6. ⢠Over time
atherosclerotic
plaques can build up
within these arteries.
⢠Caused by non
modifiable risk factors
such as
⢠Aging,
⢠Male sex,
⢠Family history and
⢠Certain ethnicities
such as being
caucasian.
PATHOPHYSIOLOGY OF ACS
7. PATHOPHYSIOLOGY OF ACS
⢠The plaque rupture and thrombus formation causes partial
occlusion causing NSTEMI
⢠Rupture of the plaque can result in total occlusion of the vessel and
thus no oxygen supply to that area.
⢠This causes STEMI.
⢠Risk factors here are modifiable such as smoking, hypertension,
dyslipidaemia, poor diet, diabetes and a sedentary lifestyle.
8. PATHOPHYSIOLOGY OF ACS
The build up of plaques can lead to a reduction of blood flow
to the cardiomyocytes leading to poor oxygen supply causing
symptoms (eg Chest pain).
10. CLINICAL PRESENTATION
ACS is a medical emergency that presents with:
⢠Central chest pain
â Described as a crushing sensation or heaviness or
chest tightness.
â Pain can radiate to the neck, jaw and left arm.
⢠Sympathetic responses of diaphoresis and
âfeeling of impending doomâ
⢠Parasympathetic responses of nausea and
vomiting.
12. INVESTIGATIONS
⢠ECG
⢠CBC
⢠Electrolytes, Renal function test (RFT)
⢠Random blood sugar (RBS)
⢠Cardiac enzymes (Troponin and CKMB)
⢠Coagulation profile
⢠Other investigations include Chest Xray and
lipid profile.
13. Importance of cardiac enzymes
Troponin is a contractile protein that is not normally found in serum;
it is released only when myocardial necrosis occurs.
14. ECG changes in ACS
⢠ECG is important to diagnose STEMI and
NSTEMI.
⢠20% are initially normal.
⢠In NSTEMI, ECG is usually normal or there is a
t wave inversion.
⢠Incidence of myocardial infarction occurs is
highest in the LAD, then RCA and left
circumflex artery.
17. NSTEMI
⢠It is called so because there is no ST segment
elevation.
ECG changes in ACS
18. ST ELEVATION
STEMI is defined as new ST elevation at the J point in at least two
contiguous leads of 2 mm (0.2 mV) or more in men or 1.5 mm (0.15
mV) in women in leads V2-V3 and/or 1 mm (0.1 mV) or more in other
contiguous limb leads
19. STEMI
⢠Usually from a complete occlusion of the
vessel leading to a transmural infarction.
⢠ST segment elevation occurs.
⢠Transmural infarction can also lead to a new
left bundle branch block.
⢠The Sgarbossa criteria are the most validated
tool to aid in the diagnosis of STEMI in the
presence of LBBB.
ECG changes in ACS
22. ANTERIOR MI
⢠ST segment elevation in the anterior leads (V3 and V4) at the J
point and sometimes in the septal or lateral leads, depending on
the extent of the MI.
⢠Reciprocal ST segment depression in the inferior leads (II, III and
aVF).
24. POSTERIOR MI
⢠ST segment depression (not elevation) in the septal and
anterior precordial leads (V1-V4).
⢠A R/S wave ratio greater than 1 in leads V1 or V2.
⢠ST elevation in the posterior leads of a posterior ECG
(leads V7-V9).
⢠Suspicion for a posterior MI must remain high, especially
if inferior ST segment elevation is also present.
25. POSTERIOR MI
⢠Isolated posterior MI is less common (3-11% of infarcts).
⢠Posterior extension of an inferior or lateral infarct implies a much
larger area of myocardial damage, with an increased risk of left
ventricular dysfunction and death.
26. The ECG leads on which an MI change appears can be
used to locate the artery that had been occluded as
shown in the table
28. Acute Coronary Syndrome
ST Elevation No ST elevation
NSTEMI Unstable angina
Electrocardiogram
Cardiac markers
DIAGNOSTIC FLOW CHART
29. MANAGEMENT
⢠This may differ with hospital or country
protocols.
⢠Initial management (MOAN)
⢠Morphine
⢠Oxygen
⢠Aspirin and clopidogrel
⢠Nitrates
30. STEMI
Emergency reperfusion through
⢠Primary percutaneous intervention (First
choice if available and early presentation).
⢠Fibrinolytic therapy using
â Streptokinase
â Alteplase
â Reteplase
MANAGEMENT
37. CONCLUSION
⢠Acute coronary syndrome is caused by partial or
complete obstruction of blood flow to the heart
muscles.
⢠It is a medical emergency and is diagnosed by
history, physical examination and investigations.
⢠ECG findings of ST elevation or depression are
commonest in ACS.
⢠Cardiac enzymes especially troponin has a high
sensitivity.
⢠Management includes fibrinolysis and
percutaneous coronary intervention.
The 2 main coronary arteries are the left main and right coronary arteries.
Left main coronary artery (LMCA). The left main coronary artery supplies blood to the left side of the heart muscle (the left ventricle and left atrium). The left main coronary divides into branches:
The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left side of the heart.
The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the outer side and back of the heart.
Right coronary artery (RCA). The right coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes, which regulate the heart rhythm. The right coronary artery divides into smaller branches, including the right posterior descending artery and the acute marginal artery. Together with the left anterior descending artery, the right coronary artery helps supply blood to the middle or septum of the heart.
Smaller branches of the coronary arteries include: obtuse marginal (OM), septal perforator (SP), and diagonals.
Angina is chest pain on exertion.
This is because when you exert yourself, the heart needs more oxygen or blood supply but because the vessels canât meet the demands of the heart you get angina as a result.
Angina: stable or unstable (there are other classification such as prinzmetal, microvascular etc)
Stable angina = chest pain comes with exertion and relieved by rest
Unstable = chest pain at rest
In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion.
Note that blood supply is from outside inside
Subendocardial infarct = zone of necrosis and zone of ischaemia proximal to the vessel- seen in NSTEMI
Transmural infarct = only zone of necrosis- seen in STEMI
Pericarditis: Sharp, piercing chest pain over the center or left side of the chest, which is generally more intense when breathing in. Shortness of breath when reclining. Heart palpitations. Low-grade fever. Sitting up and leaning forward can often ease the pain.
Endocarditis: Flu-like symptoms, such as fever and chills. A new or changed heart murmur, Fatigue. Aching joints and muscles. Night sweats.
Shortness of breath. Chest pain when you breathe.
Ruptured aortic aneurysm: Sudden, intense and persistent abdominal or back pain, which can be described as a tearing sensation. Low blood pressure. Fast pulse.
When infarction takes place it leads to death of the cardiomyocyte (coagulative necrosis).
These necrotic cardiomyocytes release certain chemicals into the blood.
Cardiac muscles are composed of actin and myosin filaments.
Actin have troponin on them that helps in muscle contraction.
Creatinine kinase MB is important for energy transfer of ATP within the cells.
These enzymes (Troponin and CKMB are released into blood when the heart muscle dies).
Troponin rises significantly and peaks at day 2 after the attack while CKMB rises but not so much and regresses faster.
Measuring cardiac markers is thus important in STEMI and NSTEMI: however these markers are unchanged in angina.
Myoglobin is released into circulation with any damage to muscle tissue
A standard 12 lead ECG consist of six limb leads called lead I, II, III, aVL, aVR and aVF. The letter âaâ stands for âaugmented,â as these leads are calculated as a combination of leads I, II and III.
The six precordial leads are called leads V1, V2, V3, V4, V5 and V6.
Left anterior descending artery supplies the anterior and part of the septum.
Left cicumflex supplies the lateral wall
Right coronary supplies the posterior and right walls.
There could be an ST segment depression or inverted T wave.
Wellens syndrome is a pattern of inverted or biphasic T waves in V2-4 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery.
LBBB = W shaped QRS wave in V1 and M shaped QRS in V6.
Three criteria are included in Sgarbossa's criteria: ST elevation âĽ1 mm in a lead with a positive QRS complex (ie: concordance) - 5 points. concordant ST depression âĽ1 mm in lead V1, V2, or V3 - 3 points. ST elevation âĽ5 mm in a lead with a negative (discordant) QRS complex - 2 points.
An inferior wall myocardial infarction â also known as IWMI, or inferior MI, or inferior ST segment elevation MI, or inferior STEMI â occurs when inferior myocardial tissue supplied by the right coronary artery, or RCA, is injured due to thrombosis of that vessel.
An anterior wall myocardial infarction â also known as anterior wall MI, or AWMI, or anterior ST segment elevation MI, or anterior STEMI â occurs when anterior myocardial tissue usually supplied by the left anterior descending coronary artery suffers injury due to lack of blood supply.
When an AWMI extends to the septal and lateral regions as well, the culprit lesion is usually more proximal in the LAD or even in the left main coronary artery.
This large anterior myocardial infarction is termed an extensive anterior.
This occurs because these ECG leads will see the MI backwards; the leads are placed anteriorly, but the myocardial injury is posterior. A R/S wave ratio greater than 1 in leads V1 or V2.
Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.
At the beginning when the inflammatory process begins (with coagulative necrosis and surrounding oedema): there is ST elevation and a peaked T wave.
12 â 24 hours after: there is neutrophil infiltration: ST elevation is still present, maybe a pathological Q wave (Q wave duration of > 40 milliseconds (one small box)) and inverted T wave.
(Q waves are considered pathological if: > 40 ms (1 mm) wide; > 2 mm deep; > 25% of depth of QRS complex; Seen in leads V1-3)
Within the first week: there is cardiomyocyte death, neutrophil death and macrophages start clearing the dead cells. Fibroblast infiltration and tissue repair. There is pathological Q wave and T wave inversion here.
Weeks to months: fibroblasts and collagen deposition = pathological Q wave.
PCI was formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter to place a stent to open up blood vessels in the heart that have been narrowed by plaque buildup
Streptokinase: Allergic reactions force the termination of many infusions. The adult dose of streptokinase for AMI is 1.5 million U in 50 mL of 5% dextrose in water (D5W) given IV over 60 minutes.
Alteplase: can be administered in an accelerated infusion (1.5 hr) using 50-mg and 100-mg vials reconstituted with sterile water to 1 mg/mL. Accelerated infusion of alteplase for AMI consists of a 15-mg IV bolus followed by 0.75 mg/kg (up to 50 mg) IV over 30 minutes and then 0.5 mg/kg (up to 35 mg) IV over 60 minutes. maximum total dose is 100 mg for patients weighing more than 67 kg.
Reteplase: The adult dose of reteplase for AMI consists of two IV boluses of 10 units each; there is no weight adjustment. The first 10-unit IV bolus is given over 2 minutes; 30 minutes later, a second 10-unit IV bolus is given over 2 minutes. Administer normal saline (NS) flush before and after each bolus.
Grace score ranges between 2 and 372.
Killip class is used to assess heart failure or pulmonary congestion in MI
The Thrombolysis in Myocardial Infarction (TIMI) Score is used to determine the likelihood of ischemic events or mortality in patients with unstable angina or nonâST-segment elevation myocardial infarction (NSTEMI). Total maximum score of 7. (Score of 0-1 = 4.7% risk - Score of 6-7 = at least 40.9% risk
Newer chest pain risk scores such as the HEART Score have been shown to better stratify risk than the TIMI Score, particularly in the undifferentiated chest pain patient.
A MACE (Major Adverse Cardiac Event) was defined as all-cause mortality, myocardial infarction, or coronary revascularization.
High risk patients would benefit from antiplatelets, anticoagulant therapy and beta blockers. Consider for glycoprotein IIb/IIIa inhibitors and revascularization using angioplasty or stenting.
Low or intermediate risk patients require continuous monitoring of cardiac enzymes and ECG and reassessment. If it becomes high risk then move to high risk management otherwise discharge home after a while with no changes for cardiologist follow up.
