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Cardiology > Ischemic Heart Disease: Part 1 > Flashcards

Ischemic Heart Disease: Part 1 Flashcards

1
Q

What is something you need to know for EKG interpretations for leads?

A

If you see ST elevation in certain leads, you should know the potential arteries affected

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2
Q

What is the classic patient with a silent MI?

A

Diabetic female

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3
Q

What does estrogen do?

A

Increases risks of blood clots, leading to a more likely cardiology.

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4
Q

What do you likely see in EKG of a silent MI?

A

Q-waves

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5
Q

What is the most common, serious, chronic, life-threatening illness?

A

Ischemic heart disease

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6
Q

What are the MC risk factors for Ischemic Hear disease?

A

genetic influences, high-fat and energy-rich diet, smoking, sedentary lifestyle

more common in low income groups

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7
Q

What is the MC cause of myocardial ischemia (MI)?

A

Atherosclerosis

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8
Q

What is the pathogenesis of an MI in a nutshell?

A

supply < demand

less supply: hypotension, Atherosclerosis, anemia, decreases supply

demand: exercise

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9
Q

What are the multifactorial causes of an MI?

A

Generally an imbalance between oxygen supply and demand
Oxygen supply → determined by blood flow
Blood flow is regulated by pressure vs. resistance ratio
Most critical factor is the radius of the blood vessel
This is influenced by atherosclerosis hardening of vessels, vascular tone, and endothelial cell dysfunction in cardiac ischemia

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10
Q

When are we most concerned about symptoms of an MI?

A

If they are symptomatic at rest - meaning that the demand is high even at rest

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11
Q

What is prinzmetal angina?

A
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12
Q

What is stable angina?

A

Have not ruptured the plaque, and it is stable.

May present with chest pain during exertion

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13
Q

What is unstable angina?

A

Not stable, or walled off block

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14
Q

What is the progression of stable angina to MI? Which of these are consider Acute coronary syndrome?

A

Stable angina –> unstable angina –> MI (stemi or NSTEMI)

unstable angina and MI (NSTEMIs, STEMIs) are EMERGENCIES, and are considered acute coronary syndrome because it needs to be addressed

Dead meat don’t beat

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15
Q

When does ACS result?

A

plaque rupture and thrombus formation. The amount of coronary blood flow restriction determines the severity:

Unstable angina - no occluded blood flow → symptoms at rest

NSTEMIs - partially impeded blood flow through the coronary vessels

STEMIs - completely impeded blood flow through the coronary vessels

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16
Q

What are the symptoms of stable angina (fixed stenosis)

A

A typical pattern; predictable

Occurs when the heart is under stress and needs more oxygen (exercise, cold, emotion)

Typically lasts 1-15 min

Goes away with rest and/or NTG

It may continue without much change for years

Not a risk at this moment and time that they will die.

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17
Q

What are the symptoms of unstable angina (Caused by a transient formation and dissolution of a thrombus)

A

Unexpected; a change in your usual pattern of stable angina

Occurs when blood flow to the heart is suddenly slowed by narrowed vessels or thrombus in the coronary arteries

It may happen at rest or with light activity. It does NOT go away with rest or nitroglycerin.

Warning sign that an MIis impending. An EMERGENCY!

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18
Q

When is something more likely to infarct and what is it?

A

Complete absence of blood supply for long time

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19
Q

Describe ischemia and symptoms?

A

Present as SOON as there is a decrease or complete absence of blood supply to myocardial tissue

Cardiac cells can tolerate mild-moderate anoxia (chest pain) for a short time without greatly affecting their function

When adequate blood flow / reoxygenation return, these cells usually return to a normal

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20
Q

Explain injury of coronary artery

A

If ischemia is severe or prolonged, the anoxic cardiac cells sustain damage and stop functioning normally

Damage to the cells still remains reversible so that injured cells remain viable and salvageable for some time

Cells may return to normal or near normal after the return of adequate blood flow and reoxygenation

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21
Q

Describe infarct

A

Severe myocardial ischemia continues because of continued complete absence of blood supply

The anoxic cardiac cells will sustain irreversible injury and die.

Dead meat don’t beat!

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22
Q

Explain the progress of ischemia to infarct

A

Ischemia –> injury –> infarct

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23
Q

What is transmural?

A

Entire transverse portion of the heart is infarcted.

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24
Q

What typically causes the NSTEMI?

A

Only a small area in the subendocardial wall of the LV, ventricular septum, or papillary muscle

Caused by a local decrease in blood supply from narrowing of a coronary artery. The subendocardial area is particularly susceptible to ischemia.

25
Q

What do you see in a NONSTEMI on an EKG?

A

EKG → ST depression or T-wave inversion (or no EKG changes)

26
Q

What causes a myocardial infarction and what do you see on an EKG?

A

Extend through the whole thickness of the heart muscle wall

Associated with atherosclerosic plaques in a coronary artery that cause complete occlusion

Labeled by the wall involved: anterior, posterior, inferior, lateral, or septal

EKG → STEMI → Q waves

Tombstoning

27
Q

What is a type 1 MI?

A

Caused by a ruptured plaque

28
Q

What is a type 2 MI?

A

Ischemia problably not from athersclerosis (like hypotension)

may have athersclerosis, but it was not caused by an MI

29
Q

What is a type 3 MI?

A

Unexpected cardiac death (don’t make it)

30
Q

What is a type 4 MI?

A

Already had a cardiac surgery like stenting

having

31
Q

What is a type 5 MI?

A

CABG

32
Q

What is silent ischemia and who is it seen in?

A

Myocardial ischemia without discomfort or pain
More common in diabetics, elderly patients, and women
Exact mechanism is unknown

33
Q

What is myocardial stunning?

A

It stuns and stops working, but the tissue is not dead - if reperfused, it will wake back up

34
Q

What is hibernating myocardium?

A

A part of their heart you cannot see, but then they do a scan (MUGA scan) that the tissue is alive and just not beating

35
Q

What happens if the right coronary artery is affected?

A

Might have troubles with the SA node because it sends it

36
Q

What is the widow maker?

A

The Left anterior descending artery because it supplies the left ventricle

37
Q

What is a way to remember what artery is doing?

A

RAMP:

R = right coronary (inferior leads)

38
Q

What is LoCA

A

L = LAD (1-4)
C = circumflex artery (lateral leads)

39
Q

What is the goal of an initial evaluation for an MI?

A
  1. High likely is ACS?
  2. What is the risk of adverse events
40
Q

What do we ask our patient if we are worried about acute coronary syndrome (unstable angina, STEMI, non-STEMI)

A

When a patient presents with chest discomfort we need:
A detailed history
An appropriate, focused physical exam
Consideration of patient risk factors

41
Q

What is angina and what typically causes this?

A

Term used to describe chest discomfort related to IHD
Remember!
Typically due to atherosclerosis

Can also be d/t vasospasm, significant anemia, LVH, congenital anomalies, AS/AR, etc.

42
Q

Why does LVH lead to chest pain?

A

more strain on the heart

43
Q

What is the typical patient for an MI? Quality, location, and timing.

A

Male >50 or female >60

Episodic chest discomfort
Quality: heaviness, pressure, squeezing, smothering, aching or choking
Rarely deemed “pain”
Location: substernal, central chest
Radiation to the arms/shoulders (left), neck, jaw, teeth, back/scapula, epigastrium
Unlikely to radiate above mandible or below epigastrium
Timing: sudden, constant

44
Q

What is the duration, setting, and severity of an MI patient?

A

MI patient - Episodic chest discomfort
Duration: 2-5 minutes, crescendo-decrescendo
Setting: typically with exertion
Severity: varies and may not correlated with extent of myocardial injury

45
Q

What makes chest symptoms better and worse?

A

Aggravating /Alleviating Factors:
Aggravating: activity/exercise, meals, stress/strong emotion, cold exposure, sexual activity, morning, supine position

Alleviating: NTG, rest
Associated S/Sx: SOB, N/V, diaphoresis, fatigue, weakness, feeling of impending doom, paresthesias, dizzy, fever

46
Q

Why do you often see early morning MIs?

A

High cortisol, which increases BP

47
Q

What are the abnormal presentation of MI to women?

A

Women may experience:
SOB, pressure or pain in the lower chest or upper abdomen, dizziness, extreme fatigue, lightheadedness, fainting, or upper back pressure

more likely to die after first heart attack :(

48
Q

What is less accurate in diagnosing an MI in a women?

A

an exercise stress test

49
Q

What is the PE of an MI?

A

sweating, panting/breathing, look sick
vitals are non-specific
sometimes new heart sounds
labored breathing
Altered LOC because of less BF to the brain (ischemia to the heart leads to hypoperfusion to the brain)

50
Q

What are some other differentials for chest pain?

A

Atherosclerosis
Stable plaque / Stenosis
Plaque rupture

Variant (Prinzmetal) Angina
Results in vasospasm
May occur at the site of an atherosclerotic plaque/lesion or, less frequently, in apparently normal vessels
Often involves the RCA
Treated with CCB and nitrates
Most common in middle-aged women
Mimics STEMI on EKG

Other

Aortic dissection
Coronary embolism
Coronary arteritis
Congenital abnormalities / anomalies
Cocaine-induced vasospasm

51
Q

How do you treat prinzmetal angina?

A

Middle aged women, treated with CCB and nitrates

52
Q

Everyone with chest pain should get what?

A

an EKG
look at previous EKGs

+/- cardiac biomarkers (usually not outpatient because it takes too long)

53
Q

What are the three categories of diagnostic testing for the CC “chest pain”?

A

Stress testing (to mimic exertion)
Coronary angiogram (aka cardiac cath)
Imaging: Echo, CT angiograms, V/Q scans, electron beam CT scan (see coronary calcification)

54
Q

What is the TIMI risk score?

A

TIMI (Thrombolysis in MI) Risk Score is used to risk stratify patients to help determine who should undergo aggressive evaluation / treatment. Event rates increase significantly as the TIMI risk score increases.

Not on test but on boards

55
Q

When do you not use a TIMI risk score?

A

If they have a STEMI, because it takes a while to work-up.

Used for unstable angina and NSTEMI

56
Q

What are the 7 independent predictors of TIMI risk score?

A

If yes to any of the following +1 point

  1. Aged ≥ 65 years
  2. ≥3 CAD risk factors (HTN, DM, HLD, smoking, + FH early MI)
  3. Prior CAD (stenosis >50%)
  4. Aspirin in last 7 days
  5. Severe angina ( >2 anginal events within 24 hours)
  6. ST deviation on admission EKG ( >0.5mm)
  7. Elevated cardiac markers (CK-MB or troponin)

don’t need to know this

57
Q

What is the HEART score?

A

History (highly suspicious - history of CAD, pain with exertion)
ECG
Age
Risk factors
Troponin

58
Q

If you get HEART score of 0-3, what is their risk of MACE in 6 weeks, what to do?

A

MACE = 2.5% risk, intervention = discharge

59
Q
A

Cardiology (22 decks)

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