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Cardiovascular > Ischemic heart disease and Acute Coronary Syndrome > Flashcards

Ischemic heart disease and Acute Coronary Syndrome Flashcards

1
Q

Which layer of the heart is most susceptible to myocardial ischemia and why is this so?

A

subendocardial layers are the most susceptible to ischemia because they undergo greater SHORTENING of subendocardial contractile units, which

1) require a greater energy supply
2) subjected to the greatest compressive forces

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2
Q

What process consumes more ATP/O2: myocardial tension development or myocardial shortening?

A

myocardial tension development

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3
Q

Explain how coronary atherosclerosis may lead to myocardial ischemia.

A

a stable plaque can turn into an unstable plaque if it is subjected to injury and/or inflammation.

The unstable plaque can undergo either

1) healing to become a stable plaque (typical angina), or it can
2) rupture and cause coronary thrombosis (Q wave infarct)

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4
Q

Explain how coronary spasms may lead to myocardial ischemia.

A

spasms can occlude a normal or atherosclerotic plaque

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5
Q

Explain how hypotension may lead to myocardial ischemia.

A

decreased diastolic pressure –> decreased coronary perfusion

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6
Q

Explain how hypoxia may lead to myocardial ischemia.

A

low PaO2 –> less oxygen delivery by coronary blood

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7
Q

Explain how anemia may lead to myocardial ischemia.

A

low Hb levels –> impaired coronary oxygen delivery

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8
Q

Explain how tachycardia may lead to myocardial ischemia.

A

decreased diastolic time –> decreased time for diastolic coronary perfusion

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9
Q

Explain how LV hypertrophy may lead to myocardial ischemia.

A

greater intramyocardial compressive forces combined with increase time and distance for blood to travel from the epicardium to the subendocardium

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10
Q

What are some factors that increase myocardial oxygen demand? (5)

A

1) tachycardia
2) HTN (increase LV wall tension necessary to pump blood out)
3) increased preload (increased wall tension/shortening)
4) increased ionotropy (greater tension/speed of contraction)
5) increased LVH (increased myocardial mass)

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11
Q

What is typical angina? variant angina?

What is stable angina? unstable angina?

A

Typical: transient chest pain that is brought on by an increase in myocardial O2 demand in the face of a fixed coronary obstruction (ie atherosclerosis). Can be stable or unstable.

Variant: (Prinzmetal angina) - transient coronary vasospasms

Stable: angina that is brought on predictably by the same amount of exercise/exertion

Unstable: angina that is changing in pattern (onset changes)

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12
Q

How does angina present differently than an acute myocardial infarction?

A

an acute MI usually, but not always, cause chest pain that is similar to that of variant angina, but it has a longer duration

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13
Q

What are some of the clinical outcomes of myocardial ischemia?

A

1) angina (typical vs variant; stable vs unstable)
2) acute myocardial infarction
3) LV dysfunction
4) heart failure (persistent ischemia causes the myocardium to infarct and scar)
5) arrhythmias

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14
Q

What causes CHRONIC coronary disease? What are the characteristic symptoms?

A

Fixed coronary artery obstruction with or without a previous infarction
symptoms range from asymptomatic -> angina -> heart failure

Physical exertion (exercise) is limited by angina

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15
Q

What causes ACUTE coronary disease? What are the characteristic symptoms?

A

acute lesion in a coronary plaque; classified as:

1) unstable angina - resulting ischemia produces new or increased chest pain, but is not severe enough to produce an infarct
2) non-STEMI - similar to unstable angina, but the ischemia is severe enough to cause a myocardial infarct
3) STEMI - lesion compounded by thrombosis, which leads to a large transmural ischemia

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16
Q

What causes sudden cardiac death?

A

arrhythmia leading to ventricular fibrillation

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17
Q

What is the levine sign?

A

clenched fist held against the anterior chest; typical of angina

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18
Q

How do patients often describe their angina?

What usually causes it?

How long does it usually last for?

A

“indescribable” - descriptions are highly variable and non-specific
Levine sign

usually brought on upon exertion

lasts 2-15minutes

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19
Q

Where does angina usually present?

A

sub-sternal; difficult to localize, but may radiate to the jaw or arms

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20
Q

What is the typical exam finding for angina?

A

S4 gallop and mitral regurtiation murmur due to decrease LV compliance during an anginal attack

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21
Q

What are the major risk factors that are suggestive of coronary disease?

A 
HTN
male
age
Type A personality
obesity
hyperlipidemia
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22
Q

How would you differentiate between coronary + non-coronary causes of angina, such as:

  • aortic dissections
  • pericarditis
  • pleural pain
A

coronary causes: insufficient myocardial oxygen supply; pain brought on upon exertion

  • aortic dissections - pain is maximal at onset and migrates as the dissection advances
  • pericarditis - pain with inspiration and lying flat
  • pleural pain - pain with inspiration
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23
Q

What are some tests that can be used to to diagnose angina?

A

1) coronary arteriography/angiography
2) resting ECG
3) myocardial perfusion scan
4) ECHO
5) exercise ECG

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24
Q

What are the possible things that can show up on an ECG in a patient with angina?

A

ST elevation: transmural ischemia
Pathological Q wave: transmural infarction
ST depression: subendocardial ischemia
Strain: LVH, electrolyte abnormalities, hyperventilation

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25
Q

Why would the myocardial perfusion scan be useful in diagnosing a patient with angina?

A

accentuates “cold spots”, or areas that have inadequate blood flow using a radioisotope dye that is preferentially taken up by myocardium that is perfused + functioning

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26
Q

Why would an ECHO be useful in diagnosing a patient with angina?

A

shows areas of myocardium that are ischemic, since the walls become hypokinetic or akinetic

27
Q

How would you treat/prevent CAD? (4)

A

Cholesterol reduction
Smoking cessation
Aspirin
Statins

28
Q

What are drug therapies that reduce LDL/ increase HDL? Which one produces the greatest decrease in LDL cholesterol and coronary mortality?

A

HMG CoA reductase inhibitors (statins)**
Bile acid sequestrants (cholestyramine)
Nicotinic Acid
Fibric Acid (gemfibrozil)

29
Q

Why is it bad to treat patients with CHF with digitalis?

A

Digitalis will reduce preload but it will also increase ionotropy, thereby increasing myocardial oxygen demand.

30
Q

What are the 3 big anti-anginal therapies?

A

1) nitrates
- venodilation -> decrease myocardial O2 demand - coronary artery dilation -> increases O2 delivery
ex: nitroglycerin, nitrates

2) b-blockers
- decrease HR/BP to decrease myocardial O2 demand
ex: propranolol, metoprolol, atenolol

3) Ca channel blockers
- prevents coronary spasms to increase O2 supply
ex: verapamil, diltiazem, nifedipine, amlodipine

31
Q

What is coronary bypass surgery?

A

procedure that restores blood flow to the heart by diverting the flow of blood around a section of a blocked artery using a vessel dissected from the body.

32
Q

What is coronary angioplasty/stenting?

A

Angioplasty - opens narrows/blocked coronary arteries to restore blood flow to the heart.

Stent - keeps the lumen open

33
Q

What are the major cases of ischemic heart disease?

A

atherosclerosis (90%)

vasospasms (10%)

34
Q

What are some of the ischemic heart disease syndromes?

A

1) angina
2) myocardial infarction
3) chronic heart disease
4) sudden death (may or may not be associated with an infarction)

35
Q

What is two different types of plaques? Which one is more likely to

A

atheromatous - necrotic, lipid rich debris; more dangerous/prone to rupture

sclerotic - fibrous + more voluminous, more stable

36
Q

How does the myocardial infarction develop?

A

The zone of necrosis begins in the subendocardium and work its way outward.

Ultimately the zone of necrosis results in scar formation

37
Q

What are the key time points of MI damage?

A

@ 10 minutes, ATP decreases by 50%
@ 40 minutes, ATP decreases by 90%

(

@ 12-24 hours, neutrophils march in
@ 48 hours, macrophages, fibroblasts, and endothelial cells appear; granulation tissue formation and collagen deposition begins to occur

38
Q

What are histological features associated with MI?

A

1) wavy fibers (dead myocardial fibers that are stretched out)
2) contraction bands (loss of nuclei)
3) hypereosinophilia (dead cells stain are more acidic)
4) coagulative necrosis
5) subendocardial sparing - oxygen from the ventricular lumen diffuses a few cell layers into the myocardium and keeps the cells alive
6) inflammation
7) mummified myocardium - islands of dead cardiac muscle surrounded by dense fibrous tissue

39
Q

What are some complications of MI?

A

arrhytmias
cardiogenic shock
CHF
rupture of papillary muscles/ventricles -> death
pericarditis (fibrinous) - due to activation of the coagulation cascade
growth of the infarct
aneurysm formation

40
Q

What is acute coronary syndrome?

A

clinical syndrome associated with new + increasing chest pain that is caused by an acute coronary lesion that causes acute myocardial ischemia

41
Q

What are the 3 subtypes of acute coronary syndrome? What can they ultimately result in?

A

acute non-occlusive ischemia

  • Unstable Angina
  • NSTEMI

acute occlusive ischemia
- STEMI

42
Q

What are the features of unstable angina in acute coronary syndrome?

ECG initial?
MI?
Enzyme pattern?
ECG final?

A

ECG initial - NO ST elevation
MI - no MI
Enzyme pattern - normal
ECG final - non-Q wave, ST depression

43
Q

What are the features of NSTEMI in acute coronary syndrome?

ECG initial?
MI?
Enzyme pattern?
ECG final?

A

ECG initial - NO ST elevation
MI - MI
Enzyme pattern - increased troponin
ECG final - non-Q wave, ST depression

44
Q

What are the features of STEMI in acute coronary syndrome?

ECG initial?
MI?
Enzyme pattern?
ECG final?

A

ECG initial - ST elevation
MI - MI
Enzyme pattern - increased troponin I
ECG final - Q wave, ST elevation

45
Q

What is the pathophysiology of ACS?

A

atherosclerotic plaque rupture and formation of a platelet plug on top of the ruptured plaque

(involves activated platelets, phospholipase A2, thrombin, thromboxane, glycoprotein IIb/IIIa)

46
Q

Review: clotting cascade

A

12 - 11 - 9 - (8) - 10
7 - (TF) - 10

10 - (5) - thrombin - fibrin - (13) - cross-linked fibrin

clotting cascade activated by tissue factor, and substances released by platelets; clot propagates as more fibrin and thrombin are generated, thus stabilizing the platelet plug

47
Q

What is the body’s natural defense against clots?

A

fibrinolysis - the subendothelial tissue releases tPA, which converts circulating plasminogen –> plasmin, which degrades fibrin.

48
Q

In what patients would you normally see Acute Coronary Syndrome?

A

commonly seen in patients with a fixed coronary obstructive disease, where acute ischemia is precipitated by supply-demand mismatch “demand ischemia”

49
Q

What are the 3 main categories of anti-thrombotic drugs? What are examples of each one?

A

1) platelet inhibitors
a) acetylsalicyclic acid (aspirin)
b) clopidogrel (plavix)
c) Eptifbatide - inhibit platelet glycoprotein IIb/IIIa

2) anticoagulants
a) heparin
b) warfarin

3) fibrinolytics
a) tPA

50
Q

How is ventricular remodeling post-MI good? bad?

A

ventricular remodeling is good in that the LV dilation and eccentric hypertrophy can initially compensate for the injured heart, but the increased tension requirements associated with the increased preload can accelerate the progression of heart failure..

51
Q

What are the initial ECG changes associated NSTEMI and STEMI? What are the final ECG changes?

A

NSTEMI:

initial: ST depression (subendocardial ischemia)
final: decreased R wave amplitude or T wave inversion

STEMI:

initial: ST elevation (transmural ischemia)
final: pathological Q waves

52
Q

What are two major serum markers of MI?

A

CKMB

Troponin I

53
Q

What are some commonalities between unstable angina + NSTEMI? Differences?

A

commonalities:

  • produced by a non-occlusive thrombus
  • symptoms of chest pain
  • ECG: normal, ST depression, or T wave inversion

differences:
- NSTEMI - occlusion is severe enough to produce biomarkers (CKMB/Troponin) that are indicative of infarction

54
Q

What are the 4 main categories of treatments that you would use to treat Unstable Angina/NSTEMI? Examples of each?

A

1) platelet inhibitors
a) acetylsalicyclic acid (aspirin)
b) clopidogrel (plavix)
c) Eptifbatide - inhibit platelet glycoprotein IIb/IIIa

2) anticoagulants
a) heparin
b) warfarin

3) Anti-ischemic
a) b-blockers
b) nitrates
c) Ca channel blockers

4) PCI (angioplasty with stent)

NOTE fibrinolytics are NOT useful

55
Q

How does one if one is experiencing STEMI or typical angina?

A

STEMI - chest pain is similar to that of typical angina, but it is

  • more severe
  • felt over a larger area
  • last longer
  • not relieved by rest or nitroglycerin
56
Q

What are some physical findings that you expect to find on a patient with STEMI?

A

RV dysfunction: JVD

LV dysfunction: gallops, mitral regurg, mumurs, crackles, cardiogenic shock (severe)

57
Q

What would you expect to find on a ECG with STEMI? Serum lab levels?

A

ECG: ST elevation -> T wave inversion + pathological Q waves

Serum markers: Troponin + CKMB

58
Q

What are the 4 main categories of treatments that you would use to treat STEMI? Examples?

A

1) anti-thrombotic
a) acetylsalicyclic acid (aspirin)
b) clopidogrel (plavix)
a) heparin

2) Anti-ischemic
a) b-blockers
b) nitrates
c) Ca channel blockers

3) Adjunct therapies
a) ACE inhibitors - prevent remodeling
b) statins - lower lipids

4) PCI (angioplasty with stent)
5) Fibrinolytics (tPA)

59
Q

What are some complications of STEMI?

A

1) LV failure (systolic/diastolic failure
2) cardiogenic shock
3) Pericarditis
4) RV infarction
5) Arrhythmias
6) Myocardial Rupture

60
Q

What is cardiogenic shock (as a complication of STEMI)?

How do you treat this?

A

when sufficient myocardium is infarcted to produce a decrease in CO and BP

treat with

  • afterload reducers
  • catecholamines
  • PCI
  • reperfusion
  • intraaortic balloon pump to artificially increase diastolic BP
61
Q

What is Dressler’s Syndrome (as a complication of STEMI)?

A

pericarditis that occurs when autoimmune antibodies form as a result of the MI attack the pericardium

62
Q

What is RV infarction (as a complication of STEMI)?

What would you find on a physical exam?
ECG? ECHO?

How do you treat this?

A

occlusion of the RCA results in an inferior infarction, resulting in LV underloading, decreased CO, and hypotension

Exam: elevated JVP
ECG: ST elevation in II, III, aVF, V1
ECHO: RV wall motion abnormality

Treatment: Fluids

63
Q

What types of arrhythmias can form (as a complication of STEMI)?

How do you treat this?

A

1) Ventricular tachyarrhytmias
2) heart block
a) Type I mobitz - AV nodal block; generally benign due to a relatively normal junctional escape rhythm
b) Type II mobitz - His purkinje block; more serious because ventricular escape rhythms are a lot sloer

when symptomatic, treat with atropine or temporal pacing

64
Q

What types of myocardial rupture can form (as a complication of STEMI)?

How do you treat this?

A

ruptures can form in

1) free wall of LV = fatal
2) ventricular septum = surgery
3) papillary muscle = surgery

Cardiovascular (8 decks)

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