Lec 16+18 Stable CAD Flashcards Preview

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Flashcards in Lec 16+18 Stable CAD Deck (69):

What is order of severity:
- MI
- asymptomatic ischemia
- unstable angina
- angina pectoris

asymptomatic ischemia --> angina pectoris --> unstable angina --> MI


What is definition ischemic heart disease?

clinical expression of imbalance between myocardial ox supply and demand


What is angina pectoris?

uncomfortable sensation in chest produced by myocardial ischemia


What is stable angina?

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%


What is variant [prinzmetal] angina?

angina occurs at rest secondary to coronary artery vasospasm

transient ST elevation on EKG


What is silent ischemia?

asymptomatic episdoes of myocardial ischemia

only detect by EKG or other lab


What is unstable angina?

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

ST depression on EKG

high risk of progression to MI


What is myocardial infarction?

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


What are the determinants of myocardial oxygen supply?

- blood O2 content
- coronary flow


What determines the O2 content of blood?

- hemoglobin level and O2 sat

- affected by lung disease, anemia, hemorrhage


What determines coronary flow?

Q = P/R
- direct relation to perfusion pressure
- indirect to vascular resistance


What determines perfusion pressure?

- 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]


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

aortic regurgitation


What determines coronary vascular resistance?

- vascular tone
- degree of coronary stenosis


What metabolic factors mediate vascular tone?

adenosine = produced in hypoxia = vasodilator


What is syndrome X?

chest pain and evidence of ischemia but normal coronary arteries

abnormal response to adenosine
microvascular dysfunction


What are endothelial factors that mediate vascular tone?

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


What 3 factors released from endothelium cause smooth muscle relaxation?

NO, prostacyclin, EDHF


What factor released from endothelium causes smooth muscle contraction?

endothelin 1


What factors act on endothelial cells to cause vasodilation?

shear stress


What factors act on endothelial cells to cause vasoconstriction?

angiotensin II


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

normal = ACh is a vasodilator

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

example of endothelial dysfunction


What are 3 major determinants of myocardial oxygen demand?

- ventricular wall stress
- heart rate
- contractility


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

wall stress = P * r / 2h

- increase by pressure overload [aortic stenosis/HTN]
- increase by volume overload [mitral regurgitation]


How does HR affect oxygen demand?

more ox required in higher HR


How does fixed atherosclerotic plaque affect coronary blood flow?

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


What does the hemodynamic consequences of arterial narrowing depend on?

- degree of stenosis
- compensatory vasodilation


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

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


At what level of stenosis is resting blood flow impaired?

90% stenosis


What dysfunction in endothelial cells in chronic CAD?

- 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


What are some causes of non-atherosclerotic myocardial ischemia?

- reduced O2 supply
- increased O2 demand


What are 2 things that can cause reduced O2 supply?

- aortic regurgitation [decrease diastolic BP --> decrease perfusion P]
- acute blood loss [GI bleeding]


What are 3 things that can cause increase O2 demand?

- tachyarrythmias = rapid aFib
- acute rise in BP = HTN crisis
- severe aortic stenosis [LV hypertrophy]


What is myocyte necrosis?

irreversible cell death with prolonged episode = infarct

- detect by cardiac imaging or Q wave on ECG


What is stunned myocardium?

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

functionally can gradually recover back to normal


What is hibernating myocardium?

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

if you revascularize you can restore ventricular function


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

- 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


What is differential diagnosis for chronic stable angina?

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

GI: associated with meal, antacids help

MSK: focal


What do you see on EKG in chronic stable angina?

ST depression or T wave inversion = myocardial ischemia

infarct = ST elevation

may be normal in most pt if not having acute episode


What is stress testing?

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


What is gold standard for chronic stable angina diagnosis?

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


What are the 2 goals for treatment of stable CAD?

- improve QOL --> reduce symptoms angina
- improve quantity of life --> reduce fatal events


What is use of nitrates in stable CAD treatment?

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


What are most common side effects nitrates?

lightheadedness, headache


What effect of nitrates on long term MI survival?

none = no mortality benefit
just for symptom release


What is use of B blockers in stable CAD treatment

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


How do nitrates affect the following:
end diastolic volume
blood pressure
heart rate
ejection time
oxygen demand

end diastolic volume: decrease
blood pressure: decrease
contractility: increase [reflex response]
heart rate: increase [reflex response]
ejection time: decrease
oxygen demand: decrease


How do beta blockers affect the following:
end diastolic volume
blood pressure
heart rate
ejection time
oxygen demand

end diastolic volume: increase
blood pressure: decrease
contractility: decrease
heart rate: decrease
ejection time: increase
oxygen demand: decrease


How do nitrates and Bblocker together affect the following:
end diastolic volume
blood pressure
heart rate
ejection time
oxygen demand

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


Which patients have greatest benefit from B-blockers?

- pts with symptoms, with prior MI, or with heart failure


Do Bblockers improve mortality or symptoms or both?

both improve mortality and symptoms


What are side effects of B blockers?

- 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


What is particular use of dihydropyridines?

coronary spasm


Why caution when use Ca channel blocker with B blocker?

may accentuate negative chronotropy and inotropy


What is effect of ranolazine?

decreases anginal frequency and improves exercise tolerance

- does not reduce mortality but does improve symtpoms


What is effect of antiplatelet therapy?

reduce risk of thrombotic complications by inhibition of platelet aggregation

= no benefit to symptoms but significant reduction mortality


Who should use thienopyridine [clopidogrel]?

pts intolerant to aspirin

inhibits platelet P2Y12 receptor

monotherapy = equivalent to aspirin, no benefit to use together


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

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


Who should get beta blockers?

post-MI, in heart failure


Who should get ACE inhibitors?

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


What 4 drugs give symptom relief in stable CAD?

- nitrates, B Blocker, CCB, ranolazine


What are the 2 methods of revascularization?

balloon angioplasty stent
coronary artery bypass graft


What are problems with previous iterations balloon angioplasty?

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


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

nope! just reduce anginal symptoms


Who should get percutaneous coronary intervention?

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


What is difference in venous vs arterial grafts?

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


Which people have greatest mortality advantage from revascularization?

- left main stenosis
- 2 vessel stenosis involving LAD
- 3 vessel CAD
- diabetic with multivessel CAD


What are advantages/disadvantages of PCI?

advantage: low risk procedure, minimal recuperation

disadvantage: need dual antiplatelet threapy = bleeding risk; higher revascularization rates


What are advantages/disadvantages of CABG?

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

disadvantages: higher procedure risk, longer recuperation