3. introduction
At rest, the cells of the cardiac
conducting system and myocardium
are polarised.
A potential difference of approx. 90
mV is present between the inside of
the cell (which is negatively charged)
and the extracellular space.
A sudden shift of calcium and/or
sodium ions across the cell
membrane triggers depolarisation,
generating the electrical signal that
travels through the conducting system
and triggers contraction of myocardial
cells.
4. Depolarisation begins in a group of specialised ‘pacemaker’
cells, called the sino-atrial (SA)node, located close to the
entry of the superior vena cava into the right atrium.
A wave of depolarisation then spreads from the SA node
through the atrial myocardium.
This is seen on the ECG as the P wave .
Atrial contraction is the mechanical response to this
electrical impulse.
5. The transmission of this electrical impulse to the
ventricles occurs through specialised conducting tissue.
Firstly, there is slow conduction through the
atrioventricular (AV) node, followed by
Rapid conduction to the ventricular myocardium by
specialised conducting tissue (Purkinje fibres).
The Bundle of His carries these fibres from the AV node
and then divides into right and left bundle branches,
spreading out through the right and left ventricles
respectively.
Rapid conduction down these fibres ensures that the
ventricles contract in a co-ordinated fashion.
6. Depolarisation of the bundle of His, bundle
branches and ventricular myocardium is
seen on the ECG as the QRS complex
Ventricular contraction is the mechanical
response to this electrical impulse.
Between the P wave and QRS complex is a
small isoelectric segment, which largely
represents the delay in transmission through
the AV node.
The normal sequence of atrial depolarisation
followed by ventricular depolarisation
(P wave followed by QRS complex) is sinus
rhythm
7. The T wave, represents recovery of the
resting potential in the cells of the conducting
system and ventricular myocardium
(ventricular repolarisation).
Because the normal conducting system
transmits the depolarising impulse rapidly to
both ventricles, the normal QRS complex is of
relatively short duration (normally less than
0.12 sec).
8. When one of the bundle branches is diseased or
damaged, rapid conduction to the corresponding
ventricle is prevented.
The depolarising impulse travels more rapidly down the
other bundle branch to its ventricle and then more
slowly, through ordinary ventricular myocardium to the
other ventricle.
This situation is called bundle branch block.
Because depolarisation of both ventricles takes longer
than normal it is seen on the ECG as a broad QRS
complex (0.12 sec or longer).
9. Depolarisation
initiated in SA node
Slow conduction
through AV node
Rapid conduction
through Purkinje
fibres
Basic electrocardiography
10. P Wave : PR Interval:
Atrial depolarization Conduction time from
atrium to ventricles
QRS Complex: T Wave:
Ventricular Ventricular
depolarization. repolarization.
.
Basic electrocardiography
13. Anatomical relations of leads in a standard 12 lead
electrocardiogram
II, III, and aVF: inferior surface of the heart
V1 to V4: anterior surface
I, aVL, V5, and V6: lateral surface
V1 and aVR: right atrium and cavity of left ventricle
14. How to monitor the ECG (1):
Monitoring leads
3-lead system
approximates to I, II, III
Colour coded
Remove hair
Apply over bone
Lead setting (II)
Gain
16. Is there any electrical Activity?
What is the QRS Rate?
What is the QRS Rhythm?
What is QRS Width?
Is there P wave?
What is the relation between P & QRS?
ECG. Interpretation
20. ECG. Interpretation
Rate
If regular
________ 300____________
Number of big square bet.RR
If irregular
a) Count 30 big square
b) Count number of R waves inside 30 big square (6seconds)
c) Number of R X 10 = HR/min
21. What is the heart rate?
(300 / 6) = 50 bpm
www.uptodate.com
22. What is the heart rate?
(300 / ~ 4) = ~ 75 bpm
www.uptodate.com
24. What is the heart rate?
33 x 6 = 198 bpm
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
25. ECG. Interpretation
R Wave
Present or no,
Width must be less than 3 small square otherwise it is wide.
If R wave not present,means Asystole or VF
P Wave :
Present or no,
If no, means atrial fibrillation, junction beat or rhythm and
premature ventricular beat or rhythm.
26. ECG. Interpretation
P-R Interval: normal length 3-5 small squares.
If more than 5 means heart block.
S-T Segment: It must be iso-electric. If raised or
depressed means ischemia. To say there is S-T
Segment changes,it must be raised 1mm in limb leads or
2 mm in chest leads(v1-v6)
27. ECG. Interpretation
T Wave :
- Increase magnitude of T (hyperacute T )
- Flat T
- Inverted T
All Are Signs of Ischemia
28. What Is This Rhythm?
This is first-degree AV block.
The P-R interval is prolonged. It is 0.31 seconds.
Definition of “prolonged P-R interval” = P-R interval is equal to or greater
than 0.2 seconds.
30. Diagnosis?
Second-degree type I AV block
Progressive lengthening of the P-R interval until a P wave is NOT followed by a QRS
complex.
Atrial rhythm is regular.
Ventricular rhythm has pauses because every 4th P wave fails to conduct into the
ventricles. (4 P waves to 3 QRS complexes = a 4:3 cycle.)
Note: Progressive prolongation of the P-R interval. This means increasing conduction
delay in AV node before the non-conducted beat.
32. Diagnosis?
Second-degree type II AV block
3 conducted beats are followed by 2 non-conducted P waves.
The P-R interval of conducted beats remains constant.
Block is usually located at the level of the bundle branches.
QRS is wide because of the block location near the bundle branches.
Cause: a serious organic lesion in the conduction pathway.
Prognosis: usually poor.
High risk for complete heart block to develop.
34. What Is This Rhythm?
Third-degree AV block at the level of the AV node (supra-nodal or
supraventricular level)
Atrial rhythm is irregular due to sinus arrhythmia at a rate of 48-70 bpm.
The atrial rate = 45-70 bpm; ventricular rate = 44 bpm. There is no constant P-R
interval. The narrow QRS complex indicates that the block is occurring above the
ventricles (supraventricular) at an upper level of the AV node.
The pathology is usually
(a) increased parasympathetic tone, which can result from drug effects such as
digoxin, or -blockers; or
(b) damage to the AV node
36. Third-degree AV block
Third-degree AV block at the supra-nodal level
Third-degree AV block with a narrow junctional escape rhythm is
usually transient and associated with a favorable prognosis.
37. What Is This Rhythm?
The wide QRS indicates that the block is occurring at the ventricular level.
There is no relation between the atrial and ventricular rhythm. Ventricular
rhythm is regular and very slow (38 bpm).
The QRS is wide because block is at the bundle branch level, usually
involving both bundle branches. The ventricular pacemaker is downstream
from that level.
Damage to both bundle branches indicates extensive conduction system
disease below the AV node. This is most often caused by extensive anterior
myocardial infarction.
38. CRITERIA FOR NORMAL
ECG
Regular rhythm
Rate for adult (60-100)
R & P waves are present with normal P-R interval
(3-5 small square)
S-T segment isoelectric
T wave upright of double size P wave.
41. Cardiac Ischemia
Definition Of The Terms:
Arteriosclerosis means thickening and lost
elasticity.
Atherosclerosis means arteriosclerosis plus
irregular inner wall due to fat deposits. So blood
flow is reduced.
Coronary heart disease means coronary
atherosclerosis plus angina or history of acute
MI.
Ischemic Heart Disease is a more general term
(poor oxygen supply to the myocardium).
45. Clinical Syndromes Of
Coronary Heart Disease
Increased Myocardial Demandial O2
Demand may exceed supply capability.
Hypoxemia, shock, anemia, etc. may reduce myocardial
oxygen supply (chest pain).
Coronary artery lesion may rapidly evolve through plaque
disruption and vessel occlusion (MI)
Variable presentation, presumptive diagnosis.
Examination may be normal and nonspecific.
48. Description
A transient discomfort (which may or may not
be perceived as pain) caused by an
inadequate blood flow and oxygen delivery to
the heart muscle.
Frequently located in the center of the chest
(called precordial or substernal) but may be
more diffuse throughout the front of the chest.
49. Causes
The most frequent cause of angina is
Coronary Atherosclerosis.
Often brought on by any factor that increases the heart
rate, including
− Exercise
− Unusual exertion
− Strong emotions
− Extreme temperatures
51. Typical symptoms
Commonly lasts from 2 to 15 minutes.
Usually described as uncomfortable pressure,fullness,
squeezing, or pain in the center of the chest
May spread to one (more often the left) or both
shoulders or arms or to the neck, jaw, back, or upper
mid portion of the abdomen (epigastrium).
As the severity of the coronary narrowing increases,
the amount of exertion needed to bring on angina
decreases
53. Atypical symptoms
Women, the elderly, and persons with diabetes often
present with angina that is more diffuse in location and
vague in description than classic angina.
May include
− Shortness of breath
− Syncope
− Lightheadedness
− Weakness
− Nausea or vomiting
− Diffuse pain
54. Treatment
Usually promptly relieved by rest or nitroglycerin.
If exertional angina is not relieved by rest or (in the
case of the patient with known CHD)1 nitroglycerin
tablet in 5 minutes, emergency medical evaluation
is required.
55. Unstable Angina
Angina in the patient with known heart disease
unrelieved or worsening after
5 minutes of rest
1 nitroglycerin tablet
1 spray dose of nitroglycerin
56. Atypical
Presentations of Angina
The elderly,
Patients with diabetes,
Women
Are more likely to present with unusual,
atypical angina without classic symptoms or
with only vague nonspecific complaints.
All three groups can present with
weakness,
shortness of breath,
syncope,
lightheadedness.
57. Acute Myocardial Infarction
Severe narrowing or complete blockage of a
diseased coronary artery. It leads to injury to
myocardium then death of the muscle.
Pain is severe may occur at rest or during sleeping
May be associated with nausea and sweating.
Pain may be atypical not relieved by rest or nitroglycerine.
59. Precipitating Events of
Heart Attack
Heart attack can occur under a wide variety of
circumstances:
Most episodes of acute coronary syndromes occur at rest
or with modest daily activity.
Heavy physical exertion is a precipitating event in a minority
of patients, perhaps 10% to 15%.
Life events with a powerful personal impact (for example,
the death of a spouse or other loved one, divorce, or loss
of job) are commonly observed before heart attack and
may be correlated.
Illicit drugs such as cocaine have clearly been shown to
cause heart attacks and ventricular arrhythmias.
60. Denial: The Deadly Response to
Heart Attack
Victims of heart attack frequently deny the possibility of
a heart attack with rationalizations such as the following:
It’s indigestion or something I ate.
It can’t happen to me. I’m too healthy.
I don’t want to bother my doctor.
I don’t want to frighten anyone.
I’ll use a home remedy.
I’ll feel ridiculous if it isn’t a heart attack.
62. The Psychology of Denial of Heart
Attack
Denial is a common reaction to emergencies such as heart attack.
The victim’s first tendency may be to deny the possibility of a heart
attack.
This denial is not limited to the victim — it may also persuade the
rescuer !!!!!.
The tendency of people involved in an emergency to deny or
downplay the serious nature of the presenting problem is a natural
one that must be overcome to provide rapid intervention and
maximize the victim’s chance of survival.
Denial of the serious nature of the symptoms delays treatment and
increases the risk of death.
The elderly, women, and persons with diabetes, hypertension, or
known CHD are most likely to delay calling the EMS system.
63. Acute Myocardial Infarction
Usually lasts for more than 15 min.
It may show signs of complications
( Hypotension, Bradycardia, Arrhythmia, Heart Failure ).
Sudden Cardiac Death (cardiac arrest), in 80% is due to
Ventricular Fibrillation, 15% Asystole and 5% Pulseless
Electrical Activity.
Cardiac enzymes : CK rises 4-6 hours after infarction, CK-
MB more specific. SGOT and LDH will rise later on.
Echocardiogram.
ECG FINDINGS
64. ECG FINDINGS
T wave changes : hyperacute, Flat, Inverted
S-T segment: elevated or depressed
Q wave: It is significant if it is more than 1 mm depth & width.
67. 12-Lead ECG Variations
in AMI and Angina
Baseline
Ischemia—tall or inverted T wave (infarct),
ST segment may be depressed (angina)
Injury—elevated ST segment, T wave
may invert
Infarction (Acute)—abnormal Q wave,
ST segment may be elevated and T wave
may be inverted
Infarction (Age Unknown)—abnormal Q wave,
ST segment and T wave returned to normal
68. Recognition of AMI
Know what to look for:
ST elevation >1 mm
3 contiguous leads
Know where to look
PT baseline
ST-segment deviation
= 4.5 mm
J point plus
0.04 second
73. Summary Of Ischaemic
Changes
Lead II, III, aVF Inferior ischaemia
Lead I, aVL ,V5, V6 Lateral ischemia
Lead V1 ,V4 Antero-lateral isch.
Lead V1,V6 Extensive anterior
77. Ventricular Tachycardia
P-waves / PR-interval
Do not exist, VENTRICULAR rhythm
QRS complex
Wide, dependent on focus
>0.12 seconds
Shockable
(VT)
78. Ventricular Fibrillation
Course vs. Fine
Remember to check patient & electrodes
VF is a lethal arrhythmia
May be secondary to hypoxia or may occur as sudden
onset
Shockable
(VF)
79.
80. Asystole (Cardiac Standstill)
Careful to check device, cables, patient, gain / sensitivity,
lead select, fine VF
Non-shockable
Asystole
Absent ventricular (QRS) activity
Atrial activity (P waves) may persist
Rarely a straight line trace
Treat fine VF as asystole
81. Asystole
Check 2 on patient:
Pulse.
Electrodes
Check 2 on monitor:
Leads (change lead)
Gain (increase QRS
size)
82. Pulseless Electrical Activity (PEA )
(Electromechanical Dissociation)
Presence of electrical complexes
No mechanical contraction of the heart
Usually b/c profound metabolic abnormality
No clearly beneficial therapy
CPR and check for reversible causes is mainstay of
treatment
Non-shockable
(PEA)
83.
84. During CPR:
Correct reversible causes
Check electrode position and contact
Attempt / verify:
IV access
airway and oxygen
Give uninterrupted compressions
when airway secure
Give adrenaline every 3-5 min
Consider: amiodarone, atropine,
magnesium
Pulseless Electrical Activity (PEA )
(Electromechanical Dissociation)
86. Management of Ischemic
Attack
Complete bed rest
Investigations ECG,CBC,BloodChemistry ,Troponin
( Cardiac enzymes), Chest X-rays.
O2 supply 2-5 L/min through nasal cannula or face mask.
Aspirin 300mg. to be chewed.
Isordil 5mg. sublingual 3x , 3-5 min apart.
Nitroglycerin infusion start by 0.5mg/h. if SBP above
90mmHg.
Morphine 3-5mg. IV if pain still severe.
87. Options for early reperfusion therapy
Percutaneous coronary intervention (PCI)
Thrombolytic drugs in absence of contra-indications.
Infuse Streptokinase 1.5 million units over 30 min.****
Treat complications ( Arrhythmia, Heart Failure,
Bradycardia , shock)
Transfer to coronary care unit.
Coronary angiography and intervention in many
patients
Management of Ischemic
Attack
88. ****
Absolute contraindications
to Thrombolytic therapy
Previous haemorrhagic stroke
Other stroke or CVA within 6 months
CNS damage or neoplasm
Active internal bleeding
Aortic dissection
Recent major surgery or trauma
Known bleeding disorder
92. Perform CPR at all times for pulseless
patients
Defibrillate VF/VT until it is no longer
present
Gain airway control and provide adequate
oxygenation and ventilation
Give IV boluses of epinephrine
Correct reversible causes
In Summary
