Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 96

THE MANAGEMENT OF ACUTE

MYOCARDIAL INFARCTION
Dr. Celeste Maycock
Consultant Emergency Physician
University Hospital of the West Indies
Associate Lecturer
FMS Department of Surgery, Radiology, Anaesthesia and Intensive Care
University of the West Indies
1
Learning Objectives

 Define Acute Coronary Syndromes

 Consider the Why? (actions), When?


(indications), How? (dose), and Watch Out!
(precautions) of medications for ischemic chest
pain patients

2
Learning Objectives (cont’d)
 Recognize significant ST-segment changes

 Know how to measure ST-segment elevation


and depression

 Know basic principles of anatomic localization of


infarct

 Know how to use the ECG to manage patients

3
Myocardial Infarction
Mortality - the problem!!

 100 patients with acute MI

 50 dead within an hour

 2 to 8 die in hospital

 10 die thereafter in the first year

4
Missed Diagnosis In A&E

 USA
 2% of patients attending an emergency room
have chest pain

 5% AMIs are inadvertently discharged home

 40% malpractice payouts are for mismanaged


chest pain cases
5
Case
 37 yr old single mom F.R. receives Christmas gift
certificate to health club

 Tough first workout

 Generalized pain

 Pain in left shoulder worse

6
Case continued
 Fourth workout
 Pain radiated down left shoulder and arm

 Felt nauseated

 Stopped exercising

 Visited Emergency Department

7
 37 year old female

 Left shoulder pain

 X-rays ordered-normal

 Intern and ED resident


 Home
 Warm up
 Take ibuprofen

8
Case continued
 At 3:12 am – ambulance called
 F.R. Looks sick and has bad indigestion c/o a weird
achy feeling in her stomach
 B/P= 110/60
 HR= 122 bpm

 History of IDDM discovered (silent MI)

 Glucometer normal

 ECG changes of STEMI in II, III and AvF


9
 Unresponsive en
route to hospital

 Autopsy thrombus
consistent with an
AMI in the right
coronary artery
10
Criteria for Acute
Myocardial Infarction (MI)
 Any one of the following criteria

 Rise or fall of biomarkers (preferably Trop) with ≥ 1 value > 99 th


percentile URL and with ≥ 1 of the following:-

Ischaemic symptoms
New ST segment / T wave changes or new LBBB
Pathological Q waves
Imaging of loss of viable myocardium
Intracoronary thrombus by angiogram or autopsy

11
Criteria Continued
 Cardiac death with h/o symptoms + presumed new ischaemic
changes / LBBB on ECG (before blood samples obtained)

 PCI related increase in cardiac biomarkers

 CABG related increase in cardiac biomarker

 Stent thrombosis seen via angiogram or at autopsy + rise/ fall of


cardiac biomarkers

12
Criteria for Prior
Myocardial Infarction
 Any one of the following:

 Pathological Q waves ± symptoms

 Imaging evidence of loss of myocardium

 Pathological findings of a healed or healing


myocardium
13
Myocardial Infarction

Non - STEMI STEMI

14
Non - STEMI

 Criteria for acute MI (positive biomarkers)

 NO ST segment elevation on ECG


 ST depression
 Dynamic T wave inversions
 No change

15
STEMI

 Criteria for acute MI (positive biomarkers)

 ST segment elevation on ECG

16
Acute Coronary Syndrome

 Spectrum of thrombotic coronary artery


diseases

 Includes
 Unstable angina
 Non–ST-elevation MI(NSTEMI)
 ST-elevation MI(STEMI)

17
Unstable angina

 Characterized by the clinical presentation of


angina ± ischemic ECG changes (ST segment
depression or new T-wave inversion)

 Is usually a historical diagnosis

 NSTEMI is similar to UA but is characterized by


positive biomarkers

18
Unstable angina
 Rest angina – angina occurring at rest and prolonged (usually
>20 mins)

 New-onset angina (within 4 – 6 weeks)

 Increasing angina – previously diagnosed angina that has


become
 More frequent
 Longer in duration
 More severe
 Resulting in the use of more GTN

19
Management of Acute Myocardial
Infarction

26
The Acute Coronary Syndrome Algorithm
(2011 American Heart Association)

27
Step 1

28
History
50% who describe these pain symptoms
have MI
 Crushing
 Dull
 Heavy
 Tight
 Pressure

31
History of the Pain
 40% who describe either of these
have MI
Burning
Indigestion
 4 times risk of MI if patient’s pain radiates to
Jaw
Shoulder
Arm

32
History : The Pain

 Timing and duration


Beware pain waking patient in early
hours
Pain lasting longer than thirty
minutes high probability for MI
 Previous episodes

33
History :The Pain
 Relationship of pain to exertion
 Associated symptoms
 Breathlessness
 Syncope
 Palpitations
 Dizziness
 Sweating and pallor
 Anxiety
 Epigastric discomfort, burping (inferior MI)
 Vomiting, nausea

34
History
 Classical presentation - 54% of patients with
AMI

 46% of patients will present in an atypical


fashion

 It is in this atypical group that a significant


number of patients with AMI will be missed

35
History: Risk Factors
 Age
 Male>35; female>45
 Race
 Smoking
 Previous MI
 Hypertension
 Diabetes mellitus
 Raised cholesterol
 Positive family history

36
Newer Risk Factors

 HIV-protease inhibitors

 Systemic Lupus

 Cocaine/Meth use

37
Examination
 Usually normal
 Features of complication
Murmurs associated with
papillary muscle rupture
Signs of congestive cardiac
failure

38
Step 2: EMS

39
Step 2: EMS
 Aspirin
 Blocks formation of thromboxane A2
 Given on suspicion ASAP
 Dose: 160 – 325 mg chewed
 C/I: True ASA allergy, recent GI bleed

 Oxygen
 Administered if dyspneic, hypoxaemic, obvious
signs of heart failure
 O2 sat < 94% or unknown
 Dose: 4 L/min
40
Step 2: EMS
 Nitroglycerin
  pain of ischemia
  preload and cardiac oxygen consumption
 Dilates coronary arteries
  cardiac collateral flow

 Dose: 1 tablet / spray s.l. every 3 to 5 mins

 C/I: Hypotension, bradycardia, tachycardia,


Inferior wall and right ventricular infarction
Recent phosphodiesterase inhibitor use
41
Step 2: EMS
 Morphine
  pain of ischemia
  anxiety

 Chest pain with ACS unresponsive to nitrates


 STEMI
 Caution in NSTEMI / UA

 Dose: 2 – 4 mg iv (titrated)

 C/I: Respiratory depression, hypotension


42
Step 3: ED assessment /
treatment

43
Fibrinolytic Checklist

44
Contraindications to
fibrinolytic use in STEMI
 Absolute
 Any prior intracranial haemorrhage
 Known structural cerebral vascular lesion (e.g. AVM)
 Known malignant intracranial neoplasm
 Ischaemic stroke within 3 months EXCEPT acute ischaemic
stroke within 3 hours
 Suspected aortic dissection
 Active bleeding or bleeding diasthesis (excluding menses)
 Significant closed head trauma or facial trauma within 3
months

45
Contraindications to
fibrinolytic use in STEMI
 Relative
 H/O chronic, severe poorly controlled HTN
 Severe uncontrolled HTN (SBP>180, DBP
>110)
 H/O prior ischaemic stroke > 3 months,
dementia, or known intracranial pathology not
covered in C/I
 Traumatic or prolonged (>10 mins) CPR or
major surgery (<3 weeks)
 Recent (within 2 to 4 weeks) internal bleeding
46
Contraindications to
fibrinolytic use in STEMI
 Relative
 Noncompressible vascular punctures
 For Streptokinase / anistreplase: prior
exposure (>5 days ago) or prior allergic rxn to
these agents
 Pregnancy
 Active peptic ulcer
 Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding
47
Step 3: ED assessment /
treatment

48
Cardiac biomarkers

 Cardiac troponin is the preferred biomarker

 More sensitive and specific than CPK, CK-MB and


myoglobin

 Reperfusion therapy should not be delayed


pending results of biomarkers

 Enzymes are insensitive during the first 4 to 6


hours of presentation 49
Cardiac Enzyme Changes with
Myocardial Infarction

30x
Enzyme
levels 20x Myoglobin
Creatine Kinase
increased 10x Troponin
above normal
6x
2x
1x
0
1 2 3 4 5 6 7 8 10 11 12 13 14
Onset of
chest pain Time (days) 50
Step 3: ED assessment /
treatment

51
Chest X-ray

 Normal

 Features of congestive heart failure


 Cardiomegaly
 Cephalization of pulmonary vessels
 Fluid in septal lines (Kerley B lines)
 Alveolar oedema (Bat’s wing)

 Clues to other causes of chest pain


52
Aortic dissection

53
54
Aortic
Calcium dissection
sign

55
Pulmonary Embolism
Hampton’s hump

56
Step 3: Immediate ED general
treatment

57
Step 4: ECG interpretation

58
ST elevation MI (STEMI)

 ST elevation in 2 or more contiguous leads

 J point elevation ≥ 2mm (0.2 mV) in men,


and ≥ 1.5 mm (0.15 mV) in women in leads V2
and V3

 J point elevation ≥ 1mm in all other leads


European Society of Cardiology/ACCF/AHA/World Heart FederationTask Force for the Universal
Definition of Myocardial Infarction (2013 ACCF/AHA Guideline for the Management of ST-
Elevation Myocardial Infarction)

59
How to Measure
ST-Segment Deviation
J point

ST-segment deviation
PT baseline

60
Blood supply to heart

 Two coronary arteries

 Left coronary

 Right coronary

61
62
63
64
Contiguous leads

 Lateral  Septal
 I, aVL, V5, V6  V1, V2

 Inferior  Anterior
 II, III, aVF  V3, V4

 Posterior
 Tall r waves and ST
depression in V1 and V2
65
STEMI – Inferior wall

66
STEMI – Anterolateral wall

67
STEMI – Inferolateral
?Posterior wall
wall involvement

68
Posterior leads

69
Left Bundle Branch Block

 Complete:
 QRS duration > 0.12s (3 small boxes)
 Terminal S in V1
 Terminal R in 1, aVL, V6
 Poor R wave progression
 ST-T waves oriented opposite to direction of
terminal QRS (secondary)

 Incomplete: QRS 0.10 – 0.12s


70
Left Bundle Branch Block

71
Hyperacute T waves

72
Evolution of ECG in
acute STEMI
 A. Normal ECG prior to MI

 B. Hyperacute T wave changes -


increased T wave amplitude and width;
may also see ST elevation

 C. Marked ST elevation with hyperacute


T wave changes (transmural injury)

 D. Pathologic Q waves, less ST elevation,


terminal T wave inversion (necrosis)
 
 E. Pathologic Q waves, T wave inversion
(necrosis and fibrosis)

 F. Pathologic Q waves, upright T waves


(fibrosis)

73
Step 4: ECG interpretation

74
ST depression
 Significant ST depressions
 ≥ 0.5 mm (0.05 mV) in ≥ 2 contiguous leads

AHA: ACLS 2011 provider manual


75
Dynamic T–wave inversions

76
Step 4: ECG interpretation

77
ECG interpretation

78
Boxes 5 – 8 (Mgt of STEMI)

79
STEMI

 Usually have complete occlusion of a coronary


artery

 Primary goal of initial treatment is early


reperfusion therapy:

 Fibrinolytics (pharmacological reperfusion)

 Primary percutaneous coronary intervention


(mechanical reperfusion)
80
Fibrinolytics
 Breaks up the fibrin network that binds
clots together

 Pts treated within 70 mins of symptom onset


have >50%  in infarct size and 75%  in
mortality rates

 The goal is a door-to-needle time of < 30 mins

81
Fibrinolytics

 Examples of Fibrinolytics:
 Alteplase (tPA, Activase),
 Anistreplase (Eminase),
 Reteplase (Retavase)
 Streptokinase (Streptase),
 Tenecteplase (TNKase)

 Agents differ in their mechanism of action,


ease of preparation and administration;
cost; need for heparin
82
Percutaneous coronary
intervention

 Coronary angioplasty ± stent placement is the


treatment of choice for the mgt of STEMI

 Performed effectively with a door-to-balloon time


<90 mins

 Skilled provider (performing >75 PCIs per year) at a


skilled PCI facility (performing >200 PCIs annually, of
which ≥ 36 are primary PCI for STEMI)
83
Percutaneous coronary
intervention

84
Percutaneous coronary
intervention

85
Boxes 9 – 12 (Mgt of NSTEMI /
UA)

86
NSTEMI / UA
 Unstable angina (UA) and NSTEMI are difficult
to distinguish initially

 Partially or intermittently occluding thrombus

 Present with similar symptoms and ECG

 An elevated biomarker separates NSTEMI from


UA
87
Adjunctive therapies
 Heparin
 Indirect inhibitor of thrombin

 Unfractionated heparin / Low molecular weight


heparin

 Disadvantage of UFH
 Need for IV
 Frequent monitoring of PTT
 Can stimulate platelet activation 
thrombocytopenia
88
Heparin

 Unfractionated heparin
 Dose: Bolus of 60 units/kg (max: 4000 units),
infusion 12 units/kg/hr (max 1000 units/hr)

89
Clopidogrel
 Oral thienopyridine prodrug

 Inhibits the adenosine diphosphate receptor on the


platelet   platelet aggregation

 Indications
 STEMI / moderate or high risk NSTEMI including those
receiving fibrinolysis
 Limited evidence in pts ≥ 75 yrs
 Pt unable to take ASA

 Dose : 300 to 600mg stat then 75mg /day


90
β - blockers
 Blocks catecholamines from binding to ß-
receptors
  HR, BP, myocardial contractility
  incidence of primary VF

 STEMI:
  rates of recurrent ischemia and reinfarction
following reperfusion therapy

91
β - blockers

 NSTEMI:
 Oral β-blocker should be started within 24 hrs of
presentation

 Contraindication:
 CCF, low cardiac output state, PR interval >0.24
seconds, second- or third-degree heart block,
active asthma, or reactive airway disease

92
Glycoprotein IIb/IIIa
inhibitors
 Inhibit the IIb/IIIa receptor on platelets ,
blocking platelet aggregation

 Indication:
 High risk UA/ NSTEMI and pts undergoing PCI

 Examples:
 Tirofiban, eptifibatide and abciximab

93
Boxes 9 – 12 (Mgt of NSTEMI /
UA)

94
ACE inhibitors

 Reduces BP by inhibiting angiotensin-


converting enzyme (ACE)

 Alters post-AMI LV remodeling

 Delay progression of heart failure

 Reduces incidence of sudden death and


recurrent MI
95
HMG Coenzyme A Reductase
Inhibitors (Statins)

  incidence of reinfarction, recurrent angina,


and arrhythmias when administered

 Initiate within 24 hours of presentation

96
Boxes 13 – 17 (Mgt of low /
intermediate risk ACS)

97
Non-invasive diagnostic test
 Indication:
 Pts suspected of having ACS but have nonischemic
ECG's and negative biomarkers

 Aim:
 Induce myocardial ischemia ± anatomic evaluation of
the coronary arteries

 CT angiography, cardiac magnetic resonance,


myocardial perfusion imaging, stress
echocardiography
98
Combination of CT angiography (CTA)
and myocardial perfusion imaging
(MPI)

99
Boxes 13 – 17 (Mgt of low /
intermediate risk ACS)

100
Management

101
Summary
 Management of ACS
 Support of cardiorespiratory function
 Rapid transport to hospital
 Early classification of the patient based on ECG
characteristics
 Patients with STEMI require prompt reperfusion;
the shorter the interval from symptom onset to
reperfusion, the greater the benefit
 UA/NSTEMI or nonspecific or normal ECGs require
risk stratification and appropriate monitoring and
therapy
105
Thank you

106
References
 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care, Circulation. 2010;
122: S787-S817 doi: 10.1161/​CIRCULATIONAHA.110.97102
 Maame Yaa A.B. Yiadom, Emergency department treatment of
acute Coronary syndromes,, Emerg Med Clin N Am 29 (2011) 699–
710
 European Society of Cardiology/ACCF/AHA/World Heart
FederationTask Force for the Universal Definition of Myocardial
Infarction (2013 ACCF/AHA Guideline for the Management of ST-
Elevation Myocardial Infarction)
 EM practice - The Diagnosis And Treatment Of STEMI In The
Emergency Department
 EM Practice - Evaluation And Management Of Non–ST–Segment
Elevation Acute Coronary Syndromes In The Emergency Department

107

You might also like