ACS Flashcards
(20 cards)
Describe the pathophysiology of Atherosclerosis (Coronary
Artery Disease).
Atherosclerosis is a chronic inflammatory condition of the arterial wall, primarily affecting medium and large arteries, such as coronary arteries.
Mechanism:
1. Endothelial Injury:
Caused by hypertension, smoking, hyperlipidemia, diabetes.
- LDL Infiltration:
LDL cholesterol enters the intima and becomes oxidized. - Inflammatory Response:
Macrophages engulf oxidized LDL → become foam cells → form fatty streaks. - Plaque Formation:
Smooth muscle proliferation, collagen deposition, and lipid core develop → fibrous plaque. - Plaque Rupture or Erosion:
Exposes thrombogenic material → platelet aggregation → thrombus formation → acute coronary event.
Define the different types of Acute Coronary Syndrome
(ACS).
ACS is a spectrum of conditions caused by sudden reduction in coronary blood flow due to atherosclerotic plaque rupture or erosion.
Types of ACS:
1. Unstable Angina (UA): Ischemia without myocardial necrosis (no elevated troponin).
- Non-ST Elevation Myocardial Infarction (NSTEMI): Ischemia with myocardial necrosis (elevated troponin) but no ST elevation on ECG.
- ST Elevation Myocardial Infarction (STEMI): Full-thickness myocardial infarction with ST elevation and elevated troponins.
What is Angina?
caused by myocardial ischemia which could either be caused by decreased myocardial oxygen supply OR increased myocardial oxygen demand
What are the causes of decreased myocardial oxygen supply?
Coronary artery diseases e.g atherosclerosis or Severe anaemia
What are the causes of increased myocardial oxygen demand?
Left Ventricular hypertrophy e.g hypertension or aortic stenosis OR Right Ventricular hypertrophy e.g pulmonary hypertension. Or Rapid tachyarrythmias.
What is stable Angina?
chest discomfort and associated symptoms precipitated by a stimulus (running, walking, cold weather, eating etc.)
minimal or non-existent symptoms at rest or with administration of sublingual nitroglycerin (GTN – glyceryl trinitrate).
What is unstable angina?
Unstable angina= ACS
It has at least one of these three features:
It occurs at rest (or with minimal exertion), usually lasting >10 min;
It is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
It occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before).
No dynamic rise and fall in troponin
Indicates high risk for coming MI.
What is the definition of a myocardial infarction?
Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin] with at least one value above the 99th percentile upper reference limit and with at least one of the following:
1. Symptoms of ischaemia.
2. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB).
3. Development of pathological Q waves in the ECG.
4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
5. Identification of an intracoronary thrombus by angiography or autopsy
What is a key feature of the levels of troponin in STEMI and NSTEMI?
rise and fall in troponin. there are two peaks
What is troponin?
Troponin I or T
Part of cardiac and skeletal muscle
Many hospitals use troponin T (high sensitivity)
Highly sensitive and specific marker of myocardial necrosis.
Use troponins in clinical context!
Troponins can be elevated in
Renal impairment
Pulmonary embolism
Critical illness- sepsis
Inflammatory disease- myo/pericarditis
Acute neurological disease
Aortic dissection
Cocaine use
After endurance exercise.
What are the symptoms ischemia?
Chest pain
Shortness of breath
Syncope
Palpitations
What does SOCRATES look like for cardiac chest pain?
S- Centre/ left side of chest
O- On exertion (though MI can be at rest)
C- Crushing/ squeezing
R- To arm/ jaw
A- Sweaty, clammy, cold, nausea and vomiting, impending sense of doom.
T- >15 mins
E- Exertion makes it worse. May be relived by GTN
S- Bad pain- >6/10. Bad enough to stop people from doing what they are doing and to wake from sleep.
What are the types of myocardial infarction?
There are 5 types but only type 1 and type 2 are clinically relevant.
Type 1:
- Caused by plaque rupture
Causes decreased or absent distal blood flow leading to myocardial necrosis
- NSTEMI and STEMI are subtypes
Type 2:
Caused by a condition, OTHER THAN CORONARY PLAQUE INSTABILITY, which cause imbalance in oxygen supply and demand.
Coronary artery spasm
Tachyarrhythmia
Bradyarrhythmia
Anaemia
Sepsis
Volume depletion
Toxins
Describe the mechanism of pathophysiology for each Acute Coronary Syndrome.
Unstable Angina:
A partially occlusive thrombus limits coronary blood flow.
No myocardial necrosis occurs, so troponin remains normal.
NSTEMI:
A partially occlusive thrombus causes subendocardial infarction.
Troponin levels are elevated due to myocyte death, but no ST elevation occurs due to incomplete damage.
STEMI:
A fully occlusive thrombus causes transmural (full-thickness) myocardial infarction.
Leads to ST elevation, troponin elevation, and wall motion abnormalities.
Describe the symptoms, clinical features and mechanisms
for the following:
- Ischaemic Heart Disease ; Myocardial Infarction ; Unstable
Angina ; Prinzmetal (Variant) Angina.
- Ischaemic Heart Disease (IHD):
Chronic atherosclerotic narrowing of coronary arteries.
Symptoms: Angina, breathlessness, fatigue.
Mechanism: Demand > supply of oxygen due to narrowed vessels. - Myocardial Infarction (MI):
Prolonged ischemia causes irreversible myocardial necrosis.
Symptoms: Crushing chest pain, radiation to arm/jaw, nausea, diaphoresis, breathlessness. - Unstable Angina:
Plaque instability with thrombus, but no infarction.
Symptoms: New-onset, worsening, or rest angina. - Prinzmetal (Variant) Angina:
Coronary vasospasm, often without significant atherosclerosis.
Symptoms: Occurs at rest, often at night or early morning.
ECG may show transient ST elevation during attacks.
List the key features of each Acute Coronary Syndrome seen in blood tests and other relevant diagnostic tests and
imaging.
Blood Tests:
Troponin I or T: Elevated in NSTEMI and STEMI, normal in unstable angina.
CK-MB: Less specific than troponin.
ECG Findings:
STEMI: ST elevation in specific leads, new LBBB, Q waves later.
NSTEMI/UA: ST depression, T-wave inversion, or normal ECG.
Imaging:
Echocardiography: Detects wall motion abnormalities.
Coronary Angiography: Visualizes coronary artery blockages.
CT Coronary Angiogram (CTCA): For stable IHD assessment.
Explain the evidence-based pharmacological treatment for
all Acute Coronary Syndromes.
Initial Management (All ACS):
1. MONA:
Morphine for pain relief.
Oxygen if O₂ saturation <94%.
Nitrates (sublingual GTN or IV) to relieve ischemia.
Aspirin 300 mg loading dose.
- Dual Antiplatelet Therapy (DAPT):
Aspirin + Clopidogrel / Ticagrelor / Prasugrel.
Continue for 12 months, then aspirin long-term. - Anticoagulation:
Fondaparinux (preferred in NSTEMI).
Unfractionated heparin if angiography is planned within 24 hrs or if STEMI. - STEMI-Specific:
Primary PCI (within 120 minutes of call to balloon time).
Thrombolysis (e.g., alteplase) if PCI unavailable.
Other Key Medications:
Beta-blockers: Reduce myocardial oxygen demand.
Statins (e.g., Atorvastatin 80 mg): Reduce cholesterol and stabilize plaques.
ACE inhibitors or ARBs: For LV dysfunction or hypertension.
Aldosterone antagonists: For heart failure or reduced EF post-MI.
Describe the short-term and long-term management of
Acute Coronary Syndromes.
Short-Term:
Admit to high-dependency or cardiac care unit.
Cardiac monitoring for arrhythmias.
Urgent PCI or fibrinolysis if STEMI.
Early initiation of DAPT, statins, beta-blockers, ACEi.
Long-Term:
Continue aspirin + secondary prevention drugs (statins, beta-blockers, ACEi).
Lifestyle modifications: Smoking cessation, diet, exercise.
Cardiac rehabilitation: Structured exercise, education, psychological support.
Control comorbidities: Diabetes, hypertension, dyslipidemia.
Outline national guidance (i.e. NICE guidelines) for Acute
Coronary syndrome.
NG185 (2020): Management of ACS with and without ST elevation.
- Recommends early risk stratification (GRACE score).
- PCI within 24–96 hours for NSTEMI depending on risk.
CG172: Focus on secondary prevention.
- Emphasizes lifestyle advice, drug therapy, and rehabilitation.
NG17: Lipid modification and statin use post-MI.
- High-intensity statin (atorvastatin 80 mg) for all post-ACS.
Describe the importance of recognising current co-
morbidities and their ability to cause Acute Coronary Syndrome
Co-morbid conditions significantly increase the risk of ACS and worsen outcomes:
Diabetes Mellitus: Accelerates atherosclerosis and increases MI risk.
Chronic Kidney Disease: Associated with vascular calcification and endothelial dysfunction.
Hypertension: Damages arterial walls and promotes plaque development.
Dyslipidemia: High LDL promotes atherosclerosis.
Smoking: Causes endothelial damage and promotes thrombosis.
Obesity and Sedentary Lifestyle: Increase metabolic risk factors and inflammation.
NICE encourages holistic assessment and management of these conditions alongside ACS treatment to reduce recurrence and mortality.
