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Ischemic Heart Disease Flashcards

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1
Q

How is angina clinically characterized?

A

Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arm.

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2
Q

What typically aggravates angina?

A

Angina is typically aggravated by exertion or emotional stress.

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3
Q

How is angina usually relieved?

A

Angina is usually relieved by rest.

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4
Q

How long does angina usually last?

A

Angina usually lasts less than 20 minutes.

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5
Q

What is the most common cause of angina?

A

The most common cause of angina is atherosclerosis.

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6
Q

What is the trend in the incidence of angina?

A

The incidence of angina is increasing in all population groups.

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7
Q

In which demographic is there a large increase in the number of angina cases?

A

There is a large increase in the number of young women experiencing angina.

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8
Q

What factors are contributing to the increased incidence of angina?

A

The Western diet and lifestyle are contributing factors to the increased incidence of angina.

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9
Q

What is a key initial event in the pathophysiology of angina?

A

Endothelial damage is a key initial event in the pathophysiology of angina.

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10
Q

What does endothelial damage lead to in the context of angina?

A

Endothelial damage leads to inflammation with plaque deposition, including cholesterol and fibrin.

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11
Q

What determines the likelihood of plaque rupture in angina?

A

The stability of the fibrous cap determines the likelihood of plaque rupture, not the size of the plaque.

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12
Q

What initiates the process of atherothrombosis?

A

Endothelial injury initiates the process of atherothrombosis.

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13
Q

What factors can cause endothelial injury in atherothrombosis?

A

Factors like hypertension, high cholesterol, smoking, and diabetes can cause endothelial injury

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14
Q

What happens during the lipid accumulation stage of atherothrombosis?

A

During lipid accumulation, LDL cholesterol penetrates the endothelium, oxidizes, and attracts monocytes.

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15
Q

How does the inflammatory response contribute to atherothrombosis?

A

Monocytes transform into macrophages, ingest oxidized LDL, and become foam cells during the inflammatory response.

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16
Q

What is formed during the plaque formation stage of atherothrombosis?

A

Foam cells aggregate into fatty streaks, smooth muscle cells migrate and produce extracellular matrix, forming a fibrous cap over the plaque during plaque formation.

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17
Q

What happens during the plaque progression stage of atherothrombosis?

A

Chronic inflammation causes plaque growth and complexity during the plaque progression stage.

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18
Q

What causes plaque destabilization in atherothrombosis?

A

Inflammation thins the fibrous cap, making it prone to rupture, which causes plaque destabilization.

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19
Q

What occurs during the thrombosis stage of atherothrombosis?

A

Rupture exposes the plaque’s contents, activating platelets and the coagulation cascade, forming a blood clot during thrombosis.

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20
Q

What are the potential clinical manifestations of thrombosis in atherothrombosis?

A

Thrombosis can block arteries, leading to conditions like heart attack, stroke, or peripheral arterial disease.

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21
Q

The end stages of atherothrombosis

A
  1. myocardial infarction
  2. ischemic stroke
  3. critical leg ischemia
  4. cardiovascular death
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22
Q

What factors increase oxygen demand in angina pectoris?

A

Factors that increase oxygen demand in angina pectoris include increased heart rate, increased systolic blood pressure (SBP), and increased wall stress.

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23
Q

What factors increase oxygen supply in angina pectoris?

A

Factors that increase oxygen supply in angina pectoris include increased coronary flow, increased hemoglobin (Hb), and increased oxygen (O2) levels.

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24
Q

What is angina pectoris?

A

Angina pectoris is a clinical syndrome characterized by chest pain or discomfort resulting from myocardial ischemia, typically due to atherosclerotic disease of the coronary arteries.

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25
What are the typical locations of chest pain or discomfort in angina pectoris?
The chest pain or discomfort is typically located behind the sternum but can also occur in the neck, jaw, shoulders, arms, or epigastrium.
26
How is the chest pain in angina pectoris usually described?
The chest pain is usually described as a squeezing, pressing, burning, or tightness sensation.
27
What are the common provoking factors for angina pectoris?
Common provoking factors include physical exertion, cold weather, large meals, and emotional stress.
28
How is angina pectoris typically relieved?
Angina pectoris is typically relieved by rest and sublingual nitroglycerin.
29
What is the usual duration of angina pectoris symptoms?
The symptoms usually last between 1 to 15 minutes.
30
What are some associated symptoms of angina pectoris?
Associated symptoms include dyspnea (shortness of breath), sweating, and nausea.
31
What are the different types of angina?
The different types of angina are stable angina, unstable angina, and variant (Prinzmetal's) angina.
32
What characterizes stable angina?
Stable angina is predictable, occurs with exertion or stress, and is relieved by rest or nitroglycerin.
33
What characterizes unstable angina?
Unstable angina is characterized by new onset, increasing frequency, duration, or severity of symptoms, or occurring at rest, indicating a higher risk of myocardial infarction.
34
What characterizes variant (Prinzmetal's) angina?
Variant (Prinzmetal's) angina is caused by coronary artery spasm, typically occurring at rest and often in cycles.
35
What is the prognosis of angina?
Angina generally has a good prognosis.
36
What type of disease is angina considered to be?
Angina is considered a primary care disease.
37
What lifestyle changes are essential for managing angina?
Essential lifestyle changes for managing angina include diet, exercise, and maintaining an ideal body weight.
38
What factors influence the prognosis of angina?
The prognosis of angina is influenced by left ventricular function, the number of coronary arteries with significant stenosis, and the extent of jeopardized myocardium.
39
How does left ventricular function affect the prognosis of angina?
Left ventricular function affects the prognosis of angina as impaired function can indicate more severe disease and a poorer prognosis.
40
How does the number of coronary arteries with significant stenosis impact prognosis?
The prognosis worsens with an increasing number of coronary arteries affected by significant stenosis, as this indicates more extensive coronary artery disease.
41
What does the extent of jeopardized myocardium indicate about prognosis?
The extent of jeopardized myocardium indicates the severity of myocardial ischemia and damage, which can impact the overall prognosis.
42
What are the typical findings on physical examination for angina?
Physical examination for angina often reveals little specific findings.
43
What should be assessed to diagnose macrovascular disease in angina?
To diagnose macrovascular disease in angina, assess for diminished peripheral pulses, bruits, and other signs of vascular disease.
44
Why is it important to consider risk factors in the diagnosis of angina?
Considering risk factors is important in diagnosing angina as they contribute to the likelihood of coronary artery disease and help guide diagnostic and management strategies.
45
What are some precipitating factors for angina?
Precipitating factors for angina include anemia, thyrotoxicosis, and tachyarrhythmias.
46
What evidence might indicate ischemic changes to the heart in angina?
Evidence of ischemic changes to the heart includes an enlarged heart, signs of heart failure, and the presence of S3/S4 heart sounds.
47
Investigations
- Resting ECG (NB) - Stress ECG if indicated - CXR - Blood -- Cholesterol -- Glucose -- Renal function if required
48
Risk factors for angina
- HPT - Diabetes - Smoking - Obesity - Age: male greater than 40, Postmeno female. - +ve family Hx Previous - - MI
49
What clinical factors are used for risk stratification in angina?
Clinical factors for risk stratification include hypertension (HPT) and diabetes
50
How does an abnormal resting ECG contribute to risk stratification in angina?
An abnormal resting ECG contributes to risk stratification by indicating potential ischemic changes or arrhythmias that may increase risk.
51
What role does left ventricular (LV) dysfunction play in risk stratification for angina?
Left ventricular (LV) dysfunction plays a role in risk stratification as it signifies impaired cardiac function, which can indicate more severe disease and higher risk.
52
What are the primary objectives of managing angina?
1. To prevent MI 2. Reduce symptoms in order to improve quality of life.
53
Management of angina by ABCDEF
- Aspirin and Anti-anginals - Beta blockers and BP - Cholesterol and Cigarettes - Diet and Diabetes - Education and Exercise - Follow up
54
What is the typical dosage range for aspirin in angina management?
The typical dosage range for aspirin in angina management is 75-150 mg/day.
55
What is the mechanism of action of aspirin in managing angina?
Aspirin is a COX inhibitor that prevents platelet thromboxane formation and inhibits platelet aggregation.
56
Why is aspirin important in the prevention of atherosclerotic plaque formation?
Aspirin is important in preventing atherosclerotic plaque formation because it inhibits platelet aggregation, which helps reduce the risk of plaque rupture and subsequent thrombosis.
57
How does aspirin help preserve endothelial function?
Aspirin helps preserve endothelial function by reducing platelet aggregation and preventing thromboxane A2 formation, which contributes to maintaining healthy endothelial cells.
58
What do controlled studies suggest about the use of aspirin in patients with stable angina?
Controlled studies suggest that aspirin should be used in all patients with stable angina, provided there are no contraindications, such as gastrointestinal issues.
59
What is the primary action of nitrates in angina management?
Nitrates are potent vasodilators that venodilate, decreasing preload and venous return, which reduces myocardial oxygen requirements.
60
What is the preferred form of nitrate administration for acute angina?
Sublingual (S/L) nitrates are preferred for acute angina due to their rapid onset of action.
61
Can nitrates be used prophylactically?
Yes, nitrates can be used prophylactically to prevent angina attacks.
62
What should be remembered about the use of nitrates regarding side effects?
Postural hypotension is a common side effect of nitrates. Additionally, headaches are common; patients should spit out the tablet when the pain subsides.
63
How can headaches from nitrate use be managed?
Paracetamol can be used to manage headaches in some patients caused by nitrate use.
64
What are common adverse effects of nitrates?
Common adverse effects of nitrates include postural hypotension, headache, and flushing.
65
What should be considered to avoid dangerous interactions when using nitrates?
Be cautious with the use of nitrates in combination with Viagra and other similar medications due to the risk of severe hypotension.
66
What are some contraindications for using nitrates?
Contraindications for using nitrates include hypotension, fixed output states, and recent use of Viagra or similar medications.
67
How do beta blockers help manage angina?
Beta blockers decrease heart rate and myocardial contraction, which in turn decreases myocardial oxygen requirements. This helps delay or avoid the onset of angina.
68
What is the target resting heart rate for patients on beta blockers for angina?
The target resting heart rate for patients on beta blockers is 55-60 beats per minute.
69
Can the heart rate be adjusted in patients with symptomatic angina?
Yes, the heart rate can be further decreased in symptomatic patients, provided there are no symptoms of bradycardia.
70
When should beta blockers be used in the management of angina?
Beta blockers should be used as a first-line treatment for angina if there are no contraindications.
71
Contraindications of beta blockers
- Asthma - COPD with reversibility - CCF?? - Heart block - Bradycardia (<50)
72
Adverse effects of beta blockers
- Impotence. - Bronchospasm. - Lethargy/ decreased exercise ability - Bradycardia/heart block. - Cold peripheries.
73
Risk modification for angina
1, lipid lowering 2. smoking cessation 3. hypertension 4. diabetes 5. obesity 6. exercise
74
lipid lowering
1. Highly beneficial role for statins. 2. Reduces risk of MI and the need for revascularisation. 3. Diet must not be overlooked!
75
Smoking cessation
1. Few randomised trials. 2. However in primary prevention setting, smoking cessation decreases risk of cardiac event by 45%. 3. Use other healthcare workers to increase rate of cessation
76
Hypertension
1. Beneficial effects on cardiac mortality confirmed in many trials. 2. Poorly controlled HPT aggravates angina. 3. Rational prescribing (B blocker) facilitates control of both.
77
Diabetes
Strict control prevents microvascular complications as well as accelerated atherosclerosis.
78
Obesity
1. Commonly associated with angina. 2. Contributes to other risk factors e.g. HPT, Diabetes, hypercholesterolaemia. 3. Wt reduction improves these risks and reduces O2 demand.
79
Exercise
Good trial data to support exercise. BP lowering, lipid improvement occur as bonus!
80
Follow Up
- Has patient’s activity decreased? - Have anginal symptoms changed? - Is therapy tolerated? - Are modifiable risks treated? - Has co-morbid illness developed?
81
Refer
- Failure of medical therapy. - ? Diagnosis. - UAP/MI - CCF symptoms or signs. - Dizziness or syncopal signs. - Poor quality of life. - Very +ve stress test.

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