Brainscape's Knowledge GenomeTM

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


See full index

_MS2 Cardio > 8/10- Clinical Manifestations of Atherosclerosis > Flashcards

8/10- Clinical Manifestations of Atherosclerosis Flashcards

1
Q

The most common cause of death in the Western world is:

A. Accidents and Suicides

B. Rheumatic Heart Disease

C. Cancers

D. Coronary Heart Disease (CHD)

E. Valvular Heart Disease

F. Stroke

A

The most common cause of death in the Western world is:

A. Accidents and Suicides

B. Rheumatic Heart Disease

C. Cancers

D. Coronary Heart Disease (CHD)

E. Valvular Heart Disease

F. Stroke

(and stroke is no. 3, so together, cardiovascular disease is no. 1 and 3)

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

When does the majority of coronary blood flow occur?

A. During systole

B. During diastole

C. Both A and B

D. Neither A nor B

A

When does the majority of coronary blood flow occur?

A. During systole

B. During diastole

C. Both A and B

D. Neither A nor B

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

The heart can increase its O2 consumption by:

A. Increasing the extraction of O2 from blood

B. Increasing coronary blood flow

C. Both A and B

D. Neither A nor B

A

The heart can increase its O2 consumption by:

A. Increasing the extraction of O2 from blood

B. Increasing coronary blood flow

C. Both A and B

D. Neither A nor B

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

Why is CHD (coronary heart disease) such an important topic of study?

A

Coronary Heart Disease is the MCC of death in the Western World

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

Important slide!

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

What is the most common etiology of CHD?

A

Atherosclerosis

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

Overall process of atherosclerosis (broadly)

A
  • Endothelial injury
  • Fatty streak formation
  • Formation of advanced lesion
  • Unstable plaque rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Coronary arteries arise from where?

A

Sinuses of Valsalva at the root of the aorta

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

Anatomical features of coronaries’ origins?

A
  • Sinus valves obstruct ostia of the coronaries in systole and open in diastole
  • Two coronaries: left (usually bifurcates into 2 arteries) and right
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which coronary artery splits? Into what?

A

Left main coronary artery

  • Left anterior descending (LAD)
  • Left circumflex artery (LCx)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Label this coronary angiogram. (this is on the right)

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

T/F: The heart is more efficient than the kidney in extracting oxygen form the blood

A

True

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

What is the heart’s consumption and of oxygen and receipt of blood compared to the kidneys?

A
  • Heart consumes 2x as much O2
  • Heart receives 4-5x less blood

Thus, the heart is more efficient in extracting O2 than the kidneys

  • In relation to its metabolic needs; the heart is relatively underperfused
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In order to increase its O2 consumption, what does the heart do?

A

Increase its blood flow (can’t really get any more efficient at extracting oxygen from blood)

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

What happens as cardiac metabolic rate increases?

A
  • Coronary vascular resistance decreases
  • Coronary blood flow (CBF) increases (up to 400%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mediator of vasodilation with increased metabolic rate?

A

Adenosine derived from ATP breakdown

  • Responsible for microvascular vasodilation and the resultant increase in CBF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the hdyraulic factors influencing CBF (coronary blood flow)?

A

During systole, cardiac contraction compresses arteries and increases resistance; coronary ostia are obstructed/partially-occluded by sinus valves

  • Coronary blood flow is maximal in diastole (more than 2/3) and minimal in systole (less than 1/3)

Autoregulation: same flow despite changes in perfusion pressure

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

What are the metabolic factors influencing CBF?

A
  • Maximal ability to extract O2 for the heart
  • Increased O2 needs can be met only by increasing CBF

Low O2 causes a switch to anaerobic metabolism that produces more lactate and local acidosis

  • This results in greater adenosine, thus leading to higher CBF (via vasodilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the autonomic factors influencing CBF?

A
  • Coronary arteries have very scant autonomic innervation (unlike atria S/PS and ventricle S-rich)
  • Autonomic factors such as circulating catecholamines cause vasodilation INDIRECTLY (by increasing local metabolites like adenosine and changing loading and contractility)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does the heart use O2 for?

A
  • Subserve basal metabolism
  • Electrical energy for depolarization
  • Mechanical work of the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What kind of metabolism does the myocardium typically undergo?

A

Normally exclusively aerobic metabolism

  • 70% from FFA oxidation
  • 30% CHO oxidation

In anoxic conditions, energy is derived from anaerobic metabolism

22
Q

What are the determinants of myocardial O2 consumption?

A
  • Heart Rate!!!
  • Wall tension
  • Contractility
  • Fenn effect (shortening against load)
23
Q

How does heart rate play into increased myocardial O2 consumption?

How much does MVO2 increase when HR doubles?

A
  • Faster HR is associated with longer relative systolic time and usually with greater contractility
  • MVO2 more than doubles with doubling of heart rate

(MVO2 = myocardial oxygen consumption)

24
Q

How does wall tension play into increased myocardial O2 consumption?

A

Wall stress/tension is affected by pressure and chamber size (recall LaPlace law = Pr/2h)

  • Wall stress and HR can be accounted for by using the double product: HR x SBP
25
Q

What is the double product? What does it measure/indicate?

A

Double product = HR x SBP

(SBP = systemic blood pressure)

  • Wall stress and HR can be accounted for by using the double product
  • HR is the most important result of stress testing (to indicate maximal test), but double product is useful too
26
Q

How does contractility play into increased myocardial O2 consumption?

A
  • Least important factor (HR is the most)

Examples that increase MVO2 via contractility:

  • Exercise
  • Digoxin
  • Ca and catecholamines
27
Q

What is the 4th determinant of MVO2 (after HR, wall tension, and contractility)?

What makes it different?

A

Fenn effect (shortening against load)

  • During fiber shortening, the energy consumed to reduce LV volume (“volume work”) is a small fraction (15%) of overall energy consumed by cardiac contraction
28
Q

How can one decrease MVO2?

A
  • Decrease HR
  • Decrease wall tension
  • Decrease contractility
29
Q

What can be done clinically to affect MVO2 determinants?

A

- Beta blockers: critically important in pts with CAD (although in acute MI, IV beta blockers may cause cardiogenic shock in acute MI)

  • Blunt HR, BP, and contractility in response to exercise
  • Effective anti-anginal drugs and reduce arrhythmias
30
Q

How may CHD present clinically?

A
  • Stable angina pectoris
  • Unstable angina pectoris
  • Myocardial infarction
  • Variant angina
31
Q

What is stable angina pectoris?

A

Retrosternal chest discomfort* (due to ischemia) reproducible at a constant level of effort

*discomfort rather than “pain”, since some experience pressure

32
Q

What is unstable angina pectoris?

A

Prolonged chest discomfort (due to ischemia) not brought on by exertion occurring more frequently than usual

33
Q

What is myocardial infarction?

A

Prolonged chest discomfort due to coronary thrombosis (resultant from prolonged ischemia and myocardial necrosis)

  • More than 20-30 min to cause cell damage from ischemia
34
Q

What is variant angina?

A

Prinzmetal’s angina

  • Rest chest discomfort with transient ST elevation (resultant from coronary spasm)
35
Q

When is exercise-induced ischemia used?

A

On pts with stable angina pectoris

  • Or pts with chest discomfort, where you’re not sure if it’s angina
36
Q

What is the pathophysiology of exercise-induced ischemia?

What is happening at rest?

What changes during exercise (and what is seen on imaging/EKG)?

A
  • At rest, blood flow is adequate despite coronary artery narrowing (from atherosclerotic CHD).
  • During exercise, increased O2 demands not met by increased flow result in ischemia manifested by chest discomfort and ST depression (ECG) or reduced myocardial perfusion (perfusion nuclear scan) or reduced wall motion (echo).
37
Q

What may be used as the stressor in a “stress test”?

A

Stress may be physical (treadmill) or pharmacologic (dobutamine, dipyridamole)

38
Q

What pharmacologics may be used for anti-ischemic therapy (list)?

A
  • Nitrates
  • Beta blockers
  • CCBs (Ca channel blockers)
  • Anti-platelet drugs (e.g. aspirin)

[Nitrates have never shown survival benefits; beta blockers much better]

39
Q

How do nitrates work in anti-ischemic therapy?

A

Reduce O2 demands

  • Reduce preload
  • Reduce wall stress
  • Increase O2 supply (dilate coronaries and relieve spasm)

Most importantly reduce myocardial O2 demand

40
Q

How do beta blockers work in anti-ischemic therapy?

A

Reduce O2 demands:

  • Reduce HR
  • Reduce wall stress
  • Reduce BP
  • Indirectly increase O2 supply (prolong diastolic coronary filling)

Most importantly reduce myocardial O2 demand

41
Q

How do CCBs work in anti-ischemic therapy?

A

CCBs are potent coronary vasodilators effective in increasing coronary blood flow and reducing MVO2

  • Use very cautiously (make sure no heart failure or decrease in ventricular function) because these diminish contractility
42
Q

How do anti-platelet drugs work in anti-ischemic therapy? Example?

A

Example = aspirin

  • Prevent clot/thrombosis formation
  • Acute treatment for acute coronary syndromes
43
Q

What are 1st line anti-ischemic treatments? 2nd line?

A

1st line: beta blockers, nitrates

2nd line: CCBs

44
Q

What can be done (non-pharm) to correct atherosclerosis?

A

- Balloon angioplasty, often followed by:

- Stenting ((done in 90% of balloon angioplasties) to prevent negative remodeling and elastic recoil)

45
Q

What is CABG?

A

Coronary artery bypass graft

46
Q

What can be done if medical management fails to control stable angina?

A

CABG or PCI are two modalities that may be considered for revascularization when medical management fails to control stable angina

(PCI = percutaneous coronary intervention; includes PTCA, stents, rotablator…)

47
Q

What may occur following older PCI/stent techniques?

What has been done in newer? At what risk?

A

30-40% restenosis

  • Due to VSM (vascular smooth muscle) proliferation (neointima proliferation)

Newer PCI (with coated stents) markedly reduce restenosis below 10%, but increases late thrombosis risk!!

48
Q

What is a negative characteristic of newer PCI with coated stents? What must be done?

A

They increase late thrombosis risk

  • Unlike PTCA, they require at least 1 yr treatment with aspirin and clopidogrel (potent platelet aggregation inhibitor)

(Don’t do if upcoming surgery)

(PTCA = percutaneous transluminal coronary angioplasty)

49
Q

Are CABG and PCI equally effective?

A

In stable CAD: both PCI and CABG do not impact survival but relieve angina

  • CABG is associated with more angina relief than PCI (b/c of more complete revascularization)

CABG preferred:

  • In diabetic pts since it achieves more complete revascularization and prolonged survival
  • In 3 vessel CHD, 2 vessel CHD with decreased EF, 2 vessel CHD with proximal LAD, and left main CHD

PCI preferred:

  • In pts with 1 or 2 vessel CHD technically amenable to PCI

*Can’t put stents in arteries that are to small

50
Q

Atherosclerosis causes fixed obstruction but may induce ___ obstruction by ____________

A

Atherosclerosis causes fixed obstruction but may induce dynamic obstruction by altering vasomotor tone or through plaque rupture

_MS2 Cardio (35 decks)

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