Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology - Cardiovascular > Atherosclerosis, Chronic Stable Angina, and Acute Coronary Syndromes > Flashcards

Atherosclerosis, Chronic Stable Angina, and Acute Coronary Syndromes Flashcards

1
Q

What is the first stage of the increasing size of the atheroma / what is this called? When can the vessel lumen start getting smaller?

A

Positive remodeling -> vessel gets larger due to plaque formation, but the vessel is not stenosed at all
-> lumen shrinks once the plaque occupies greater than 40% of the circular intima

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What region of the atherosclerotic plaque is most vulnerable to rupture?

A

The shoulder region -> where the inflammatory cells are flanking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three factors which increase myocardial oxygen demand?

A
  1. Increased heart rate
  2. Increased myocardial contractile (inotropic state, i.e. via catecholamines)
  3. Increased wall tension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do preload and afterload increases affect myocardial oxygen demand?

A

By increasing wall tension, they increase myocardial oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

At what critical stenosis of vessels does chronic stable angina occur? What will happen to vessels downstream the stenosis?

A

> 70% is usually, but there can be a wide range of symptomatic vs nonsymptomatic depending on the coronary flow reserve / myocardial O2 demands.

Downstream the stenosis: Dilation of blood vessels to increase blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why do patients with atherosclerotic stenosis of the epicardial coronary arteries experience angina?

A

They stenosis causes a significant decrease in the coronary flow reserve (CFR), and as a result these patients are not able to increase their coronary blood flow during stress to manage the new oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Prinzmetal angina? Is it associated with atherosclerosis?

A

Angina caused by coronary artery vasospasm and resultant constriction of blood flow

It can occur with or without atherosclerosis, and is associated with cocaine use, deficient NO production, smoking, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What ECG finding will Prinzmetal angina show?

A

ST segment elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a good, rapid measure of myocardial oxygen demand?

A

Rate Pressure Product (RPP)

RPP = HR * SBP

SBP = systolic blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give another possible cause of myocardial ischemia other than atherosclerosis or coronary artery vasospasm?

A

Reduced oxygen carrying capacity of the blood (hypoxemia)

-> i.e. severe anemia, or elevated carboxyhemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the most common anginal symptoms?

A

Retrosternal chest discomfort, may localize to epigastrium, arms, shoulders, or neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What precipitates angina and what makes it better?

A

Precipitates: Exertion, eating, emotional stress, or exposure to cold (shoveling snow)

Palliates: Rest or nitroglycerin after 1-5 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is unstable angina defined?

A

New onset angina of at least class III severity (within 2 months of initial presentation), increase in frequency or severity, or angina at REST.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some atypical presentations of angina and who is most likely to present with these?

A

Nonspecific arm pain, dyspnea alone, etc

This is called “anginal equivalent”

Most common in: Women, diabetics, and elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most characteristic ECG change in stable angina?

A

1mm or more ST segment depression measured 80 seconds from the J point (end of QRS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does a myocardial perfusion scintigraphy test work?

A

Inject thallium into blood at rest, and see distribution of radioactive tracer in myocardial wall.

Next, do the same during exercise. Areas of lower radioactive tracer uptake a poorly perfused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

During an echocardiograph for angina, what are we checking for?

A

Wall movement abnormalities -> areas which are poorly perfused will not contract as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the workup protocol for a low risk vs high risk patient when checking for angina?

A

Low risk: Exercise test alone (ECG findings in exertion)

High risk: Exercise test + imaging studies, including scinitgraphy, echocardiograph, etc

19
Q

What is the gold standard test for coronary artery stenosis?

A

Coronary angiography

20
Q

What is the general treatment plan for chronic stable angina?

A

Beta blocker. Use non-DHP calcium channel blocker if not working or contraindicated

Use sublingual nitroglycerin for acute events

21
Q

What is the general treatment plan for Prinzmetal angina?

A

Use DHP calcium channel blockers (relax the coronary arteries), with sublingual nitroglycerin for acute events.

22
Q

Give two mechanical treatments for angina?

A
  1. PCI - percutaneous coronary intervention - stent the problematic vessel, will not totally relieve problem because plaque will be caked on wall or contents will embolize into microvasculature
  2. Coronary artery bypass graft - if multiple vessels involved
23
Q

What are the three mean coronary artery branches?

A
  1. Left anterior descending
  2. Left circumflex
  3. Right coronary artery

1/2 are branches of the left coronary

24
Q

What areas does the left anterior descending artery supply?

A
  1. Anterior wall of LV
  2. Anterior 2/3 of interventricular septum
  3. Anterior LV papillary muscle (dual supply with circumflex)
  4. Anterolateral wall
25
Q

What does the left circumflex artery supply?

A
  1. Posterolateral LV

2. Anterior LV papillary muscle (dual supply with circumflex)

26
Q

What areas are either perfused by right coronary or left circumflex artery depending on right or left dominant heart? What is the more common type of heart?

A
  1. Inferior LV
  2. Posterior left bundle branches
  3. AV node (/proximal HIS bundle)

Most commonly right-dominant hearts

27
Q

What areas does the right coronary artery supply (other than the right / left dominant areas?

A
  1. Anterior right ventricle
  2. Posterior 1/3 of interventricular sptum
  3. Posterior wall of LV
  4. Posteromedial papillary muscle of LV
28
Q

How do you differentiate between unstable angina and NSTEMI?

A

Unstable angina: Acute coronary syndrome without myocardial necrosis

NSTEMI: Acute coronary syndrome with myocardial necrosis -> cardiac markers (troponins) will be elevated

29
Q

How does unstable angina / NSTEMI differ from STEMI?

A

STEMI is associated with ST elevation due to COMPLETE epicardial artery occlusion

NSTEMI / Unstable angina will only be partially occluded

30
Q

What causes the majority of ACS?

A

Acute thrombus forming on a ruptured atherosclerotic plaque

31
Q

What symptoms are most compatible with infarction due to ACS?

A

Prolonged chest discomfort >30 minutes, with radiation to left arm or neck.

  • > precipitated by exertion and relieved by rest / nitroglycerin
  • > nausea, vomiting, diaphoresis, palpitations are common
32
Q

What are common atypical presentations for ACS in women and elderly patients?

A

Women - SHARP pain, fatigue, weakness, nonspecific complaints

Elderly - altered mental status

33
Q

If a patient has new lower extremity edema or elevated jugular venous pressure, what coronary artery is likely occluded? What other signs will be associated often?

A

RCA infarct -> loss of RV function

Includes bradycardia, heart block, no S4 / pulmonary rales (LV is working better than RV), 3rd degree AV block, and mitral valve regurgitation (it supplies posteromedial papillary muscle)

34
Q

What is the first heart sound to appear in ischemia and why?

A

S4 - diastolic dysfunction, ventricular stiffness leads to reduced compliance for blood rushing in during atrial systole

35
Q

In what type of infarct will hypotension be significant? How does this differ from other infarcts?

A

LAD -> supplies anterior left ventricle, unable to pump blood into systemic circulation.

Other infarcts will have less marked functional LV decreases -> increased tachycardia and catecholamine drive may lead to hypertension.

36
Q

In what type of MI can a dyskinetic cardiac bulge be palpated?

A

Anterior wall MI (LAD)

37
Q

What will happen to the T wave in transmural ischemia?

A

T wave will be inverted

  • > subendocardium will repolarize before the epicardium because Ito1 channels will not work as well in epicardium (help with rapid repolarization)
  • > normal repolarization is epicardium -> subendocardium
38
Q

What other ECG change occurs in transmural infarction other than ST elevation?

A

Q wave appears -> right atrial depolarization seems relatively more significant because the infarcted section of the LV has no electrical conductance.

39
Q

Why should serial troponins be drawn in the hospital? When do their numbers peak / turn back to baseline?

A

Because they may be negative very early on in infarction

Increase within 3-6 hours, peak at 48 hours, and return to baseline around 7-10 days

40
Q

Other than troponins and CK-MB, what is one level you should measure to guide medication in ACS?

A

Lipid level profile -> guides statin usage

41
Q

In what ACS’s should thrombolytic therapy be used?

A

Only in STEMI, and only if PCI capability is unavailable for greater than 90 minutes.

Must be done within 12 hours of symptoms onset.

42
Q

When should PCI be performed and why is it superior to thrombolytics?

A

Within 90 minutes door to needle

Provides greater overall patency, gives a lower risk of bleeding, and gives instant knowledge of the extent of underlying disease

43
Q

What should be done to help patient where PCI fails or they develop a rupture in LV, papillary muscle, or IV septum?

A

Emergency coronary artery graft bypass surgery (CAGB)

44
Q

Should PCI be done in NSTEMI or unstable angina?

A

Yes, this is okay -> just no thrombolytic therapy unless STEMI

Pathophysiology - Cardiovascular (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions