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Cardio All My Notes > Ischemia (Acute Coronary Syndromes and stable angina ) > Flashcards

Ischemia (Acute Coronary Syndromes and stable angina ) Flashcards

1
Q

What is the most common cause of Acute Coronary Syndromes?

A

a thrombus from an atherosclerotic plaque blocking a coronary artery. lead to decrease oxygen supply and increase oxygen supply.

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2
Q

What is the common mechanism underlying all Acute Coronary Syndromes?

A

the rupture or erosion of the fibrous cap of a coronary artery plaque.

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3
Q

What happens when the fibrous cap of a coronary artery plaque ruptures or erodes?

A

it leads to platelet aggregation and adhesion.

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4
Q

What are the consequences of platelet aggregation and adhesion in Acute Coronary Syndromes?

A

Platelet aggregation and adhesion in Acute Coronary Syndromes result in localized thrombosis, vasoconstriction, and distal thrombus embolization.

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5
Q

How does thrombus formation and vasoconstriction contribute to myocardial ischemia?

A

reduce coronary blood flow, leading to myocardial ischemia.

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6
Q

What is the difference between unstable angina, NSTEMI, and STEMI?

A
  • Unstable angina is characterized by subtotal occlusion, supply-led ischemia without infarction, and a high (50%) risk of myocardial infarction (MI) in the subsequent 30 days.
  • NSTEMI is also characterized by subtotal occlusion about 90% and infraction if lefted untreated for 30 min .
  • STEMI is characterized by complete occlusion thus immediate infraction.
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7
Q

What are the four types of MI, and what distinguishes them?

A

Type 1: Traditional MI due to an acute coronary event.
Type 2: Ischemia secondary to increased demand or reduced supply of oxygen.
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischemic event.
Type 4: MI associated with PCI (percutaneous coronary intervention), coronary stenting, or CABG (coronary artery bypass grafting).

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8
Q

What are the symptoms commonly associated with severe crushing central chest pain at rest?

A
  • Pain that radiates to the jaw and arms, similar to angina but more prolonged and
  • not relieved by GTN (glyceryl trinitrate).
  • They are also associated with sweating, nausea, and often vomiting.
  • The duration of pain is typically 30 minutes or longer.
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9
Q

Which groups of individuals are at higher risk of atypical presentation or silent MI?

A

Answer: the elderly, and patients with diabetes are at higher risk of atypical presentation or silent MI.

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10
Q

What are the possible symptoms of atypical or silent MI?

A

milder symptoms (without chest pain), especially in younger women, such as shortness of breath, fatigue, body aches, and an overall feeling of illness.

Other symptoms may include an unusual feeling or mild discomfort in the back, chest, arm, neck, or jaw (without chest pain), heartburn, nausea/vomiting, abdominal pain.

  • It is important to note that these symptoms may occur up to a month before the occurrence of an MI and can include fatigue, sleep disturbance, shortness of breath, anxiety, indigestion, and palpitations.
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11
Q

What is the significance of xanthelasma as a sign?

A

Answer:
* Xanthelasma is a sign of atherosclerosis.

  • It is a yellowish deposit of cholesterol that forms on the eyelids and is associated with the presence of atherosclerotic plaques.
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12
Q

What are the ECG changes observed in STEMI?

A

Answer: include

  • ST segment elevation in leads consistent with an area of ischemia.
  • A new Left Bundle Branch Block (LBBB) can also diagnose a STEMI.
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13
Q

What are the ECG changes observed in NSTEMI?

A

Answer:
* may be normal or may show ST segment
depression in a specific region,

  • deep T-wave inversion, and
  • pathological Q waves suggesting a deep infarct (a late sign).
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14
Q

What are the possible ECG findings in unstable angina?

A

Answer:
* may be normal or may include non-specific changes,
* abnormal T waves, or
* ST depression.

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15
Q

What ECG findings indicate a posterior myocardial infarction (MI)?

A

Answer:
ST depression with tall R waves in V2-V3 indicates a posterior MI and
* elevation in V7 -V9

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16
Q

What ECG findings suggest an anterior MI?

A

Answer: include ST segment elevation in the leads corresponding to the anterior region of the heart (typically leads V2-V4).

  • Effecting the left anterior decending artery
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17
Q

What are the initial management strategies for unblocking the artery in Acute Coronary Syndromes?

A

Answer: The initial management strategies include administering
* morphine (with metoclopramide),
* providing oxygen if hypoxic,
* using nitrates if the patient is hypertensive or in acute left ventricular failure (LVF),
* administering aspirin, and
* prescribing ticagrelor or clopidogrel.

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18
Q

What is the definitive management approach for STEMI?

A

Answer:
* percutaneous coronary intervention (PCI) if available within 2 hours of pain onset.
* If PCI is not available within 2 hours, thrombolysis can be considered.

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19
Q

What is the definitive management approach for NSTEMI?

A

Answer: involves risk stratification based on ECG changes, troponin levels, and past medical history.
* All patients receive continuing aspirin and fondaparinux (anticoagulant).
* High-risk patients may undergo PCI and receive tirofiban (antiplatelet),
* while low-risk patients may be discharged after repeat negative troponin and followed up.

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20
Q

What are the lifestyle modifications recommended for secondary prevention in Acute Coronary Syndromes?

A

Answer: The lifestyle modifications include
* participating in a cardiac rehab program,
* making dietary modifications,
* increasing exercise, and quitting smoking.
* It is also important to have good control of blood pressure, cholesterol, and diabetes.

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21
Q

What medications are part of the secondary prevention regimen for Acute Coronary Syndromes (DABS)?

A

Answer: The medications for secondary prevention are:
* Dual antiplatelet therapy with aspirin for life and 6-12 months of a P2Y12 inhibitor (e.g., ticagrelor).
* ACE inhibitor (ACEi).
* β-blocker, which should be started within 24 hours of confirmed ACS.
* Statin.

Other medications include
* GTN for angina symptoms and
* aldosterone antagonists for patients with symptoms and/or signs of heart failure and left ventricular systolic dysfunction.

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22
Q

In which patient populations does CABG (coronary artery bypass grafting) have a survival advantage over PCI (percutaneous coronary intervention)?

A

Answer: CABG has a survival advantage over PCI in patients who areover 65 years old, have diabetes, or
have complex 3 vessel disease.

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23
Q

What is the conduit of choice for the left anterior descending coronary artery in CABG?

A

Answer: The left internal mammary artery

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24
Q

What are some arrhythmias that can occur as complications of Acute Coronary Syndromes?

A

Answer: include bradycardia, heart block, and tachyarrhythmias such as ventricular fibrillation.

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25
Q

What are some structural complications that can occur after an MI?

A

Answer: include
* SUdden cardiac death (SCD)
* ventricular septal defect (VSD),
* mitral regurgitation,
* ventricular wall rupture leading to cardiac tamponade (typically occurring 5-10 days post-MI), and
* the formation of a left ventricular mural thrombus that may result in systemic emboli.

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26
Q

What is Dressler’s syndrome?

A

Answer:
* Dressler’s syndrome is pericarditis that usually occurs around 2-3 weeks after an MI.

  • It is characterized by localized immune response causing pericarditis.
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27
Q

What are the types of functional damage that can occur as complications of Acute Coronary Syndromes? 3

A

Answer: include

  • acute ventricular failure (left, right, or both),
  • chronic cardiac failure, and
  • cardiogenic shock.
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28
Q

Why are anti-platelet medications like aspirin, clopidogrel, and ticagrelor the mainstay of treatment for Acute Coronary Syndrome?

A

Answer:
* ACS is usually caused by a thrombus from an atherosclerotic plaque blocking a coronary artery.

  • When a thrombus forms in a fast-flowing artery, it is predominantly composed of platelets.
  • Anti-platelet medications help prevent platelet aggregation and clot formation, reducing the risk of further blockage in the coronary arteries.
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29
Q

Which coronary artery supplies the right atrium, right ventricle, inferior aspect of the left ventricle, and posterior septal area?

A

Answer:
The Right Coronary Artery (RCA)
supplies the right atrium, right ventricle, inferior aspect of the left ventricle, and posterior septal area.

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30
Q

Which coronary artery supplies the left atrium and the posterior aspect of the left ventricle?

A

Answer: The Circumflex Artery
supplies the left atrium and the posterior aspect of the left ventricle.

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31
Q

Which coronary artery travels down the middle of the heart and supplies the anterior aspect of the left ventricle and the anterior aspect of the septum?

A

Answer:
The Left Anterior Descending (LAD)
artery travels down the middle of the heart and supplies the anterior aspect of the left ventricle and the anterior aspect of the septum.

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32
Q

How is NSTEMI diagnosed based on troponin levels and ECG changes?

A

Answer: NSTEMI is diagnosed when there are raised troponin levels and other ECG changes such as ST depression, T wave inversion, or pathological Q waves.

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33
Q

What is a “silent MI” and who is more likely to experience it?

A

Answer:

  • A “silent MI” refers to a myocardial infarction (MI) that occurs without typical chest pain symptoms.
  • Diabetic patients are more likely to experience a silent MI.
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34
Q

Which leads on the ECG correspond to different heart areas supplied by specific coronary arteries?

A

Answer:
* The leads I, aVL, V3-6 correspond to the anterolateral heart area supplied by the left coronary artery.
* The leads V1-4 correspond to the anterior heart area supplied by the left anterior descending (LAD) artery.
* The leads II, III, aVF correspond to the inferior heart area supplied by the right coronary artery.

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35
Q

What are some alternative causes of raised troponins, other than acute coronary syndrome?

A

Answer: include
* chronic renal failure,
* sepsis,
* myocarditis,
* aortic dissection, and
* pulmonary embolism.

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36
Q

What is the purpose of percutaneous coronary intervention (PCI) also called coronary angioplasty?

A

Answer:

  • PCI is a procedure that involves inserting a catheter into the patient’s brachial or femoral artery and guiding it to the coronary arteries using X-ray guidance.
  • It is used to identify and treat blockages in the arteries by widening the gap with balloons or using devices to remove or aspirate the blockage.
  • Stents are often placed to keep the artery open.
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37
Q

What is the BATMAN mnemonic for acute NSTEMI treatment?

A

Answer: BATMAN stands for:
1. Beta-blockers,
2. Aspirin (300mg stat dose),
3. Ticagrelor (180mg stat dose),
4. Morphine (titrated to control pain),
5. Anticoagulant (Fondaparinux unless high bleeding risk), and
6. Nitrates (e.g., GTN) to relieve coronary artery spasm.

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38
Q

How is the GRACE score used in NSTEMI?

A

Answer: The GRACE score is used to assess the risk of death or repeat MI within 6 months after an NSTEMI.

  • Patients with a medium or high risk score are considered for early PCI within 4 days of admission to treat underlying coronary artery disease.
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39
Q

Q: What is the recommended daily dose of aspirin for secondary prevention in patients post-MI?

A

A: The recommended dose is 75mg once daily.

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40
Q

Besides aspirin, what are some other antiplatelet options for secondary prevention in MI patients?

A

A: Clopidogrel or ticagrelor can be used as additional antiplatelet medications for up to 12 months.

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41
Q

Q: What is the recommended dose of atorvastatin for secondary prevention in MI patients?

A

A: The recommended dose is 80mg once daily.

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42
Q

Q: Which class of medications, such as ramipril, is recommended for ACE inhibition in secondary prevention of MI?

A

A: are recommended for secondary prevention, and the dose should be titrated as tolerated up to 10mg once daily.

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43
Q

Q: Which beta blocker is commonly used in secondary prevention of MI?

A

A: Atenolol is a commonly used beta blocker, but other beta blockers can be used as well, titrated to the highest tolerated dose.

44
Q

Q: Which medication is used as an aldosterone antagonist for secondary prevention in MI patients with clinical heart failure?

A

A: Eplerenone is an aldosterone antagonist used for secondary prevention, and the dose is titrated to 50mg once daily.

45
Q

Q: What is the distinction between Type 1 and Type 2 MI?

A

A:
* Type 1 MI refers to a traditional MI caused by an acute coronary event,
* while Type 2 MI is ischemia secondary to increased demand or reduced supply of oxygen, not primarily caused by thrombotic acute coronary syndromes.

46
Q

Q: How does smoking contribute to the development of ischemic heart disease?

A

A: Smoking increases endothelial injury and plaque formation, which can further narrow the coronary vessels and reduce blood flow.

47
Q

Question 1: What is the pathophysiology of stable angina?

A

Answer: Stable plaque with a strong fibrous cap occluding ≥ 70% of the lumen.

48
Q

Question 2: How would you describe the chest pain in stable angina?

A

Answer: characterized as “squeezing, tight choking.”

49
Q

What type of ischemia is seen in patients with stable angina?

A

Answer: Patients with stable angina have subendocardial ischemia.

  • The endocardial layer is the farthest layer from the coronary blood vessels; thus, it is the most
    susceptible to ischemia
50
Q

Question 1: What is the pathophysiology of unstable angina?

A

Answer:
characterized by an unstable plaque with a weak fibrous cap that is prone to rupture.

The exposed fatty center of the plaque leads to thrombus formation, resulting in occlusion of ≥ 90% of the lumen.

51
Q

Question 2: How would you describe the chest pain in unstable angina?

A

Answer: Chest pain in unstable angina occurs at rest and worsens with exertion.

52
Q

Question 3: What type of ischemia is seen in patients with unstable angina?

A

Answer: Patients with unstable angina also have subendocardial ischemia.

53
Q

Question 1: What is the pathophysiology of subendocardial infarcts/NSTEMI?

A

Answer:

  • Subendocardial infarcts/NSTEMI are caused by an unstable plaque with a weak fibrous cap that can rupture.
  • Thrombus formation occurs when platelets attach to the exposed fatty center of the plaque, leading to occlusion of ≥ 90% of the lumen.
54
Q

Question 4: What is the pathophysiology of transmural infarct/STEMI?

A

Answer:

  • Transmural infarcts/STEMI are also caused by an unstable plaque with a weak fibrous cap that can rupture.
  • Thrombus formation occurs when platelets attach to the exposed fatty center of the plaque, leading to occlusion of 100% of the lumen.
55
Q

Question 7: What is the characteristic feature of vasospastic angina/Prinzmetal’s angina?

A

Answer:
The chest pain in vasospastic angina/Prinzmetal’s angina is not related to or caused by atherosclerosis.

  • It typically occurs in young females with a history of illicit drug use, smoking, alcohol abuse, or triptan use.
  • Chest pain often occurs at night.
56
Q

Question 8: What is the underlying pathophysiology of vasospastic angina?

A

Answer:
Chest pain due to vasoconstriction of coronary vessels, narrowing the lumen and causing ischemia to the entire myocardium (“transmural” ischemia).

57
Q

Question 9: What diagnostic features are associated with vasospastic angina?

A

Answer:

  • ST elevation on an EKG,
  • negative troponins (a marker of destruction/infarction), and
  • reproduction of symptoms by acetylcholine, ergonovine, or
  • hyperventilation.
58
Q

Question 10: What is the recommended treatment for vasospastic angina?

A

Answer:

  • Treatment involves prescribing calcium channel blockers or nitroglycerin to dilate blood vessels.
  • Beta blockers should be avoided to prevent worsening vasoconstriction.
59
Q

stable angina and acute coronary syndrome (unstable angina, NSTEMI, and STEMI)?

A

Answer:
The duration of chest pain is shorter in stable angina, typically lasting 5-10 minutes.

In acute coronary syndrome, including unstable angina, NSTEMI, and STEMI, the duration of chest pain is usually greater than 10 minutes.

60
Q

Question 7: What is the significance of atypical (silent) presentations in certain populations?

A

Answer: Atypical (silent) presentations of ischemic heart disease may occur in specific populations such as
* diabetics (due to neuropathy affecting specific nerves),
* the elderly, and individuals post-heart transplant (due to alterations in nerve signaling).

These populations may not experience typical chest pain symptoms, and other signs or symptoms should be considered in their evaluation.

61
Q

Question 3: How does left ventricular MI affect blood pressure?

A

Answer:
1. Left ventricular MI can lead to hypotension.
2. With decreased blood volume in the left ventricle, there is less blood being pumped into the aorta, resulting in decreased ejection fraction and subsequently causing hypotension.
3. Hypotension can further decrease perfusion to organs.

62
Q

Question 4: What is reflex tachycardia, and why does it occur in left ventricular MI?

A

Answer: Reflex tachycardia is an autonomic nervous system response triggered by hypotension.
* In left ventricular MI, the decreased cardiac output leads to hypotension.
* To compensate for the decreased cardiac output and blood pressure, the autonomic nervous system increases heart rate (tachycardia) to improve cardiac output.
* This reflex response is known as reflex tachycardia.

63
Q

Question 5: What is the significance of S4 heart sounds in left ventricular MI?

A

Answer:
* S4 heart sounds may be heard in left ventricular MI.
* This sound occurs when the ventricles become stiff due to infarction.

64
Q

What is sudden cardiac death, and how can it occur in the first 24 hours following myocardial infarction (MI)?

A

Answer:
* Sudden cardiac death refers to an abrupt loss of cardiac function.
* It can occur due to the increased cell permeability in the area of infarction.
* This increased permeability allows an abnormal influx of cations (such as calcium and sodium) into the cells, leading to abnormal depolarization and generation of abnormal electric potentials.
* These abnormal electrical signals can cause the ventricles to contract irregularly, potentially leading to
* premature ventricular contractions (PVCs),
* ventricular tachycardia (VT), and
* ultimately ventricular fibrillation (VF).

65
Q

Question 2: What is cardiogenic shock, and what can cause it in the first 24 hours following an MI?

A

Answer:
* Cardiogenic shock is a condition characterized by inadequate cardiac output to meet the body’s demands, resulting in systemic hypoperfusion.
* It can occur if there is a significant infarct in a major vessel, particularly in the left ventricle.
* This can lead to severe hypotension, which causes reduced blood flow to the extremities and can manifest as cold extremities.

66
Q

Question 3: What is flash pulmonary edema, and how does it relate to myocardial infarction?

A

Answer:
* Flash pulmonary edema is the rapid accumulation of fluid in the lungs due to increased pressure in the pulmonary circulation.
* In the context of myocardial infarction, blood backing up into the pulmonary circulation can occur, leading to flash pulmonary edema.
* This can result in symptoms such as sudden onset of shortness of breath and hypoxia.
* To compensate for the decreased cardiac output, reflex tachycardia may occur to maintain an adequate cardiac output.

67
Q

Question 4: What are the potential complications that can occur between 24 hours and 3 days following an MI?

A

Answer:
1. Ventricular septal defect (VSD): In the septum, weak tissue resulting from an infarction can lead to rupture and the formation of a VSD, allowing blood to flow from the left ventricle into the right ventricle.

  1. Free wall rupture: Infarction in the left ventricle can weaken the tissue, and if it ruptures, blood can accumulate in the pericardial cavity, leading to cardiac tamponade.
  2. Papillary muscle rupture: Papillary muscles, which attach to the valves via chordae tendineae, can become weak and rupture due to an infarction. If this occurs in the left heart, it can cause mitral valve regurgitation.
  3. Left ventricular pseudoaneurysm: In cases of free wall rupture, blood can collect in the pericardium and form a pseudoaneurysm. This can increase the risk of mural thrombus formation.
68
Q

Question 5: What is the significance of left ventricular pseudoaneurysm following an MI?

A

Answer:
* refers to the formation of a localized outpouching in the left ventricular wall due to a free wall rupture.

  • This pseudoaneurysm can accumulate blood in the pericardial cavity.
  • The presence of blood stasis in this area increases the risk of thrombus formation (mural thrombus), which can lead to embolic complications if dislodged.
69
Q

Question 2: What is a left ventricular aneurysm, and when does it typically occur following an MI?

A

Answer:
* is a bulging or outpouching of the weakened area of the left ventricle following an infarction.

  • During the healing process after an MI, the soft granulation tissue is gradually replaced by fibrous tissue.
  • In some cases, the fibrous tissue may “bulge out” or form an aneurysm.
  • This typically occurs between 14 days to 1 month after the MI.
70
Q

Question 1: What are the diagnostic tools used in ischemic heart disease?

A

Answer: The diagnostic tools used in ischemic heart disease include the
* 12-lead electrocardiogram (EKG) and
* biomarkers such as troponin and CK-MB.

71
Q

Question 5: What are troponin and CK-MB, and how are they used as biomarkers in myocardial infarction?

A

Answer:

  • Troponin (specifically troponin I and troponin T) and CK-MB are molecules found within myocardial cells.
  • When there is tissue destruction, such as in myocardial infarction, these biomarkers leak out of the cells into the bloodstream.
  • Troponin is highly specific for myocardial tissue, while CK-MB is more specific for heart tissue compared to other organs.
  • Troponin and CK-MB levels typically take 12-24 hours to reach their peak, similar to the time course of myocardial infarction.
  • CK-MB levels may normalize more quickly than troponin.
  • These biomarkers can be used to assess the presence of myocardial infarction and determine the timing of the event.
72
Q

when to use CK-MB insted of Troponin

A

If a patient experiences new chest pain after an infarction, CK-MB levels can be ordered since troponin levels may still remain elevated and have not yet normalized.

73
Q

What is the significance of a positive stress test in the diagnostic evaluation?

A

Answer:
* A positive stress test indicates a higher likelihood of significant coronary artery disease.

  • In such cases, elective cardiac catheterization may be considered.
74
Q

What does the NSTE-ACS mnemonic stand for in relation to the TIMI Score?

A

Answer:

  • NSTE-ACS stands for Non-ST-Segment Elevation Acute Coronary Syndrome.
  • It is used in the TIMI Score to determine the need for catheterization based on various risk factors.
75
Q

What are some risk factors included in the TIMI Score mnemonic?

A

Answer:
The risk factors included in the TIMI Score mnemonic are age ≥65, elevated cardiac markers (troponins), ST segment depression on ECG, and the presence of at least three risk factors such as diabetes, hypertension, smoking, or age.

76
Q

What are the criteria for considering catheterization based on the TIMI Score?

A

Answer: A TIMI Score of ≥2 indicates an increased risk and the need to consider catheterization.

77
Q

What are the criteria for medically managing and reevaluating patients based on the TIMI Score?

A

Answer: A TIMI Score of 0-1 indicates a lower risk, and these patients can be managed medically with reevaluation.

78
Q

What is the Diamond Classification of Chest Pain used for in determining the need for stress testing?

A

Answer: The Diamond Classification of Chest Pain is used to evaluate stable angina.
It includes factors such as anginal chest pain, age/gender, substernal chest pain,

worsened chest pain with exertion, and relief with nitroglycerin.

79
Q

What is the importance of stress testing in patients with flow-limiting stenosis?

A

Answer:
* Stress testing is important in patients with flow-limiting stenosis to assess the presence of ischemia.
* It cannot diagnose a myocardial infarction (MI) but helps determine if there is a significant blockage causing inadequate blood flow.

80
Q

Which patients should undergo stress testing?

A

Answer:
* Stress testing is appropriate for patients with an intermediate probability of coronary artery disease (CAD).
* It is not recommended for patients with a high or low probability of CAD.
* Those with a high probability should undergo catheterization.

81
Q

How is target heart rate determined during stress testing?

A

Answer: Target heart rate is calculated as 85% of the maximum heart rate (HR). Maximum HR can be estimated using the formula: 220 - Age.

82
Q

What are the key indicators of a positive stress test based on EKG, Echo, and MPI?

A

Answer:

  1. EKG: ST segment depression or T wave inversion indicates a positive result.
  2. Echo: Wall motion abnormality indicates a positive result.
  3. MPI (myocardial perfusion imaging): Cold spots (areas of poor perfusion) indicate a positive result.
83
Q

When is pharmacologic stress testing used, and what medications are commonly used?

A

Answer:
* Pharmacologic stress testing is used when patients are unable to perform the exercise aspect of stress testing.
* Medications used include dobutamine for stress echocardiography and adenosine/dipyridamole for myocardial perfusion imaging (MPI).

84
Q

How does dobutamine work in stress echocardiography?

A

Answer: Dobutamine binds to β1 receptors (act as agonist) on myocardial and nodal cells, leading to increased heart rate, stroke volume, contractility, and oxygen demand.

85
Q

What is the mechanism of action of adenosine and dipyridamole in pharmacologic stress testing for MPI?

A

Answer:
* Adenosine and dipyridamole are vasodilators.
* They cause dilation of healthy blood vessels, allowing easy blood flow.
* However, they do not work on diseased vessels, leading to “coronary steal syndrome” where blood is “stolen” by healthy vessels, leaving diseased vessels starved and potentially ischemic.

86
Q

What is the goal of the treatment of ischemic heart disease?

A

The goal is to decrease the risk of
plaque formation and

thrombosis.

87
Q

What is the role of platelets in forming thrombosis?

A
  • Platelets play a role in thrombosis by adhesion and activation at the site of plaque rupture.
  • They secrete molecules such as ADP, TXA2 (Thromboxane A2), and 5-HT,
  • which can cause platelet aggregation and increase stickiness.
88
Q

What is the mechanism of action of aspirin in reducing thrombosis?

A
  • Aspirin irreversibly inhibits Cyclooxygenase-1 (COX-1),
  • which inhibits the production of Thromboxane A2 (TXA2).
  • This inhibition reduces platelet aggregation .
89
Q

What are some examples of P2Y12 receptor inhibitors used as antiplatelet medications?

A

Examples include clopidogrel (Plavix), ticagrelor (Brilinta), and prasugrel.

90
Q

What is the mechanism of P2Y12 receptor inhibitors?

A

P2Y12 receptor inhibitors bind to the adenosine diphosphate (ADP) P2Y12 receptor on platelets, leading to a decrease in platelet aggregation and stickiness. (NOT PREVENT )

91
Q

How does heparin work as an anticoagulant?

A
  • Heparin binds to antithrombin III, enhancing its activity.
  • Antithrombin III inhibits thrombin and factor X, decreasing coagulation and clot formation.
92
Q

What are the two types of heparins commonly used?

A
  • Unfractionated heparin (given intravenously or subcutaneously) and
  • low molecular weight (LMW) heparin
    LMW heparin is preferred in many cases.
93
Q

What is the role of statins in reducing thrombosis?

A

Statins do not directly reduce thrombosis but rather decrease plaque formation.

They are HMG-CoA reductase inhibitors , which ideally decrease LDL cholesterol and increase HDL cholesterol, leading to a reduction in plaque formation and potentially lowering the risk of future thrombosis.

94
Q

When is ACE-I recommended in the long-term treatment of patients with ischemic heart disease?
.

A
  • ACE-I are recommended in long-term treatment if the patient’s blood pressure can tolerate them.
  • They help lower blood pressure and
    • reduce cardiac remodeling, especially in patients who have had a myocardial infarction (MI)
95
Q

What is the mechanism of action of nitroglycerin in reducing oxygen demand? 2

A
  • Nitroglycerin is a vasodilator that causes dilation of the venous system, leading to decreased preload and decreased oxygen demand.
  • It also vasodilates the coronary vessels, increasing perfusion to ischemic cardiac tissue.
96
Q

What are the contraindications for nitroglycerin?

A

Nitroglycerin should be avoided in patients who are preload dependent, such as those with right ventricular myocardial infarction .
It is contraindicated in patients taking phosphodiesterase inhibitors
and those with aortic stenosis.

97
Q

What is the mechanism of morphine in reducing oxygen demand? 2

A
  • Morphine is a vasodilator that causes venous dilation, decreasing preload and oxygen demand.
  • It also causes arterial dilation, reducing afterload and oxygen demand.
  • However, it should be used cautiously as some studies suggest it may have adverse effects on outcomes.
98
Q

What are some examples of calcium channel blockers used in reducing oxygen demand?

A

Examples include
amlodipine,
nicardipine,
nimodipine, and
nifedipine,
which are mainly dihydropyridines.

99
Q

What are the contraindications for calcium channel blockers?

A

Calcium channel blockers should be avoided in patients with decompensated heart failure (weak heart). BECAUSE THE HEART CAN NOT CONTRACT WELL

100
Q

What is the preferred type of stent used in PCI?

A

Drug-eluting stents (DES) are the most common and preferred type of stents used in PCI. They release antirestenotic drugs that inhibit excessive intimal hyperplasia and reduce the risk of restenosis.

101
Q

What is the recommended duration of dual antiplatelet therapy (DAPT) after stent placement?

A
  • DAPT should be continued for at least a year after stent placement.
  • It typically consists of a combination of clopidogrel or ticagrelor with aspirin.
102
Q

When is coronary artery bypass graft surgery (CABG) indicated?

A

CABG is indicated in cases of left main stem coronary artery stenosis, significant stenosis (≥70%) of the proximal left anterior descending artery with 2-3 vessel occlusion, severe chest pain with 2-3 vessel disease, and NSTEMI or unstable angina not responding to maximal medical treatment.

103
Q

What are the types of grafts used in CABG?

A

Arterial grafts, such as the
radial artery and
internal thoracic artery, and
venous grafts,
particularly the saphenous vein, are used in CABG procedures.

104
Q

What is the mechanism of alteplase in thrombolysis?

A

Alteplase is a tissue plasminogen activator (TPA) that converts plasminogen to plasmin, leading to fibrinolysis.

105
Q

What are the contraindications for thrombolysis?

A

Thrombolysis is contraindicated in cases of active bleeding,
* prior intracranial hemorrhage ,
* recent surgery, and
* severe hypertension.

Cardio All My Notes (13 decks)

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