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Cardiovascular > IHD, Part 1 > Flashcards

IHD, Part 1 Flashcards

1
Q

what is the most common, serious, chronic, life-threatening illness in the U.S?

A

IHD

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2
Q

what % of the population has a sustained MI?

A

3-4%

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3
Q

MC risk factors of IHD

A
  1. genetic influences
  2. high-fat and energy-rich diet
  3. smoking
  4. sedentary lifestyle
  5. In the U.S, growing among low-income groups
    - Primary prevention has prolonged age of disease development
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4
Q

What is the most MCC of myocardial ischemia?

A

atherosclerotic CAD

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5
Q

Mechanism of Myocardial Ischemia

A

Multifactorial
1. Generally an imbalance between oxygen supply and demand
2. Oxygen supply → determined by blood flow
- Blood flow is regulated by pressure vs. resistance ratio
- Most critical factor is radius of blood vessel

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6
Q

pathogenesis of IHD

A
  1. Ischemic heart disease = MI
  2. supply < demand
    - If heart muscle is not perfused with blood, it cannot get properly oxygenated, and ischemia results
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7
Q

the radius of the blood vessel is influenced by what factors?

A

atherosclerosis hardening of vessels
vascular tone
endothelial cell dysfunction in cardiac ischemia

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8
Q

what are the 4 types of IHD? which are acute coronary syndrome (ACS)?

A
  1. Prinzmetal Angina
  2. Stable Angina
  3. Unstable Angina (ACS)
  4. Myocardial Infarction (ACS)
    - stemi
    -nstemi
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9
Q

stable, fixed plaque that reduces vessel diameter and when demand goes up, supply is limited, leading to symptoms
what is this called?

A

stable angina

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10
Q

ACS results when there is _____ and _____.

A

plaque rupture
thrombus formation

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11
Q

The amount of coronary blood flow restriction determines the severity:

A
  1. Unstable angina - no occluded blood flow → sx at rest
  2. NSTEMIs - partially impeded blood flow through the coronary vessels
  3. STEMIs - completely impeded blood flow through the coronary vessels
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12
Q

differences between stable vs unstable angina

A
  1. stable - Fixed stenosis
    - 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
  2. unstable - Caused by a transient formation and dissolution of a thrombus
    - 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 MI is impending. An EMERGENCY!
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13
Q

After occlusion of a Coronary Artery, the myocardium evolves through various stages and degrees of severity of impairment:

A

ischemia –> injury –> infarct

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14
Q
  • Present as soon as there is a decrease or complete absence of blood supply to myocardial tissue; immediate phase
  • Cardiac cells can tolerate mild-moderate anoxia for a short time without greatly affecting their function
  • When adequate blood flow / reoxygenation return, these cells usually return to a normal
    what is this stage/degree of severity of impairment?
A

ischemia

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15
Q
  • 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
    what is this stage/degree of severity of impairment?
A

injury

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16
Q
  • Severe myocardial ischemia continues because of continued complete absence of blood supply
  • The anoxic cardiac cells will sustain irreversible injury and die.
    what is this stage/degree of severity of impairment?
A

infarct

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17
Q

what results in necrosis of a portion of the myocardium

A

irreversible myoardial injury

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18
Q

ACUTE MI suggests the infarct is how old?

A

<3-5 d

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19
Q

Patients may present after the 5 day window with an old MI demonstrating symptoms such as ?

A

heart failure
Q waves have already developed on EKG

20
Q

Types of Myocardial Infarctions:

A
  1. Subendocardial / NSTEMI / Non-Q Wave MI
  2. Transmural / STEMI / Q Wave MI
21
Q

which MI
- Involves small area in the subendocardial wall of the LV, ventricular septum, or papillary muscle
- Caused by local decrease in blood supply from narrowing of a coronary artery. The subendocardial area is particularly susceptible to ischemia.
- EKG → ST depression or T-wave inversion (or no EKG changes)

A

Subendocardial / NSTEMI / Non-Q Wave MI

22
Q

which MI
- 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
- Typically much more severe; high risk of complications

A

Transmural / STEMI / Q Wave MI

23
Q

MI Classifications

A
  1. Type 1 - Spontaneous MI related to ischemia d/t primary coronary event (plaque erosion and/or rupture, fissuring, dissection)
  2. Type 2 - MI secondary to ischemia d/t either ↑ oxygen demand or ↓ decreased supply (e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, HTN, or hypotension)
  3. Type 3 - Sudden unexpected cardiac death
  4. Type 4 - MI associated with coronary angioplasty or stents
  5. Type 5 - MI associated with CABG
24
Q

other forms of MI

A
  1. Silent Ischemia
    - MI without discomfort or pain
    - MC in DM, elderly patients, and women
    - Exact mechanism is unknown
  2. Myocardial Stunning
    - Reversible myocardial dysfunction following reperfusion of an ischemic insult
    - Initially appears to be permanently damaged but following early reperfusion, contractile function returns to normal
  3. Hibernating Myocardium
    - A result of prolonged reduction in blood flow from coronary artery disease
    - Causes ventricular contractile dysfunction that will improve once blood flow improves
25
Q

often accompanied by a ↓ HR b/c of involvement of the sinus node. Long term effects are usually less severe than those of an anterior wall MI.
EG leads - II, III, aVF
which coronary artery/myocardium was involved?

A

RCA and/or LCx
IWMI

26
Q

anterior wall performs the main pump function and decay of the function of this wall will lead to ↓ BP, ↑ HR, shock and on a longer term, HF
ECG leads - V1-V4
which coronary artery/myocardium was involved?

A

LAD
AWMI

27
Q

if ECG leads involved are I, aVL, V5, V6, which coronary artery/myocardium is involved?

A

LCX / lateral wall LV

28
Q

for the Goal for Initial Evaluation, what are the 2 questions to consider:

A
  1. how likely is ACS
  2. what is the risk of adverse events?
29
Q

When a patient presents with chest discomfort we need:

A
  1. A detailed history
  2. appropriate, focused PE
  3. Consideration of patient risk factors
  4. Estimate the probability of significant CAD
    (high, intermediate, or low)
30
Q

Term used to describe chest discomfort related to IHD

A

Angina Pectoris

31
Q

possible causes of angina

A
  1. Typically d/t atherosclerosis
  2. also be vasospasm, significant anemia, LVH, congenital anomalies, AS/AR, etc.
32
Q

typical presentation of “chest pain”

A
  1. Male >50 or female >60
  2. Episodic chest discomfort
    - Quality: heaviness, pressure, squeezing, smothering, aching or choking
    — Rarely deemed “pain”
    - Location: substernal, central chest
    — Radiation to arms/shoulders (left), neck, jaw, teeth, back/scapula, epigastrium - Unlikely to radiate above mandible or below epigastrium
    - Timing: sudden, constant
    - Duration: 2-5 minutes, crescendo-decrescendo
    - Setting: typically with exertion
    - Severity: varies and may not correlated with extent of myocardial injury
    - 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
33
Q

abnormal pt presentation of chest pain

A
  1. Women may experience:
    - SOB, pressure or pain in the lower chest or upper abdomen, dizziness, extreme fatigue, lightheadedness, fainting, or upper back pressure
  2. Exercise stress test may be less accurate in women
  3. Women are are more likely to die after their first heart attack
34
Q

PE of chest pain

A
  1. Vitals – hypotension or HTN, Tachy or Brady, nonspecific fever
  2. General – anxious, restless, diaphoretic, pallor, confusion
  3. Neck – JVD in RV infarct
  4. CV – arrhythmia, muffled heart sounds, S4 gallop, JVD, new heart sounds / murmurs, diminished peripheral pulses, pericardial rub
  5. Pulm – pulmonary rales or wheezing, pulmonary edema, labored breathing if in LV failure
  6. Neuro – look for signs of altered level of consciousness, CVA
35
Q

Chest Pain ddx

A
  1. Coronary Artery Associated - Myocardial O2 supply-demand mismatch
    - Atherosclerosis
    - Variant (Prinzmetal) Angina
    - other: Aortic dissection , Coronary embolism, Coronary arteritis, Congenital abnormalities, Cocaine-induced vasospasm
  2. Non-coronary causes of myocardial O2 supply- demand mismatch
    - Hypotension
    - HTN
    - Hypertrophic CM
    - Severe myocardial hypertrophy
    - Severe AS/AR
    - Pericarditis
    - In response to ↑ metabolic demands (hyperthyroidism, marked anemia, or paroxysmal tachyarrhythmias)
  3. Non-ischemic myocardial injury
    - Myocarditis
    - Non-ischemic cardiomyopathy
    - Cardiac contusion
    - Cardiotoxic drugs
    - Multifactorial causes: Takotsubo Cardiomyopathy, PE, severe HF, sepsis
  4. pulm - pulmonary embolus, pneumothorax, pneumonia, pleuritis, pulmonary HTN / cor pulmonale
  5. Chest wall - Costochondritis, fibrositis, rib fracture, sternoclavicular arthritis, Herpes zoster
  6. GI - esophagitis, spasm, reflux, rupture, peptic ulcer, pancreatitis, colic, cholecystitis, choledocholithiasis, cholangitis
  7. psych - anxiety, affective disorders, somatoform
36
Q

Variant (Prinzmetal) Angina is treated with what meds?

A

CCB and nitrates

37
Q

Variant (Prinzmetal) Angina is Mc in who?

A

middle-aged women

38
Q

Diagnostic Testing for “Chest Pain” Patient

A
  1. EKG +/- cardiac biomarkers
  2. stress testing
  3. coronary angiogram (cardiac cath)
  4. imaging
    - CT angiogram
    - Echo (TTE and TEE)
    - CT angiogram or V/Q Scan
    - Electron beam CT scan
39
Q

types of stress testing

A
  • Exercise stress test alone
  • Exercise stress test with nuclear imaging component
  • Pharmacologic Stress test with nuclear imaging component
  • Exercise stress test with imaging (Stress Echo)
40
Q

If a pt comes in with a compliant of chest pain, what imaging would you order for coronary calcification?

A

Electron beam CT scan

41
Q

How to risk stratify pts to help determine who should undergo aggressive evaluation / tx?

A

TIMI Risk Score

  1. ≥65
  2. ≥3 CAD risk factors (HTN, DM, HLD, smoking, + FH early MI)
  3. Prior CAD (stenosis >50%)
  4. ASA 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)

0-2: Low risk
3-4: Intermediate risk
5 or more: High risk

41
Q

If a pt comes in with a compliant of chest pain, what imaging would you order to r/o a PE?

A

Ct angiogram or V/Q scan

41
Q

What is HEART Score?

A

For cardiac risk assessment of major adverse cardiac event (MACE)

  • History
  • EKG
  • Age
  • Risk Factor
  • Troponion

<3: d/c
4-6: admit for observation
>7: admit w/ early invasive strategies

42
Q

what makes a pt to have a high likelihood of ACS secondary to CHD in pts without ST-segment elevation?

A
  1. primary sx is pain or discomfort in chest or left arm AND current pain is similar to pain of prior documented angina/MI
  2. has known CHF / MI
  3. transiet mitral regurg / hypotension / diaphoresis / pulmonary edema / rales
  4. new transiet ST deviation (≥1mm)
  5. new t-waves inversion in multiple precordial leads
  6. elevated troponion
42
Q

what makes a pt to have an intermediate likelihood of ACS secondary to CHD in pts without ST-segment elevation?

A

absence of high-likelihood features, normal troponin, plus 1 of the following:

  • primary sx is pain or discomfort in chest or L arm
  • > 70
    male
  • DM
  • extracardiac vascular dz
  • fixed Q waves
  • ST depression 0.5-1mm or T-wve inversion >1mm
43
Q

what makes a pt to have a low likelihood of ACS secondary to CHD in pts without ST-segment elevation?

A

no high or intermediate-likelihood features, normal troponin

may have of the following and STILL be low likelihood:

  • hx of sx of probably ischemic
  • used coke
  • T-wave flattening or inversion <1mm

Cardiovascular (24 decks)

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