2. Case scenario
A 60-year-old man presented to emergency department following the onset of chest pain approximately
two hours earlier. He had tried several doses of sublingual glyceryl trinitrates (GTN) but his pain had not
resolved. He had became increasingly breathlessness and clammy , with a tight crushing pain across his
chest and left shoulder .
PMH:
MI with CABG 2 years.
Hypertensive for 4 years. Angina 5 years. Diabetes mellitus 2 years.
FHx:
Both parents had HTN. Father had heart attack in his early 50’s and died in his 70’s of a second heart
attack; mother died a few years later from a stroke
Diagnosis ?
Investigations ?
Treatment ?
Complications ?
3. Learning Objectives
By the end of this tutorial you must be able to
1-identify the coronary artery and blood supply of the heart
2- define acute coronary syndrome and list the risk factors
3- illustrate pathophysiology of acute coronary syndrome
4- take proper focused history of chest pain
5-deffrentiate between all DD of chest pain
6- identify ECG changes during myocardial ischemia
7-treat acute coronary syndrome as emergency and long term management
4. Acute coronary syndrome
Acute coronary syndromes (ACS) encompass a spectrum of unstable
coronary artery disease
Patients with ACS include those whose clinical presentations cover the
following diagnoses:
Unstable angina
Non-ST-elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI).
9. Lesser Factors
• Obesity
• Physical inactivity or sedentary lifestyle
• Stress, lack of social support, depression
• Homocysteine ;It is amino acid, may have an effect on atherosclerosis by damaging the inner lining of arteries and
promoting blood clots.
• Postmenopausal estrogen deficiency
• High carbohydrate intake Alcohol consumption Lipoprotein A
• Consumption of hardened fat (Diet ; high in satuarted fats and cholestrol is associated with high TG,LDL, VLDL.)
• Chlamydiae pneumonia infection
10. pathophysiology
An imbalance between the supply of oxygen and the myocardial
demand resulting in myocardial ischaemia
Supply
Atheroma, thrombosis, spasm, embolus
Demand
Anaemia, hypertension, high cardiac output (thyrotoxicosis, myocardial
hypertrophy)
11. Response to injury hypothesis
ATHEROSIS
Accumulation of cholesterol within the vessel wall intima. Smooth muscle cell proliferation
SCLEROSIS
Expansion of fibrous tissue
INFLAMMATION
Chronic inflammatory cells migrate into wall, release cytokines
GROWTH FACTORS/INFLAMMATORY MEDIATORS
Pathogenesis of Atheroma
1. Fatty streak development
2. Atheromatous plaque development
3. Thrombus development
12.
13. MI : Sequence of events
usually resulting from acute plaque changes (fissuring ulceration ,rupture or
erosion ) -> exposed collagen -> plt aggregation -> thrombus formation ->
thrombus evolved -> vaso-occlosion -> ischemia (prolonged ) -> myocardial
infarction
14.
15. Pathophysiology of all 3 is the same
Unstable Angina (UA)
ST depression, T Wave inversion or normal
No enzyme release
Non-Transmural Myocardial Infarction (NTMI or SEMI)
ST depression, T Wave inversion or normal
No Q waves
CPK, LDH + Troponin release
Transmural Myocardial Infarction (AMI)
ST elevation
+ Q waves
CPK, LDH + Troponin release
16. Clinical presentation
Acute central chest pain, lasting >20min, often associated with nausea,
sweatiness, dyspnoea, palpitations. ACS without chest pain is called
‘silent’; mostly seen in elderly and diabetic patients.
Silent MIs may present with: syncope, pulmonary oedema, epigastric pain
and vomiting, post-operative hypotension or oliguria,
acute confusional state, stroke, and diabetic hyperglycemic states
17. Focused history of chest pain
Personal data
Age, sex, occupation
Chief complain
Chest pain for …
History of presenting complain
SOCRATES
Site of pain: Central, retrosternal, diffused Onset: sudden or gradual Character: crushing, stabbing, heavy
Radiation: to arm, shoulder, neck or jaw Associations: shortness of breath, nausea, sweating, palpitation
Timing: Duration
Exacerbating and alleviating factors: Worse with respiration or movement, changing in position Relieving factor: by rest, analgesia or GTN
Severity: (mild, moderate, severe) out of 10
If patient is known case of angina or chest pain in the past, relation of pain with exercise
Cough, tachypnea, orthopnea, syncope, lower limp edema history of trauma
18. Systemic review:
Full systemic review
Especially: Cough, hemoptysis, fever, heartburn, weight loss, symptoms of heart failure
Past medical history;
Similar condition angina, any previous heart attack or stroke other cardiac diseases DM hypertension
hypercholesterolemia renal disease obesity
Oseophgeal diseases PUD asthma DVT
Family history;
Similar condition DM hypertension cardiac diseases sudden death hypercholesterolemia obesity Renal
disease
Social history:
Socioeconomic status Social surrounding Social habit (smoking ,alcohol)
health insurance
Drug history:
Allergy Long term medication (aspirin, nitrite ...) Current medication
19. Differential Diagnosis of Chest pain
Ischemic heart disease (acute coronary syndromes, stable angina)
Pleurisy
Esophageal disease (GERD, diffuse oseophgeal spasm)
Musculoskeletal chest pain
Dissection of the aorta
Disease of the spine
Herpes zoster
Nonspecific chest pain
PE
pneumothorax
Pericarditis
20. PHYSICAL EXAMINATION
patients usually appear restless and in distress.
The skin is warm and moist.
Breathing may be labored and rapid. Fine crackles, coarse crackles, or rhonchi may be heard when auscultating the lungs.
an increased blood pressure related to anxiety or a decreased blood pressure caused by heart failure.
The heart rate may vary from bradycardia to tachycardia.
When the patient is placed in the left lateral decubitus position, abnormalities of the precordial pulsations can be felt. These abnormalities
include a lack of a point of maximal impulse or the presence of diffuse contraction.
On auscultation, the first heart sound may be diminished as a result of decreased contractility.
A fourth heart sound is heard in almost all patients with MI, whereas a third heart sound is detected in only about 10% to 20% of patients.
Transient systolic murmurs may be heard
After about 48 to 72 hours, many patients acquire a pericardial friction rub
Patients with right ventricular infarcts may present with jugular vein distension, peripheral edema, and an elevated central venous pressure.
21. Investigations
General (routine investigations ): CBC , RFT , RBS , U.G , ESR
Specific investigation :
Lipid profile
TFT
Electrocardiogram ECG
Serum Markers of Infarction (Troponin I and T , CK-MB)
Chest x-ray
23. Serum Markers of Infarction
Certain proteins are released into circulation during an MI
Creatine kinase CK rises in plasma within 4 to 8 hours, peaks at 24 hours,
returns to normal by 48 hours to 72 hours
Not specific for myocardial damage: skeletal muscle trauma and IM
injection, and hypothyroidism
24. CK-MB
CK-MB isoenzyme is more specific for diagnosis of AMI Not influenced by
skeletal muscle injuries
CK-MB rises and peaks slightly earlier than total CK and returns to normal
within 36 – 72 hours
May be elevated in: myocarditis after surgery, hypothyroidism, repetitive
cardioversion
Acute MI: CK-MB is greater than 2.5% of total serum CK
Serum CK and CK-MB isoenzyme should be measured on admission, then
12 and 24 hours later in diagnostic evaluation of an acute MI
25. Troponin
Troponin I and T are sensitive and highly specific markers of acute MI
Levels begin to rise within 3 hours after onset of infarction and remain
elevated for several days
Higher Troponin I levels or early (+) of Troponin T assay correlate with
greater short-term mortality
26.
27. ECG
Five-step (and nine-step) process
• The five-step process (and nine-step) is a logical and systematic process for analyzing ECG tracings
1. Determine the rate. (Is it normal, fast, or slow?)
2. Determine the regularity. (Is it regular or irregular?)
3. Assess the P waves. (Is there a uniform P wave preceding each QRS complex?)
4. Assess the QRS complexes. (Are the QRS complexes within normal limits? Do they appear normal?)
5. Assess the PR intervals. (Are the PR intervals identifiable? Within normal limits? Constant in duration?)
6. Assess the ST segment. (Is it a flat line? Is it elevated or depressed?)
7. Assess the T waves. (Is it slightly asymmetrical? Is it of normal height? Is it oriented in the same direction as the
preceding QRS complex?)
8. Look for U waves. (Are they present?)
9. Assess the QT interval. (Is it within normal limits?)
28.
29. The ECG can help identify the presence of
ischemia, injury, and/or infarction of the heart
muscle.
• The three key ECG indicators are:
∞ Changes in the T wave (peaking or inversion).
∞ Changes in the ST segment (depression or elevation).
∞ Enlarged Q waves or appearance of new Q waves.
• ST segment elevation is the earliest reliable sign that myocardial infarction has occurred
and tells us the myocardial infarction is acute.
• Pathologic Q waves indicate the presence of irreversible myocardial damage or past
myocardial infarction.
• Myocardial infarction can occur without the development of Q waves.
30.
31.
32. Identifying the location of myocardial
ischemia, injury, and infarction
ECG changes Coronary artery
anterior myocardial
infarction.
Leads V1, V2, V3, and
V4
Left anterior
descending
septal infarctions. Leads V1, V2, and V3 Left anterior
descending
Lateral infarction leads I, a VL, V5, and
V6.
Left circumflex
Inferior infarction leads II, III, and aVF. Right coronary
Posterior infarctions reciprocal changes in
leads V1 and V2.
Left c, rt coronary
37. Treatment
the goals of pharmacotherapy for IHD as general
Decrease amount of myocardial necrosis
a. Preserve LV function b. Prevent HF
• Prevention of major adverse cardiac events( death & non fatal MI)
• Pain relief
Treatment of acute life threatening complications
Modifying risk factors
Improve the quality of life
Prevent coronary artery reocclussion
38. immediate goals of therapy include:
(1) relief of ischemic chest discomfort : (oxygen,nitrate,morphine)
(2) early restoration of blood flow (reperfusion)
To the infarct-related artery to prevent infarct expansion:(asprin&PCI or fibrinolytics)
(3) prevention of coronary artery reocclusion &systemic embolization:(anticoagulants).
(4) Prevention of complications and death:
(long term use of aspirine,B blocker,ACEI)
(5) maintenance of normoglycemia
39. According to the American College of Cardiology/American Heart
Association
(ACC/AHA) practice guidelines, early pharmacologic therapy should
include:
(1) intranasal oxygen (if oxygen saturation is less than 90%)
(2) sublingual (SL) nitroglycerin (NTG) (3) aspirin (4) aβ-blocker
(5) unfractionated heparin (UFH) or enoxaparin
(6) fibrinolysis in eligible candidates.
Morphine is administered to patients with refractory angina as an analgesic and venodilator
that lowers preload.
These agents should be administered early while the patient is still in the emergency
department.
7)An angiotensin-converting enzyme (ACE) inhibitor should be started within 24 hours of
presentation, particularly in patients with left ventricular ejection fraction (LVEF) ≤40%,
signs of heart failure, or an anterior wall MI, if there are no contraindications
40.
41.
42. For patients with STE ACS primary PCI (with either balloon angioplasty or stent
placement) is the treatment of choice for reestablishing coronary artery blood flow when the
patient presents within 3 hours of symptom onset.
Primary PCI may be associated with a lower mortality rate than fibrinolysis, possibly
because PCI opens more than90% of coronary arteries compared with less than 60%
opened with fibrinolytics. The risks of intracranial hemorrhage (ICH) and major bleeding
are also lower with PCI than with fibrinolysis
If a patient undergoes PCI,
UFH is discontinued immediately after the procedure..
43. For patients undergoing primary PCI, clopidogrel is administered as a 300- to 600-mg
loading dose followed by a 75 mg/day maintenance dose, in combination with aspirin 325
mg once daily, to prevent subacute stent
thrombosis and long-term cardiovascular events.
Abciximab is a first-line GP IIb/IIIa inhibitor for patients undergoing primary PCI who
have not received fibrinolytics. It should not be administered
to STE ACS patients who will not be undergoing PCI. .
44. Complications of myocardial infarction
Heart failure
Rupture of free wall of infarcted ventricle (usually fatal)
Rupture of the interventricular septum (ventricular septal defect)
Mitral regurgitation
Arrhythmias
Heart block
Pericarditis
Thromboembolism
Dressler’s syndrome
Ventricular aneurysm
45. Prognosis
Prognosis is variable depending on factors such as age and size of infarct.
Fifty per cent of patients die during the acute event, many before
reaching hospital. A further 10% die in hospital, and of the survivors a
further 10% die in the next 2 years.
48. References
Wilkinson, Ian et al. Oxford Handbook Of Clinical Medicine. Oxford: Oxford
University Press, 2017.
"Myocardial Infarction: Practice Essentials, Background,
Definitions." Emedicine.medscape.com. N.p., 2017. Web. 8 Oct. 2017.
Pharmacotherapy Handbook Seventh Edition Barbara G. Wells, PharmD, FASHP,
FCCP, BCPP & Joseph T. DiPiro, PharmD, FCCP
Essentials of clinical medicine KUMAR and CLARK’S – FIFTH EDITION
