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X Clin Med II Exam 1 > Ischemic Heart > Flashcards

Ischemic Heart Flashcards

1
Q

Coronary artery disease

A

Pathologic process affecting coronary arteries (atherosclerosis)

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2
Q

Coronary heart disease

A

Includes angina pectoris, MI, silent myocardial ischemia and mortality from CAD

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3
Q

Cardiovascular disease

A

Pathologic process affecting entire arterial circulation

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4
Q

Myocardial infarct

A

Irreversible death of heart muscle due to prolonged lack of oxygen

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5
Q

What is the role of nitric oxide?

A

Inhibits plaque formation, anti-inflammation

Damage leads to development of atherosclerosis

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6
Q

Major risk factors of IHD

A

Diet, HTN, DM, dyslipidemia (high LDL, low HDL, high TAGs), cigarettes
Also can be male, older, FH, obesity, metabolic syndrome

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7
Q

When are atypical sxs of IHD more common?

A

Women, elderly and pts with DM

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8
Q

Transient vs prolonged ischemia

A

Transient may lead to angina pectoris and prolonged cal lead to MI

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9
Q

What is another name for stable angina?

A

Angina pectoris

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10
Q

What is the pain like in a stable angina?

A

Not pain (heaviness, pressure, squeezing, choking)
Substernal so Levine’s sign
Can radiate to arms, neck, jaw, epigastrium, mid-back

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11
Q

How long does the pain in a stable angina last?

A

2-10 min (crescendo-decrescendo)

Usually with rest of sublingual nitro

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12
Q

What are atypical sxs of angina?

A

Dyspnea (common in women), nausea, fatigue or faintness

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13
Q

What sxs are not likely to be ischemia or angina?

A

Sharp, fleeting stabs of chest pain

Prolonged, dull ache in left precordial area

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14
Q

What exactly is stable angina?

A

Exertional or stress-related chest or arm discomfort that resolves with rest or nitro

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15
Q

Diagnostic tests done for stable angina

A

12 lead EKG (may have ST and T wave changes that occur during episodes of chest pain)

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16
Q

What is the Bruce protocol?

A

For exercise stress tests where speed/incline adjusted every 3 min to get HR to 85% of maximum

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17
Q

What are we looking for in stress testing?

A

EKG changes, decreased myocardial perfusion in nuclear imaging, drop in SBP >10 or any other sxs

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18
Q

When can exercise stress testing be unreliable?

A

Women, elderly, obesity, debility, bundle branch block, pacemaker

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19
Q

What are the indications for a pharmacologic stress test?

A

Pt unable to exercise, not able to achieve target HR with exercise or high likelihood of false positive

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20
Q

Gold standard for diagnosisng CAD

A

Angiography

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21
Q

What is the focus of IHD tx?

A

Treat signs and sxs of established IHD, rather than preventing it

22
Q

What is the optimal diet?

A

Plant based (grains, legumes, veggies, fruits, <15% calories from fat)

23
Q

What types of meds are used for stable angina?

A

Meds to decrease O2 demand, meds that increase oxygen supply, antiplatelets, statins, revascularization

24
Q

What are meds that decrease O2 demand?

A

Nitrates (preload reduction), betablockers (afterload reduction) and calcium channel blockers (afterload reduction)

25
Q

First line tx for chronic angina

A

Beta blockers

26
Q

Meds that increase O2 supply

A

Nitrates (.3-.6 mg sublingually or spray), CCBs

27
Q

What are the antiplatelet meds?

A

Aspirin (every pt on this unless contra), clopidogrel or a combo

28
Q

What do statins do?

A

Stabilize plaques to reduce clinical events, slow progression and induce regression of atherosclerosis

29
Q

What are the acute coronary syndromes?

A

Unstable angina, non-st segment elevation MI or ST segment elevation MI

30
Q

What is the presentation of ACS?

A

Ischemic pain, SOB, weakness, nausea, anxiety, sense of doom and may see those atypical sxs

31
Q

Potentially fatal ddx of chest pain

A

Aortic dissection, PE, pneumothorax, perforated viscous in GI, cocaine abuse

32
Q

Presentation of unstable angina

A

Ischemic discomfort and 1 of 3:
Occurs at rest, >10 min
Severe and of new onset (4-6 wks)
Occurs with crescendo pattern (gets worse)

33
Q

What is Prinzmetal’s angina?

A

Ischemic sxs secondary to vasospasm
Usually younger pts
Chest pain at rest with transient ST segment elevation
Tx: nitrates and CCBs

34
Q

Possible pathophysiologic processes of UA or NSTEMI

A

Plaque rupture or erosion with superimposed nonocclusive thrombus (most common)
Dynamic obstruction (coronary artery spasm)
Progressive mechanical obstruction
UA secondary to increased myocardial O2 demand/decreased supply

35
Q

Stress testing in UA/NSTEMI

A

Only in situations where there is no evidence for infarction (normal enzymes) but diagnosis unclear

36
Q

Clinical features of unstable angina

A

No elevation of CK-MB or troponin (no myocardial cell necrosis)

37
Q

Clinical features of non-ST elevation MI

A

Definite elevation of CK-MB and/or troponin (no ST elevation)

38
Q

Txs for UA/NSTEMI

A

Bedrest with monitoring, MONA, beta blockers, antiplatelets, anticoagulation with heparin, statins, PCI
(STEMI is very similar)

39
Q

TIMI variables for risk stratification of UA/NSTEMI

A 
Age > 65
>3 risk factors of CHD
Prior coronary stenosis >50%
ST segment deviation on admitted EKG
>2 anginal episodes in 24 hrs
Increaesd cardiac biomarkers
Aspirin in last 7 days
1 pt for each
40
Q

Interpretation of TIMI risk score

A

As it increases, it increases the number of events that occur over 14 days

41
Q

Who is at an increased risk for STEMI?

A

Ppl with multiple risk factors or history of UA

42
Q

Identifiable precipitating factors of STEMI

A

Vigorous exercise, extreme stress, medical/surgical illness

43
Q

Common causes of STEMi

A

Rupture of vulnerable plaque (complete occlusion of coronary artery)
Slowly developing stenosis of coronary artery

44
Q

Diagnostics for STEMI

A

12 lead EKG, CXR, biomarkers, CBC, lipid panel, cardiac imaging, angiogram

45
Q

EKG changes and cardiac markers for UA, STEMI and NSTEMI

A

UA: negative biomarkers and either!
STEMI: positive markers and ST segment elevation
NSTEMI: positive markers and no ST elevation

46
Q

What is MONA?

A

Management of IHD
Oxygen first
Then nitro or morphine if that doesn’t work
Antiplatelet therapy to limit size of infarct

47
Q

When must you start thrombolytic therapy?

A

Within first 12 hrs of STEMI (so 30 min after dx)

48
Q

Absolute contraindications of thrombolytic therapy

A

Hx of intracranial hemorrage, stroke in last year, poorly controlled HTN, suspected dissection, active internal bleeding

49
Q

What is revascularization indicated for?

A

STEMI (can be more effective than thrombolytics if doc is good)

50
Q

Complications post mI

A

Recurrent ischemia, pump failure, ventricular arrhythmias, pericarditis, mural thrombus, cardiac rupture, depression

51
Q

Management post MI

A

Risk stratification, treat risk factors, beta blockers/aspirin or ACE/ARB is LV dysfunction

X Clin Med II Exam 1 (7 decks)

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