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Cardiology > Ischemic Heart Disease and ACS > Flashcards

Ischemic Heart Disease and ACS Flashcards

1
Q

What type of angina can chronic ischemic herat disease lead to and why?

A

Stable angina. This is because after each ischemic episode, inflammatory factors are released in the area, leading to platelet aggregation and eventual healing. Over time, process repeats itself and the lumen of the vessel narrows, leading to stenosis or obstruction.

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2
Q

What are the complications of MI that can occur from 4-7 days after MI? (3)

A

This is the acute inflammation stage in which macrophages enter the ischemic area and eat dead/necrotic debris. This is also when the wall is the weakest. Possible complications:

1) Rupture of ventricular free wall → cardiac tamponade.
2) Rupture of IV septum → left to right shunt
3) Rupture of papillary muscle →mitral insufficiency

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3
Q

Histological changes in myocardium 1-7 days after MI

A

Acute inflammation. In 1-3 days, presence of neutrophils. In 4-7 days, presence of macrophages

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4
Q

What is the mechanism of SK fibrinolytic agent and why is it not used?

A

Mechanism: SK attaches to plasminogen to transform plasminogen → plasmin, which dissolves clot. However, SK attaches not only to plasminogen in the clot but to all circulating plasminogens (nonspecific).

Not used anymore because it only dissolves about 50% of clot.

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5
Q

Histological changes in myocardium less than 4 hours after MI

A

None

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6
Q

What are different types of ischemic herat disease?

A

1) Angina pectoris (stable, unstable, variant)
2) Chronic ischemic heart disease
3) MI
4) Sudden cardiac death
* 5) Silent ischemia*
* 6) Syndrome X*

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7
Q

If EKG at rest or stress test doesn’t detect MI but you are still suspicious of an MI, what can you do?

A

Can do myocardial perfusion imaging, in which during rest and exercise, an isotope is injected into pt’s heart. Can visualize where obstructions occur this way.

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8
Q

What is silent ischemia?

A

Type of ischemic syndrome; pts don’t have warning system of ischemia (pain); thus, their heart becomes ischemic without pain.

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9
Q

What does TIMI risk score measure? How is it measured?

A

How likely that ACS is present and risk of death. Out of 7 points; if patient has specific risk factors (e.g. age >65, presence of smoking, DM, HTN/ known CAD etc) then patient accrues points → higher risk of ACS/ death.

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10
Q

What are the common ways that people describe chest pain related to an MI?

A

1) Like elephant sitting on my chest
2) Burning sensation
3) Choking feeling in throat
4) Tooth ache
5) Bra is too tight

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11
Q

What is the most common cause of ischemic heart disease/ ischemia?

A

Atherosclerosis.

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12
Q

What is the mechanism behind tPA as a fibrinolytic agent?

A

Attaches to plasminogen in the clot and transforms it to plasmin, which dissolevs the clot.

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13
Q

What factors affect coronary vascular resistance? (5)

A

1) External compression
2) Arterial tone (Metabolic Factor, Endothelial factors, Neural factors)

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14
Q

How long does pain episodes from angina pectoris last unless it has progressed to ongoing infarction?

A

5-10 minutes

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15
Q

What estimates perfusion pressure of coronary arteries and why? What can decrease perfusion pressure?

A

Aortic diastolic pressure because the coronary artery perfusion occurs during diastole, due to unimpaired blood flow. Conditions that decrease aortic diastolic pressure (e.g. hypotension) also decrease coronary perfusion pressure, which may lession myocardial oxygen supply.

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16
Q

Even though blood freely circulates in the coronary vessels, why don’t they clot?

A

The endothelium produces substances that prevent clotting (e.g. block clotting factors, thrombin formation, etc.)

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17
Q

What causes unstable angina episodes?

A

Acute atherosclerotic plaque rupture that leads to acute thrombosis with incomplete occlusion of coronary artery.

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18
Q

What two factors determine coronary bloodflow and which is the main determinant of bloodflow?

A

1) Perfusion pressure
2) Resistance: main determinant.

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19
Q

Why are cardiac enzymes elevated in the blood after an MI?

A

Because in MI, there is irreversible damaged to the myocytes, which results in membrane damage. In response, the enzymes from the myocytes leak out into the blood.

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20
Q

How does myocardial tissue get damaged in chronic ischemic heart disease?

A

Contractile cardiac tissue gets replaced with non-contractile fibrous tissue after each ischemic attack.

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21
Q

2 main mechanisms of cell death/ arrhythmias in MI

A

1) No oxygen → Anaerobic metabolism
2) No oxygen → no ATP production → Impaired Na+/K+ ATPase

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22
Q

What are the EKG/ cardiac marker changes during unstable angina episode?

A

EKG may/may not show ST depression and/or TWI.

There will be no elevation in troponin bc this is a reversible injury and therefore no injury to cell membrane → no leakage of cardiac enzymes.

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23
Q

Definition of STEMI

A

Occlusive thrombus with ST elevation and serum markers

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24
Q

What is coronary artery bypass?

A

Using a vein or mammary artery to connect aorta to the myocardium due to obstruction in coronary artery.

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25
Q

What two main factors determine myocardial O2 supply and which one has a greater influence in balancing oxygen supply with demand of the heart?

A

1) O2 content
2) Coronary blood flow

Coronary blood flow is the main determining factor for balancing oxygen supply/demand of the heart. This is bc unless pt is anemic or has lung disease, O2 content will be constant. However, coronary blood flow is more dynamic.

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26
Q

In regards to coronary blood flow, what are the two ways the ischemic heart disease can result?

A

Decrease in coronary blood inflow (arterial perfusion) or decrease in coronary blood outflow (venous drainage)

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27
Q

How does stable angina affect troponin levels and why?

A

No elevation in troponin- this is a reversible injury to the myocytes; as a result, there is no membrane damage and cardiac enzymes do not leak.

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28
Q

What happens to cardiac enzymes Troponin and CK-MB when reperfusion occurs?

A

Peaks earlier than usual

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29
Q

What is the first line tx of variant angina?

A

Ca2+ channel blocks (e.g. Diltiazem)

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30
Q

How does a decrease in coronary blood outflow/ venous drainage away frmo myocardial capillary beds lead to ischemia and hypoxic injury?

A

Becuase there is decreased clearance and accumulation of toxic metabolites within the myocardium

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31
Q

What are the triggers of variant angina episodes and why?

A

1) Triptans
2) Tobacco
3) Cocaine

All of these induce vasoconstriction, which could induce/ worsen coronary artery vasospasm.

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32
Q

Why is statin given as soon as patient with suspected MI walks into ER?

A

It lowers cholesterol. Although it takes time for the drug to lower cholesterol levels, patients that are given statins in addition to other MI tx (e.g. angioplasty) do markedly better than patients who are not given statins.

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33
Q

What is more specific for MI diagnosis, Troponin I or CK-MB and why?

A

Troponin I because it is only found in myocardium. CK-MB is found in both cardiac and skeletal muscle and is not as specific for MI diagnosis.

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34
Q

How do endothelial factors induce vasodilation of coronary blood vessels?

A

In response to binding of vasodilation agonists such as ACh, serotoinin, and thrombin to endothelial cell, the endothelial cell produces vasodilatory factors like NO, which goes to the smooth muscle cell to form cGMP → relaxation

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35
Q

What do pathologic Q waves indicate?

A

Old transmural infarct

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36
Q

How does endothelial dysfunction by atherosclerosis lead to coronary thrombus?

A

Endothelial damage leads to decrease in their antithrombotic effects and vasodilatory effects. This results in increased likelihood of coronary thombosis.

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37
Q

Definition of NSTEMI (2)

A

Option #1) Partially occlusive thrombus with ST segment depression and/or TWI with + serum biomarkers

Option #2) Occlusive thrombus (transient ischemia) with ST depression and/or TWI with + serum biomarkers

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38
Q

What are two main mechanisms of coronary thrombus formation in relation to atherosclerosis?

A

Atherosclerosis leads to coronary thrombus in two main angles- via plaque rupture, and dysfunctional endothelium.

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39
Q

Unstable angina and cause

A

CP that occurs at rest and exertion. Usually due to rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery.

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40
Q

Once patient is diagnosed with STEMI, what is the first thing to do within 90 minutes?

A

Emergency catheterization of balloon angioplasty (PCI)

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41
Q

Histological changes in myocardium 1-3 weeks after MI

A

Granulation tissue with plump fibroblasts, collagen, and BVs.

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42
Q

What EKG changes/ cardiac enzymes are present during episode of Prinzmetal angina?

A

ST elevation but no elevation of troponin levels (unlike MI)

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43
Q

What are the causes of coronary blood flow interruption (risk factors for ischemic heart disease)

A

1) Atherosclerotic narrowing of coronary blood vessel
2) Thrombus formation in coronary blood vessel
3) Coronary vasospasms (e.g. seen in prinzmetal angina pectoris)

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44
Q

How does stable agina usually progress?

A

Pts usually develop unstable agina and/or get an MI

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45
Q

If a pt is diangosed with NSTEMI, what are the different courses to take as treatments?

A

First, do a risk assessment (e.g. TIMI score). If risk is high, then go on to invasive strategies (e.g. PCI or CABG). If risk is low, can treat more conservatively by using meds.

46
Q

What is it called when patient makes a clinched chest over the chest to describe the chest pain? What is it indicative of?

A

Levine’s sign; indicative of MI.

47
Q

EKG findings/ cardiac enzymes in unstable angina episdoes

A

No ST elevation- EKG may be normal or show new TWI or ST depression

Normal serum biomarkers

48
Q

What is the gold standard way to see if pt has MI?

A

Coronary angiography- inject dye directly into coronary arteries by cannulating arteries like brachial artery, radial artery, femoral artery.

49
Q

How is stable angina relieved?

A

By rest or adminstration of nitrates

50
Q

Women with variant angina have history of what condition?

A

Migraine HA, which are also associated with arterial vasospasms

51
Q

When is a stress test indicated for a pt?

A

If a patient has a normal EKG but presents with all the signs and sx of an MI, there is still high suspicion for an MI diagnosis. Thus, the patient can take a stress test (exercise) to increase HR and contractility, which makes the heart demand more blood flow/ O2. When looking at an EKG at this time, it may show characteristic MI changes (e.g. T wave inversions, ST segment changes).

52
Q

How is Prinzmetal angina related to atherosclerosis, thrombus formation, or physical activity?

A

Angina itself does not have any relation to these factors, although patient may have atherosclerosis.

53
Q

What are the different ways in which plaque rupture (via atherosclerosis) lead to coronary thrombus formation (2)

A

1) Exposure of subendothelial collagen + increased turbulent blood flow leads to platelet aggregation
2) Rupture causes activation of coagulation cascade via release of tissue factors

54
Q

Why is arterial tone important for coronary artery blood flow?

A

The myocardium always extracts maximal oxygen that it could; thus, the only way to get more oxygen is by increasing blood flow to the heart. The way to do this is by altering arterial tone (vasodilating) thereby decreasing resistance for coronary blood flow.

55
Q

How do endothelial cells influence clotting?

A

It can produce substances such as NO and prostacyclin that prevent platelets from aggregating so that it doesn’t obstruct coronary arteries.

56
Q

What does ST elevation indicate?

A

Transmural infarct (STEMI)

57
Q

What is percutaneous coronary intervention (PCI)

A

AKA balloon angioplasty. Procedure that uses a catheter to place a small structure a stent to open up blood vessels (via balloon) in the heart that have been narrowed by plaque buildup (atherosclerosis).

58
Q

How can reinfarction between 3-10 days post MI be diagnosed?

A

Re-elevation of CK-MB.

59
Q

What ligand for endothelial cell is both a vasoconstricor and vasodilator for coronary vessels? When is it a constrictor vs. dilator?

A

Thrombin. When it acts with other vasodilators (e.g. ACh, Serotonin), it induces endothelial cell to produce molecules that vasodilate the coronary blood vessels. When it acts alone, it induces vasoconstriction of coronary blood vessels by producing endothelin 1

60
Q

What is the timeline of rise, peak, and drop for CK-MB?

A

Rise: 6-12 hours after onset of MI

Peak: 16-24 hours

Return to normal: within 2-3 days

61
Q

What do ST depression indicate?

A

Subendocardial infarct (NSTEMI)

62
Q

What does chronic ischemic heart disease eventually lead to and why?

A

CHF; the heart becomes progressively dilated and eventually, the contractility decreases resulting in dilated cardiomyopathy, which leads to CHF.

63
Q

How does increase in anaerobic metabolism after MI affect the hypoxic cells?

A

Increases in anaerobic metabolism results in increased H+ → chromatin clumping/ protein denaturation → cell death

64
Q

What is MI and what is it usually caused by?

A

necrosis (irreversible death) of cardiac myocytes. Usually caused by rupture of atherosclerotic plaque with thrombosis and complete occlusion of coronary artery.

65
Q

What do laboratory tests look for in order to help diagnose an MI? When is each lab value looked at? (advantages of each)

A

Elevated cardiac enzymes:

1) Troponin I + T: most sensitive and specific marker (gold standard for MI). This stays high in the blood for 7-10 days; thus, it cannot detect reinfarction but it is still highly diagnostic for a MI.
2) CK-MB: creatine kinase enzyme found exclusively in cardiac muscle. This enzyme stays in the blood for relatively short amount of time (3 days). Thus, this can be used for reinfarction.
3) LDH- when this is released by myocardium, it stays in the blood for a very long time. Thus, if pt comes in with MI that occurred awhile ago (e.g. 2 weeks, this marker can be used.

66
Q

ACEI, Aspirin, Beta blockers, Clopidogrel, Low molecular weight heparin, statins, nitrates

A

Agents used to tx acute unstable angina and NSTEMI

67
Q

What is unstable angina defined by in regards to occlusion, EKG changes, and serum biomarkers?

A

Unstable angina: Partial occlusive thrombus, ST segment depression and/or TWI, and no serum biomarkers

68
Q

What does CK-MB enzyme do?

A

Reversibly transfers phosphate group from creatine phoshate to ADP

69
Q

Why can’t troponin I be used to diagnose a second re-infarctoin between 3-10 days post MI?

A

Because between 3-10 days, troponin is still evelated from first infarction

70
Q

How much of a decrease in lumen is necessary to cause unstable angina?

A

90% decrease

71
Q

What are the risk factors for ischemic heart disease?

A

Same as atherosclerosis, since it is the main cause:

  • Modifiable risk factors: HTN, hyercholesterolemia, smoking, DM
  • Nonmodifiable risk factors: Age, male sex/postmenopausal females, genetics (e.g. family history)
72
Q

Stable angina and cause

A

CP that arises with exertion or emotional stress; occurs due to atherosclerosis of coronary arteries with less than 70% stenosis that cannot meet metabolic demands of myocardium during exertion.

73
Q

How does nitroglycerin help chest pain?

A

It is a powerful dialator; when taken under the tongue, it dilates coronary arteries as well as the veins in the legs. As a result, there is less blood coming back to the heart (decrease preload) ⇒ tension decreases and heart doesn’t have to work as hard.

74
Q

How does imparied Na+/K+ ATPase affect cells after MI?

A

Na+ leaks into cell while K+ leaks out; therefore, there is an altered membrane potential, leading to arrythmias. Because there is not much Na+ outside of the cell, the Na+/Ca2+ exchanger doesn’t work, so Ca2+ builds up inside of the cell, inducing cell death.

75
Q

Imbalance between what two factors causes ischemic heart disease, and what most often causes this imbalance?

A

Imbalance between myocardial oxygen supply and myocardial oxygen demand. Imbalance is most often caused by atherosclerosis.

76
Q

How is pain control achieved in the setting of unstable agina, NSTEMI, or STEMI?

A

Nitrogylcerin and morphine

77
Q

What is the timeline of troponin I’s rise, peak, and drop?

A

Rise: 3-4 hours after onset of MI

Peak: 18-36 hours

Remains elevated for 7-10 days

Returns to normal: within 10-14 days

78
Q

What is the cause of chronic ischemic heart disease?

A

Due to chronic mistmatch between myocardial O2 demand and supply, leading to chronic ischemic damage (with or without infarct)

79
Q

What is common cause of why stable angina has decreased ability to perfuse the myocardium?

A

It is usually due to a fixed, high grade stenosis of the coronary artery due to a stable atherosclerotic plaque.

80
Q

Histological changes months after MI

A

Fibrosis/ scar

81
Q

How does external compression affect coronary vascular resistance?

A

During systole, the contraction of surrounding myocardium compresses the coronary vessels, leasing to increased resistance and therefore decreased flow.

82
Q

Clopidogrel, Ticlopidine, and Prasugrel are examples of what and what are their mechanisms of action?

A

Anti-platelet drugs. They prevent activation of platelets once they adhere to the endothelium, preventing them from the next step, aggregation. More specifically, these drugs bind the P2Y receptors on the outside of the platelet, which is necessary for activation.

83
Q

Pain caused by decrease in myocardial perfusion that presents as tightness, squeezing, or heaviness in chest area

A

Angina pectoris

84
Q

How do metabolic factors affect coronary blood flow?

A

When there is an increased oxygen demand by the myocardium/ not enough oxygen supplied, ATP cannot be formed. As a result, ADP turns into AMP, which releases adenosine. Adenosine is a powerful vasodilator, vasodilating the coronary arteries. This decreases resistance of the coronary arteries and increases blood flow. Other metabolic factors that induce vasodilation include lactate, acetate, H+, CO2.

85
Q

How do endothelial cells induce vasoconstriction of coronary vessels?

A

Vasoconstrictor ligands such as Thrombin, angiotensin II, epi bind to endothelial cell which activates production of endothelin-1 within the endothelium. This is acts on smooth muscle cells of coronary vessels → constriction.

86
Q

2 advantages of measuring myoglobin levels in the setting of suspected MI

A

1) Serum myoglobin levels rise quickly after an MI, unlike CK-MB or troponin which rise several hours after an MI
2) Elevated levels of myoglobin several hours after an MI have high sensitivity and low specificity and has a high negative predictive value (people who test negative truly don’t have the disease). As a result, patients who test negative most likely do not have an MI.

87
Q

Histological changes in myocardium 4-24 hours after MI

A

Coagulative necrosis- removal of nucleus; pykhosis, karyorrhexis, karyolysis (hallmarks)

88
Q

In regards to myocardial demand for oxygen and supply, when does myocardia ischemia occur?

A

occurs when myocardial oxygen demand > oxygen supply

89
Q

Diaphoresis, N/V, SOB, fatigue, retrosternal pain, and pain in left arm and/or jaw are sx of what?

A

ACS

90
Q

What are the consequences of endothelial cell damage by atherosclerosis?

A

Damage to endothelial cells decreases production of substances like prostacyclin and NO which leads to:

1) More vasoconstriction (since prostacyclin and NO are vasodilators)
2) Increased risk of platelet aggregation

91
Q

Which biomarker is the most specific for cardiac necrosis?

A

Cardiac troponin I

92
Q

Histological changes 2-4 weeks after MI

A

Resorption, fibrosis

93
Q

How does decrease in coronary blood inflow into myocardial capillary beds to ischemia/hypoxic injury?

A

Bc it leads to decreased delivery of O2 and nutrietns into the myocardium

94
Q

EKG/ cardiac enzyme findings in NSTEMI

A

1) No persistent ST elevation- EKG may be normal or only show minor changes
2) Increased troponins (indicating infarction)- 24 hrs of sx onset

95
Q

If hospital doesn’t have emergency PCI available within 90 minutes, what is the next step for a pt diagnosed with STEMI?

A

Fibrinolytic therapy (e.g. tPA)

96
Q

What is/isn’t a small thrombus (non-flow limiting) + no EKG changes + healing and plaque enlargement

A

not an acute coronary syndrome.

97
Q

What type of drugs are contraindicated in pts with variant angina and why?

A

Triptans because they induce vasoconstriction which may trigger/ worsen coronary artery vasospasm.

98
Q

When do variant angina episdoes occur the most?

A

At rest, especially at night and early in the morning.

99
Q

What is wall stress dependent on? (think of formula)

A

S= P*r/2h

Wall stress is directly correlated with pressure and radius, while it is indirectly correlated with thickness.

100
Q

During stabla agina episodes, what does EKG show?

A

ST depression

101
Q

What steps lead to infarction in an MI (4)

A

1) Rupture of atheroscleroptic plaque in coronary artery
2) Occlusive thrombosis
3) Prolonged ischemia
4) infarction

102
Q

What precipitates vasospasm, and is used as a confirmation of dx of Prinzmetal angina?

A

Ergonovine

103
Q

Variant angina (aka Prinzmetal angina) and cause

A

Episodic CP unrelated to exertion. Due to coronary artery vasospasm, transiently but completely cutting off blood supply. Thus, whenever BV get claped down by vasospams, pt experiences pain.

104
Q

How do endothelial factors influence coronary blood flow?

A

The endothelium releases factors that regulate arterial tone, which in turn influence resistance, and therefore affects coronary blood flow.

105
Q

What is wall stress and how does it influence myocardial O2 demand?

A

Wall stress is the force that tries to pull the myocardial fibers apart. Energy is needed to maintain the fibers together, and oxygen is needed. When wall stress is increased, more oxygen is needed by the heart to maintain the fibers. Thus, anything that increases wall stress increases O2 demand, while anyhting that decreases wall stress decreases O2 demand.

106
Q

What are the main factors that influence myocardial O2 demand? (3)

A

1) wall stress
2) HR
3) Contractility

107
Q

How does % stenosis of coronary artery affect flow and how does this relate to angina?

A

Up until 70% of stenosis, vasodilatory capabilities of coronary arteries can compensate and allow enough flow to the myocardium for its oxygen demand. Thus, there will be no sx of angina at rest or even during exertion. However, when there is greater than 70% of stenosis, vasodilation may/may not be able to compensate. If stenosis is close to 70%, vasodilation will compensate and pt will have no angina sx at rest. However, this pt may have angina during exertion because when there is increased O2 demand, the flow cannot increase as much as it should due to the stenosis. As a reuslt, this pt will have stable angina. If stenosis is large like close to 90%, vasodilation will not be able to compensate blood flow/O2 at rest, and pt may have angia sx at rest as well.

108
Q

How do neural factors affect coronary blood flow?

A

They regulate coronary arteriolar tone, which affects resistance and therefore coronary blood flow. It mainly acts via the SNS. When alpha receptors are activated, it causes vasoconstriction, which increases resistance of coronary arteries, thereby decreasing coronary blood flow. When beta-2 receptors are activated, it causes vasodilation, which decreases resistance of coronary arteries, thereby decreasing coronary blood flow.

109
Q

EKG/ cardiac enzyme findings in STEMI

A

EKG: Persistent ST elevation or new LBBB

Cardiac enzyme: increased Troponin

110
Q

What are the 3 types of ACS and what are the EKG/cardiac enzyme changes for each?

A

1) STEMI: Persistent ST elevation and increased troponin
2) NSTEMI: No changes in EKG or ST depression/TWI with increased troponins
3) Unstable angina: NO changes in EKG or ST depression/ TWI with non-elevated serum biomarkers

Cardiology (21 decks)

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