ST elevation myocardial infarction (STEMI) results from plaque rupture or erosion leading to an occlusive thrombus. This causes myocardial cell death spreading from inner to outer layers of the heart wall. Reperfusion therapy such as primary percutaneous coronary intervention (PCI) or fibrinolytic drugs are the main treatments aimed at saving ischemic heart muscle. For PCI, the door-to-balloon time should be ≤90 minutes, while for fibrinolytics the door-to-needle time should be ≤30 minutes. General management includes intensive care monitoring, IV access, analgesia, oxygen supplementation, and investigations to guide treatment and prognosis.

1. ST Elevation Myocardial
Infarction (STEMI)
1

2. Pathophysiology
Plaque rupture or erosion, lead to the formation of
an occlusive thrombus – lasting long enough to
cause significant myocardial necrosis.
The wave of necrosis spread from the
subendocardium to the subepicardial region –
subendocardial infarction to transmural infarction.
2

3. 3

4. 4

5. 5

6. Natural history of a coronary thrombus :-
1. Spontaneous lysis over few days
2. Persistent permanent occlusion (20-30%)
3. Partial lysis
6

7. Symptomatology
 Severe retrosternal chest pain
 Classical radiation to left upper limb
 Marked diaphoresis
 Pale and clammy
 No response to GTN
7

8. • In the elderly or diabetic patients the presentation
is atypical:
– Fatigue
– Dyspnoea
– Presyncope, Syncope
– Confusion & disorientation
– Epigastric burning
8

9. The ECG
• Q wave
• ST segment
• T wave
9

10. Chest leads from a patient
with acute anterior ST segment elevation myocardial infarction (STEMI). A, In the earliest
phase of the infarction, tall, positive (hyperacute) T waves are seen in leads V2 to V5. B,
Several hours later, marked ST segment elevation is present in the same leads (current
of injury pattern), and abnormal Q waves are seen in leads in V1 and V2.
10

11. Acute inferior wall infarction. Notice the ST elevations in leads II, III, and aVF and the
reciprocal ST depressions in leads I and aVL . Abnormal Q waves are also present in
leads II, III, and aVF
11

12. ECG – pitfalls in diagnosis
The initial ECG can be normal or non
diagnostic (ie. Minor changes) in 1/3 of the
cases.
12

13. ECG localization of infarction
 The ECG changes are seen in the lead that
face the infarct.
 The other leads will show the reciprocal
changes.
13

14. 14
Courtesy: Kumar and Clarke Clinical Medicine 8th edition

15. 15

16. Plan of management:
1. General management
a) Intensive care
b) Monitoring
c) IV access
d) Analgesia
e) Oxygen supplementation
f) Anxiolysis
g) Investigations
2. Reperfusion therapy
3. Rehabilitation and secondary prevention.
16

17. When should I admit a patient to the
CCU?
How long should I keep him in CCU?
1. All patients with (i) anterior infarcts or (ii)
multisite infarcts should be admitted to the CCU
at least for the first 48 hrs.
2. Uncomplicated inferior infarcts (with no RV
involvement) also will ideally need CCU care for
at least 24 hrs but should not be given
preference when a choice to be made.
Continued…
17

18. 3. Where the history suggests an AMI but the ECG
is normal, CCU care is not imperative (as the
mortality in these cases is less than 1%)
4. Any patient who has no evidence of AMI (on
ECG and / or biochemical markers) at 12 hrs
may be transferred out of CCU.
5. Uncomplicated infarcts (with no persistent
ischaemic type of chest discomfort, LVF, heart
block, hypotension or arrhythmia ) may be
transferred out of CCU after 48 hrs.
Continued…
18

19. 5. If any complication is present, the patient
should ideally be kept in the CCU until 24hrs
after stabilization.
6. Unstable patients already in CCU must not be
transferred out to make room for a patient
deemed to be more seriously ill. Such a policy
will only lead to partially stabilized patients
being constantly transferred out with loss of
cost-benefit in the long run.
7. No age limit for CCU admission is
recommended.
19

20. What are the first few things I should
perform in the CCU as general
management?
1. Bed rest is essential
2. Allow the patient to adopt the position of
maximal comfort, but do not allow feet to be
dependant. (This can aggravate hypotension)
Continued….
20

21. 3. Attach the patient to a continuous monitoring
system. Keep the chest area free of electrodes
so that the area is available for resuscitation if
an arrest were to occur. For monitoring – use
limb leads or MCL lead.
4. Insert IV line. The IV line must be in upper limb
at a site that is central as possible.
[If iv access is in the lower limbs, cardiac drugs
given at the site may not reach the heart or may
take long time to reach the heart when the
circulation is compromised]
Continued….
21

22. Veins over a joint are best avoided as the IV lines may
get displaced if the patient were to get restless.
Do not waste time on ‘cut downs’. If the upper limb veins
are “difficult” to visualize, place a gauze wad soaked in
warm water with or without GTN spray, which will often
dilate the vein.
In case of difficulty, a CVP line would be quicker if
expertise is available.
*Note: In large infarctions and if complications are likely,
it is judicious to keep two IV lines patent.
5. Use veins at compressible sites.
22

23. MCL lead
23

24. Plan of management:
1. General management
a) Intensive care
b) Monitoring
c) IV access
d) Analgesia
e) Oxygen supplementation
f) Anxiolysis
g) Investigations
2. Reperfusion therapy
3. Rehabilitation and secondary prevention.
24

25. Why reduce pain?
• To relieve the distress
• To lower the adrenergic drive – so to reduce the
infarct size, VT, Vascular resistance, BP.
How should the pain of AMI be
relieved?
1. Morphine would be the analgesic of choice. *If
pain is severe and patient is of moderate or
large body build -Morphine 5mg iv. Slow iv
injection is required at 1mg per minute. (Intra
muscular injections should be avoided.)
Continued….
25

26. • lf one of the following are present, the first
dose should only be 2.5mg iv
(a) Small body build
(b) Elderly patient
(c) Already received hypnotic drug(s)
(d) Chronic respiratory disease.
2. Assess the pain after 10 (5-15) minutes.
Administer morphine as 2.5 mg iv aliquots
every 10 minutes until adequate analgesia is
achieved.
Continued….
26

27. 3. Usual maximum dose of morphine is 15mg. However, in
the presence of severe pain, patients may require up to
20 - 25mg iv, as the threshold of morphine tolerance
rises with severe pain. Do not exceed this limit.
4. The other centrally acting analgesics such as pethidine,
pentozocine may be used only if morphine is
contraindicated. These drugs tend to increase the
pulmonary vascular resistance and are not the preferred
agents in AMI. Pethidine- 50mg / im. Repeat 25mg
every 15 minutes up to a maximum of 100mg.
5. Morphine causes
(1) Respiratory depression - Use Ambu bag ventilation
and give antidote: Naloxone 100 micrograms every 2
minutes up to 250mcg. (Maximum dose is 3
micrograms/kg).
Continued….
27

28. (2) Vomiting
(3) Histamine release
with wheeze.
(4) Hypotension - correct with N saline 100ml
iv over 10 minutes
(5) Bradycardia & heart block - use iv atropine
When giving morphine as in No. 3 above, always
check to these side effects before each dose. Even
before the first dose, the above contraindications
must be gone over as a check list.
Continued….
28
Administer antihistamine
eg: promethazine 25mg im
or metoclopramide 10 mg
iv along with morphine
morphine

29. 6. If any contraindication for morphine exists, the
best analgesic would be inhalation of nitrous
oxide(N2O)
This is given as a 50% mixture with Oxygen (O2).
The patient's face mask is connected to both O2 ,
N2O cylinders and both are opened to the same
flow rate. The patient breathes this mixture for 3-5
minutes and when drowsiness occurs or pain is
relieved, the inhalation is ceased.
Continued….
29

30. Side effects:- Rarely marrow suppression is noted after
prolonged administration only, leading to megalosblastic
anaemia
Nitrous Oxide is contraindicated in pneumothorax as it
leaks into these air filled spaces increasing the tension
within.
Continued….
30

31. 7. If morphine is contraindicated and nitrous oxide is
unavailable, medozolam (Dormicum) may be used to
sedate the patient.
8. The NSAIDS/ COX -2 inhibitors should not be given in
AMI because of possible prothrombotic effects. They
should he omitted if the patient was already taking
these drugs for some other indication.
31

32. Plan of management:
1. General management
a) Intensive care
b) Monitoring
c) IV access
d) Analgesia
e) Oxygen supplementation
f) Anxiolysis
g) Investigations
2. Reperfusion therapy
3. Rehabilitation and secondary prevention.
32

33. How should oxygen be given in AMI?
1. All patients may be offered O2 supplementation via nasal
prongs. This may be given for the initial 6 hours. Do not
give beyond 6 hrs unless 4 below is present.
If the patient prefers to be without it, oxygen may be
omitted
The O2 flow rate is to be at 2- 4 L min.
2. Check pulse oximetry. If SaO2 is below 90%, oxygen must
be given via the face mask.
-Use 12L/min via face mask.
Continued…..
33

34. 34

35. 35

36. 3. If SaO2 is over 90%, there is no evidence of benefit of O2
supplementation.
4. Oxygen must not be given to any patient with evidence
of CO2 retention because respiratory drive may be
dependent on hypoxia in these patients.
5. However, if a patient at risk of CO2 retention develops
pulmonary oedema, O2must NOT be withheld.
Continued…
36

37. 6. Supraphysiological doses of O2 may cause peripheral
vasoconstriction but in most patients this is of no clinical
relevance.
7. Class of evidence for O2 therapy in AMI as follows:-
Class I - (i) Overt pulmonary congestion
(ii) Arterial oxygen desaturation (SaO2 <90%)
Class IIa - All uncomplicated AMI patients for first 6 hrs.
37

38. Plan of management:
1. General management
a) Intensive care
b) Monitoring
c) IV access
d) Analgesia
e) Oxygen supplementation
f) Anxiolysis
g) Investigations
2. Reperfusion therapy
3. Rehabilitation and secondary prevention.
38

39. How do I achieve sedation &
anxiolysis in AMI?
1. The patient (and relatives) should be reassured and
relieved of anxiety.
2. (a) Diazepam -5mg orally is recommended as a nocte dose
for at least the first 3 - 5 days, if the patient is unable to
sleep.
(b) Thereafter it may be continued until the patient is able
to have a restful sleep without it.
Note: There is only class IIb level of evidence for the routine
use of sedation/anxiolytics.
3. If the patient is markedly anxious, a small dose of
diazepam (eg. 2.5mg) or chlordiazepoxide (librium) -10mg
may be used on a t.d.s basis for 3 days or so.
Continued…..
39

40. 4 (a) If patient is confused & violent - a safely used drug in
AMI would be haloperidol (2mg iv and going upto 10mg iv
for the first dose).
(b) Haloperidol iv dose may be repeated in 4 hrs time.
The total dose should not exceed 18mg in 24 hrs.
5. IV medozolam may be used for quick sedation.
6. The use of these drugs in elderly must be with caution.
40

41. Other tests required
– Troponin assay
– FBC
– Serum electrolytes
– RBS
– Lipid profile
– Chest Xray
– Bed side 2D echo (i.e. point of care)
(you may see RWMA or detect evidence of dissection,
pericarditis, pulmonary embolism)
41

42. Plan of management:
1. General management
a) Intensive care
b) Monitoring
c) IV access
d) Analgesia
e) Oxygen supplementation
f) Anxiolysis
g) Investigations
2. Reperfusion therapy
3. Rehabilitation and secondary prevention.
42

43. Time is muscle
Minutes mean muscle
Hence least delay must occur from FMC (First
Medical Contact). Necrosis starts in 15-30 minutes
but all is not lost until 6 hrs.
The main stay of therapy is Reperfusion to save
the salvageable myocardium.
43

44. 44

45. Cross section of the left ventricle showing the difference between a subendocardial
infarct, which involves the inner half of the ventricular wall, and a transmural
infarct, which involves the full thickness (or almost the full thickness) of the wall.
As discussed in the text, pathologic Q waves may be a marker of transmural
infarction. However, not all transmural myocardial infarctions produce abnormal Q
waves; in some cases, subendocardial (nontransmural) infarctions are associated
with Q waves
45

46. Clinical features suggesting viable
(salvageable) myocardium
• Continuous pain
• Persistence of ST segment elevation
• Some degree of contraction on
echocardiography
If these are present, reperfusion must not be
denied solely on guideline based time windows.
46

47. Reperfusion strategies
1. Invasive strategy
This is the ideal treatment in PCI capable centers if
the Door to Balloon time is ≤ 90 minutes. The time
from onset of pain must be < 120 minutes.
2. Pharmacologic strategy
This is the treatment in PCI non capable centers. The
door to needle time is ≤ 30 minutes
3. Pharmaco-invasive strategy
This strategy involves transfer. You commence on the
pharmacological strategy and transfer the patient to
a PCI capable center for invasive therapy.
47

48. Invasive Strategy
Primary PCI
If a large thrombus is present you can aspirate out
the thrombus load.
It is usual to treat the IRA (Infarct Related Artery)
only.
So the other lesion have to be attended to later.
Implanting a stent is usual.
(cost- Rs.350,000- Rs.550,000)
48

49. 49

50. Pharmacologic strategy
• This is achieved by the use of Fibrinolytic agents.
• Pre hospital fibrinolysis (in the transport
ambulance) is the current concept.
(Telemedicine, Paramedics)
Golden first hour
50

51. Fibrinolytic agents:
a. Fibrin specific agents
• Tenecteplase (TNK-t-PA) [cost Rs.65,000]
• Alteplase
• Reteplase
b. Non fibrin specific agents
• Streptokinase [cost Rs.6,000]
• Urokinase
51

52. Why must you know whether your
fibrinolytic agent is Fibrin specific or
not?
If fibrin specific- you must follow up with
Enoxaparin.
If not fibrin specific- it is not mandatory. However
the current protocols have advised Enoxaparin
even for non fibrin specific fibrinolysis
Hence after Streptokinase LMWH is mandatory.
52

53. What are the ECG criteria for
thrombolytic therapy?
The ECG criteria are valid only in the context of a suggestive
history. As thrombolytic therapy is indicated only for STEMI,
these ECG changes are also valid for making the diagnosis of
STEMI.
1. ST segment elevation in 2 or more contiguous leads.
Inferior leads - 1mm or more
Right ventricular leads - 1mm or more
Anterior leads - 2mm or more (However, if the
history is suggestive even 1mm elevation is now taken as
significant)
Continued….
53

54. • The ST elevation is to be convex upwards
• There should be no initial positive notch
• The T waves could be very tall with the proximal limb
merging with the upward ST.
2. True posterior pattern in V I, V2 (i.e upright QRS complex with
upright T waves) confirmed by ST changes in V7 - V9. *If the
history is suggestive of AMI but EGG is doubtful, always
record V7-V9.
Continued…….
54

55. ECG criteria Lives saved per 100
treated
LBBB
Anterior ST elevation
Inferior ST elevation
49
37
8
3. Left bundle branch block- if this is a new / presumed new
change, it is very significant.
4. Diagnosis of acute changes in the presence of pre
existing LBBB is difficult and consists of the new
appearance a ‘q’ wave in leads where the complex is
predominantly positive, and/or the movement of the ST
segment in the same direction as the terminal QRS axis.
5.
55

56. 56

57. 57

58. How do I reduce the door to needle time?
1. The door to needle (or, door to drug) time must
ideally be reduced to 30 minutes or less.
2. For this reason-
* Patients with chest pain should be exempted
from formal registration and filling in BHTs
etc.
* They should not subjected to detailed history
taking and physical examinations.
Continued…..
58

59. 3. The door to needle time of 30 minutes is roughly
divided into 3 equal periods :
• 10 minutes - from time of presentation to the
emergency department to performing the 12 leads
ECG.
• 10 minutes - If ST elevations are present, for a quick
assessment of contraindications for SK, achieving
venous access and administering aspirin.
• 10 minutes - Mixing and commencing the
administration of streptokinase
4. It is only after commencing the SK infusion that the
patient should be transferred to a CCU [i.e. SK infusion
must commence in the emergency units].
59

60. What is the method of administering
Streptokinase?
1. When the patient is thought to require Streptokinase in
view of his cardiac status, go over the list of
contraindications first.
2. Administer 250mg of hydrocortisone iv as a bolus dose.
(This is optional and is not followed by many. Perhaps
its use should be restricted to cases where some allergy
is expected.)
3. Set up the Streptokinase infusion system of 100ml
Saline + 2 vials of Streptokinase. Make sure that there is
no flocculation in the solution.
Continued…..
60

61. 4. Start the infusion slowly at 6 drops/minute Watch for
signs of anaphylactic reactions for the first 5 minutes. A
medical officer is responsible for this monitoring,
5. Once the iv sensitivity testing is completed, the drip
rate is increased. (Drip rate: 110ml in 1 hour would work
out to about 2ml per minute = 30 drops per minute).
6. After the completion of the SK infusion, success of
reperfusion must assessed.
61

62. What are the contraindications for
thrombolytic therapy?
Absolute contraindications
1. Active internal bleeding
2. CNS neoplasm
3. Haemorrhagic stroke at any time
4. Other strokes within past six months
5. GI bleeding within last month
6. Aortic dissection
62

63. Relative contraindications
1. Blood pressure >180/110 mmHg
2. Severe trauma/ major surgery within past 2-3 wks.
3. CRP over 10 mts – especially with rib fractures.
4. Pregnancy or within one week of delivery.
5. Active malignancy
6. Severe hepatic dysfunction.
7. Severe renal dysfunction.
8. Known bleeding disorder.
9. Age>75 yrs. (Gusto I)
10. SK given within 5-6 months.
11. Dementia.
12. Acute Pancreatitis
13. Puncture of non compressible artery within past 2 weeks.
14. Infective Endocarditis.
15. Active cavitating pulm TB.
16. Intracardiac thrombi.
17. TIA
63

64. Non – contraindications:
1. Proliferative diabetic retinopathy
2. Warfarin therapy (INR<2)
3. Menstrual bleeding.
64

65. Assessment of Reperfusion After Fibrinolysis
TIMI 3 flow after fibrinolytic therapy predicts subsequent short- and long-term survival.
Traditional variables that have been used to assess the angiographic response to fibrinolytic
therapy are imprecise and have included an improvement in or relief of chest pain,
resolution of ST elevation, and the presence of reperfusion arrhythmias (e.g., accelerated
idioventricular rhythm). The relatively sudden and complete relief of chest pain coupled
with 70% ST resolution (in the index lead showing the greatest degree of elevation on
presentation) is highly suggestive of restoration of normal myocardial blood flow.
65

66. • Complete (or near complete) ST-
segment resolution at 60 or 90 minutes
after fibrinolytic therapy is a useful
marker of a patent infarct artery.
• Conversely, partial or absent improvement in the extent of ST
elevation is not as accurate in predicting a “closed artery”. Lack of
improvement in ST resolution is associated with worse prognosis. The
combination of 50% ST resolution and the absence of reperfusion
arrhythmias at 2 hours after treatment predicts TIMI flow <3.
66

67. • Lack of resolution of ST elevation by at
least 50% in the worst lead at 60 to 90
minutes should prompt strong
consideration of a decision to proceed
with immediate coronary angiography
and “rescue” PCI.
67

68. • Transfer of Patients With STEMI to a PCI-
Capable Hospital for Coronary
Angiography After Fibrinolytic Therapy:
Recommendations:
68

69. Immediate transfer to a PCI-capable hospital for
coronary angiography is recommended for suitable
patients with STEMI who develop cardiogenic shock
or acute severe HF, irrespective of the time delay
from MI onset. (Level of Evidence: B) evidence of
failed reperfusion or reocclusion after fibrinolytic
therapy (Level of Evidence: B)
69

70. • Transfer to a PCI-capable hospital for
coronary angiography is reasonable for
patients with STEMI who have received
fibrinolytic therapy even when
hemodynamically stable and with clinical
evidence of successful reperfusion.
Angiography can be performed as soon as
logistically feasible at the receiving
hospital, and ideally within 24 hours, but
should not be performed within the first 2 to
3 hours after administration of fibrinolytic
therapy. (Level of Evidence: B)
70

71. How do I manage hypotension
caused by streptokinase infusion?
Some degree of hypotension is almost inevitable with
streptokinase.
1. Check BP at 10 minute intervals, once SK infusion is
commenced.
2. If a drop in BP is found, check for signs of peripheral
hypoperfusion. If patient is not symptomatic, do NOT
stop the SK infusion.
3. Position with head down and feet up by 15°.
4. Commence a N.saline infusion. Give 100ml over 10
minutes
Continued…..
71

72. 5. Reduce rate of SK infusion but do not stop it. The SK
infusion is to be stopped only if BP falls further and if
the fall can be halted by N.Saline infusion.
6. Once SK infusion is stopped, give further 150 N. saline
over 15 minutes. If picks up, restart SK infusion (after 15
minutes of N.Saline)
7. Attempt to give at least 750,000 units of SK (ie . Half of
the full dose of 1.5 M units )
72

73. How do I deal with neurological
signs or symptoms while on SK?
1. The following and symptoms must be is looked for while
thrombolytics are being given:
I. Headache (not related to nitrate therapy)
II. Alteration of level of Consciousness.
III. Focal neurological signs
2. If any of the above is seen, the following steps must be
taken immediately
I. Stop infusion of SK at once.
II. Stop infusion of heparin, if in progress.
III. Arrange for CT scan as soon as possible.
3. Reverse the bleeding tendency,
4. Early referral to a neurologist is imperative as 30 day
mortality is 60% in the subset of patients with cerebral
hemorrhage
73

74. How do I deal with anaphylactic
reactions caused by Streptokinase?
1. If any of the following clinical features occur during
streptokinase infusion, anaphylaxis/ anaphylactoid reaction
should be presumed and treated as such.
1. Wheezing
2. Skin eruption
3. Itching
4. Severe drop in BP.
2. Stop SK infusion immediately.
74

75. 3.Adrenaline must be used with caution in the setting of AMI but
must not be withheld in true systemic anaphylaxis:
IM adrenaline (preferred route) 1 in 100 (1mg/ml) 0.3ml or
Slow IV adrenaline (only if the circulation is grossly impaired)
1 in 10,000 3ml
4.Administer hydrocortisone 200mg iv stat. Repeat the steroid
injection every 10minutes until the clinical improvement occurs
up to a total of 1000mg of Hydrocortisone.
75

76. How do I manage bleeding
complications due to thrombolytic
therapy?
1. When any evidence of bleeding is present, attempt to
classify the situation as,
– Minor bleeds
– Major bleeds
2. Minor bleeds – If possible achieve haemostasis. If
bleeding is only very minor, continue the SK infusion
until at least half the dose is given. However, if bleeding
is likely to be dangerous, discontinue the SK infusion at
once. Subsequently, assess the patient as given for
major bleeds.
Continued….
76

77. 3. Major bleeds-
Stop SK infusion at once.
Reverse the abnormal clotting state by the use of
FFP. Give 2 units of FFP over one hour and check
coagulation parameters. Repeat FFP until bleeding
ceases.
Have fresh blood as reserve.
If bleeding continues, use aprotinin.
Dose 200,000 KIU over 10 minutes. (KIU=Kallikrein
Inactivation Units)
Repeat in 1hour if required.
If bleeding continues, setup an aprotinin infusion while
fresh blood infusion too continues.
Continued….
77

78. Add aprotinin 800,000 KIU in 400 ml of N.Saline and drip at 6-8
drops/minute.
If aprotinin is not available tranexamic acid may be given by slow
IV injection.
0.5g – slow iv over 10 minutes
(May be given t.d.s as required).
In grave life threatening bleeding, Human fibrinogen concentrate
is recommended. If not available, you may use Cryoprecipitates.
These are specifically prepared to provide factor VIII but contain
adequate amounts of fibrinogen too and hence are useful.
4. Haemorrhagic stroke is one instance of a major bleed. If
headache or altered level of consciousness occurs, treat as for
haemorrhagic stroke. Confirm diagnosis by CT scan if possible.
Obtain neurological opinion.
Note:- Local action of tranexaemic acid could be used for gum
bleeds ect. although not given in standard indications.
78

79. Monitoring for bleeding
a) Overt bleeding
b) Latent bleeding – best detected by pallor, Hb,
PCV
79

80. How do I assess reperfusion
following thrombolytic therapy?
1. Abrupt cessation of chest pain, which occurs after
completion of the SK infusion suggests satisfactory
reperfusion. However, this must be confirmed by ECG.
2. ST segment recovery is, so far, the best indicator of
reperfusion.
[In fact it is marginally better than coronary angiography in
predicting outcome after SK therapy].
• The ST elevation in lead (s) with greatest elevation
should fall by 50% in 60-90 min after fibrinolytic
therapy.
• Alternatively, we can take the sum of total ST elevations
in all leads. If this figure falls by 50% after SK, it
indicates good perfusion.
Continued….. 80

81. 3. Biochemical markers are also used to assess reperfusion. The
markers rise sharply with good reperfusion due to the “wash
out” phenomenon. This is not recommended in our setting as the
information obtained does not justify the cost in most instances.
4. Reperfusion arrhythmias – the common ones are AIVR &
S.bradycardia. AIVR needs no treatment. Sinus bradycardia is to
be treated.
*Reperfusion arrhythmias is too far infrequent to be of real value
in determining success of reperfusion.
81

82. Success of SK in achieving reperfusion is only 30%.
Success of tenecteplase is 60-65 %
82

83. What are the methods of infusing
other thrombolytic agents?
1. rtPA (Alteplase)
Total dose of rtPA is 100mg
 If within 6 hrs, a front loaded regimen is used:
IV bolus of 15mg tPA
Followed by, IV infusion of 50mg - Over 30 minutes
IV infusion of 35mg- Over 60 minutes
Total 100mg Total 90 minutes
 If within 6-12 hrs, the infusion is to be over 3 hours.
IV bolus of 10mg tPA
Followed by, IV infusion of 50mg - Over 60 minutes
IV infusion of 40mg- Over 120 minutes
Total 100mg Total 3 hours
83

84. 2. Reteplase
10U IV bolus over 2 minutes, then 30 minutes later 10U IV bolus over 2 minutes (i.e.
double bolus)
Note: incompatible with heparin; stop heparin during bolus or use alternative IV site.
3. TNK-tPA: Tenecteplase®:
Weight based, administer by IV bolus over 5 seconds.
Weight Dose Volume
<60kg 30mg 6cc
60-70kg 35mg 7cc
70-80kg 40mg 8cc
80-90kg 45mg 9cc
>90kg 50mg 10cc
Note: Incompatible with dextrose solutions. All agents should be followed by sc
enoxaparin.
84

85. How do I diagnose a RV infarction?
1. The following clinical triad in the presence of an acute
inferior STEMI, indicates RV infarction :-
I. Hypotension
II. Clear lung fields
III. Elevated JVP
2. ECG changes are few,
a) ST elevation> 1mm in V4R.
Within 10 hours, this ST elevation can fully resolve.
The inverted T waves, however would persist.
b) ST elevation>1mm in V1 and V2 may also indicate a
RV infarction, if an inferior infarction co-exists.
Continued….
85

86. How should a RV infarction be
managed?
1. The patient should be well hydrated.
• Check JVP –If the JVP is normal, the patient should be
well hydrated using oral fluids
• If JVP is low – iv fluids are necessary.
2. IV fluids must be given as follows, if invasive
haemodynamic monitoring is not being performed.
• 200ml N.Saline to be given over 10minutes (i.e. 100ml
over 5 minutes)
Continued….
86

87. If the patient tolerates this volume repletion without
evidence of pulmonary oedema, but systolic BP is still below
90mmHg, more fluids must be given as follows:
1000ml N.Saline – over 1hr.
Check the haemodynamic response and continue upto
2000ml over 2hrs.
3. If the BP remains below 90mmHg even after 2200ml of fluids
as given above, commence a dobutamine infusion.
Dobutamine – 5 micrograms/kg/minute and increased every
10 minutes as required.
87

88. Complications of AMI
There are 8 main complications of AMI. They are as follows:
I. Ischaemic complications
i. Reinfarction
ii. Post MI unstable angina
iii. Second infarction
II. Infarct area complications – aneurysm formation
III. Haemodynamic complications – Pulmonary oedema,
Cardiogenic shock
IV. Myomalacia related complications – MR, VSD, Cardiac
rupture
V. Pericarditis and effusions
VI. Immunolgic complications – Dressler’s syndrome
VII. Thromboembolic complications
VIII. Arrhythmic complications
88

89. Remodelling and Ventricular aneurysm formation
89

90. Remodelling ctd…
The infarcted segment thins & stretches = Infarct
expansion (occurs in few days)
This causes wall stress at the edges: Hence the
remainder of the LV dilates and hypertrophies =
remodeling (may go on for years)
• ACE-I reduce aneurysm formation.
• Complications of aneurysms
– LVF
– Thromboembolism (from mural thrombus)
– VT
90

91. Anticoagulants
Why give them?
– Reduce thromboembolic events
– Prevents reinfarction
Given for 8 day or until discharge or coronary
revascularization.
91

92. TIMI risk score for STEMI
92

93. Secondary prevention
This is an important concept.
One episode of ACI indicates the higher susceptibility of that
patient to develop acute decompensation.
Drugs : Aspirin
Beta blockers
ACE-I
Statins
Life style: smoking
exercise
diet
weight reduction
psychological rehabilitation
Co morbidities: Diabetes Mellitus, Hypertension, Chronic Kidney
Disease
93

94. Cardiac rehabilitation
94

95. Psychological rehabilitation
Emotional problems are very common:
Denial
Anxiety
Depression
95

96. What is the protocol for physical
activity after an AMI?
1. (a) Strict bed rest is recommended for at least 12 hrs.
(b) If no complications are present and the infarction is “small” (ie. 3
leads or less involved) –they may use a bedside commode after 12 hrs.
(c) If no complications are present but the infarct involves more than 3
leads – it may be prudent to extend the bed rest period up to 24 hrs.
2. Early ambulation is now the policy for uncomplicated infarcts.
After 24hrs- Walk around the bed
48hrs- Wash face, shave, sit out in a chair.
72hrs – Walk around ward for 3-5minutes.
96hrs – Walk around ward for 10-15minutes & attend to all normal
activities.
120hrs- Fit for discharge after ‘modified’ stress test.
3. The majority of symptoms that occur during early ambulation are related
to ‘postural hypotension’. Hence the initial stage of mobilization should
be under supervision of a nurse or physiotherapist.
Continued….
96

97. 4. In the case of larger infarcts, patients should be discouraged from
keeping their feet dependent even when seated (as hypotension can
ensue). However the seated up position itself is beneficial as it
reduces the PCWP slightly. Hence the ideal position for these
patients is the ‘propped up’ position and ‘seated up’ with lower
limbs kept straight and elevated.
5. Early ambulation is best done under telemetric monitoring &
preferably with BP monitoring.
6. Early ambulation offers much psychological benefit to patients.
7. The ‘Valsalva’ like exertions such as straining at stool etc. must be
avoided until full recovery.
97

98. What is an easy pre discharge checklist to
keep in mind?
A - Aspirin
Antianginal drugs
ACE inhibitors
B - Blood pressure
Beta blockers
Body mass index (i.e. weight)
C - Cigarette smoking
Cholestrol levels & statins
Clinical risk stratification
D - Dietary advise
Daily activities including sexual intercourse & driving
Diabetes
E - Exercise program
Exercise ECG dates
Employment – when to return 98

99. International classification of
myocardial infarction (MI)
99