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Adult Clinical Medicine > Coronary Heart Disease > Flashcards

Coronary Heart Disease Flashcards

1
Q

What are modifiable risk factors for coronary heart disease?

A
  1. Smoking
  2. Dyslipidemia
  3. Diabetes
  4. Hypertension
  5. Lack of physical activity
  6. Diet
  7. Obesity
  8. Socioeconomic factors
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2
Q

What are non-modifiable risk factors for coronary heart disease?

A
  1. FHx: event in 1st degree relative 55 or younger M or 65 for female
  2. Age 45 or older M, 55 for female
  3. Sex: under age 60: M over F
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3
Q

Describe the pathophysiology of Coronary heart disease

A
  1. gradual narrowing of the arterial lumen from plaque building at sights of endothelial injury (ie. HTN or smoking)
  2. Macrophages, recruited to the site, ingest oxidized LDL and become foam cells.
  3. Activated foam cells lead to endothelial disruption, increased localized inflammatory response, more LDL and macrophage uptake and the cycle continues.
  4. The resulting disruption to the endothelium is now a plaque
  5. Plaque may continue to accumulate lipoproteins or it may stabilize and form a fibrous cap
  6. When plaque rupture occurs, foreign material from within the plaque is spilled into the blood, triggering thrombus formation.
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4
Q

The formation of arterial plaque starts with the movement of ____ into the arterial wall at sights of endothelial injury arising from various insults, such as hypertension or smoking

A

oxidized LDL particles

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5
Q

Describe the actual event leading to infarction

A

it is a SUDDEN rupture of arterial plaque

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6
Q

Activated foam cells lead to __, ___, __, and ___

A

endothelial disruption,

increased localized inflammatory response,

more LDL and

macrophage uptake and the cycle continues.

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7
Q

Plaques that form ____ have the potential to rupture

A

without a fibrous cap

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8
Q

The vulnerability of plaque to rupture is related to many factors such as:

A
  1. plaque with high lipid content is more prone to rupture
  2. pts inflammatory state
  3. resting BP
  4. others
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9
Q

compare a stable and unstable plaque

A

Stable: thick fibrous cap which protects it from rupture
-narrow lumen leads to classic sx of chronic angina

Unstable: thin fibrous cap and is prone to rupture
-resultant thrombus formation causes the spectrum of ACS

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10
Q

DDX for chest pain

A
  1. ACS
  2. stable angina
  3. MSK CP
  4. GI
  5. psychiatric
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11
Q

what is angina pectoris

A
  • chest pain or discomfort secondary to coronary ischemia

- an imbalance in myocardial oxygen supply and demand

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12
Q

Coronary ischemia is essentially an imbalance in __ and __

A

myocardial oxygen supply and demand

*Thus, a person with CHD and luminal narrowing may be asymptomatic at rest but the increased myocardial oxygen demands placed on the heart by an activity such as walking up stairs or shoveling snow are sufficient to cause ischemia and pain.

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13
Q

compare stable and unstable angina

A

Stable angina: Most common. Follows a predictable pattern:

  • Worsened by exercise,
  • relieved by rest, nitroglycerin.
  • Duration: Less than 20 minutes.

Unstable angina: Does not follow a pattern:

  • Can occur without exertion and
  • not be relieved by rest or nitroglycerin.
  • A medical emergency.
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14
Q

What is variant or Prinzmetal’s angina

A
  • Rare.
  • Usually occurs at rest, typically between midnight and early morning.
  • Due to coronary artery vasospasm in the absence of atherosclerosis

**must r/o atherosclerosis

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15
Q

What is microvascular angina?

A
  • Normal coronary arteries and no identifiable cause.
  • Attributed to inadequate circulation in coronary microvasculature.

**must have a normal cardiac angiogram

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16
Q

Terms often used by patients to describe chest pain

A

squeezing, tightness, pressure, constriction, band-like, fullness in the chest, burning, heartburn, know in the chest, lump in throat, ache, weight on chest, toothache, bra too tight

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17
Q

Terms often used by patients to describe pain that is NOT angina

A
  1. sharp
  2. knife-like
  3. stabbing
  4. pins and needles
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18
Q

Characteristics of angina pectoris

A
  1. gradual onset over several minutes
  2. substernal but not felt in a specific spot
  3. diffuse, difficult to localize
  4. Levine’s sign
  5. Constant, not changing with position or respiration
  6. Should not be reproducible with palpation
  7. Often radiates to other parts of the body
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19
Q

Angina pectoris often radiates to where?

A
  • most often on right side of body
    1. shoulder
    2. arms
    3. wrist
    4. fingers
    5. neck
    6. throat
    7. mandible and teeth
    8. back
  • *NOT maxilla
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20
Q

What is Levine’s sign?

A

Levine’s sign is a clenched fist held over the chest to describe angina pectoris. Although this is considered a classic sign of cardiac ischemia, multiple studies suggest that Levine’s sign has very poor sensitivity and that its absence should not influence clinical decision making.

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21
Q

Angina pectoris can be associated w/ other symptoms including:

A
  1. Shortness of breath
  2. Diaphoresis, “clamminess”
  3. Fatigue
  4. Nausea
  5. Dizziness, lightheadedness,
  6. Belching, “indigestion”
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22
Q

Large study of 430,000 patients with confirmed MI found that one-third had no chest pain on presentation.*
These patients presented with:

A
  1. dyspnea alone
  2. n/v
  3. palpitations
  4. syncope
  5. cardiac

*much less likely to be diagnosed with a confirmed MI. As a result, this group of patients experienced much higher in-hospital mortality. The point here is that the absence of classic angina pectoris does not rule out acute coronary syndrome as a possible diagnosis.

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23
Q

describe the evaluation of angina pectoris

A
  1. QUICKLY determine if ACS or stable angina
  2. ECG w/in 10 min if pt experiencing ongoing CP
  3. thorough H/P and PE, time permitting
  4. Exercise stress test: any pt w/ chronic stable angina should be tested if there are no contraindications to testing
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24
Q

Low risk factors for angina pectoris

A
  1. stable angina
  2. no CHF
  3. normal resting EKG
  4. normal LVF
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25
Q

High right factors for angina pectoris

A
  1. unstable angina
  2. CHF
  3. Q waves or ischemic ST-T wave changes on resting ECG
  4. depressed systolic function
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26
Q

Management of chronic stable angina must involve risk factor modification and lifestyle changes such as:

A
  1. smoking cessation
  2. dietary modification
  3. increased activity
  4. lipid goals:
    LDL less than 100
    TG less than 200
    HDL over 40
    BP less than 130/85
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27
Q

Chronic stable angina – Medical management:

A
  1. Directed at increasing O2 supply and decreasing demand
  2. Nitrates
  3. Beta-blockers
  4. Ca2+ channel blockers
  5. ASA
  6. Statins
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28
Q

describe the use of nitrates for chronic stable angina

A
  1. Venodilation leading to decreased venous return to the heart –> decreased LV wall stress –> decrease in myocardial O2 demand. Arterial dilation –> dilation of stenotic vessel and collateral vessels –> increased BF to myocardium.
  2. Short-acting sublingual forms: Nitro 0.3-0.6 mg taken for acute attacks. (Major side effect: HA)
  3. Long-acting preparations: Tablets, patches, ointment…for prophylaxis of attacks. Limited by tolerance.
29
Q

describe the use of beta-blockers for chronic stable angina

A
  1. Decrease HR and force of contraction –> decreased myocardial O2 demand
  2. Cardioselective forms preferred (e.g. metoprolol, atenolol), titrate to resting heart rate of 50-60.
  3. Avoid in asthmatics
  4. Taper over 7-10 days to discontinue
  5. Can be used in combination with nitrates
30
Q

describe the use of Ca2+ channel blockers for chronic stable angina

A
  1. Decrease HR and force of contraction, decrease afterload –>decreased myocardial O2 demand
  2. Caution in patients with LV dysfunction (negative inotrope)
  3. Can be a substitute in patients with contraindication to BB
  4. Taper over 7-10 days to discontinue
31
Q

describe the use of ASA for chronic stable angina

A
  1. Inhibits prostaglandin synthesis –> decreased vasoconstriction and platelet activity.
  2. Dose: From 75 mg qd up to 325 qd.
  3. Anti-anginal drugs relieve symptoms but do not affect mortality (except BB in MI)…aspirin, however, significantly affects mortality.
  4. Unless contraindicated…ALL patients with angina should be on ASA qd.
32
Q

describe the use of statins for chronic stable angina

A
  1. Lower LDL levels, increase HDL (smaller effect), also provide cardioprotective effect aside from lipid-lowering: Likely due to plaque-stabilization.
  2. Goal LDL-C in Angina: 100mg/dL
  3. Unless contraindicated: All patients with angina should be on a statin, regardless of their baseline LDL.
33
Q

Describe the medical management for variant angina

A
  1. Calcium channel blockers and long-acting nitrates
  2. Smoking cessation is paramount!

*Beta-blockers are contraindicated!!!!

34
Q

Acute coronary syndrome is a spectrum of presentations due to myocardial ischemia, including;

A
  1. unstable angina,
  2. non-ST elevation myocardial infarction (NSTEMI), and
  3. ST elevation myocardial infarction (STEMI).
35
Q

Unlike chronic stable angina, all of the conditions in the spectrum of acute coronary syndromes are associated with:

A

unstable plaque and, without intervention, progression to more serious disease is likely

36
Q

Describe the evaluation of ACS

A
  1. Start initial treatment as soon as you suspect ACS! (don’t delay while you obtain a more thorough hx)
  2. Careful history and exam if pt is stable
  3. ECG, CXR, serum cardiac markers
  4. categorize short-term risk of fatal or non-fatal Mi using guidelines
37
Q

who typically presents with atypical angina sx

A
  1. young
  2. female
  3. elderly
  4. diabetics
38
Q

How does angina typically present in women

A
  1. More atypical descriptions
  2. More symptoms in the jaw area
  3. More non-pain related symptoms
  4. Rate pain as more intense than men
  5. Use different words to describe pain (e.g. “sharp”)
39
Q

When are serum cardiac markers best drawn

A

in in-pt or ED bc Levels rise following myocardial injury

40
Q

Why is serial analysis of serum cardiac markers essential?

A

-10-15% of ER patients in whom acute infarction is eventually diagnosed have normal levels on the first sample tested.

41
Q

What are the serum cardiac markers?

A
  1. CK-MB*
  2. Troponins*
  3. Myoglobin (low cardiac specificity but high sensitivity, can be used to r/o MI)
  4. Lactate dehydrogenase (rarely used)
42
Q

describe when CK-MB is detectable and when should it be drawn

A
  1. Detectable 4-6 hours after onset of myocardial injury
  2. Levels peak in 12-24 hours
  3. Normalizes in 2-3 days
  4. Levels are drawn on admission to the ER, then at 6 and 12 hours
43
Q

When is CK-MB useful?

A
  1. Assess reinfarction or infarct extension bc levels normalize quickly (2-3 days)
    * levels do not predict infarct size
44
Q

describe when troponin I and T is detectable and when should it be drawn

A
  1. Detectable 3-6 hours after onset of myocardial injury
  2. Levels peak in 12-24 hours
  3. Normalizes in 2 weeks, useful as a late marker of recent acute MI
  4. Levels are drawn on admission to the ER, then at 6 & 12 hours
45
Q

When is troponin useful?

A
  1. The preferred markers for the diagnosis of myocardial injury – most sensitive for early infarction
  2. best late marker for recent acute MI
  3. Prognostic value: Higher levels = more myocardial injury
46
Q

There is increased risk of death in patients who have the following signs during or shortly after an acute MI:

A
  1. hypotension
  2. tachycardia
  3. pulmonary edema/crackles
  4. new murmur (MR)
  5. new heart sounds (S3)
  6. diminished peripheral pulses
47
Q

three types of acute coronary syndrome:

A
  1. unstable angina,
  2. non-ST elevation myocardial infarction (NSTEMI), and
  3. ST elevation myocardial infarction (STEMI)
48
Q

3 clinically distinct forms of unstable angina

A
  1. New-onset exertional angina
  2. Angina of increasing frequency or duration or refractory to nitroglycerine
  3. Angina at rest

*ECG changes may be evident but typically only when chest pain is present.

49
Q

What distinguishes unstable angina from the two forms of myocardial infarction is:

A

there is no elevation in cardiac markers with unstable angina.

*Thus, unstable angina does not cause measurable myocardial injury.

50
Q

Unlike unstable angina, myocardial infarction, by definition, includes significant ____. It is important to keep in mind there one cannot distinguish unstable angina from myocardial infarction until ___ are measured.

A

elevations in cardiac markers

cardiac markers

51
Q

What characterizes a NSTEMI

A
  1. Implies non-transmural infarction
  2. Prolonged chest pain with significant elevations in CK-MB or Troponins
  3. No ST elevation
  4. May have ECG changes suggestive of ischemia: ST depression or new T wave inversion
52
Q

What characterizes a 1STEMI

A
  1. Implies transmural infarction
  2. Prolonged chest pain with significant elevations in CK-MB or Troponins
  3. New LBBB with ACS symptoms is STEMI unless cardiac markers remain normal
  4. ST segment elevation on ECG:
53
Q

treatment of ACS

A
  1. Immediate: MONA
    - Morphine: 2-4mg IV bolus, then 2-8mg q5-15 min
    - Oxygen:
    - Nitrates: SL nitro 0.4mg q 5 min x3
    - ASA: 160-325mg chewed

*In the outpatient setting, these measures are typically initiated while waiting for EMS to arrive. –> do not use other forms of opiates (IM or oral) if IV is not available

54
Q

What is the treatment of unstable angina with a normal ECG and serum markers?

A
  1. Continue to monitor in the ED or observation unit
  2. Continue symptomatic support
  3. Repeat ECG at 6 and 12 hours
  4. If no evidence of ischemia or infarct –> perform stress test
  5. If evolves into NSTEMI or STEMI, treat appropriately
55
Q

What is the treatment of a NSTEMI

A
  1. Heparin, preferably low molecular weight heparin: Enoxaparin (Lovenox) –> anti-thrombin effect
  2. Beta-blocker
  3. IV nitroglycerine, if persistent pain
  4. Clopidogrel (Plavix) –> platelet inhibitor
56
Q

NSTEMI is considered high risk if there is:

A
  1. ST depression
  2. persistent CP
  3. hemodynamically instability

*In the case of high risk NSTEMI, evolution to STEMI is considered likely and a percutaneous coronary intervention, or PCI, is often indicated.

57
Q

Describe PTCA

A

“Balloon Angioplasty” : Usually involves placement of a stent. Stent re-stenosis is prevented by life-long ASA and clopidogrel (Plavix) for up to one year.

58
Q

In most cases of PCI what other drugs are used:

A
  1. a platelet inhibitor in the GP IIb/IIIa class is used just before the intervention is performed.
  2. To prevent stent re-stenosis, patients are generally placed on lifelong aspirin and 6 to 12 months of clopidogrel (Plavix).
59
Q

Describe the treatment of a STEMI

A
  1. Beta-blocker
  2. IV nitroglycerine, if persistent pain
  3. IV heparin
  4. Clopidogrel (Plavix) –> platelet inhibitor
  5. Primary PCI: goal: less than 90 minutes
  6. Or Thrombolysis with t-PA (tissue plasminogen activator): goal : less than 30 minutes

*In high-volume centers, with “door-to-balloon” times under 90 minutes, PCI is superior to thrombolytic therapy

60
Q

In high-volume centers, with “door-to-balloon” times under ___, PCI is superior to thrombolytic therapy

A

90 minutes

61
Q

Long-term risk factor modifications one should reinforce with a patient who just had a MI

A
  1. Instruction on smoking cessation
  2. Instruction on optimal weight, diet, and daily exercise
  3. Lipid-lowering therapy (statin)
  4. A fibrate or niacin if HDL less than 40 mg/dL
  5. Hypertension control to a BP of less than 130/85
  6. Tight control of hyperglycemia in diabetics
62
Q

What meds should a person be on after an MI for long-term risk factor modification

A
  1. Statin
  2. fibrate or niacin
  3. ASA 75-325mg qd
  4. clopidogrl 75mg qd when ASA is not tolerated bc ofhypersensitivity or GI intolerance
  5. Combined ASA + clopidogrel for 9 months after NSTEMI
  6. BB unless contraindicated
  7. ACE inhibitor for pts w/ CHF, LV dysfucntion (EF less than 40%), HTN, or diabetes
  8. tight glycemic control
63
Q

How are stressors used in non-invasive CHD evaluation?

A
  1. exercise treadmill
  2. pharmacologic agents:
    - Dobutamine
    - Dipyridamole (persantine)
    - Adenosine

*used for diagnostic and prognostic assessment

64
Q

Methods for detecting ischemia on stress tests include:

A
  1. EKG
  2. radionuclide (thallium or technitium) perfusion scan
  3. echocardiography
65
Q

Describe the Exercise stress test (stress treadmill)

A
  1. Patient is monitored by “real time” ECG while walking on a treadmill.
  2. The speed and incline are increased every 3 minutes until the patient:
    - can no longer tolerate the test (the “exercise response”)
    - has an abnormal non-ECG response (e.g insufficient increase in HR or BP)
    - has diagnostic changes on ECG (ST depression).

*This can also be also be combined with radionuclide (Usually Thallium) myocardial perfusion scanning.

66
Q

Under ideal circumstances, the _____ of CHD should be assessed prior to making any decisions about testing.

A

pretest probability of CHD

67
Q

How do you determine if stress testing is appropriate based on different pretest probabilities

A

High (over 75%): non-invasive tests have poor negative predictive value –> consider angiography

Low (less than 25%): non-invasive tests have poor positive predictive value –> consider not testing

Intermediate (25-75%): non-invasive tests can be valuable for diagnosis and risk assessment

68
Q

Pretest probability of CHD in patients takes into account patients w/ chest pain according to:

A
  1. age,
  2. gender, and
  3. symptoms (atypical vs typical)
69
Q

Once you have determined that stress testing is appropriate, how do you determine what test to choose

A
  1. normal baseline EKG, able to tolerate exercise–> exercise stress treadmill
  2. normal baseline EKG, unable to tolerate exercise–> pharmacologic stress test
  3. ECG abnormalities (ST depression at rest, WPW, LVH) able to tolerate exercise–> exercise imaging test (stress thallium or stress echo)
  4. ECG abnormalities (ST depression at rest, WPW, LVH) unable to tolerate exercise–> pharmacologic stress test (persantine)

Adult Clinical Medicine (26 decks)

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