NURSING 2005_Ischaemic Heart Disease_1 Slide PP Flashcards

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1
Q

Front

A

Back

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2
Q

<h1>Page 01</h1>

<br></br>What is another term for Acute Coronary Syndrome?

A

Ischaemic heart disease.

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3
Q

<h1>Page 01</h1>

<br></br>What type of angina is characterized by predictable chest pain during physical activity or stress?

A

Stable angina.

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4
Q

<h1>Page 01</h1>

<br></br>What type of angina is characterized by unpredictable chest pain that can occur at rest or with minimal physical exertion?

A

Unstable angina.

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5
Q

<h1>Page 01</h1>

<br></br>What is another term for a heart attack?

A

Myocardial infarction.

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6
Q

<h1>Page 01</h1>

<br></br>Which type of myocardial injury is potentially reversible?

A

Reversible.

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7
Q

<h1>Page 01</h1>

<br></br>Which type of myocardial injury is not reversible?

A

Irreversible.

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8
Q

<h1>Page 02</h1>

<br></br>What is the site of atherosclerotic plaque development?

A

Coronary arteries.

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9
Q

<h1>Page 03</h1>

<br></br>What is angina?

A

Angina is chest pain or discomfort that occurs when the heart muscle doesn’t get enough oxygen-rich blood.

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10
Q

<h1>Page 03</h1>

<br></br>What are the common symptoms of angina?

A

Chest pain, pressure, or discomfort, often described as a squeezing or tightness in the chest.

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11
Q

<h1>Page 03</h1>

<br></br>What triggers angina?

A

Physical exertion, emotional stress, extreme cold or hot temperatures, heavy meals, and smoking.

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12
Q

<h1>Page 03</h1>

<br></br>How is stable angina usually relieved?

A

By rest or medication, such as nitroglycerin.

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13
Q

<h1>Page 04</h1>

<br></br>What is angina pectoris?

A

Chest pain caused by insufficient oxygen to the heart.

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14
Q

<h1>Page 04</h1>

<br></br>What is the cause of angina pectoris?

A

Blockage of a coronary artery leading to ischaemia and hypoxia.

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15
Q

<h1>Page 04</h1>

<br></br>What determines the phenotype of angina pectoris?

A

The degree of blockage in the coronary artery.

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16
Q

<h1>Page 04</h1>

<br></br>What causes the pain in angina pectoris?

A

Myocardial ischaemia.

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17
Q

<h1>Page 04</h1>

<br></br>What leads to the imbalance between myocardial oxygen supply and demand in angina pectoris?

A

Blockage of a coronary artery causing ischaemia and hypoxia.

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18
Q

<h1>Page 05</h1>

<br></br>What is stable angina?

A

Stable angina is stable atherosclerotic plaque combined with vasoconstriction.

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19
Q

<h1>Page 05</h1>

<br></br>What is the most common type of angina?

A

Stable angina.

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20
Q

<h1>Page 05</h1>

<br></br>What are the characteristics of the plaque in stable angina?

A

Plaque with small necrotic core and thick fibrous cap, with low chance of rupture.

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21
Q

<h1>Page 05</h1>

<br></br>What is the typical cause of stable angina?

A

Exercise or stress.

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22
Q

<h1>Page 05</h1>

<br></br>What kind of blockage is present in stable angina?

A

Only partial blockage.

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23
Q

<h1>Page 05</h1>

<br></br>What is the nature of atherosclerotic narrowing in stable angina?

A

Fixed.

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24
Q

<h1>Page 06</h1>

<br></br>What happens to the heart when at rest in stable angina?

A

It gets an adequate supply of blood.

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25
Q

<h1>Page 06</h1>

<br></br>What happens to the heart with exercise in stable angina?

A

It needs to beat harder to meet the demands of the body.

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26
Q

<h1>Page 06</h1>

<br></br>What is required for the ventricles during exercise in stable angina?

A

They need more blood.

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27
Q

<h1>Page 06</h1>

<br></br>What prevents the increased demand for blood from being met in stable angina?

A

Narrowing of the vessel.

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28
Q

<h1>Page 06</h1>

<br></br>What is the result of myocardial ischaemia in stable angina?

A

Pain.

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29
Q

<h1>Page 06</h1>

<br></br>When does the pain subside in stable angina?

A

With rest, after the increased demand on the heart is over.

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30
Q

<h1>Page 06</h1>

<br></br>How do symptoms deteriorate over time in stable angina?

A

As plaque increases in size.

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31
Q

<h1>Page 06</h1>

<br></br>What reduces the amount of exercise or stress needed for symptoms to come on in stable angina?

A

Less exercise/stress.

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32
Q

<h1>Page 06</h1>

<br></br>Why doesn’t stable angina normally progress to unstable angina?

A

Because the plaques have different structures.

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33
Q

<h1>Page 07</h1>

<br></br>What are the characteristics of unstable angina?

A

Larger plaques, more plaques, unstable plaques, associated thrombi.

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34
Q

<h1>Page 07</h1>

<br></br>What is the difference in blood flow in unstable angina compared to stable angina?

A

Blood flow is not adequate at rest, leading to pain without exertion.

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35
Q

<h1>Page 07</h1>

<br></br>Why is unstable angina considered more serious and unpredictable?

A

Due to the higher chance of plaque rupture and worsened ischaemia and hypoxia.

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36
Q

<h1>Page 07</h1>

<br></br>What symptoms are associated with unstable angina?

A

Nausea, shortness of breath, sweating.

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37
Q

<h1>Page 07</h1>

<br></br>How is unstable angina different from stable angina in terms of relief?

A

It is not relieved by rest or medication.

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38
Q

<h1>Page 07</h1>

<br></br>What is the risk associated with unstable angina?

A

Risk of having a myocardial infarction.

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39
Q

<h1>Page 07</h1>

<br></br>What effect does atherosclerotic plaque with overlying non-occlusive thrombus have on the coronary artery lumen?

A

Significantly reduces the size of the coronary artery lumen.

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40
Q

<h1>Page 08</h1>

<br></br>What is the characteristic of unstable angina related to atherosclerotic narrowing?

A

Fixed atherosclerotic narrowing with a non-occlusive thrombus.

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41
Q

<h1>Page 08</h1>

<br></br>What happens when there is significant narrowing of the coronary artery in unstable angina?

A

It prevents sufficient blood flow at rest, leading to myocardial ischemia.

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42
Q

<h1>Page 08</h1>

<br></br>What may unstable angina progress to if the thrombus expands to completely block the coronary artery?

A

Myocardial infarction.

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43
Q

<h1>Page 08</h1>

<br></br>How does atherosclerotic plaque with overlying non-occlusive thrombus affect the coronary artery lumen in unstable angina?

A

It significantly reduces the size of the coronary artery lumen.

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44
Q

<h1>Page 09</h1>

<br></br>What are the characteristics of stable angina?

A

Varying degrees of vessel occlusion, leads to ischaemia and hypoxia, blood flow isn’t completely blocked, tissue receives enough oxygen to be kept alive but is under strain.

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45
Q

<h1>Page 09</h1>

<br></br>What are the characteristics of unstable angina?

A

Varying degrees of vessel occlusion, leads to ischaemia and hypoxia, blood flow isn’t completely blocked, tissue receives enough oxygen to be kept alive but is under strain, but the final step to necrosis isn’t reached, making it reversible.

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46
Q

<h1>Page 09</h1>

<br></br>What happens if sufficient perfusion is restored in angina?

A

Normal function is restored.

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47
Q

<h1>Page 09</h1>

<br></br>What is the final step to necrosis in unstable angina?

A

It isn’t reached, making angina reversible.

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48
Q

<h1>Page 09</h1>

<br></br>What does ischaemia lead to in both stable and unstable angina?

A

Hypoxia and infarction (necrotic cell death).

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49
Q

<h1>Page 10</h1>

<br></br>What are the risk factors for atherosclerosis?

A

Hypertension, high LDL, smoking, and alcohol.

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50
Q

<h1>Page 10</h1>

<br></br>What are the modifiable risks that can act as an initiating insult for atherosclerosis?

A

Hypertension, high LDL, smoking, and alcohol.

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51
Q

<h1>Page 10</h1>

<br></br>What factors can worsen plaques that are already present in atherosclerosis?

A

Hypertension, high LDL, smoking, and alcohol.

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52
Q

<h1>Page 10</h1>

<br></br>What are the risk factors to decrease in order to prevent angina?

A

Hypertension, high LDL, smoking, and alcohol.

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53
Q

<h1>Page 11</h1>

<br></br>What is the pharmacological treatment for angina involving Glyceryl trinitrate (GTN)?

A

Oral tablets, IV or spray.

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54
Q

<h1>Page 11</h1>

<br></br>What is GTN a prodrug of?

A

Nitric oxide.

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55
Q

<h1>Page 11</h1>

<br></br>How does GTN act in the body?

A

By dilating blood vessels.

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56
Q

<h1>Page 11</h1>

<br></br>What is the effect of GTN on coronary blood flow?

A

It improves coronary blood flow.

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57
Q

<h1>Page 11</h1>

<br></br>How does GTN relieve ischaemia?

A

By dilating coronary arteries.

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58
Q

<h1>Page 11</h1>

<br></br>What is the mechanism by which GTN reduces pain?

A

By dilating coronary arteries and improving coronary blood flow.

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59
Q

<h1>Page 11</h1>

<br></br>What type of vasodilator is GTN?

A

Quick-acting vasodilator.

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60
Q

<h1>Page 12</h1>

<br></br>What is the mechanism of action of statins like Simvastatin?

A

Inhibiting an enzyme that synthesizes cholesterol in the liver.

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61
Q

<h1>Page 12</h1>

<br></br>What is the role of cholesterol (LDL) in atherosclerotic plaque development?

A

It serves as building blocks for atherosclerotic plaque development.

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62
Q

<h1>Page 12</h1>

<br></br>How does Simvastatin affect cholesterol production?

A

It lowers cholesterol production.

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63
Q

<h1>Page 12</h1>

<br></br>What is the effect of Simvastatin on LDL uptake in liver cells?

A

It increases LDL uptake in liver cells.

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64
Q

<h1>Page 12</h1>

<br></br>How does the action of Simvastatin contribute to decreased plaque burden?

A

By reducing circulating LDLs, which means less building blocks for atherosclerotic plaque development.

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65
Q

<h1>Page 13</h1>

<br></br>What is the pharmacological treatment for angina using aspirin?

A

Aspirin is used as an anti-platelet agent to reduce platelet aggregation and prevent thrombus formation.

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66
Q

<h1>Page 13</h1>

<br></br>How does aspirin work to prevent thrombus formation in angina?

A

It reduces platelet aggregation.

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67
Q

<h1>Page 13</h1>

<br></br>What is the effectiveness of low-dose aspirin in reducing thrombus formation?

A

Very effective.

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68
Q

<h1>Page 14</h1>

<br></br>What is the mechanism of action of beta-blockers in the treatment of angina?

A

They antagonize (block) catacholamines and block the ability of the sympathetic nervous system to increase heart rate, leading to decreased cardiac output and blood pressure.

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69
Q

<h1>Page 14</h1>

<br></br>How do beta-blockers affect heart rate and blood pressure?

A

They decrease heart rate and blood pressure.

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70
Q

<h1>Page 14</h1>

<br></br>What is the effect of beta-blockers on the workload of the heart?

A

They decrease the workload of the heart.

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71
Q

<h1>Page 14</h1>

<br></br>What is the primary action of beta-blockers on arteries?

A

They dilate arteries.

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72
Q

<h1>Page 15</h1>

<br></br>When are surgical treatments for angina considered?

A

When medications are ineffective or the condition worsens.

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73
Q

<h1>Page 15</h1>

<br></br>What does bypass surgery do in the context of angina?

A

It bypasses blood flow around the area of atherosclerotic plaque.

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74
Q

<h1>Page 15</h1>

<br></br>How does bypass surgery remove the risk of occlusive thrombus formation?

A

By removing blood flow from the narrowed coronary artery.

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75
Q

<h1>Page 15</h1>

<br></br>What risk does bypass surgery remove in relation to myocardial infarction?

A

It removes the risk of myocardial infarction.

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76
Q

<h1>Page 16</h1>

<br></br>What is the purpose of balloon angiography in the context of angina?

A

To increase the size of the lumen and improve blood flow in a narrowed coronary artery.

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77
Q

<h1>Page 16</h1>

<br></br>How does balloon angiography impact the diseased artery?

A

It increases blood flow through the diseased artery.

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78
Q

<h1>Page 16</h1>

<br></br>What is the risk associated with balloon angiography in relation to plaque?

A

It does not impact plaque, so there is still a risk of future events.

79
Q

<h1>Page 17</h1>

<br></br>What are some non-pharmacological treatments for angina?

A

Healthy diet, avoiding saturated fat, regular physical activity, maintaining a healthy weight, reducing consumption of alcohol and smoking, and maintaining normal blood pressure.

80
Q

<h1>Page 18</h1>

<br></br>What is another name for Myocardial Infarction?

A

Heart attack.

81
Q

<h1>Page 18</h1>

<br></br>What is the main cause of Myocardial Infarction?

A

Blockage of blood flow to the heart.

82
Q

<h1>Page 18</h1>

<br></br>What are the common symptoms of Myocardial Infarction?

A

Chest pain, shortness of breath, and sweating.

83
Q

<h1>Page 18</h1>

<br></br>What is the immediate treatment for Myocardial Infarction?

A

Aspirin and nitroglycerin.

84
Q

<h1>Page 18</h1>

<br></br>What is the ongoing treatment for Myocardial Infarction?

A

Medications, lifestyle changes, and cardiac rehabilitation.

85
Q

<h1>Page 19</h1>

<br></br>What is myocardial infarction (MI) commonly known as?

A

Heart attack.

86
Q

<h1>Page 19</h1>

<br></br>What causes the death of heart tissue in myocardial infarction?

A

Prolonged lack of blood flow and oxygen.

87
Q

<h1>Page 19</h1>

<br></br>What is the cause of infarction of the myocardium in myocardial infarction?

A

Prolonged insufficient blood supply.

88
Q

<h1>Page 19</h1>

<br></br>What can cause necrosis of the myocardium in myocardial infarction?

A

Atherosclerotic narrowing with occlusive thrombus.

89
Q

<h1>Page 19</h1>

<br></br>What is the result of unstable angina in relation to myocardial infarction?

A

It can lead to myocardial infarction.

90
Q

<h1>Page 19</h1>

<br></br>What happens to the rest of the heart during a myocardial infarction?

A

It will continue to function.

91
Q

<h1>Page 19</h1>

<br></br>What compensatory mechanisms are activated during myocardial infarction?

A

Mechanisms to maintain cardiac output (same as for heart failure).

92
Q

<h1>Page 20</h1>

<br></br>How can myocardial infarction be classified based on ECG abnormalities?

A

Based on the presence/absence of ST elevation.

93
Q

<h1>Page 20</h1>

<br></br>What does NSTEMI stand for and what does it indicate?

A

NSTEMI stands for Non-ST elevation myocardial infarction, indicating partial or transient blockage resulting in necrosis and less damage.

94
Q

<h1>Page 20</h1>

<br></br>What does STEMI stand for and what does it indicate?

A

STEMI stands for ST elevation myocardial infarction, indicating complete obstruction by a thrombus resulting in necrosis and extensive damage.

95
Q

<h1>Page 20</h1>

<br></br>What is the difference between NSTEMI and STEMI in terms of blockage?

A

NSTEMI is associated with partial or transient blockage, while STEMI is associated with total blockage in a major coronary artery.

96
Q

<h1>Page 21</h1>

<br></br>What is the cardinal symptom of myocardial infarction?

A

Heavy, squeezing, crushing chest pain.

97
Q

<h1>Page 21</h1>

<br></br>Where may the pain from myocardial infarction radiate to?

A

Left arm, jaw, neck, or shoulder blades.

98
Q

<h1>Page 21</h1>

<br></br>How is the chest pain from myocardial infarction affected by vasodilators?

A

Not relieved well / at all by vasodilators (i.e. GTN).

99
Q

<h1>Page 21</h1>

<br></br>What causes shortness of breath in myocardial infarction?

A

Increased oxygen demand and decreased oxygen supply.

100
Q

<h1>Page 21</h1>

<br></br>What results from increased sympathetic nervous system stimulation in myocardial infarction?

A

Indigestion.

101
Q

<h1>Page 21</h1>

<br></br>What compensatory responses occur in myocardial infarction due to decreased oxygen supply?

A

Tachycardia and tachypnea - increased heart rate and respiratory rate.

102
Q

<h1>Page 21</h1>

<br></br>What are the catecholamine responses in myocardial infarction?

A

Coolness in extremities, perspiration, anxiety, restlessness.

103
Q

<h1>Page 21</h1>

<br></br>What percentage of individuals with myocardial infarction may have asymptomatic or vague symptoms?

A

Approximately 20%.

104
Q

<h1>Page 22</h1>

<br></br>What are the ECG abnormalities associated with myocardial infarction?

A

ST depression, T inversion, and ST elevation.

105
Q

<h1>Page 22</h1>

<br></br>What are the serum markers of myocardial injury used for diagnosis?

A

Cardiac markers.

106
Q

<h1>Page 22</h1>

<br></br>Which enzyme is used as a cardiac marker for myocardial injury?

A

Creatine kinase - MB isoenzyme.

107
Q

<h1>Page 22</h1>

<br></br>What cell contents are used to diagnose myocardial infarction?

A

Troponin.

108
Q

<h1>Page 22</h1>

<br></br>What does an echocardiogram show in the case of myocardial infarction?

A

Reduced ejection fraction.

109
Q

<h1>Page 22</h1>

<br></br>When is coronary angiography usually performed in the case of myocardial infarction?

A

In the acute phase when angioplasty or emergency heart surgery is imminent.

110
Q

<h1>Page 23</h1>

<br></br>What are some ECG abnormalities associated with myocardial infarction?

A

ST-segment elevation, T-wave inversion, and Q-wave formation.

111
Q

<h1>Page 24</h1>

<br></br>What is the definition of myocardial infarction (MI)?

A

Infarction of the myocardium due to prolonged myocardial ischaemia.

112
Q

<h1>Page 24</h1>

<br></br>What is the consequence of prolonged myocardial ischaemia?

A

Chest pain and death of heart tissue leading to a heart attack.

113
Q

<h1>Page 24</h1>

<br></br>What happens during the healing process of myocardial infarction?

A

Scar tissue is laid down to wall off the necrotic tissue, and the dead tissue is replaced with scar tissue.

114
Q

<h1>Page 24</h1>

<br></br>How does scar tissue differ from the rest of the myocardium?

A

It doesn’t function like the rest of the myocardium, as it is not contractile tissue, leading to impaired pumping.

115
Q

<h1>Page 24</h1>

<br></br>What does the white region in a healed myocardial infarct represent?

A

Scar tissue.

116
Q

<h1>Page 25</h1>

<br></br>What is the pathophysiology of myocardial infarction?

A

Rupture of an unstable atherosclerotic plaque in a coronary artery leading to acute plaque event, region of myocardial tissue death, occlusive thrombus, and narrowed coronary artery.

117
Q

<h1>Page 26</h1>

<br></br>What happens to cells in response to hypoxia during myocardial infarction?

A

They switch to anaerobic respiration.

118
Q

<h1>Page 26</h1>

<br></br>What is created as a result of anaerobic respiration during myocardial infarction?

A

An acidic environment.

119
Q

<h1>Page 26</h1>

<br></br>What drives an increase in intracellular sodium during myocardial infarction?

A

The acidic environment.

120
Q

<h1>Page 26</h1>

<br></br>What drives an increase in intracellular calcium during myocardial infarction?

A

The acidic environment.

121
Q

<h1>Page 26</h1>

<br></br>Over what time period does necrosis develop during myocardial infarction?

A

3 - 12 hours.

122
Q

<h1>Page 26</h1>

<br></br>Over what time period is weak tissue connective tissue laid down during myocardial infarction?

A

3 - 4 days.

123
Q

<h1>Page 26</h1>

<br></br>Within what time frame does the new tissue heal into non-contractile connective tissue during myocardial infarction?

A

Within 3 months.

124
Q

<h1>Page 27</h1>

<br></br>What are the immediate complications of myocardial infarction?

A

Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.

125
Q

<h1>Page 27</h1>

<br></br>What are the sub-acute complications of myocardial infarction?

A

Free wall rupture, LV thrombus, arrhythmia, cardiac failure.

126
Q

<h1>Page 27</h1>

<br></br>What are the chronic complications of myocardial infarction?

A

Ongoing cardiac failure, arrhythmia, LV aneurysm.

127
Q

<h1>Page 27</h1>

<br></br>What are the acute complications of myocardial infarction?

A

Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.

128
Q

<h1>Page 27</h1>

<br></br>What complications can occur in the immediate or delayed phase of myocardial infarction?

A

Acute (immediate/hours) and sub-acute (days) complications.

129
Q

<h1>Page 28</h1>

<br></br>What is free wall rupture in the context of myocardial infarction?

A

It is the rupture of the weakened and necrotic heart tissue post-MI, leading to cardiac tamponade.

130
Q

<h1>Page 28</h1>

<br></br>Why is it important for patients to be kept on bed rest post-MI?

A

To prevent free wall rupture and cardiac tamponade due to the weak and susceptible heart tissue.

131
Q

<h1>Page 28</h1>

<br></br>What is cardiac tamponade in the context of MI complications?

A

It is the accumulation of blood around the heart within the pericardial sac, leading to obstructive shock and is life-threatening.

132
Q

<h1>Page 28</h1>

<br></br>What is the most common timing for free wall rupture post-MI?

A

3 - 5 days post-MI.

133
Q

<h1>Page 28</h1>

<br></br>What does the yellow region in myocardial infarct indicate?

A

Necrotic tissue.

134
Q

<h1>Page 29</h1>

<br></br>What are the complications of myocardial infarction related to heart structure rupture?

A

Interventricular septum rupture, rupture of the division between the left and right ventricles, papillary muscle rupture, and rupture of muscle which anchors AV leaflets to the heart wall.

135
Q

<h1>Page 29</h1>

<br></br>What happens as a result of the mixing of oxygenated and deoxygenated blood in the heart?

A

Impaired AV valves opening/closing and regurgitation of blood back into atrium on the affected side.

136
Q

<h1>Page 30</h1>

<br></br>What is LV aneurysm?

A

It is an abnormal dilation of the wall of the left ventricle.

137
Q

<h1>Page 30</h1>

<br></br>Where does LV aneurysm form?

A

At a site of weakened myocardium following MI and functional tissue loss.

138
Q

<h1>Page 30</h1>

<br></br>How may LV aneurysm impair blood flow?

A

It may impair blood flow out of the heart.

139
Q

<h1>Page 30</h1>

<br></br>What prevents LV aneurysm from rupturing?

A

It is usually lined with scar tissue.

140
Q

<h1>Page 31</h1>

<br></br>What is arrhythmia?

A

Irregular or ‘out-of-step’ rhythms due to impaired electrical activity.

141
Q

<h1>Page 31</h1>

<br></br>When can arrhythmia occur after a myocardial infarction?

A

It can occur early (hours) or late (months) after the infarction.

142
Q

<h1>Page 31</h1>

<br></br>What can the death of critical myocardial tissue in the conduction system lead to?

A

Abnormal heart rhythm.

143
Q

<h1>Page 31</h1>

<br></br>What are the two types of abnormal heart rhythm that can occur due to myocardial infarction?

A

Atrial or ventricular.

144
Q

<h1>Page 31</h1>

<br></br>What happens if ventricular arrhythmia occurs?

A

The heart won’t pump sufficient blood out.

145
Q

<h1>Page 31</h1>

<br></br>What is responsible for cardiac arrest in the context of myocardial infarction?

A

Arrhythmia.

146
Q

<h1>Page 31</h1>

<br></br>Is arrhythmia rapidly fatal?

A

Yes, it is rapidly fatal.

147
Q

<h1>Page 32</h1>

<br></br>What is the consequence of MI of the ventricles?

A

Reduced ability to pump out sufficient blood.

148
Q

<h1>Page 32</h1>

<br></br>What can result from continued high ESV in the left ventricle?

A

Blood backs up in veins and capillaries of the lungs.

149
Q

<h1>Page 32</h1>

<br></br>What is the term for the condition where fluid is pushed from the veins into the alveoli?

A

Pulmonary oedema.

150
Q

<h1>Page 32</h1>

<br></br>What are the manifestations of left sided heart failure?

A

Fatigue, shortness of breath, coughing up fluid.

151
Q

<h1>Page 32</h1>

<br></br>What is the sequence of progression from left heart failure to right heart failure?

A

Left heart failure to right heart failure to peripheral oedema.

152
Q

<h1>Page 33</h1>

<br></br>What is cardiogenic shock?

A

Failure of the heart to pump out sufficient cardiac output.

153
Q

<h1>Page 33</h1>

<br></br>What happens to the body in cardiogenic shock?

A

It no longer gets enough blood due to ventricular dysfunction.

154
Q

<h1>Page 33</h1>

<br></br>How is cardiogenic shock defined?

A

As sustained low blood pressure.

155
Q

<h1>Page 33</h1>

<br></br>What can cause cardiogenic shock?

A

It can be an acute consequence of an extreme heart attack or a result of late-stage heart failure.

156
Q

<h1>Page 33</h1>

<br></br>What are the consequences of cardiogenic shock?

A

It causes damage to essential organs around the body, for example, ischemic stroke in the brain.

157
Q

<h1>Page 33</h1>

<br></br>Is cardiogenic shock life-threatening?

A

Yes, it is life-threatening.

158
Q

<h1>Page 34</h1>

<br></br>What is the immediate treatment acronym for Myocardial Infarction?

A

MOAN (Morphine, Oxygen, Aspirin, Nitrates).

159
Q

<h1>Page 34</h1>

<br></br>What is the purpose of Morphine in the immediate treatment of Myocardial Infarction?

A

For pain relief.

160
Q

<h1>Page 34</h1>

<br></br>Why is Oxygen administered in the immediate treatment of Myocardial Infarction?

A

To provide oxygen to the heart tissue.

161
Q

<h1>Page 34</h1>

<br></br>What is the role of Aspirin in the immediate treatment of Myocardial Infarction?

A

To prevent clotting from blood stasis.

162
Q

<h1>Page 34</h1>

<br></br>How do Nitrates contribute to the immediate treatment of Myocardial Infarction?

A

By improving blood flow via vasodilation (e.g. GTN).

163
Q

<h1>Page 35</h1>

<br></br>What is the goal of revascularization treatment for myocardial infarction?

A

To remove obstruction and restore blood flow to the coronary artery.

164
Q

<h1>Page 35</h1>

<br></br>What is the function of tissue plasminogen activator (tPA) in myocardial infarction treatment?

A

To dissolve the thrombus occluding the coronary artery.

165
Q

<h1>Page 35</h1>

<br></br>How do bypass grafts contribute to myocardial infarction treatment?

A

They redirect blood flow around the plaque area.

166
Q

<h1>Page 35</h1>

<br></br>What is the purpose of balloon angioplasty in myocardial infarction treatment?

A

To open up the artery.

167
Q

<h1>Page 35</h1>

<br></br>How does a stent contribute to myocardial infarction treatment?

A

It opens up the artery.

168
Q

<h1>Page 36</h1>

<br></br>What is the goal of ongoing treatment for myocardial infarction?

A

To prevent clot recurrence and future occlusive events.

169
Q

<h1>Page 36</h1>

<br></br>How does aspirin contribute to ongoing treatment for myocardial infarction?

A

It reduces platelet aggregation.

170
Q

<h1>Page 36</h1>

<br></br>What is the role of anticoagulants like Heparin and Warfarin in ongoing treatment for myocardial infarction?

A

They reduce the clotting potential of the blood.

171
Q

<h1>Page 36</h1>

<br></br>How can exercise contribute to ongoing treatment for myocardial infarction?

A

It can lower cholesterol and reduce vasoconstriction.

172
Q

<h1>Page 36</h1>

<br></br>What role does a balanced diet play in ongoing treatment for myocardial infarction?

A

It ensures sufficient nutrient intake.

173
Q

<h1>Page 36</h1>

<br></br>How does smoking cessation contribute to ongoing treatment for myocardial infarction?

A

It prevents nicotine-induced vasoconstriction and increased blood pressure, which can lead to myocardial infarction.

174
Q

<h1>Page 37</h1>

<br></br>What is meant by the term ‘ischaemic heart disease’?

A

A condition characterized by reduced blood supply to the heart muscle.

175
Q

<h1>Page 37</h1>

<br></br>What are the factors that contribute to ischaemic heart disease?

A

Factors such as high cholesterol, high blood pressure, smoking, diabetes, and obesity.

176
Q

<h1>Page 37</h1>

<br></br>What are the clinical features of stable angina, unstable angina, and myocardial infarction?

A

Stable angina: chest pain with exertion, Unstable angina: chest pain at rest, Myocardial infarction: prolonged chest pain, shortness of breath, nausea, and sweating.

177
Q

<h1>Page 37</h1>

<br></br>How can myocardial infarction and chronic ischaemic heart disease lead to heart failure?

A

By causing damage to the heart muscle, reducing its ability to pump effectively.

178
Q

<h1>Page 37</h1>

<br></br>What are the immediate and long-term complications of myocardial infarction?

A

Complications include arrhythmias and rupture of the heart muscle.

179
Q

<h1>Page 38</h1>

<br></br>What are the two broad categories of Ischaemic Heart Disease?

A

Angina and Myocardial Infarction.

180
Q

<h1>Page 38</h1>

<br></br>What causes temporary myocardial ischaemia?

A

Exertion increasing the demand for O2 and inability to supply enough through narrowed artery.

181
Q

<h1>Page 38</h1>

<br></br>What is the cause of stable angina?

A

Atherosclerotic narrowing within a coronary artery.

182
Q

<h1>Page 38</h1>

<br></br>What is unstable angina caused by?

A

Atherosclerotic narrowing within a coronary artery with non-occlusive thrombus.

183
Q

<h1>Page 38</h1>

<br></br>What are the immediate complications of myocardial infarction?

A

Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.

184
Q

<h1>Page 38</h1>

<br></br>What are the delayed complications of myocardial infarction?

A

Free wall rupture, LV thrombus, arrhythmia, cardiac failure.

185
Q

<h1>Page 38</h1>

<br></br>What happens to the tissue in an old, healed infarct?

A

Dead tissue is removed and replaced with scar tissue, appearing white.

186
Q

<h1>Page 38</h1>

<br></br>What happens when plaque and clot completely block the lumen of an artery?

A

It completely stops blood flow through the artery.

187
Q

<h1>Page 39</h1>

<br></br>What are the delayed complications of myocardial infarction?

A

Ongoing cardiac failure, arrhythmia, LV aneurysm.

188
Q

<h1>Page 39</h1>

<br></br>What are the acute complications of myocardial infarction?

A

Arrhythmia, acute heart failure, pulmonary oedema, cardiogenic shock, myocardial rupture, LV thrombus.

189
Q

<h1>Page 39</h1>

<br></br>What is myocardial rupture and when is it most common post-MI?

A

Myocardial rupture is when tissue is weak and necrotic, and it is most common 3-5 days post-MI.

190
Q

<h1>Page 39</h1>

<br></br>What are the consequences of rupture of the anterior wall post-MI?

A

Rupture of the anterior wall can lead to cardiac tamponade and obstructive shock.

191
Q

<h1>Page 39</h1>

<br></br>What is the cause of pulmonary oedema post-MI?

A

Pulmonary oedema is associated with the failure of the left ventricle to pump out enough blood it receives from the lungs.

192
Q

<h1>Page 39</h1>

<br></br>What are the consequences of arrhythmias post-MI?

A

Arrhythmias post-MI can lead to premature contractions and ventricular fibrillation.

193
Q

<h1>Page 39</h1>

<br></br>What is LV aneurysm and how does it form?

A

LV aneurysm is the dilation of the wall of the left ventricle, forming at a site of weakened myocardium following MI and tissue loss.

194
Q

<h1>Page 39</h1>

<br></br>What are the consequences of cardiogenic shock post-MI?

A

Cardiogenic shock can lead to inadequate perfusion of the tissues within the body.