ECG on ST segement elevations

1. ST Segment Elevations : Always a
marker of myocardial infarction ?
Review article
Chairperson :Prof. DR. Chandrasekhara .P
M.V.J.Medical College & R.H.
By: Dr. M. Ramesh Babu

2. About journal
• Indian heart journal .
• Volume 65,Number 4, july-august 2013.
• G. Coppola a, P. Carita` a, E. Corrado a, A.
Borrelli b, A. Rotolo a, M. Guglielmo a, C.
Nugara a, L. Ajello a,*, M. Santomauro c, S.
Novo a .
• on behalf of the Italian Study Group of
Cardiovascular Emergencies of the Italian Society
of Cardiology, University of Palermo , Italy

3. Introduction

4. Introduction

5. Conduction system

6. 6
Introduction

7. 7
E C G

8. ST segment
• ST segment – interval between depolarization
and repolarization of the ventricles.
• ST can be evaluated by using a baseline
reference both the PQ and the TP segments.
• PQ segment may be altered by atrial lesions
(i.e. valvular diseases, acute pericarditis or
atrial infarction).
• In limb leads, the ST segment is isoelectric in
>75% of healthy adults.

9. ST Segment
ST segment <2mm in chest leads
ST segment not more than 0.5 mm in limb leads

10. ST segment
• The magnitude of ST deviation is related to the
amplitude of QRS complex and is higher and
more common in young adults of male gender.
• In non-pathological conditions,the elevation can
reach even 0.3 mV in V2-V3, while is rarely more
than 0.1 mV in the other precordial leads.
• In the MI, ST segment elevation is believed to
represent a “current of injury” From damaged
cells that are partially depolarized to the healthy
myocardium.

11. ST segment
• In presence of currents of injury, each compensation of
the TQ segment induces a displacement of ST segment
in a higher position and leads to an elevation.
• The ST segment represents the phase two (plateau) of
the action potential (AP): it is possible to suppose that
any modification of AP may result in an ST segment
deviation.
• In some non-ischemic conditions (such as the Brugada
Syndrome), the speed of AP in the epicardial surface
seems to be lower than in the endocardial one.

12. How to measure ST segment?

13. Abnormalities of ST segment
• 1 . Depression of the ST segment.
• 2. Elevation of the ST segment.
• Depression of the ST segment
• Commonest abnormality mostly marked in V5 and V6 ,
especially V 5.
• The basic mechanism giving rise to ST segment
depression is injury to the subendocardial region of the
left ventricle.
• ST segment force or vector is always deviated towards
the surface of injury.

14. Forms of ST segment depression
• 1. Horizontally of the ST segment:
• One of the earliest sign of coronary insuffiency is
the development of ST segment change
horizontally.
• The ST segment becomes isoelectric for an
appreciable period , usually 0.12sec or longer.
• 2. Upward sloping ST segment:
• This is a form of junctional ST segment
depression where only the proximal part of the
ST segment – its junction with the QRS complex –
is depressed.

16. Forms of Junctional ST segment
• A hypothetical parabola joining the distal limb of
the P wave , the PR segment , the ST segment and
the proximal limb of the T wave will be smooth
and unbroken.
• It is usually still difficult or impossible to separate
the ST segment from the T wave since no ST-T
junctional angle has developed.
• A hypothetical parabola will be broken and step-
like.
• A distinct angle between the ST segment and the
T wave is usually present so that the two can be
defined and seperated.

18. Plane ST segment depression
• Depression of a horizontal ST segment results in
plane ST segment depression .
• This is always associated with a sharp angled ST-T
junction and hence a clear seperation of the ST
segment from the proximal limb of the T wave.

19. Down – sloping ST segment
• This refers to an ST segment which is already
depressed at its proximal origin, and then
slopes even further downward.
• Reflects a severe form of impaired coronary
blood flow.
• Its a transient form and may occur during the
spontaneous attacks of angina pectoris
(Heberden’s angina) /precipitated by exercise.
• The greater the depression worse the
prognosis.

21. Elevation of ST segment
• Spontaneous/ exercise induced in following conditions:
• Coronary spasm –basic mechanism of prinzmetal’s
angina.
• Organic stenosis of the coronary arteries.
• Left ventricular aneurysm.
• Impaired left ventricular function- common finding in
MI patients.
• ST segment elevation is usually the expression of
transmural myocardial injury, which is dominantly
epicardial.
• Vector directed to the surface of the injury.

23. NATURAL VARIANTS
Early repolarization / BER
• Benign early repolarization (BER), is a non-
pathological condition,(1% of general population
and 48% of patients referred to an emergency
point of care for chest pain).
• Possible mechanisms: “hypervagotonia”,
“asthenic habitus”, and an early start of the
repolarization in the epicardial surface before the
end of depolarization in the entire myocardium.

24. Cont..
• In BER, the ECG shows an elevated ST segment
that presents a concave slope in more than one
lead.
• A notch (or a little delay) in the terminal portion
of the QRS complex, associated with the presence
of high and concordant T waves, is also
detectable.
• The elevation is usually < 0.2 mV (80-90% of the
cases) but in some patients it can reach even 0.5
mV.

27. Cont.
• Only in 2% of the cases, an elevation >0.5 mV is
found.
• The highest elevation is usually observed in
precordial leads (fromV2 -V5); if it is confined to
limb leads a different diagnosis should be
evaluated.
• The aspect of T waves (which are typically tall,
peaked and concordant) may resemble that one
detected in acute myocardial infarction (AMI),
especially in the case of posterior involvement.
• D/D’S:pericarditis.

28. Cont.
• In patients with acute pericarditis, at least at
the beginning, there is a frequent depression
of PR segment, especially in V6 with a
specular elevation in aVR, not present in BER.
• ST segment elevation is usually more
pronounced and prone for dynamic changes in
pericarditis than in BER.

29. LV hypertrophy and hypertrophic
cardiomyopathy
• LVH is a very common condition that is
associated with ST segment elevation.
• As in LBBB, the repolarization pattern is
discordant to the QRS. The elevation is more
commonly observed in leads V2-V3 and is
usually <0.3 mV with minor in V4-V6.

30. cont .
• ECG shows high voltage of R waves in antero-
lateral leads associated to Q waves in anterior
and inferior leads.
• The T waves, usually being very deep and
inverted in V2-V4, may resemble a non-Q AMI.
Rarely, a real ST elevation might be seen.

31. ECG hypertrophic cardiomyopathy

32. LBBB
• In this condition ST segment and T-waves are usually
discordant with the QRS, since they are directed in
opposite directions.
• A concordant ST segment shift should always be
referred to a myocardial lesion and considered as
strongly indicative of MI.
• In discordant ST elevation of the J point 0.5 mV in V1-
V2 is strongly suggestive of MI in the presence of LBBB.
• The same ST changes have been observed in 7.3% of a
population of 124 patients with LBBB without MI.

33. LBBB
• In the same group, a direct correlation
between QRS amplitude and entity of the ST
segment elevation was found.
• Moreover, in LBBB, the QRS/T ratio appears to
be more predictive than the amplitude of ST
elevation.
• When this ratio is near to or < 1, the
probability to an MI is high.

34. LBBB
Criteria for diagnosing acute AWMI with LBBB:
• 1. ST elevation in at least one lead of >1mm
concordant to the positive QRS complex (5
points).
• 2. ST depression of >1 mm in V1-V3 (3 points).
• 3. discordant ST elevation > 5mm in at least one
leads with a predominant negative QRS (2
points).
• A total > or = to 3 points is s/o an acute MI in
presence of LBBB.

36. LBBB
• An Acute IWMI with LBBB can be diagnosed
routinely as there is no masking effect of the
LBBB in the inferior leads.

37. LBBB
Diagnosing old AWMI with LBBB
• Presence of LBBB may mask features of old
AWMI.
• Presence of Q waves in leads V5-V6 ,I or AVL in
presence of LBBB S/O old AWMI.
• Notching of 50 ms on the ascending limd of the S
wave of leads V3-V5 ( Cabrera’s sign).
• Notching in the upstroke of R wave in leads I, AVL
or V6 ( Champan’s sign) are considered indicators
of old AWMI in presence of LBBB.

39. Artifacts
Leads malpositioning:
• Usually, during stress test and in emergency
point of care, even the peripheral electrodes
are positioned on the chest (Mason-Likar
disposition).
• Sometimes, this kind of disposition may alter
the Einthoven Triangle leading to possible
alterations of the ST segment.

40. Artifacts
• During electrical cardioversions or the
adminisration of a DC shock by an implantable
cardioverter defibrillator, a transient ST
segment elevation is rarely observed.
• A consistent ST elevation for more than 2 min
may indicate a myocardial lesion

41. Atrial Flutter 2:1(a) after a DC shock (b).

42. In Cardiovascular diseases
Pericarditis.
• Although pericardium is electrically inactive, its
infection and/or inflammation may affect the
external part of epicardium and cause significant
ECG modifications.
• In Acute pericarditis :
• Earliest sign is tall and symmetrical T waves.
• Abnormalities in ST segment – elevated concave
upward ST segment (saddle shaped) with tall and
peaked T wave . Vector is towards the injured
tissue.
• Sinus tachycardia.

44. Acute pericarditis
ST elevation is seen only in contiguous leads (regional lead group such as anterior,
inferior or lateral/apical) with a frequent depression in the reciprocal leads.

45. Cont..
• In sub acute pericarditis:
• ST segment will become convex upward with
isoelectric T wave.
• In chronic pericarditis :
• Low to inverted T waves in most leads.
• Diminshed amplitude of all the ECG
deflexions.
• Potential electrical alterns.

46. In Myocarditis
• It is defined as the inflammation of the
myocardium.
• Clinically ranges from subclinical disease
(asymptomatic ECG abnormalities) to fulminant
heart failure presenting as a new onset
cardiomyopathy.
• It should be considered in young patients
symptomatic for acute, ischemic-like chest pain
associated with ECG abnormalities and global
(rather than segmental) left ventricular
dysfunction on ECHO.

47. Cont.
• The ECG changes, despite angiographically
documented absence of coronary vessels
involvement, vary from ST segment upsloping in
contiguous leads, T waves inversions, widespread
ST segment depressions.
• Increase of the VAT
• Rough or irregular deflexions
• Pathological q waves
• Increased QRS duration
• Atypical intraventricular conduction defect.

49. ECG myocarditis

50. Aortic dissection
• May sometimes be associated with an ST
segment elevation due to the involvement of the
ostia of coronary arteries, to cardiogenic shock
after tamponade or to pre-existing coronary
artery disease.
• In other cases, it is possible to observe a
phenomenon called “wandering ST”, which is a
marker of the disease progression and is
characterized by the transient elevation of the ST
segment in some leads that reappears in other
leads.

51. Ventricular aneurysm
• The persistence of the typical pattern of the
fully evolved phase of myocardial infarction- Q
wave ,raised ST segment and inverted T wave
– for 3 months or longer after the acute attack
suggests the ventricular aneurysm.

53. Prinzmetal’s angina
• It is associated with elevation of ST segment.
• The modifications of ST segment, although transient,
are the same of STEMI, since they result from
transmural ischemia.
• ECG manifestations:
• Elevation ST segment frequently manifests in leads V2-
V6 amplitude from 4mm to 40mm.
• Higher the elevation higher the severity.
• Abnormal T waves – the T wave becomes pointed and
widened.
• Abnormal QRS complexes – an increase in the
amplitude of the R wave ,a diminution in the depth of
the S wave, intraventricular conduction defects like
LBBB and RBBB.

54. Prinzmetal’s angina
Transient elevation of ST segment in inferior leads in patients symptomatic for chest
pain and histamine fish poisoning.

55. Prinzmetal’s angina
Transient elevation of ST segment in inferior leads in patients symptomatic for chest
pain who was going to be transferred in the surgery room for an orthopedic
intervention.

56. Brugada Syndrome and arrhytmogenic
right ventricular cardiomyopathy/dysplasia
• Osher and Wolff, for the first time in 1953,
described a persistent ST elevation in
precordial leads without ischemia or any other
possible explanation.
• In 1992, Brugada et al described a syndrome
which was characterized by RBBB, ST segment
elevation in leads V1 to V3 and sudden cardiac
death in subjects <65 years.

57. Cont.
• The imbalance between inwards and
outwards ionic currents at phase I defines the
pathological substrate for Brugada.
• This channelopathy is a rare conidition.
• Originally, 3 patterns of Brugada syndrome
were described.
• But only the type I that is charecterized by a
RBBB pattern, ST segment elevation with
coving, can be confused with MI.

58. Cont.
• In type I Brugada syndrome,- maximum ST
elevation-In v1 or V2 , coved ST segment with
J point elevation fallowed by negative T wave.
• In type II – saddle back configuration with
high takeoff of ST segment ,ending in positive
or biphasic T wave without touching baseline.
• In type III – ST segment elevation of <0.1mv
with either of the morphologies.

60. Wolff Parkinson White Sndrome
• WPW syndrome is an electrocardiographic syndrome
which is the expression of an anomalous AV conduction
pathway , congenital in origin.
ECG changes:
• A short PR interval.
• A slurred , thickened, initial upstroke of the QRS complex,
which is termed as delta wave.
• A relatively normal- narrow- ensuing terminal QRS
deflexion.
• Slightly widening of the QRS complex as a whole.
• Secondary ST segment and T wave changes i.e. changes
which are secondary to the abnormal intraventricular
conduction of pre-excition , may be confused with
myocardial disease.

62. ARVC/D
• Arrhythmogenic right ventricular
cardiomyopathy/dysplasia (ARVC/D) is a
genetically determined heart muscle disorder
that is characterized by the fibro-fatty
replacement of right ventricle myocardium in
the so called “triangle of dysplasia”.
• The disease has a variable expression but even in
its concealed form individuals are often
asymptomatic but may be at risk of sudden
cardiac death especially during exertion.

63. Cont.
• The (major and minor) criteria for the diagnosis,
which are based on structural, histological, ECG,
arrhythmic and familial features, have been
recently revised.
• Notably, in subjects with ARVC/D, there is often
an elevation of ST segment which is similar to
that detectable in Brugada syndrome and
represent a challenge in differentiating between a
real Brugada syndrome or an acute ischemia.

64. ECG ARVC/D
Arrhythmogenic right ventricular cardiomyopathy/dysplasia.

65. Pulmonary diseases
• PTE: Obstruction of the blood flow through
the lungs leads to an increased pressure
overload in the right chambers.
• Major PTE results whenever the combination
of embolism size and underlying
cardiopulmonary status interact to produce
hemodynamic instability.

66. Cont.
• As the result of pressure overload in the right
ventricle, the ECG usually shows
tachycardia/atrial fibrillation, right bundle branch
block and/or the pattern S1Q3T3, which is
considered suggestive,even if not specific.
• Occasionally, an STsegment elevation in right
precordial leads is also possible.
• The evidence of Q waves in DIII and aVF (but not
in DII) without ST elevation in the same leads may
allow to differentiate a PTE from an MI.

67. Pulmonary thromboembolism

68. Acute pulmonary embolism
• ECG changes:
• Low amplitude deflexions.
• Rt. Arterial enlargement.
• Rt. Ventricular enlargement.
• Rt. Ventricular Myocardial ischaemia.
• Rt. Ventricular myocardial injury.
• RBBB.
• Arterial tachyarrthmias.

69. ECG changes in frontal leads
• S1,Q3,T3 Pattern.
• S-T segment depression in standard leads I and II.
• A “ stair case “ ascent of the ST segment in leads I
and II, consists of flattening of the initial part of
the ST segment and T wave,fallowed by a more or
less sharp rise and then again flattening of the
terminal portion of T.
• Rt. Axis deviation.
• RBBB.
• Tall peaked P waves in lead II.

71. S1 Q3 T3
• S1 (LEAD I) is a frequent manifestation of acute pulmonary
embolism.
• Usually changes in few hours to a deep and narrow
deflexion.
• This may regress within 24 hrs or return normal gradual
over weeks.
• A deep prominent q wave in lead III – is an important
component of triad of APE.
• Q wave forms q R complex, q S complex does not forms.
• This q wave does not fullfill pathological q wave criteria.
• T wave inversion in lead III is almost always associated with
the S1 Q3 abnormality.

73. SI SII SIII Syndrome
• As a normal variant in healthy individuals who
have no evidence of heart disease.
• As an expression of RV dominance like in TOF,
pulmonary atresia, cor pulmonale, transposition
of great vessels.
• In Anterior wall MI especially apical wall
infarction.
• In straight back syndrome – a congenital anomaly
the upper dorsal vertebral column is lost.

74. Atelectasis and pulmonary metastases
• Atelectasis is the collapse of lung tissue and results in
reduced (or absent) gas exchange and oxygen absorption to
healthy tissue.
• The ECG with ST segment elevation usually shows
development of a deep S wave in lead I and a new Q wave
in lead III.
• The T waves are, however, normal and the classic “SIQ3T3
pattern” observed in patients with PTE is not present.
• Pulmonary hypertension may be able to overload the right
ventricle and results in ST segment changes in inferior
leads.
• Pulmonary metastases are another cause of ST segment
alterations in patients without cardiac artery diseases.

75. Gastrointestinal diseases
• Acute pancreatitis
• Differentiation of acute pancreatitis from an acute coronary
syndrome is difficult.
• Pancreatitis itself may indeed produce minor transient
ECG changes that frequently involve T waves (inversions) or
ST segment (depression).
• However, sometimes typical changes, such as ST segment
elevation without underlying cardiac pathology may be
recorded.
• The metabolic abnormalities, such as hypocalcemia,
hypernatremia, hypokalemia, hypomagnesemia and insulin-
induced hypoglycemia that often characterize the acute
pancreatitis,may be involvedin the genesis of these
electrocardiographic features.

76. Cont.
• ST segment elevation and in particular
coronary vasospasm, exacerbation of prior
coronary artery disease or formation of
thrombus in the coronary arteries due to the
increased platelet adhesiveness or to
coagulopathy induced by pancreatic enzyme.

77. Acute cholecystitis
• Acute cholecystitis is another acute abdominal
condition,which can produce an ST segment
elevation that mimics AMI.
• Gallbladder distension is able to increase
heart rate, arterial blood pressure and plasma
renin levels

78. Drug induced ST segment elevation
• Many drugs may have cardiac effects through
various mechanisms.
• Some drugs can have a “direct” effect by
stimulating cardiac receptors or by inducing
anatomic damage or inflammation.
• Some others may “indirectly” interfere with the
activity of autonomous nervous system.
• A lot of cardiac side effects and ECG modification
can be associated with drug consumption.

79. Cont.
• When an ST segment elevation (or an ECG
modification) without a clear clinical setting is
detected, the presence of a drug interaction
should be always excluded.
• For example, clozapine, which intensively acts on
nervous system, may cause
hypotension,tachycardia, ST displacement
(depression and/or elevation) and myocarditis.
• In such cases, clozapine should be no longer
administrated.

80. Elevation of ST segment during
treatment with clozapine.

81. Digitalis effect
• Digitalis effects on myocardial repolarization, consists of 4 ECG
changes.
• 1. Effect on ST segment- characteristic inverse check mark
configuration of the S-T segment manifests in leads which have
dominantly upright QRS complexes, i.e. in leads with tallest R
waves.
• When this inverse check mark effect on ST segment appears in
leads with the tallest R waves as well as in leads with dominantely
negative QRS deflexions s/o digitalis toxity.
• Therapuetic administation of digitalis diminishes the magnitude of
the T wave but does not change its direction.
• With digitalis toxicity T wave amplitude diminishes and also changes
the direction.
• Shortening of Q-T interval.
• Abnormal cardiac rhythms ( II deg. A-v block and ven.extrasystoles,
v.t).

83. Potassium effect (hyperkalaemia)
• Progressive diminution and eventual disappearance of
the P wave.
• Widening of the QRS complex.
• A bizarre intraventricular conduction defect like RBBB.
• Tall , widened and characteristically shaped T wave.
The proximal limb of T wave is steeper than distal limb.
• With high k+ levels ST segment disappers and becomes
the ascending limb of the S wave forms continous
vertical line with proximal limb of T wave.
• Virtual disappearance of the ST segment.

86. Hypokalaemia
• Progressive diminution with eventual
diaspearance of the T wave.
• Progressive increase in the amplitude of the U
wave.
• First and second degree AV block
(wenckenbach type).
• Depression of the ST segment. The depression
may be horizontal or concave – upward.

88. Calcium effect(Hypocalcemia)
• Prolongation of Q-T interval due increase in
duration (0.50-0.60 sec).
• Elongation ST segment that has increased
horizontally and duration (0.3-0.34) ends in a
T wave.
• T wave occasionally become inverted,
sometimes deeply and increased in amplitude.

90. Hypercalcaemia
• Shortening of the Q-T interval.
• Shortening of the ST segment , virtually
disappears and incorporated into the T wave.
• The ST segment sometimes slightly elevated
and gives rise to a impression of epicardial
injury.

92. Hemorrhagic cerebrovascular disease
• ECG changes are usually observed in patients with
acute cerebrovascular pathology such as strokes or
subarachnoid hemorrhages.
• Subarachnoid hemorrhage is generally due to the
rupture of an aneurysm and is characterized by
headache, rushing, nausea and loss of consciousness.
• The sympathetic neuronal activation, which is
consequent to the increase of intracranial pressure,
seems to play an important pathogenic role.
• The ECG modifications may sometimes resemble an
MI.

93. Cont.
• The most common abnormalities are prolongation of QT
interval, inversion of T waves and appearance of abnormal
U wave.
• The literature has reported cases of ST segment elevation in
absence of coronary artery disease; they are probably
related to the catecholamine effect on myocytes or to
spasm of the epicardial coronary arteries, which at least
may even cause a real myocardial ischemia.
• This situation may be also seen in pheochromocytoma,
cocaine abuse or emotional stress.
• Sometimes the subarachnoid hemorrhage may also induce
an ST segment elevation without the release of markers of
myocardial necrosis nor anatomical necrosis, as confirmed
by the autopsy.
• Elevation of ST segment during treatment with clozapine.

94. ECG during acute subarachnoid
hemorrhage

95. Myocardial infarction
• Myocardial infarction results in ischaemia,
injury and necrosis.
• Infarction process evolves through 3 phases:
• 1. hyperacute phase
• 2. fully evolved phase
• 3. chronic stabilized phase.

97. Fully evolved phase
• The infarcted regions consists of a central core of
necrosis ,surrounded by injured tissue,which in
turn is surrounded by a zone of ischaemic tissue.
• The myocardial necrosis is represented by a QS
complex.
• The myocardial injury is represented by an
elevated and coved or convex- upward ST
segment.
• The myocardial ischaemia is reflected by an
inverted , symmetrical and pionted T wave which
is increased in magnitude.

99. Myocardial necrosis
• 1.QS complex : is totally negative QRS complex,
with no ensuring positivity.
• QS complexes of myocardial necrosis are evident
in leads V2-V4.
• Necrotic tissue is electrically inert and cannot be
activated or depolarized.it constitutes a
transmural infarction ,an electrical ‘hole’ or
‘window’ within the muscle wall.
• QRS vectors are directed away from a necrotic or
infracted myocardium.

100. Myocardial necrosis
• 2. A Q r complex is the manifestation of a deep
wide pathological Q wave which is fallowed by a
small r wave.
• This terminal positivity reflects the depolarization
of remaining viable myocardial tissue in the
infarcted ventricular wall.
• This will occur when the infarction results in
endocardial or epicardial rinds of necrosis.
• 3.Attentuation of R wave amplitude without
associated pathological Q wave is a frequent
manifestation with MI, yet tends to be a
neglected diagnostic parameter.

101. ECG effects of myocardial injury
• Myocardial injury is reflected by deviation of the
ST segment , deviated towards the surface of the
injured tissue- epicardial surface.
• The ST segment in the fully evolved phase of the
infarction are coved or convex upward.
• Reciprocal and indicative changes:
• The coved and elevated ST segments of an acute
myocardial infarction are termed indicative
changes.
• The depressed ST segments associted with an
acute myocardial infarction are termed reciprocal
changes.

103. ECG effects of myocardial ischaemia
• Myocardial ischaemia is reflected in leads
oriented to the ischeamic region by inverted,
symmetrical and pointed T waves which are
frequently also increased in magnitude.
• T wave vector is directed away from the
region of myocardial ischaemia.

104. Hyperacute phase of myocardial
infarction
• The hyperacute phase of MI occurs before the
fully evolved phase and usually within a few
hours of the onset of the infarction.
• ECG changes:
• 1. increased ventricular activation time.
• 2. increased amplitude of the R wave.
• 3. slope elevation of the ST segment.
• 4. tall and widened T waves.

106. Cont.
• Increased ventricular activation time: i.e. delay
in the onset of the intrinscoid deflexion- the time
from beginning of the QRS complex to the apex of
the R wave.
• Time is delayed beyond 0.45sec – 0.6sec.
• This is illustrated in leads AVL , V5 and V6.
• Increased amplitude of the R wave:
• R wave becomes taller , particularly noticeable in
cases of the hyperacute phase of inferior wall MI
(leads II,III,AVF).
• The increased ventricular activation time and tall
R wave are due to acute injury block.

107. Cont.
• Slope elevation of the ST segment:
• The ST segment straight upward sloping then becomes
elevated.
• The very earliest sign of this manifestation may merely
be a straightening of the ST segment without any
elevation.
• Tall and widened T waves:
• The T wave becomes very tall and wide , it exceeds the
amplitude of associated R wave.
• The monophasic deflexion , it is difficult to separate all
3 deflexions( R, ST and T waves ).
• Reciprocal ST segment depression usually occurs in
leads to the uninjured surface.
• Prinzmetal’s angina may have identical presentation to
the hyperacute phase of MI. (resolves within 20 min.).

108. Cont.
• Significance of hyperacute phase:
• During this phase that the complication of
primary ventricular fibrillation is most likely to
occur.
• Indication for intense vigilance and coronary
care monitoring.
• The greater the elevation of the ST segment ,
and taller the T wave , the more potentially
critical situation.

109. cont
• Chronic stabilized phase:
• The elevated ST segment gradually returns to
the baseline , becoming predominantly
isoelectric once again.
• The inverted T wave gradually regains its
positivity.
• The QRS complex may regain some of its
previous positivity.

111. Sub endocardial infarction
• ECG findings are not as definitive or clear-cut as
that of transmural or even epicardial infarction.
• The diagnosis is made by clinico- ECG correlation.
• Clinico-biochemical correlation.
• In ECG depressed ST segment with deeply
inverted T waves in mid,lateral precordial and in
standard leads I and II.
• These abnormal changes persist for several days.

113. conclusions
• ST segment is a important marker for MI but
also a significant finding in lot of other
diseases.

114. Thank you