Certain drugs ( eg digoxin, nicotine, amphetamines, caffeine) can also
cause junctional drsrhythmias.

 In junctional escape rhythm the HR is 40 to 60 beats/min
 It is 61 to 100 b/min in accelerated junctional rhythm and 101 to 180 b/min
in junctional tachycardia.
 Rhythm is regular.
 The p wave is abnormal in shape and inverted, or it may be hidden in the
QRS complex .
 The PR interval is less than 0.12 sec when the p wave precedes the QRS
complex .
 The QRS complex is usually normal.

 Junctional escape rhythm serve as a safety mechanism when the SA node
has not been effective.
 Escape rhythm such as this should not be suppressed.
 Accelerated junctional rhythm is due to sympathetic stimulation to
improve CO.
 Junctional tachycardia indicates a more serious problem.
 This rhythm may reduce CO , causing the patient to become
hemodynamically unstable (eg hypotensive).

 If a patient has symptoms with a junctional escape rhythm , atropine can
be used.
 In accelerated junctional rhythm and junctional tachycardia caused by
drug toxicity, the drug is stopped .
 In the absence of digitalis toxicity, beta adrenergic blockers , calcium
channel blockers ,and amiodarone are used for rate control.
 Cardioversion should not be used .

 First degree AV block is a type of AV block in which every impulse is
conducted to the ventricles but the time of AV conduction is prolonged.
 After the impulse moves through the AV node , the ventricles usually
respond normally.
 First –degree AV block is associated with MI, CAD, rheumatic fever,
hyperthyroidism , electrolyte imbalance(eg hypokalemia), vagal
stimulation and drug such as digoxin, ,beta adrenergic blockers, calcium
channel blockers and flecainide.

 HR is normal and rhythm is regular .
 The P wave is normal, the PR interval is prolonged (greater than 0.20
second) and the QRS complex usually has a normal shape and duration .
 CLINICAL SIGNIFICANCE :
 Is not usually not serious but can be a sign of higher degrees of AV block .
 Patients with first degree AV block are asymptomatic

 There is no treatment for first degree AV block.
 Changes to potentially causative situations may be considered.
 Monitor patients for any new changes in heart rhythm (eg more serious
AV block)

 Mobitz 1 or wenckebach heart block include a gradual lengthening of the
PR interval.
 It occurs because of a prolonged AV conduction time until an atrial
impulse is nonconducted and a QRS complex is blocked.
 Type 1 AV block most commonly occurs in the AV node, but it can also
occurs in the His-purkinje system.
 CLINICAL ASSOCIATION
 Type 1 AV block may result from drugs such as digoxin or β-adrenergic
blockers .
 It may also associated with CAD and other disease that can slow AV
conduction.

 Atrial rate is normal , but ventricular rate may be slower because of
nonconducted or blocked QRS complex resulting in bradycardia.
 Once a ventricular beat is blocked , the cycle repeats itself with
progressive lengthening of the PR interval until another QRS complex is
blocked.
 Ventricular rhythm is irregular .
 The P wave has a normal shape .
 The QRS complex has a normal shape and duration .

 Type 1 AV block is usually a result of myocardial ischemia or inferior MI.
 In some patients ( eg acute MI) it may be a warning sign of a more serious
AV conduction disturbance (eg complete heart block )
 TREATMENT :
 If the patient is symptomatic , atropine is used to increase HR or a
temporary pacemaker may be needed , especially if the patient has had an
MI.
 If the patient is asymptomatic the rhythm is closely observed with a
transcutaneous pacemaker on standby .
 Bradycardia is more likely to become symptomatic when hypotension , HF
or shock is present.

 Mobitz 2 heart block a P wave is nonconducted without progressive PR
lengthening .
 This usually occurs when a block in one of the bundle branches is present.
 In which certain number of impulses from the SA node are not conducted
to the ventricles.
 This occurs the ratio 2:1,3:1, and so on (eg two P waves to one QRS complex
, three P waves to one QRS complex) .
 It may occurs with varying ratio .

 TYPE 2 AV block is associated with
 Rheumatic heart disease
 CAD
 Anterior MI
 Drug toxicity

 Ventricular rhythm may be irregular .
 The PR interval may be normal or prolonged in duration and remains
constant on conducted beats.
 The QRS complex is usually greater than 0.12 second because of bundle
branch block.
 Often progress to 3rd degree AV block associated with poor prognosis.
 Reduced HR frequently results in decreased CO with subsequent

 Hypotension and myocardial ischemia.
 Type 2 AV block is an indication for therapy with a permanent pacemaker.
 Treatment :
 Temporary pacemaker necessary before the insertion of a permanent
pacemaker.
 If the patient become symptomatic ( hypotension , angina)

 or complete heart block , constitutes one form of AV dissociation in
which no impulses from the atria are conducted to the ventricles.
 The atria are stimulated and contract independently of the ventricles.
 The ventricular rhythm is an escape rhythm , and the ectopic pacemaker
may be above or below the bifurcation of the bundle of His .
 Severe heart disease including
 CAD
 MI

 Myocarditis
 Cardiomyopathy
 Systemic disease such as
 Amyloidosis
 Scleroderma
 Drugs can cause AV block
 Digoxin
 β-adrenergic blockers
 Calcium channel blockers

 The atrial rate is usually a sinus rate of 60 to 100 b/min.
 If it is in the AV node, the rate is 40 to 60 b/min, and if it is in the His –
purkinje system , it is 20 to 40 b/min.
 The PR interval is variable , and other is no relationship between the P
wave and QRS complex.
 Reduced CO with subsequent ischemia
 HF

 Shock
 Syncope
 Bradycardia
 Even period of asystole
 TREATMENT :
 Atropine
 Dopamine
 Epinephrine (temporary measures to increase HR and BP)
 Patient need a permanent pacemaker as soon as possible.

 PVC is a contraction coming from an ectopic focus in the ventricles.
 It is the premature (early) occurrence of a QRS complex .
 A PVC is wide and distorted in shape compared with a QRS complex
coming down the normal conduction pathway.
 PVCs that arise from different foci appear different in shape from each
other and are called multifocal PVCs .
 PVCs that have the same shape are called unifocal PVCs
 When every other beat is a PVC , the rhythm is called ventricular
bigeminy.

 When every third beat is a PVC , it is called ventricular trigeminy.
 Two consecutive PVCs are called a couplet.
 VT occurs when there are three or more consecutive PVCs .
 R-on-T phenomenon occurs when a PVC falls on the T wave of a preceding
beat .
 This is especially dangerous because the PVC is firing during the relative
refractory phase of ventricular repolarization .
 Excitability cardiac cells increase during this time , and the risk for the
PVC to start VT or ventricular fibrillation is great

 PVCs are associated with stimulant
 Caffeine
 Alcohol
 Nicotine
 Aminophylline
 Epinephrine
 Isoproterenol
 digoxin

 Electrolyte imbalances
 Hypoxia
 Fever
 Exercise
 Emotional stress
 Disease states associated with PVCs include
 MI
 Mitral valve prolapse
 HF
 CAD

 HR varies according to intrinsic rate and number of PVCs.
 Rhythm is irregular because of premature beats.
 The P wave is rarely visible and is usually lost in the QRS complex of the
PVC .
 Retrograde conduction may occur, and the P wave may be seen after the
ectopic beat.
 The PR interval is not measurable
 The QRS complex is wide and distorted in shape, lasting more than 0.12
sec .
 The T wave is generally large and opposite in direction to the major
direction of the QRS complex

 In heart disease , PVCs may reduce the CO and lead to angina and HF
depending on frequency.
 Because PVCs in CAD or acute MI indicate ventricular irritability ,
assess the patients physiologic response to PVCs.
 TREATMENT :
 OXYGEN therapy for hypoxia
 Electrolyte replacement
 Assessment of the patients hemodynamic status
 β adrenergic blockers
 Procainamide
 amiodarone

 It occurs when an ectopic focus or foci fire repeatedly and the ventricles
takes control as the pacemaker.
 Different forms of VT exist , depending on QRS configuration.
 Monomorphic VT has QRS complexes that are the same in shape, size,
and direction.
 Polymorphic VT occurs when the QRS complexes gradually change back
and forth from one shape , size, and direction to another over a series of
beat.
 Polymorphic VT associated with a prolonged QT interval .

 VT may be sustained (longer than 30 sec) or nonsustained (less than 30
sec ).
 The development of VT is an ominous sign
 It is a life-threatening dysrhythmia because of decreased CO and the
possibility of development of VF , which is lethal
 VT associated with
 MI
 CAD

 Significant electrolyte imbalances,
 cardiomyopathy,
 mitral valve prolapse
 Long QT syndrome
 Drug toxicity
 Central nervous system disorder
 Can be seen in patient who have no evidence of cardiac disease.

 Ventricular rate is 150 to 250 b/min
 Rhythm may be regular or irregular
 AV dissociation may be present , with P wave occurring independently of
the QRS complex.
 The atria may be depolarized by the ventricles in a retrograde fashion.
 The P wave is usually buried in the QRS complex , and the PR interval is
not measurable.
 The QRS complex is distorted in appearance and wide ( greater than 0.12
sec in duration )
 The T wave is in the opposite direction of the QRS complex

 VT can be stable( patient has a pulse )
 Unstable ( patient is pulseless )
 Sustained VT causes a severe decrease in CO because of decreased
ventricular diastolic filling times and loss of atrial contraction.
 Hypotension
 Pulmonary edema
 Decreased cerebral blood flow
 Cardiopulmonary arrest

 If the VT is monomorphic and the patient is clinically stable (eg pulse is
present) and has preserved left ventricular function
 IV procainamide, sotalol, amiodarone is used
 These drugs can also be used if the VT is polymorphic with a normal
baseline QT interval
 Polymorphic VT with a prolonged baseline QT interval is treated with IV
magnesium, isoproterenol , phenytoin .
 Drugs that prolong the QT interval ( eg dofetilide ) should be
discontinued.

 VT without a pulse is a life-threatening situation .
 It is treated in the same manner as VF
 CPR and rapid defibrillation are the first line of treatment ,followed by
the administration of vasopressors ( epinephrine ) and
antidysrhythmics ( eg amiodarone ) if defibrillation is unsuccessful.
 An accelerated idioventricular rhythm (AIVR) can develop when the
intrinsic pacemaker rate ( SA node or AV node ) becomes less than that
of a ventricular ectopic pacemaker.
 The rate is between 40 to 100 b/ min .
 Commonly associated with acute MI and reperfusion of the
myocardium after thrombolytic therapy or angioplasty of coronary
arteries

 Is a severe derangement of the heart rhythm characterized on ECG by
irregular waveforms of varying shapes and amplitude.
 This represents the firing of multiple ectopic foci in the ventricle.
 Mechanically the ventricle is simply “quivering” with no effective
contraction , and consequently no CO occurs.
 VF is a lethal dysrhythmia.
 Occurs in acute MI and myocardial ischemia and in chronic disease such
as HF and cardiomyopathy

 It may occur during cardiac pacing or cardiac catheterization procedure
because of catheter stimulation of the ventricles.
 Electric shock
 Hyperkalemia
 Hypoxemia
 Acidosis
 Drug toxicity

 HR is not measurable .
 Rhythm is irregular and chaotic.
 The P wave is not visible , and the PR interval and the QRS interval are
not measurable.
 VF result in an unresponsive , pulseless, and apneic state.
 if it is not rapidly treated the patient will not recover.

 CPR and ACLS with the use of defibrillation and definite drug therapy (eg
epinephrine , vasopressin )
 There should be no delay in using a defibrillator once available

 Asystole represents the total absents of ventricular electrical activity
 Occasionally P waves are seen
 No ventricular contraction occurs because depolarization does not occur
 Patient are unresponsive, pulseless, apneic
 Asystole is the lethal dysrhythmia that require immediate treatment
 VF may masquerade as Asystole
 Always assess the rhythm in more than one lead

 Asystole is usually a result of advance cardiac disease, a severe cardiac
conduction system disturbance or end stage HF
Clinical significance
 Generally the patient with Asystole has end stage HD or has a prolonged
arrest and cannot be resuscitated
Treatment
 CPR with initiation of ACLS measures
 This include definitive drug therapy with Epinephrine and/or Vasopressin
and intubation

 The PEA is a situation in which organized electrical activity is seen on the
ECG but there is no mechanical activity of the ventricles and the patient
has no pulse
 It is most common dysrhythmias seen after defibrillation
 Prognosis poor unless the underline causes quickly identified and treated

 The most common lying cause of
PEA include,
 hypovolemia
 Hypoxia
 Metabolic acidosis
 Hyperkalemia
 Hypokalemia
 Hypoglycemia
 Hypothermia
 Toxins
 Cardiac tamponade
 Thrombosis
 Tension pneumothorax
 Trauma

 Treatment begins with CPR followed by drug therapy Ex: Epinephrine and
intubation

 The sudden cardiac death refers to death from a cardiac cause
 Most SCD result from ventricular dysrhythmias, specifically VT, VF

 Defibrilation is the treatment of choice to end VF and pulseless VT
 Rapid defibrillation within 2 minutes is critical to a successful patient
outcomes
 Defibrilation involves the passage of an electric shock through the heart to
depolarise the cell of the myocardium
Goal
Following repolarization of myocardial cells will allow the SA node to
resume the role of pace maker

Monophasic
 It deliver energy in one direction
 Initial shock with 360 joules
Biphasic
 Deliver energy in 2 direction
 Deliver successful shocks at lower
energies (120-200 joules)and with
fewer post shock ECG
abnormalities than monophasic
defibrillators

 Hand-free multifunction defibrillator pads are available and are placed on
the chest
 Connect cable form the pads to the defibrillator
 Charge and discharge the defibrillator using buttons on the defibrillator
 All personals are clear before discharging the defibrillator

 Synchronized cardioversion is the therapy of choice for the patient
with ventricular tachydysrhythmias ( eg VT with pulse) or
supraventricular tachydysrhythmias ( eg atrial fibrillation with a rapid
ventricular response)
 A synchronized circuit in the defibrillator delivers a shock that is
programmed to occur on the R wave of the QRS complex of the ECG.
 If synchronized cardioversion is done on a nonemergency basis (the
patient is awake and hemodynamically stable), the patient is sedated (
IV midazolam) before the procedure.
 If a patient with supraventricular tachycardia or VT with a pulse
becomes hemodynamically unstable , synchronized cardioversion
should be performed as quickly as possible

 Start the initial energy for synchronized cardioversion at 50 to 100 joules (
biphasic defibrillator) and 100 joules ( monophasic defibrillator ) and
increase if needed.
 If the patient become pulseless or the rhythm changes to VF , turn the
synchronizer switch off and performed defibrillation.

 The implantable cardioverter defibrillator is an important technology for
patients who
1. Have survived SCD
2. Have spontaneous sustained VT
3. Have syncope with inducible VT or VF during EPS
4. Are at high risk for future life threatening dysrhythmias ( eg have
cardiomyopathy)
The ICD consists of a lead system placed via subclavian vein to the
endocardium

 A battery powered pulse generator is implanted subcutaneously , usually
over the pectoral muscle on the patient nondominant side.
 The pulse generator is similar in size to a pacemaker
 The ICD sensing system monitors the HR and rhythm identifies VT or VF
 After sensing system detects a lethal dysrhythmias , the device delivers 25
joules or less shock to the patient heart
 If the first shock is unsuccessful , the device recycles and can continue to
deliver shocks.
 These device use algorithms that detect dysrhythmia and determine the
appropriate response.

 They also provide backup pacing for bradydysrthmias that may occur after
defribrillation.
 Preprocedure and postprocedure nursing care of the patient undergoing
ICD placement is similar to the care of a patient undergoing permanent
pacemaker implantation.
 Leaflet

 Use electrical energy to” burn” or ablate areas of the conduction system as
definite treatment of tachydysrhythmias .
 Ablation therapy is done after EPS has identified the sources of the
dysrhythmia .
 An electrode tipped ablation catheter ablates accessory pathways or
ectopic sites in the atria, the AV NODE ,and the ventricles.
 Catheter ablation is considered the nonpharmacologic treatment of
choice for atrial dysrhythmias resulting in rapid ventricular rates and AV
nodal re-entrant tachycardia refractory to drug therapy

ECG Monitoring (Basic of ECG)

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