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Applied Pathophysiology > Coronary Artery Disease II > Flashcards

Coronary Artery Disease II Flashcards

1
Q

Acute Coronary Syndrome (ACS)

A

a term used to describe a range of conditions associated with sudden, reduced BF to the heart

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2
Q

CAD branches into…

A

Stable Angina or Acute Coronary Syndromes (branches into Unstable Angina –> NSTEMI or STEMI)

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3
Q

When does STEMI occur?

A

occurs by developing a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis

this causes a full thickness damage of heart muscle

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4
Q

STEMI’s account for __% of myocardial infarction (MI; heart attacks)

A

70%

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5
Q

When does NSTEMI occur?

A

occurs by developing a COMPLETE occulsion of a MINOR coronary artery or a PARTIAL OCCLUSION of a MAJOR coronary artery previously affected by atherosclerosis

this causes a partial thickness damage of heart muscle

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6
Q

NSTEMI’s account for __% of MI

A

30%

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7
Q

Remember? Stable Angina results from…

A
  1. occlusion of the artery by a stable atherosclerotic plaque
  2. a stable atherosclerotic plaque > 70%
    — autoregulation –>
    arteriolar dilation occurs but is INSUFFICIENT to allow reserve coronary blood flow for exertion 6
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8
Q

In contrast, unstable angina (more stable) results from…

A
  1. an unstable atherosclerotic plaque

fatty streaks become fibrous plaques which ultimately advance to weakened plaques vulnerable to rupture

  1. can be <50% stenosis
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9
Q

What is a Fibrous Cap Rupture?

A
  • due to shearing forces of blood flow
  • ***Not all plaques rupture; “vulnerable plaques”
    or “high risk plaques” include:

– large, lipid-rich core
– core consistency (i.e. less viscous)
– thin fibrous cap (less “protection”)
– increased inflammation in fibrous cap (post mortem studies found more macrophages in culprit lesions than in stable angina plaques)

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10
Q

Distinguish b/t Vulnerable & Stable Plaque

A

Vulnerable plaque - associated with unstable angina (can rupture)
- lipid core (larger)
- fibrous cap (smaller)

Stable plaque - associated with stable angina (won’t rupture with BF)
- lipid core (smaller)
- fibrous cap (larger

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11
Q

Types of clots –>

A

types of MI

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12
Q

White Clot

A

More PLATELETS than fibrin

INCOMPLETE artery occlusion

More common in NSTEMI

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13
Q

Red Clot

A

More FIBRIN than platelets

Usually COMPLETE artery occlusion

More common in STEMI

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14
Q

____ is much worse than ______

A

STEMI

NSTEMI

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15
Q

Unstable Angina

A
  • platelet aggregation
  • worse than stable angina
  • not as bad as MI
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16
Q

ST-SEGMENT ELEVATION MI (STEMI)

A
  • thrombosis
  • completely occludes coronary artery
  • thrombus is reddish (fibrin-rich)

(happen in bigger C.A)

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17
Q

NON-ST SEGMENT ELEVATION MI (NSTEMI)

A
  • thrombosis does not occlude coronary artery (therefore smaller than STEMI)
  • thrombus is grayish-white (platelet-rich)
  • embolism blocks downstream microvascular artery
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18
Q

_____ thickness damage of heart muscle in NSTEMI

A

PARTIAL

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19
Q

_____ thickness damage of heart muscle in STEMI

A

FULL

(larger C.A. occulusion, lead to MI more severely can lead to HF even)

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20
Q

What are the Signs & Symptoms of ACS?

A

same as stable angina, except
* they can start to occur at rest (unstable angina)
* they do not get better with rest nor nitrates

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21
Q

What are the Symptoms of Unstable Angina?

A

PAIN
* often described as discomfort
* squeezing, pressure, burning, tightness, heavy weight on chest (elephant)
* Levine sign “fist in the center of the chest”
* gradual in onset; intensity increases over minutes (non-cardiac pain is usually the opposite)

Radiation of pain
* arms, shoulders, neck, jaw, back, throat, teeth, upper abdomen (C7-
T4)
* tend to have the same quality of chest discomfort with recurrent ischemic episodes (i.e. same location and intensity); increase in severity is a warning sign of unstable angina/acute coronary syndromes

Shortness of breath
* dysfunction of the heart leads to mild pulmonary congestion

Bradycardia
* slowheartrate<60bpm
* lesscommon
* blood supply to AV node impaired

Tachycardia
* stress/panic and release of catecholamines (to try and compensate for reduced oxygen supply)

Nausea/vomiting
* vagus nerve stimulation

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22
Q

Differentiating ACS

A

Stable Angina - resolves with rest, short duration

ACS - does not resolve with rest, severe pain, long duration

  • STEMI (ST-segment elevation)
  • Troponin T & CK (ST-segment depression, T wave inversion; therefore inactive MI or maybe had it before)
    – NSTEMI (Trop T elevated (necrosis)
    – Unstable Angina (Trop T normal (no necrosis)

Basically, is the ischemia enough to cause sufficient heart damage to release detectable amounts of troponin T?

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23
Q

What is Troponin?

A
  • Complex of three regulatory proteins (troponins C, I & T)
  • Integral to muscle contraction in cardiac & skeletal muscle (not smooth muscle)
  • Two subtype isoforms (cardiac I and T) are VERY SENSITIVE AND SPECIFIC
    indicators of damage to cardiac muscle

(associated with Ca2+)

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24
Q

What is Creatine Kinase (myocardial band)?

A
  • Enzyme that facilitates transfer of high energy phosphate groups (via ATP and ADP)
  • Found in skeletal muscle, cardiac muscle and the brain
  • In muscle injury and when myocytes die, the muscle will release CK enzymes
    (marker for muscle injury)
  • NOT SPECIFIC to cardiac muscle, so we no longer use CK-MB for cardiac
    diagnostics
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25
Q

Necrosis:

A

cell membrane ruptures & cell content release into EC space & then ??

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26
Q

What is High-Sensitivity Troponin-T Test?

A
  • Is a marker of CARDIAC MYOCYTE DEATH (dying heart cells)
  • HIGH results indicate that there has been DAMAGE to the heart
  • In emergency, this test is ordered at presentation and then every 8 hours until first positive result
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27
Q

When can levels of Troponin become elevated?

A

Levels of troponin can become elevated in the blood within 3 or 4 hours after heart injury and may remain elevated for 10 to 14 days. In people with angina, an elevated troponin may indicate that their condition is worsening and they are at increased risk of a heart attack.

28
Q

Could you get increase of troponin levels in blood?

A

earlier point ???

29
Q

What are the drugs used in ACS?

A
  • relieve ischemia and ischemic pain
  • disrupt or prevent further occlusion/clotting
  • correct hemodynamic abnormalities (blood pressure, atherosclerosis)
30
Q

What are the drugs used for management of ACS?

A

Morphine - Pain relief

Nitrates - Ischemia relief

Aspirin - Prevent clotting

Beta-blockers - Ischemia relief

Thienopyridines (clopidogrel,
prasugrel) or
ticagrelor - Prevent clotting

GP IIb/IIIa inhibitors - Prevent clotting

Heparin - Prevent clotting

Fibrinolytics - Break up clots (tenectoplase,
alteplase)

Statins (once stable) - Lower cholesterol

ACEIs (once BP stable) - BP control/prevent future events

31
Q

Slide 26 & 28

A

done

32
Q

TIMI Risk Scores (US/NSTEMI)

A

One Point awarded for each of the following:
- Age ≥ 65 years
- 3 or more of the following heart disease risk factors:
– Smoking
– Hypercholesterolemia
– Hypertension
– Diabetes
– Family history of premature cardiovascular
events/death
- Known coronary artery disease (≥50% stenosis)
- ASA use in past 7 days
- ≥2 episodes of chest discomfort in the past 24 hours
- ST-segment depression ≥0.5mm (on ECG)
- Positive biochemical marker for infarction

33
Q

What is considered Low Risk for TIMI?

A

0-2 points

0-8.3% risk of death/MI or severe ischemia

34
Q

What is considered Moderate Risk for TIMI?

A

3-4 points

13.2-19.9% risk of death/MI or severe ischemia

35
Q

What is considered High Risk for TIMI?

A

5-7 points

26.2-40.9% risk of death/MI or severe ischemia

36
Q

What is the Reperfusion Therapy?

A

ST-SEGMENT ELEVATION MI
* thrombosis
* completely occludes coronary artery
* thrombus is reddish (fibrin-rich)

  1. mechanically disrupt clot – PCI (mech. way)
  2. dissolve clot – thrombolytics (aka fibrinolytics)
    eg. streptokinase, alteplase, tenecteplase, reteplase (pharmacological way)
37
Q

What is Angiography (or coronary angiogram)?

A

A catheter is inserted through artery in forearm, thigh, upper groin or neck and threaded to the coronary artery in question

A dye is released, allowing for X-rays to illuminate the arteries and show areas of poor blood flow

38
Q

What is a Percutaneous Coronary Intervention?

A

A tiny catheter runs from the femoral artery (or jugular vein depending on side of heart) to the affected area

A balloon at the tip squashes the atherosclerotic plaque and holds the artery open

A bare-metal or drug eluting stent is placed, like a little cage to keep the artery open
- b/c otherwise it’ll close after taking it out (so stent stays in; therefore this will cause it to narrow again)

will leave a scar which will affect heart function after the procedure ??

39
Q

What is Coronary Revascularization (Bypass)?

A
  • Harvest a blood vessel (great saphenous vein, left internal mammary artery (LIMA))
  • Sew one end of the vessel above the blocked coronary artery and one end below “by-passing” the blockage to restore blood flow
  • The number of blockages determine how many bypasses need to be done
    (i.e. triple, quadruple, quintuple)
40
Q

What is the Graded Severity of Stable Angina?

A

less severe

  • triggered by activities that increase myocardial oxygen demand and lasts for 2-5 minutes
  • described as discomfort rather than pain
41
Q

What is the Graded Severity of Unstable Angina?

A

At least 1 of these features:
* occurs at rest (or minimal exertion) and lasts for more than 20 minutes
* severe and described as frank pain of new onset (i.e. within 1 month)
* occurs with a new pattern – more severe, prolonged, or occurs with less exertion than previous angina

ischemia IS NOT severe enough to produce myocardial necrosis so there is no release of biochemical markers (eg. troponins T or I, creatine kinase (CK) myocardial band)

42
Q

What is the order of Graded Severity for CAD?

A

Stable Angina < Unstable Angina < Myocardial Infraction < NSTEMI < STEMI

43
Q

What is the least and most stable CAD?

A

stable angina

STEMI

44
Q

____% of patients with myocardial infarction die before they can reach the hospital

A

33-50%

45
Q

What is a major reason why 33-50% of patients with myocardial infarction die before they can reach the hospital

A

Lethal arrhythmia –> Sudden cardiac death

46
Q

How many cardiomyocytes in heart?

A

24% –> cardiomyoctes are huge

SA node has highest signal, it can inhibit in AV node

47
Q

Cardiac arrhythmia:

A

refers to a group of conditions that cause the heart to beat irregular, too slowly, or too quickly.

(heart no longer beats normally)

48
Q

What are the types of Cardiac arrhythmia’s?

A
  • Tachycardia - >100
  • Bradycardia - < 60
  • Irregular heartbeat, also known as a flutter or fibrillation
  • Early heartbeat, or a premature contraction
49
Q

Tachycardia:

A

This refers to a fast heartbeat — a resting heart rate greater than 100 beats a minute.

  • Tachycardias in the atria
  • Tachycardias in the ventricles
50
Q

What are Tachycardias in the atria?

A
  • Atrial flutter
  • Atrial fibrillation
  • Supraventricular tachycardia (SVT)
51
Q

Atrial flutter:

A

is caused by a re-entry circuit within the right atrium. The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a fairly predictable atrial rate of around 300 bpm (range 200-400).

If one signal impulse is high enough it’ll lead to re-entry

NOT P wave (replaced normal P wave)

52
Q

Atrial Fibrillation:

A

A rapid heart rate caused by chaotic electrical impulses in the atria. These signals result in rapid, uncoordinated, weak contractions of the atria
- many impulses (fire at diff. positions & strength)

53
Q

Supraventricular tachycardia (SVT):

A

is usually caused when electrical impulses originating at or above the atrioventricular node, or AV node are out of synch.

  • happen above or at AV node

(NO P wave at all)

54
Q

Tachycardias in the ventricles:

A

Ventricular tachycardia

Ventricular fibrillation

Long QT syndrome

55
Q

Ventricular fibrillation:

A

Ventricular fibrillation occurs when rapid, chaotic electrical impulses cause the ventricles to quiver ineffectively instead of pumping necessary blood to the body. This serious problem is fatal if the heart isn’t restored to a normal rhythm within minutes.

56
Q

Long QT syndrome:

A

Long QT syndrome is a heart disorder that carries an increased risk of fast, chaotic heartbeats.

57
Q

Ventricular tachycardia:

A

is a rapid, regular heart rate that originates with abnormal electrical signals in the ventricles. The rapid heart rate doesn’t allow the ventricles to fill and contract efficiently to pump enough blood to the body.

(reversibel (abnormal impulse in ventricle)

58
Q

Ventricular fibrillation:

A

occurs when rapid, chaotic electrical impulses cause the ventricles to quiver ineffectively instead of pumping necessary blood to the body. This serious problem is fatal if the heart isn’t restored to a normal rhythm within minutes.

  • more severe (will flatline mostly likely in next few)
  • no regular wavelength at all (fire at diff. times & strength)
59
Q

The long QT syndrome (LQTS):

A

is a disorder of myocardial repolarization characterized by a prolonged QT interval on the electrocardiogram (ECG). It is often inherited and present from birth. It can also be caused by certain medications.

60
Q

The long QT syndrome (LQTS) symptoms may include:

A
  • Fainting
  • Dizziness
  • Seizures
  • Abnormal rate and rhythm of the heartbeat
61
Q

Bradycardia:

A

This refers to a slow heartbeat — a resting heart rate less than 60 beats a minute

62
Q

What are the Bradycardia disorders?

A

Sick sinus syndrome

Conduction block

63
Q

Sick sinus syndrome:

A

Sinus node isn’t sending impulses properly and the heart rate may be slow (bradycardia).

64
Q

Conduction block:

A

A block occurs along the electrical transduction pathways, often in or near the AV node.

65
Q

What is a major treatment of Bradycardia?

A

Pacemaker

66
Q

Bradycardia is…

A

normal waves but just slow

Applied Pathophysiology (34 decks)

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