NURSING 2005_Ischaemic Heart Disease_1 Slide PP Flashcards
(194 cards)
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Front
A
Back
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<h1>Page 01</h1>
<br></br>What is another term for Acute Coronary Syndrome?
A
Ischaemic heart disease.
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<br></br>What type of angina is characterized by predictable chest pain during physical activity or stress?
A
Stable angina.
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<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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<br></br>What is another term for a heart attack?
A
Myocardial infarction.
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<br></br>Which type of myocardial injury is potentially reversible?
A
Reversible.
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<br></br>Which type of myocardial injury is not reversible?
A
Irreversible.
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<br></br>What is the site of atherosclerotic plaque development?
A
Coronary arteries.
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<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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<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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<br></br>What triggers angina?
A
Physical exertion, emotional stress, extreme cold or hot temperatures, heavy meals, and smoking.
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<br></br>How is stable angina usually relieved?
A
By rest or medication, such as nitroglycerin.
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<br></br>What is angina pectoris?
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Chest pain caused by insufficient oxygen to the heart.
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<br></br>What is the cause of angina pectoris?
A
Blockage of a coronary artery leading to ischaemia and hypoxia.
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<br></br>What determines the phenotype of angina pectoris?
A
The degree of blockage in the coronary artery.
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<br></br>What causes the pain in angina pectoris?
A
Myocardial ischaemia.
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<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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<h1>Page 05</h1>
<br></br>What is stable angina?
A
Stable angina is stable atherosclerotic plaque combined with vasoconstriction.
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<br></br>What is the most common type of angina?
A
Stable angina.
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<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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<br></br>What is the typical cause of stable angina?
A
Exercise or stress.
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<br></br>What kind of blockage is present in stable angina?
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Only partial blockage.
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<br></br>What is the nature of atherosclerotic narrowing in stable angina?
A
Fixed.
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<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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What happens to the heart with exercise in stable angina?
It needs to beat harder to meet the demands of the body.
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What is required for the ventricles during exercise in stable angina?
They need more blood.
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What prevents the increased demand for blood from being met in stable angina?
Narrowing of the vessel.
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What is the result of myocardial ischaemia in stable angina?
Pain.
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When does the pain subside in stable angina?
With rest, after the increased demand on the heart is over.
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How do symptoms deteriorate over time in stable angina?
As plaque increases in size.
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What reduces the amount of exercise or stress needed for symptoms to come on in stable angina?
Less exercise/stress.
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Why doesn't stable angina normally progress to unstable angina?
Because the plaques have different structures.
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What are the characteristics of unstable angina?
Larger plaques, more plaques, unstable plaques, associated thrombi.
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Page 07
What is the difference in blood flow in unstable angina compared to stable angina?
Blood flow is not adequate at rest, leading to pain without exertion.
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Why is unstable angina considered more serious and unpredictable?
Due to the higher chance of plaque rupture and worsened ischaemia and hypoxia.
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What symptoms are associated with unstable angina?
Nausea, shortness of breath, sweating.
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How is unstable angina different from stable angina in terms of relief?
It is not relieved by rest or medication.
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What is the risk associated with unstable angina?
Risk of having a myocardial infarction.
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What effect does atherosclerotic plaque with overlying non-occlusive thrombus have on the coronary artery lumen?
Significantly reduces the size of the coronary artery lumen.
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What is the characteristic of unstable angina related to atherosclerotic narrowing?
Fixed atherosclerotic narrowing with a non-occlusive thrombus.
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What happens when there is significant narrowing of the coronary artery in unstable angina?
It prevents sufficient blood flow at rest, leading to myocardial ischemia.
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What may unstable angina progress to if the thrombus expands to completely block the coronary artery?
Myocardial infarction.
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How does atherosclerotic plaque with overlying non-occlusive thrombus affect the coronary artery lumen in unstable angina?
It significantly reduces the size of the coronary artery lumen.
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What are the characteristics of stable angina?
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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What are the characteristics of unstable angina?
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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Page 09
What happens if sufficient perfusion is restored in angina?
Normal function is restored.
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What is the final step to necrosis in unstable angina?
It isn't reached, making angina reversible.
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What does ischaemia lead to in both stable and unstable angina?
Hypoxia and infarction (necrotic cell death).
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Page 10
What are the risk factors for atherosclerosis?
Hypertension, high LDL, smoking, and alcohol.
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What are the modifiable risks that can act as an initiating insult for atherosclerosis?
Hypertension, high LDL, smoking, and alcohol.
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What factors can worsen plaques that are already present in atherosclerosis?
Hypertension, high LDL, smoking, and alcohol.
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What are the risk factors to decrease in order to prevent angina?
Hypertension, high LDL, smoking, and alcohol.
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What is the pharmacological treatment for angina involving Glyceryl trinitrate (GTN)?
Oral tablets, IV or spray.
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What is GTN a prodrug of?
Nitric oxide.
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How does GTN act in the body?
By dilating blood vessels.
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What is the effect of GTN on coronary blood flow?
It improves coronary blood flow.
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How does GTN relieve ischaemia?
By dilating coronary arteries.
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What is the mechanism by which GTN reduces pain?
By dilating coronary arteries and improving coronary blood flow.
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What type of vasodilator is GTN?
Quick-acting vasodilator.
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What is the mechanism of action of statins like Simvastatin?
Inhibiting an enzyme that synthesizes cholesterol in the liver.
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What is the role of cholesterol (LDL) in atherosclerotic plaque development?
It serves as building blocks for atherosclerotic plaque development.
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How does Simvastatin affect cholesterol production?
It lowers cholesterol production.
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What is the effect of Simvastatin on LDL uptake in liver cells?
It increases LDL uptake in liver cells.
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How does the action of Simvastatin contribute to decreased plaque burden?
By reducing circulating LDLs, which means less building blocks for atherosclerotic plaque development.
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Page 13
What is the pharmacological treatment for angina using aspirin?
Aspirin is used as an anti-platelet agent to reduce platelet aggregation and prevent thrombus formation.
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How does aspirin work to prevent thrombus formation in angina?
It reduces platelet aggregation.
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What is the effectiveness of low-dose aspirin in reducing thrombus formation?
Very effective.
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What is the mechanism of action of beta-blockers in the treatment of angina?
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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How do beta-blockers affect heart rate and blood pressure?
They decrease heart rate and blood pressure.
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What is the effect of beta-blockers on the workload of the heart?
They decrease the workload of the heart.
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What is the primary action of beta-blockers on arteries?
They dilate arteries.
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When are surgical treatments for angina considered?
When medications are ineffective or the condition worsens.
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What does bypass surgery do in the context of angina?
It bypasses blood flow around the area of atherosclerotic plaque.
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How does bypass surgery remove the risk of occlusive thrombus formation?
By removing blood flow from the narrowed coronary artery.
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What risk does bypass surgery remove in relation to myocardial infarction?
It removes the risk of myocardial infarction.
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What is the purpose of balloon angiography in the context of angina?
To increase the size of the lumen and improve blood flow in a narrowed coronary artery.
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How does balloon angiography impact the diseased artery?
It increases blood flow through the diseased artery.
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What is the risk associated with balloon angiography in relation to plaque?
It does not impact plaque, so there is still a risk of future events.
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What are some non-pharmacological treatments for angina?
Healthy diet, avoiding saturated fat, regular physical activity, maintaining a healthy weight, reducing consumption of alcohol and smoking, and maintaining normal blood pressure.
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What is another name for Myocardial Infarction?
Heart attack.
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What is the main cause of Myocardial Infarction?
Blockage of blood flow to the heart.
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What are the common symptoms of Myocardial Infarction?
Chest pain, shortness of breath, and sweating.
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What is the immediate treatment for Myocardial Infarction?
Aspirin and nitroglycerin.
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What is the ongoing treatment for Myocardial Infarction?
Medications, lifestyle changes, and cardiac rehabilitation.
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What is myocardial infarction (MI) commonly known as?
Heart attack.
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What causes the death of heart tissue in myocardial infarction?
Prolonged lack of blood flow and oxygen.
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What is the cause of infarction of the myocardium in myocardial infarction?
Prolonged insufficient blood supply.
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What can cause necrosis of the myocardium in myocardial infarction?
Atherosclerotic narrowing with occlusive thrombus.
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What is the result of unstable angina in relation to myocardial infarction?
It can lead to myocardial infarction.
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What happens to the rest of the heart during a myocardial infarction?
It will continue to function.
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What compensatory mechanisms are activated during myocardial infarction?
Mechanisms to maintain cardiac output (same as for heart failure).
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How can myocardial infarction be classified based on ECG abnormalities?
Based on the presence/absence of ST elevation.
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What does NSTEMI stand for and what does it indicate?
NSTEMI stands for Non-ST elevation myocardial infarction, indicating partial or transient blockage resulting in necrosis and less damage.
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What does STEMI stand for and what does it indicate?
STEMI stands for ST elevation myocardial infarction, indicating complete obstruction by a thrombus resulting in necrosis and extensive damage.
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What is the difference between NSTEMI and STEMI in terms of blockage?
NSTEMI is associated with partial or transient blockage, while STEMI is associated with total blockage in a major coronary artery.
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What is the cardinal symptom of myocardial infarction?
Heavy, squeezing, crushing chest pain.
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Where may the pain from myocardial infarction radiate to?
Left arm, jaw, neck, or shoulder blades.
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How is the chest pain from myocardial infarction affected by vasodilators?
Not relieved well / at all by vasodilators (i.e. GTN).
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What causes shortness of breath in myocardial infarction?
Increased oxygen demand and decreased oxygen supply.
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What results from increased sympathetic nervous system stimulation in myocardial infarction?
Indigestion.
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What compensatory responses occur in myocardial infarction due to decreased oxygen supply?
Tachycardia and tachypnea - increased heart rate and respiratory rate.
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What are the catecholamine responses in myocardial infarction?
Coolness in extremities, perspiration, anxiety, restlessness.
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What percentage of individuals with myocardial infarction may have asymptomatic or vague symptoms?
Approximately 20%.
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What are the ECG abnormalities associated with myocardial infarction?
ST depression, T inversion, and ST elevation.
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What are the serum markers of myocardial injury used for diagnosis?
Cardiac markers.
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Which enzyme is used as a cardiac marker for myocardial injury?
Creatine kinase - MB isoenzyme.
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What cell contents are used to diagnose myocardial infarction?
Troponin.
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What does an echocardiogram show in the case of myocardial infarction?
Reduced ejection fraction.
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When is coronary angiography usually performed in the case of myocardial infarction?
In the acute phase when angioplasty or emergency heart surgery is imminent.
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What are some ECG abnormalities associated with myocardial infarction?
ST-segment elevation, T-wave inversion, and Q-wave formation.
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What is the definition of myocardial infarction (MI)?
Infarction of the myocardium due to prolonged myocardial ischaemia.
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What is the consequence of prolonged myocardial ischaemia?
Chest pain and death of heart tissue leading to a heart attack.
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What happens during the healing process of myocardial infarction?
Scar tissue is laid down to wall off the necrotic tissue, and the dead tissue is replaced with scar tissue.
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How does scar tissue differ from the rest of the myocardium?
It doesn't function like the rest of the myocardium, as it is not contractile tissue, leading to impaired pumping.
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What does the white region in a healed myocardial infarct represent?
Scar tissue.
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What is the pathophysiology of myocardial infarction?
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.
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What happens to cells in response to hypoxia during myocardial infarction?
They switch to anaerobic respiration.
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What is created as a result of anaerobic respiration during myocardial infarction?
An acidic environment.
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What drives an increase in intracellular sodium during myocardial infarction?
The acidic environment.
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What drives an increase in intracellular calcium during myocardial infarction?
The acidic environment.
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Over what time period does necrosis develop during myocardial infarction?
3 - 12 hours.
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Over what time period is weak tissue connective tissue laid down during myocardial infarction?
3 - 4 days.
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Within what time frame does the new tissue heal into non-contractile connective tissue during myocardial infarction?
Within 3 months.
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What are the immediate complications of myocardial infarction?
Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.
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What are the sub-acute complications of myocardial infarction?
Free wall rupture, LV thrombus, arrhythmia, cardiac failure.
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What are the chronic complications of myocardial infarction?
Ongoing cardiac failure, arrhythmia, LV aneurysm.
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What are the acute complications of myocardial infarction?
Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.
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What complications can occur in the immediate or delayed phase of myocardial infarction?
Acute (immediate/hours) and sub-acute (days) complications.
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What is free wall rupture in the context of myocardial infarction?
It is the rupture of the weakened and necrotic heart tissue post-MI, leading to cardiac tamponade.
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Why is it important for patients to be kept on bed rest post-MI?
To prevent free wall rupture and cardiac tamponade due to the weak and susceptible heart tissue.
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What is cardiac tamponade in the context of MI complications?
It is the accumulation of blood around the heart within the pericardial sac, leading to obstructive shock and is life-threatening.
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What is the most common timing for free wall rupture post-MI?
3 - 5 days post-MI.
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What does the yellow region in myocardial infarct indicate?
Necrotic tissue.
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What are the complications of myocardial infarction related to heart structure rupture?
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.
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What happens as a result of the mixing of oxygenated and deoxygenated blood in the heart?
Impaired AV valves opening/closing and regurgitation of blood back into atrium on the affected side.
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What is LV aneurysm?
It is an abnormal dilation of the wall of the left ventricle.
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Where does LV aneurysm form?
At a site of weakened myocardium following MI and functional tissue loss.
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How may LV aneurysm impair blood flow?
It may impair blood flow out of the heart.
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What prevents LV aneurysm from rupturing?
It is usually lined with scar tissue.
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What is arrhythmia?
Irregular or 'out-of-step' rhythms due to impaired electrical activity.
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When can arrhythmia occur after a myocardial infarction?
It can occur early (hours) or late (months) after the infarction.
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What can the death of critical myocardial tissue in the conduction system lead to?
Abnormal heart rhythm.
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What are the two types of abnormal heart rhythm that can occur due to myocardial infarction?
Atrial or ventricular.
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What happens if ventricular arrhythmia occurs?
The heart won't pump sufficient blood out.
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What is responsible for cardiac arrest in the context of myocardial infarction?
Arrhythmia.
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Is arrhythmia rapidly fatal?
Yes, it is rapidly fatal.
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What is the consequence of MI of the ventricles?
Reduced ability to pump out sufficient blood.
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What can result from continued high ESV in the left ventricle?
Blood backs up in veins and capillaries of the lungs.
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What is the term for the condition where fluid is pushed from the veins into the alveoli?
Pulmonary oedema.
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What are the manifestations of left sided heart failure?
Fatigue, shortness of breath, coughing up fluid.
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What is the sequence of progression from left heart failure to right heart failure?
Left heart failure to right heart failure to peripheral oedema.
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What is cardiogenic shock?
Failure of the heart to pump out sufficient cardiac output.
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What happens to the body in cardiogenic shock?
It no longer gets enough blood due to ventricular dysfunction.
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How is cardiogenic shock defined?
As sustained low blood pressure.
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What can cause cardiogenic shock?
It can be an acute consequence of an extreme heart attack or a result of late-stage heart failure.
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What are the consequences of cardiogenic shock?
It causes damage to essential organs around the body, for example, ischemic stroke in the brain.
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Is cardiogenic shock life-threatening?
Yes, it is life-threatening.
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What is the immediate treatment acronym for Myocardial Infarction?
MOAN (Morphine, Oxygen, Aspirin, Nitrates).
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What is the purpose of Morphine in the immediate treatment of Myocardial Infarction?
For pain relief.
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Why is Oxygen administered in the immediate treatment of Myocardial Infarction?
To provide oxygen to the heart tissue.
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What is the role of Aspirin in the immediate treatment of Myocardial Infarction?
To prevent clotting from blood stasis.
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How do Nitrates contribute to the immediate treatment of Myocardial Infarction?
By improving blood flow via vasodilation (e.g. GTN).
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What is the goal of revascularization treatment for myocardial infarction?
To remove obstruction and restore blood flow to the coronary artery.
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What is the function of tissue plasminogen activator (tPA) in myocardial infarction treatment?
To dissolve the thrombus occluding the coronary artery.
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How do bypass grafts contribute to myocardial infarction treatment?
They redirect blood flow around the plaque area.
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What is the purpose of balloon angioplasty in myocardial infarction treatment?
To open up the artery.
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How does a stent contribute to myocardial infarction treatment?
It opens up the artery.
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What is the goal of ongoing treatment for myocardial infarction?
To prevent clot recurrence and future occlusive events.
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How does aspirin contribute to ongoing treatment for myocardial infarction?
It reduces platelet aggregation.
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What is the role of anticoagulants like Heparin and Warfarin in ongoing treatment for myocardial infarction?
They reduce the clotting potential of the blood.
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How can exercise contribute to ongoing treatment for myocardial infarction?
It can lower cholesterol and reduce vasoconstriction.
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What role does a balanced diet play in ongoing treatment for myocardial infarction?
It ensures sufficient nutrient intake.
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How does smoking cessation contribute to ongoing treatment for myocardial infarction?
It prevents nicotine-induced vasoconstriction and increased blood pressure, which can lead to myocardial infarction.
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What is meant by the term 'ischaemic heart disease'?
A condition characterized by reduced blood supply to the heart muscle.
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What are the factors that contribute to ischaemic heart disease?
Factors such as high cholesterol, high blood pressure, smoking, diabetes, and obesity.
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What are the clinical features of stable angina, unstable angina, and myocardial infarction?
Stable angina: chest pain with exertion, Unstable angina: chest pain at rest, Myocardial infarction: prolonged chest pain, shortness of breath, nausea, and sweating.
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How can myocardial infarction and chronic ischaemic heart disease lead to heart failure?
By causing damage to the heart muscle, reducing its ability to pump effectively.
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What are the immediate and long-term complications of myocardial infarction?
Complications include arrhythmias and rupture of the heart muscle.
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What are the two broad categories of Ischaemic Heart Disease?
Angina and Myocardial Infarction.
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What causes temporary myocardial ischaemia?
Exertion increasing the demand for O2 and inability to supply enough through narrowed artery.
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What is the cause of stable angina?
Atherosclerotic narrowing within a coronary artery.
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What is unstable angina caused by?
Atherosclerotic narrowing within a coronary artery with non-occlusive thrombus.
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What are the immediate complications of myocardial infarction?
Arrhythmia, acute heart failure, pulmonary edema, cardiogenic shock.
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What are the delayed complications of myocardial infarction?
Free wall rupture, LV thrombus, arrhythmia, cardiac failure.
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What happens to the tissue in an old, healed infarct?
Dead tissue is removed and replaced with scar tissue, appearing white.
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What happens when plaque and clot completely block the lumen of an artery?
It completely stops blood flow through the artery.
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What are the delayed complications of myocardial infarction?
Ongoing cardiac failure, arrhythmia, LV aneurysm.
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What are the acute complications of myocardial infarction?
Arrhythmia, acute heart failure, pulmonary oedema, cardiogenic shock, myocardial rupture, LV thrombus.
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What is myocardial rupture and when is it most common post-MI?
Myocardial rupture is when tissue is weak and necrotic, and it is most common 3-5 days post-MI.
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What are the consequences of rupture of the anterior wall post-MI?
Rupture of the anterior wall can lead to cardiac tamponade and obstructive shock.
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What is the cause of pulmonary oedema post-MI?
Pulmonary oedema is associated with the failure of the left ventricle to pump out enough blood it receives from the lungs.
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What are the consequences of arrhythmias post-MI?
Arrhythmias post-MI can lead to premature contractions and ventricular fibrillation.
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What is LV aneurysm and how does it form?
LV aneurysm is the dilation of the wall of the left ventricle, forming at a site of weakened myocardium following MI and tissue loss.
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What are the consequences of cardiogenic shock post-MI?
Cardiogenic shock can lead to inadequate perfusion of the tissues within the body.
