Brainscape's Knowledge GenomeTM

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


See full index

Cardio Exam 1 > Lec 16+18 Stable CAD > Flashcards

Lec 16+18 Stable CAD Flashcards

1
Q

What is order of severity:

  • MI
  • asymptomatic ischemia
  • unstable angina
  • angina pectoris
A

asymptomatic ischemia –> angina pectoris –> unstable angina –> MI

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

What is definition ischemic heart disease?

A

clinical expression of imbalance between myocardial ox supply and demand

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

What is angina pectoris?

A

uncomfortable sensation in chest produced by myocardial ischemia

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

What is stable angina?

A

chronic pattern of angina associated with physical activity or emotional upset usually radiates to L arm or jaw

relieved by rest w/in minutes or nitroglycerin

temporary ST depression on EKG
no permanent mycocardial damage = reversible

usually when stenosis > 70%

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

What is variant [prinzmetal] angina?

A

angina occurs at rest secondary to coronary artery vasospasm

transient ST elevation on EKG

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

What is silent ischemia?

A

asymptomatic episdoes of myocardial ischemia

only detect by EKG or other lab

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

What is unstable angina?

A

increase frequency + duration of angina at low exertion or at rest

ST depression on EKG

high risk of progression to MI

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

What is myocardial infarction?

A

region of myocardial necrosis usually due to prolonged cessation blood supply from acute thrombus at site of coronary atherosclertic stenosis + complete occlusion of coronary artery

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

What are the determinants of myocardial oxygen supply?

A
  • blood O2 content

- coronary flow

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

What determines the O2 content of blood?

A
  • hemoglobin level and O2 sat

- affected by lung disease, anemia, hemorrhage

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

What determines coronary flow?

A

Q = P/R

  • direct relation to perfusion pressure
  • indirect to vascular resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What determines perfusion pressure?

A
  • coronary perfusion occurs during diastole
  • can be approximated by diastolic pressure in aorta

decrease by anything that: decreases diastolic P [hypotension or aortic regurgitation] OR increases LVEDP [diminishes flow]

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

What are some conditions that decrease diastolic pressure and thus perfusion pressure?

A

hypotension

aortic regurgitation

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

What determines coronary vascular resistance?

A
  • vascular tone

- degree of coronary stenosis

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

What metabolic factors mediate vascular tone?

A

adenosine = produced in hypoxia = vasodilator

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

What is syndrome X?

A

chest pain and evidence of ischemia but normal coronary arteries

abnormal response to adenosine
microvascular dysfunction

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

What are endothelial factors that mediate vascular tone?

A

endothelium-dependent vasodilators: ACh, serotonin, thrombin, sheer stress –> cause endothelium to produce NO, prostacyclin, EDHF

endothelium-dependent vasoconstrictors: Thrombin, angiotensin II, epinephrin –> cause endothelium to produce endothelin I

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

What 3 factors released from endothelium cause smooth muscle relaxation?

A

NO, prostacyclin, EDHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What factor released from endothelium causes smooth muscle contraction?

A

endothelin 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What factors act on endothelial cells to cause vasodilation?

A

ACh
serotonin
shear stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What factors act on endothelial cells to cause vasoconstriction?

A

thrombin
angiotensin II
epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does endothelial response to ACh changed in normal vs at risk?

A

normal = ACh is a vasodilator

in pt with lots of risk factors for heart disease –> give ACh –> vasoconstriction

example of endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 3 major determinants of myocardial oxygen demand?

A
  • ventricular wall stress
  • heart rate
  • contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is ventricular wall stress? What are some states that increase it?

A

wall stress = P * r / 2h

  • increase by pressure overload [aortic stenosis/HTN]
  • increase by volume overload [mitral regurgitation]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does HR affect oxygen demand?

A

more ox required in higher HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does fixed atherosclerotic plaque affect coronary blood flow?

A

increases resistance
mostly by reduction in lumen diameter
also by length of lesion
R= L / r^4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does the hemodynamic consequences of arterial narrowing depend on?

A
  • degree of stenosis

- compensatory vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

At what level of stenosis is maximal blood flow decreased under conditions of stress?

A

70% stenosis = stable angina, fine in normal but when you exert yourself you don’t have enough O2 to support increased need

29
Q

At what level of stenosis is resting blood flow impaired?

A

90% stenosis

30
Q

What dysfunction in endothelial cells in chronic CAD?

A
  • impaired release of endothelium-dependent vasodilators in response to normal stimuli
  • impaired vasodilatory effects of adenosine + other metabolites
  • vasoconstriction over vasodilation [usually opposite]
  • loss of inherent antithrombic effect of endothelial cells –> promotes thrombosis
31
Q

What are some causes of non-atherosclerotic myocardial ischemia?

A
  • reduced O2 supply

- increased O2 demand

32
Q

What are 2 things that can cause reduced O2 supply?

A
  • aortic regurgitation [decrease diastolic BP –> decrease perfusion P]
  • acute blood loss [GI bleeding]
33
Q

What are 3 things that can cause increase O2 demand?

A
  • tachyarrythmias = rapid aFib
  • acute rise in BP = HTN crisis
  • severe aortic stenosis [LV hypertrophy]
34
Q

What is myocyte necrosis?

A

irreversible cell death with prolonged episode = infarct

  • detect by cardiac imaging or Q wave on ECG
35
Q

What is stunned myocardium?

A

episode of systolic dysfunction after some degree of transient ischemia but no necrosis

functionally can gradually recover back to normal

36
Q

What is hibernating myocardium?

A

chronic dysfunction, has many years of CAD and chronic lack of O2 supply –> abnormal ventricular function

if you revascularize you can restore ventricular function

37
Q

What should you look for in history for diagnosis of chronic stable angina?

A
  • sensation pain/pressure in chest
  • diffuse localization can radiate to left arm/neck
  • lasts few min
  • associated: SOB, fatigue, nausea, diaphoresis
  • precipitated by physical activity or emotional stress
38
Q

What is differential diagnosis for chronic stable angina?

A

cardiac spasm= occurs only at rest
pericarditis = positional / bad with deep inspiration

GI: associated with meal, antacids help

MSK: focal

39
Q

What do you see on EKG in chronic stable angina?

A

ST depression or T wave inversion = myocardial ischemia

infarct = ST elevation

may be normal in most pt if not having acute episode

40
Q

What is stress testing?

A
  • try to induce stress by exercise or pharmacologic so you can look at EKG or echo or nuclear perfusion to check for ischemia
41
Q

What is gold standard for chronic stable angina diagnosis?

A

coronary angiography
= need contrast media, visualize lumen but can’t assess atherosclerotic disease in vascular wall to look for vulnerability

42
Q

What are the 2 goals for treatment of stable CAD?

A
  • improve QOL –> reduce symptoms angina

- improve quantity of life –> reduce fatal events

43
Q

What is use of nitrates in stable CAD treatment?

A

venodilation –> reduce LV volume –> lower wall stress + ox demand

44
Q

What are most common side effects nitrates?

A

lightheadedness, headache

tolerance

45
Q

What effect of nitrates on long term MI survival?

A

none = no mortality benefit

just for symptom release

46
Q

What is use of B blockers in stable CAD treatment

A

inhibit B receptors –> decrease HR and contractility [B1]; vasoconstriction in vasculature and bronchial tree [B2]

–> decrease myocardial ox demand by slowing HR + decrease force of contraction + increase ox supply by increase duration of diastole

47
Q 
How do nitrates affect the following:
end diastolic volume
blood pressure
contractility
heart rate
ejection time
oxygen demand
A 
end diastolic volume: decrease
blood pressure: decrease
contractility: increase [reflex response]
heart rate: increase [reflex response]
ejection time: decrease
oxygen demand: decrease
48
Q 
How do beta blockers affect the following:
end diastolic volume
blood pressure
contractility
heart rate
ejection time
oxygen demand
A 
end diastolic volume: increase
blood pressure: decrease
contractility: decrease
heart rate: decrease
ejection time: increase
oxygen demand: decrease
49
Q 
How do nitrates and Bblocker together affect the following:
end diastolic volume
blood pressure
contractility
heart rate
ejection time
oxygen demand
A 
end diastolic volume: no effect or decrease
blood pressure: decrease
contractility: little/none
heart rate: decrease
ejection time: little/no effect
oxygen demand: big decrease
50
Q

Which patients have greatest benefit from B-blockers?

A
  • pts with symptoms, with prior MI, or with heart failure
51
Q

Do Bblockers improve mortality or symptoms or both?

A

both improve mortality and symptoms

52
Q

What are side effects of B blockers?

A
  • bronchospasm –> caution in asthmatics
  • decompensated LV dysfunction –> make it worse = DO NOT USE IN DECOMPENSATED LV
  • significant bradycardia
  • fatigue
  • sexual dysfunction
  • may mask reflex tachycardia from hypoglycemia
53
Q

What is particular use of dihydropyridines?

A

coronary spasm

54
Q

Why caution when use Ca channel blocker with B blocker?

A

may accentuate negative chronotropy and inotropy

55
Q

What is effect of ranolazine?

A

decreases anginal frequency and improves exercise tolerance

  • does not reduce mortality but does improve symtpoms
56
Q

What is effect of antiplatelet therapy?

A

reduce risk of thrombotic complications by inhibition of platelet aggregation

= no benefit to symptoms but significant reduction mortality

57
Q

Who should use thienopyridine [clopidogrel]?

A

pts intolerant to aspirin

inhibits platelet P2Y12 receptor

monotherapy = equivalent to aspirin, no benefit to use together

58
Q

What is effect of lipid lowering therapy on pt with stable angina?

A

lower risk for death/MI in pt at risk or wtih established CAD

59
Q

Who should get beta blockers?

A

post-MI, in heart failure

60
Q

Who should get ACE inhibitors?

A

post MI, with LV dysfuntion, in heart failure, DM, chronic kidney disease, HTN

61
Q

What 4 drugs give symptom relief in stable CAD?

A
  • nitrates, B Blocker, CCB, ranolazine
62
Q

What are the 2 methods of revascularization?

A

balloon angioplasty stent

coronary artery bypass graft

63
Q

What are problems with previous iterations balloon angioplasty?

A

balloon alone –> get elastic recoil, restenosis

bare metal –> get restenosis due to inflammation and proliferation smooth muscle around it

drug eluting –> coated with anti-proliferative, inhibits restonosis but also delays normal endothelialization –> increase risk for thrombosis
= need long term DAPT

64
Q

Is there reduction in death from stent [percutaneous coronary intervention]?

A

nope! just reduce anginal symptoms

65
Q

Who should get percutaneous coronary intervention?

A

pt with refratory symptoms despite optomizing medical therapy OR intolerant to medical therapy

66
Q

What is difference in venous vs arterial grafts?

A

venous = from saphenous; patency at 10 yrs 50%

arterial = from raidal, internal mammary; very high patency 90% at 10 yrs = used for left main stenoses

67
Q

Which people have greatest mortality advantage from revascularization?

A
  • left main stenosis
  • 2 vessel stenosis involving LAD
  • 3 vessel CAD
  • diabetic with multivessel CAD
68
Q

What are advantages/disadvantages of PCI?

A

advantage: low risk procedure, minimal recuperation
disadvantage: need dual antiplatelet threapy = bleeding risk; higher revascularization rates

69
Q

What are advantages/disadvantages of CABG?

A

advantages = complete revascularization, no need for long term anti-platelet therapy, proven mortality benefit in certain pts

disadvantages: higher procedure risk, longer recuperation

Cardio Exam 1 (16 decks)

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