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ACS Flashcards

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1
Q

What does the term “Acute Coronary Syndrome” (ACS) refer to? .

A

(STEMI),
(NSTEMI),
unstable angina

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2
Q

How is unstable angina different from NSTEMI?

A

NSTEMI and Unstable Angina both has ischemic symptoms but an elevation in troponins is seen in NSTEMI.

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3
Q

What is ischaemic heart disease, and how is it related to ACS?

A

Ischaemic heart disease (also known as coronary artery disease) involves the gradual build-up of fatty plaques within the coronary arteries, leading to decreased blood flow and oxygen delivery to the myocardium. This can result in ACS events like STEMI, NSTEMI, and unstable angina.

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3
Q

Why may unstable angina and NSTEMI be indistinguishable initially?

A

Because a rise in troponins may take several hours to appear, making it difficult to differentiate between unstable angina and NSTEMI early on. Both are treated similarly until troponin results are available.

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4
Q

What are the two main problems caused by ischaemic heart disease?

A

Gradual narrowing of arteries: Reduced blood and oxygen delivery during exertion, causing angina.

Risk of plaque rupture: Sudden rupture of fatty plaques leading to artery occlusion and ischemia in the myocardium.

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5
Q

What is angina and how is it related to ACS?

A

Angina is chest pain caused by insufficient oxygen reaching the myocardium, often due to narrowed coronary arteries during exertion.

It is a symptom of ischaemic heart disease, which can progress to ACS.

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6
Q

What happens when a fatty plaque ruptures in a coronary artery?

A

Plaque rupture can lead to sudden occlusion of the artery, blocking blood flow and preventing oxygen from reaching the affected area of the myocardium, potentially leading to a heart attack (STEMI or NSTEMI).

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7
Q

What are the modifiable risk factors for ACS?

A

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

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8
Q

What are the unmodifiable risk factors for ACS?

A

Increasing age
Male gender
Family history of cardiovascular disease

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9
Q

What is the initial trigger for endothelial dysfunction in ischaemic heart disease?

A

Endothelial dysfunction is triggered by factors such as smoking, hypertension, and hyperglycaemia.

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10
Q

What changes occur in the endothelium during ischaemic heart disease?

A

Pro-inflammatory effects
Pro-oxidant effects
Proliferation
Reduced nitric oxide bioavailability

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11
Q

How do low-density lipoprotein (LDL) particles contribute to the pathophysiology of ischaemic heart disease?

A

LDL particles infiltrate the subendothelial space, where they contribute to the formation of fatty plaques.

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12
Q

What role do monocytes play in the development of atherosclerotic plaques?

A

Monocytes migrate from the blood into the subendothelial space, where they differentiate into macrophages. These macrophages then phagocytose oxidized LDL, transforming into foam cells

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13
Q

What is the role of smooth muscle proliferation in atherosclerotic plaque formation?

A

Smooth muscle cells proliferate and migrate from the tunica media into the intima, leading to the formation of a fibrous capsule that covers the fatty plaque, stabilizing it.

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14
Q

What happens when foam cells die in the context of ischaemic heart disease?

A

The death of foam cells can propagate the inflammatory process, further contributing to the development of atherosclerotic plaques.

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15
Q

What is the classic symptom of ACS?

A

The classic and most common symptom of ACS is chest pain. It is typically central or left-sided and may radiate to the jaw or left arm.

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16
Q

How is the chest pain in ACS typically described by patients?

A

heavy, constricting, or “like an elephant on my chest.”

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17
Q

Can patients with ACS present with different types of chest pain?

A

Yes, in clinical practice, patients may present with a variety of chest pain types, and ACS-related pain can be confused with other causes like dyspepsia.

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18
Q

Are there certain patient groups who may not experience chest pain in ACS?

A

Yes, patients such as diabetics and the elderly may not experience chest pain, or may have atypical presentations.

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19
Q

What are other common symptoms of ACS besides chest pain?

A

Dyspnoea (shortness of breath)
Sweating
Nausea and vomiting

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20
Q

What physical signs are often present in ACS?

A

Tachycardia (fast heart rate)
Normal or mildly altered vital signs (e.g., pulse, blood pressure, temperature, oxygen saturation)

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21
Q

What signs might indicate complications of ACS, such as cardiac failure?

A

If complications like cardiac failure develop, signs of heart failure may appear.

Pale and clammy skin
Abnormal heart sounds or pulmonary congestion.

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22
Q

What are the two most important investigations for assessing a patient with chest pain in ACS?

A

ECG (Electrocardiogram)

Cardiac markers ( troponin)

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23
Q

Which ECG leads correspond to anterior wall myocardial infarction (MI), and which coronary artery is affected?

A

ECG Leads: V1-V4

Coronary Artery: Left anterior descending (LAD)

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24
Which ECG leads correspond to inferior wall myocardial infarction (MI), and which coronary artery is affected?
ECG Leads: II, III, aVF Coronary Artery: Right coronary artery (RCA)
25
Which ECG leads correspond to lateral wall myocardial infarction (MI), and which coronary artery is affected?
ECG Leads: I, V5-V6 Coronary Artery: Left circumflex artery (LCx)
26
What is the primary goal of treatment once a diagnosis of ACS has been made?
Prevent worsening (further occlusion of the coronary vessel) Revascularize the vessel if occluded (especially for STEMI) Treat pain
27
What is the MONA mnemonic used for in ACS management?
Morphine Oxygen (only if oxygen saturation is <94%) Nitrates Aspirin
28
When should oxygen therapy be administered in ACS patients according to current guidelines?
Oxygen should be given only if oxygen saturation is <94%, as per British Thoracic Society guidelines
29
What is the priority of management for patients with STEMI?
The priority is to revascularize the blocked vessel, either through thrombolysis or percutaneous coronary intervention (PCI).
30
What is the preferred treatment for STEMI in modern practice?
Percutaneous coronary intervention (PCI), which involves balloon angioplasty and, often, stent placement to prevent further occlusion.
31
How is the management of NSTEMI different from STEMI?
For NSTEMI, a risk stratification tool (e.g., GRACE) is used. High-risk or unstable patients may undergo coronary angiography during admission, while lower-risk patients may have it at a later date.
32
What second antiplatelet drugs are commonly used in addition to aspirin in STEMI management?
Clopidogrel Prasugrel Ticagrelor
33
What are the key components of secondary prevention for patients who have had an ACS?
Secondary prevention includes lifelong therapy with: Aspirin A second antiplatelet (e.g., clopidogrel) Beta-blocker ACE inhibitor Statin
34
What are the criteria for diagnosing STEMI on ECG?
Clinical symptoms of ACS (≥ 20 minutes) Persistent ST-segment elevation in ≥ 2 contiguous leads: V2-V3: ≥ 2.5 mm (men under 40), ≥ 2.0 mm (men over 40), ≥ 1.5 mm (women) Other leads: ≥ 1 mm ST elevation New left bundle branch block (LBBB)
35
What is the management for a patient with STEMI?
Coronary reperfusion therapy: PCI (Percutaneous coronary intervention) within 12 hours if available within 120 minutes. Fibrinolysis if PCI is not available within 120 minutes of symptom onset. Dual antiplatelet therapy: Aspirin + another drug (e.g., prasugrel if no oral anticoagulants, clopidogrel if on oral anticoagulants). PCI procedure: Radial access preferred. Use drug-eluting stents. Thrombus aspiration considered. Complete revascularization for multivessel disease without cardiogenic shock.
36
What should be given to STEMI patients undergoing PCI prior to the procedure?
Prior to PCI, patients should receive dual antiplatelet therapy: Aspirin + prasugrel (if not on an oral anticoagulant) or clopidogrel (if on an oral anticoagulant).
37
What is the preferred anticoagulant during PCI for radial access?
Unfractionated heparin is used with bailout glycoprotein IIb/IIIa inhibitors (GPI) if necessary.
38
What anticoagulant is used during PCI with femoral access?
Bivalirudin is used with bailout glycoprotein IIb/IIIa inhibitors (GPI) if necessary.
39
How should fibrinolysis be used in STEMI management?
Fibrinolysis should be administered within 12 hours if PCI cannot be performed within 120 minutes. If the ECG does not show resolution of ST elevation 60-90 minutes post-fibrinolysis, PCI should be considered.
40
What should be monitored after fibrinolysis in STEMI patients?
An ECG should be repeated after 60-90 minutes to check for resolution of ST elevation. If ST elevation persists, PCI should be considered.
41
What is the initial antithrombin treatment for NSTEMI/unstable angina patients who are not having immediate angiography and are not at high risk of bleeding?
Fondaparinux should be offered to these patients.
42
Which risk assessment tool is commonly used for NSTEMI/unstable angina, and what factors does it consider?
The GRACE score is used, considering: Age Heart rate Blood pressure Cardiac and renal function Cardiac arrest on presentation ECG findings Troponin levels
43
When should unfractionated heparin be used in NSTEMI/unstable angina management?
Immediate angiography is planned. The patient's creatinine is > 265 µmol/L.
44
How is the GRACE score used in NSTEMI/unstable angina management, and how are patients stratified?
The GRACE score predicts 6-month mortality and helps stratify patients: Lowest: ≤ 1.5% mortality Low: > 1.5% to 3.0% Intermediate: > 3.0% to 6.0% High: > 6.0% to 9.0% Highest: > 9.0%
45
Who should have immediate coronary angiography in NSTEMI/unstable angina?
Clinically unstable patients (e.g., hypotensive) should have immediate coronary angiography.
46
Who should have coronary angiography within 72 hours in NSTEMI/unstable angina management?
Patients with a GRACE score > 3% (i.e., those at intermediate, high, or highest risk) should have coronary angiography within 72 hours.
47
When should coronary angiography be considered for NSTEMI/unstable angina patients during hospitalization?
Coronary angiography should be considered if ischaemia develops after admission.
48
What dual antiplatelet therapy should be given prior to PCI for NSTEMI/unstable angina patients?
If the patient is not on an oral anticoagulant: use prasugrel or ticagrelor. If the patient is on an oral anticoagulant: use clopidogrel.
49
What anticoagulant therapy is recommended for NSTEMI/unstable angina patients undergoing PCI?
Unfractionated heparin should be given to all patients undergoing PCI.
49
What is the conservative management approach for NSTEMI/unstable angina patients not undergoing immediate angiography?
For conservative management, further drug therapy includes: Dual antiplatelet therapy (aspirin + another drug): If the patient is not at high risk of bleeding: use ticagrelor. If the patient is at high risk of bleeding: use clopidogrel.
50
What are the poor prognostic factors in ACS?
Age Development or history of heart failure Peripheral vascular disease Reduced systolic blood pressure Killip class Initial serum creatinine concentration Elevated initial cardiac markers Cardiac arrest on admission ST segment deviation
51
What is the Killip class system, and how is it used in ACS prognosis?
The Killip class is a system used to stratify risk post-myocardial infarction based on clinical signs of heart failure. The classes and their associated 30-day mortality rates are: Class I: No clinical signs of heart failure (6% mortality) Class II: Lung crackles, S3 (17% mortality) Class III: Frank pulmonary edema (38% mortality) Class IV: Cardiogenic shock (81% mortality)
52
What is the first-line drug therapy for stable angina according to NICE guidelines?
Aspirin (unless contraindicated) Statin (unless contraindicated) Beta-blocker or calcium channel blocker (based on comorbidities, contraindications, and patient preference)
52
What is the role of sublingual glyceryl trinitrate in angina management?
Sublingual glyceryl trinitrate is used to abort angina attacks.
53
Which type of calcium channel blocker should be used as monotherapy for stable angina?
A rate-limiting calcium channel blocker, such as verapamil or diltiazem, should be used as monotherapy.
54
What type of calcium channel blocker should be used in combination with a beta-blocker for stable angina?
A long-acting dihydropyridine calcium channel blocker, such as amlodipine or modified-release nifedipine, should be used in combination with a beta-blocker.
55
Why should verapamil not be prescribed concurrently with beta-blockers? .
Verapamil and beta-blockers should not be used together due to the risk of complete heart block
56
What should be done if there is a poor response to the initial angina treatment?
If the response to initial treatment is poor, increase the medication to the maximum tolerated dose (e.g., atenolol 100mg once daily).
57
What is the next step if a patient with stable angina remains symptomatic after monotherapy with a beta-blocker or calcium channel blocker? .
If the patient remains symptomatic, add the other drug (e.g., add a calcium channel blocker if on a beta-blocker, or add a beta-blocker if on a calcium channel blocker)
58
What should be considered if a stable angina patient cannot tolerate the addition of a beta-blocker or a calcium channel blocker?
Consider one of the following drugs: Long-acting nitrate Ivabradine Nicorandil Ranolazine
58
When is it appropriate to add a third drug in patients with stable angina?
Add a third drug (e.g., ivabradine, nicorandil, ranolazine) while the patient is awaiting assessment for PCI or CABG if on both a beta-blocker and calcium-channel blocker.
59
How can nitrate tolerance be managed in patients using nitrates for angina?
asymmetric dosing interval (for standard-release isosorbide mononitrate) to maintain a daily nitrate-free period of 10-14 hours. This effect is not seen with once-daily modified-release isosorbide mononitrate.
59
What is the first-line antiplatelet therapy for medically treated acute coronary syndrome (ACS)?
Aspirin (lifelong) Ticagrelor (12 months)
60
What is the second-line antiplatelet therapy for ACS (medically treated) if aspirin is contraindicated?
Clopidogrel (lifelong)
61
What is the first-line antiplatelet therapy for patients undergoing percutaneous coronary intervention (PCI)?
Aspirin (lifelong) Prasugrel or Ticagrelor (12 months)
62
What is the second-line antiplatelet therapy for PCI if aspirin is contraindicated?
Clopidogrel (lifelong)
63
What is the first-line antiplatelet therapy for transient ischemic attack (TIA) and Ischemic stroke?
Clopidogrel (lifelong)
64
What is the second-line antiplatelet therapy for TIA and ischemic stroke?
Aspirin (lifelong) and Dipyridamole (lifelong)
65
What is the mechanism of action of thrombolytic drugs?
Thrombolytic drugs activate plasminogen to form plasmin, which in turn degrades fibrin and helps break up thrombi.
65
What are the primary uses of thrombolytic drugs?
-ST elevation myocardial infarction (STEMI) - Acute ischaemic stroke - Pulmonary embolism (strict inclusion criteria apply)
66
What are examples of thrombolytic drugs?
- Alteplase - Tenecteplase - Streptokinase
67
What are the contraindications to thrombolysis?
- Active internal bleeding - Recent haemorrhage, trauma, or surgery (including dental extraction) - Coagulation and bleeding disorders - Intracranial neoplasm - Stroke within the last 3 months - Aortic dissection - Recent head injury - Severe hypertension
68
What are the common side effects of thrombolytic drugs?
- Haemorrhage - Hypotension (more common with streptokinase) - Allergic reactions (may occur with streptokinase)
69
Syndrome X
Features angina-like chest pain on exertion ST depression on exercise stress test but normal coronary arteries on angiography Management nitrates may be beneficial
70
What are the different forms of myopathy caused by statins?
Myopathy includes myalgia, myositis, rhabdomyolysis, and asymptomatic raised creatine kinase.
71
How do statins work to lower cholesterol levels?
Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
72
What are the risk factors for myopathy when taking statins?
Advanced age female sex low body mass index presence of multisystem disease (e.g., diabetes mellitus).
73
Which statins are more likely to cause myopathy: lipophilic or hydrophilic? A
Lipophilic statins (e.g., simvastatin, atorvastatin) are more likely to cause myopathy than hydrophilic statins (e.g., rosuvastatin, pravastatin, fluvastatin).
74
When should liver function tests (LFTs) be checked in patients on statins?
LFTs should be checked at baseline, 3 months, and 12 months. Treatment should be stopped if serum transaminases rise to and persist at 3 times the upper limit of the reference range.
75
What is the effect of statins on patients with a history of intracerebral hemorrhage?
Statins may increase the risk of intracerebral hemorrhage in patients with a history of stroke, but this effect is not seen in primary prevention. Statins should be avoided in patients with a history of intracerebral hemorrhage
76
Which class of drugs is known to interact with statins and should lead to temporary discontinuation of statin therapy?
Macrolides (e.g., erythromycin, clarithromycin) interact with statins and should lead to discontinuation until the course is completed. Macrolides inhibit cytochrome P450 3A4 (CYP3A4) enzymes by , which can lead to increased plasma concentrations of statins metabolised by this pathway, leading to adverse effects of statins.
77
Are statins safe to use during pregnancy?
contraindicated during pregnancy. Statins inhibit HMG-CoA reductase, reducing synthesis. Cholesterol is crucial for fetal development, especially for the formation of cell membranes and steroid hormones. Statins are also not recommended during breastfeeding due to unknown effects on the infant.
78
Who should receive a statin according to NICE guidelines?
All people with established cardiovascular disease (e.g., stroke, TIA, ischemic heart disease, peripheral arterial disease) should receive a statin.
79
What is the threshold for starting statins in primary prevention based on cardiovascular risk?
Statins should be considered for people with a 10-year cardiovascular risk of 10% or more.
79
Should patients with type 2 diabetes be assessed for statin therapy?
Yes, patients with type 2 diabetes should be assessed using the QRISK2 tool to determine if they need statin therapy.
80
Which patients with type 1 diabetes should be considered for statin therapy?
Patients with type 1 diabetes who were diagnosed more than 10 years ago, are over 40, or have established nephropathy should be considered for statin therapy.
81
Why should statins be taken at night?
Should be taken at night because the majority of cholesterol synthesis occurs during the night, especially true for simvastatin.
82
What is the recommended dose of atorvastatin for primary prevention of cardiovascular disease?
20 mg of atorvastatin for primary prevention.
82
What is the recommended dose of atorvastatin for secondary prevention of cardiovascular disease?
The recommended dose is 80 mg of atorvastatin for secondary prevention.
83
When does myoglobin begin to rise after a myocardial infarction, and how long does it take to return to normal?
Myoglobin rises within 1-2 hours, peaks in 6-8 hours, and returns to normal in 1-2 days.
84
What is the significance of CK-MB in myocardial infarction, and how long does it take to return to normal?
CK-MB is useful for detecting reinfarction as it returns to normal after 2-3 days. It begins to rise 2-6 hours after infarction, peaks at 16-20 hours, and returns to normal in 2-3 days.
84
What is the time course for CK levels after a myocardial infarction?
CK rises within 4-8 hours, peaks at 16-24 hours, and returns to normal in 3-4 days.
84
What is the time course for troponin T after a myocardial infarction?
Troponin T begins to rise 4-6 hours after infarction, peaks in 12-24 hours, and remains elevated for 7-10 days.
84
How does AST behave after a myocardial infarction?
AST rises 12-24 hours after infarction, peaks at 36-48 hours, and returns to normal in 3-4 days.
85
What is the time course for LDH levels following a myocardial infarction?
LDH rises 24-48 hours after infarction, peaks at 72 hours, and returns to normal in 8-10 days.
85
Which cardiac enzyme is the first to rise after a myocardial infarction, and which remains elevated the longest?
Myoglobin is the first to rise (1-2 hours), while troponin T remains elevated the longest (7-10 days).
86
Which cardiac enzyme is most useful for detecting reinfarction after the initial event?
CK-MB is most useful for detecting reinfarction, as it returns to normal within 2-3 days, making it a good indicator of reinfarction.
87
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93
Where is Nicotinic acid (niacin) used as a treatment ?
Limited use due to side effects Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia. It lowers cholesterol and triglyceride concentrations while raising HDL levels.
94
Adverse effects of niacin?
flushing: mediated by prostaglandins impaired glucose tolerance myositis

cardiology (6 decks)

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