9 - The Heart: Ischemic Heart Disease Flashcards

1
Q

Ischemic Heart Disease (IHD): Defined

A

Imbalance between the myocardial supply (perfusion) and cardiac demand for oxygenated blood

Starts with Angina –> ends with MI

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2
Q

IHD: IHD Syndromes (4)

A
  1. MI
  2. Angina Pectoris (chest pain)
  3. Chronic IHD with heart failure
  4. Sudden cardiac death (consequence of MI)
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3
Q

IHD: Angina Pectoris - Defined

A

Characterized by chest pain – interpreted differently as ‘constricting’, ‘squeezing’ and so on

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4
Q

IHD: Angina Pectoris - Types

A

Stable (typical) – relieved by rest but precipitated by physical activity; pain relieved by sublingual nitroglycerine and rest tested by treadmill

Prinzmetal – due to spasm of coronary artery, good response to nitroglycerine

Unstable – increasing in frequency, impending MI, dangerous type within 30 minutes

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5
Q

IHD: Angina Pectoris - Types

A

Stable (typical) – relieved by rest but precipitated by physical activity; pain relieved by sublingual nitroglycerine and rest tested by treadmill

Prinzmetal – due to spasm of coronary artery, good response to nitroglycerine

Unstable – increasing in frequency, impending MI, dangerous type within 30 minutes

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6
Q

IHD: MI - Incidental and Risk Factors A

A

A. Coronary Arterial Occlusion
- Atheromatous plaque leads to intra plaque hemorrhage or rupture

Mnemonics: HAS LIPIDS

H- Hereditary 
A- Age 
S- Sex
L- Lipid ( hyperchelestrol)
I- Inactivity ( Sedentary life style)
P- Pressure ( Hypertension)
I –increased weight ( Obesity)
D- Diabetes
S- Smoking
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7
Q

IHD: MI - Incidental and Risk Factors A

A

A. Coronary Arterial Occlusion
- Atheromatous plaque leads to intra plaque hemorrhage or rupture

Mnemonics: HAS LIPIDS

H- Hereditary 
A- Age 
S- Sex
L- Lipid ( hyperchelestrol)
I- Inactivity ( Sedentary life style)
P- Pressure ( Hypertension)
I –increased weight ( Obesity)
D- Diabetes
S- Smoking
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8
Q

IHD: MI - Non-Atheromatous Conditions (6)

A
  1. Vasospasm (cocaine)
  2. Emboli
  3. Ischemia without evident atherosclerosis
  4. Sickle cell disease
  5. Shock
  6. Vasculitis
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9
Q

IHD: MI - Patterns: Transmural (3)

A

Caused by occlusion of epicardial vessels

*FULL THICKNESS

Atherosclerosis, plaque changes and superimposed thrombus

**ECG: ST Segment ELEVATION/Q wave

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10
Q

IHD: MI - Patterns: Transmural (3)

A

Caused by occlusion of epicardial vessels

*FULL THICKNESS

Atherosclerosis, plaque changes and superimposed thrombus

**ECG: ST Segment ELEVATION/Q wave

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11
Q

IHD: MI - Patterns: Subendocardial (3)

A

Necrosis limited to *inner 1/3 to one half of the ventricular wall

Follows plaque disruption secondary to thrombolysis

*Non-ST elevation infarcts” –> No Q waves (no myocyte death)

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12
Q

IHD: MI - Patterns: Subendocardial (3)

A

Necrosis limited to *inner 1/3 to one half of the ventricular wall

Follows plaque disruption secondary to thrombolysis

*Non-ST elevation infarcts” –> No Q waves (no myocyte death)

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13
Q

IHD: MI - Supply, Frequency, Region

A
  1. LAD - 40-50%
  2. RCA - 30-40%
  3. Left circumflex - 15-20%
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14
Q

IHD: MI - Morphology

A

Difficult to identify if TTC stains VIABLE tissue leaving necrotic tissue unstained

Older infarcts easy to ID and represent ischemic coagulative necrosis

Inflammatory cells seen in infarct

Myocytolysis

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15
Q

IHD: MI - Morphology

A

Difficult to identify if TTC stains VIABLE tissue leaving necrotic tissue unstained

Older infarcts easy to ID and represent ischemic coagulative necrosis

Inflammatory cells seen in infarct

Myocytolysis within 6 hours

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16
Q

IHD: MI - Enzymes

A

1st check Troponin I –> after 2-3 hrs, sustained for 2 weeks; highly specific but not sensitive

CKMB: released immediately (2-3 hours), peaks at 2nd day, and is normal by 3rd day

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17
Q

IHD: MI - Enzymes

A

1st check Troponin I –> after 2-3 hrs, sustained for 2 weeks; highly specific but not sensitive

CKMB: released immediately (2-3 hours), peaks at 2nd day, and is normal by 3rd day

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18
Q

IHD: MI - Microscopy 1st day

A

Vascular congestion within 3 hours

Swelling and Redness - Acidophilia within 6 hours

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19
Q

IHD: MI - Microscopy 24 hrs

A

Red and swollen - full coagulative necrosis

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20
Q

IHD: MI - Microscopy 48 hrs

A

Yellowing of infarct due to macrophages

21
Q

IHD: MI - Microscopy 3 days

A

Yellow infarct surrounded by red border due to fibroblast proliferation

22
Q

IHD: MI - Microscopy 1-3 weeks

A

Yellow infarct due to collagen

23
Q

IHD: MI - Microscopy 3 months

A

Grey, white scar due to fibrosis

24
Q

IHD: MI - Microscopy 3 months

A

Grey, white scar due to fibrosis

25
Q

What occurs in the first hour of MI?

A

Cell death because of arrhythmia (monitor ever 50 minutes)

Palpate pulse (Vtach, AFIb)

26
Q

What can occur on the 7th day of MI and also what’s a good enzyme to confirm this?

A

Re-infarction/Ventricular rupture due to weak scar that isn’t fully formed by all of the collagen

So, ventricle isn’t strong enough to withhold the hemodynamic force

CKMB great to confirm this

27
Q

IHD: MI - Reperfusion infarcts

A

Usually hemorrhagic (red infarcts)

Irreversibly injured myocytes exhibit contraction bands
Intensely eosinophilic stripes ( closed sarcomeres)

28
Q

IHD: MI - C/F (4)

A
  1. Severe chest pain radiating to left shoulder
  2. ‘Silent’ MI refers to no pain by elderly and diabetics
  3. Diaphoresis
  4. Atypical presentations include **Abdominal epigastric pain mimicking severe colic and back pain
29
Q

IHD: MI - C/F (4)

A
  1. Severe chest pain radiating to left shoulder
  2. ‘Silent’ MI refers to no pain by elderly and diabetics
  3. Diaphoresis
  4. Atypical presentations include **Abdominal epigastric pain mimicking severe colic and back pain
30
Q

IHD: MI - Diagnosis with Enzymes (4)

A

CKMB, cTnT, and cTnI is first 3-12 hrs.

CKMB and cTnI peak at 12 hr.

CKMB returns to normal 48-72hrs

cTnI in 5-10 days

cTnT in 5-14 days

31
Q

IHD: MI - Consequences and complications (1 of 3) - Contractile Dysfunction

A

Left ventricular failure leads to congestion and edema of lung: massive infarct leads to cardiogenic shock and has high mortality

32
Q

IHD: MI - Consequences and complications (2 of 3) - Arrhythmias within 1 hour of MI can cause death

A

Sinus bradycardia
Tachycardia
Heart block
Ventricular fibrillation

33
Q

IHD: MI - Consequences and complications (3 of 3) - Myocardial rupture after 7 days

A

Necrotic ventricle is vulnerable and ruptures and causes hemopericardium and cardiac tamponade and immediate death

Rupture of ventricular septum causes acute VSD and left to right shunts

34
Q

IHD: MI - Consequences and complications - 1. Contractile Dysfunction

A

Left ventricular failure leads to congestion and edema of lung: massive infarct leads to cardiogenic shock and has high mortality

35
Q

IHD: MI - Consequences and complications - 2. Arrhythmias within 1 hour of MI can cause death

A

Sinus bradycardia
Tachycardia
Heart block
Ventricular fibrillation

36
Q

IHD: MI - Consequences and complications - 3. Myocardial rupture after 7 days

A

Necrotic ventricle is vulnerable and ruptures and causes hemopericardium and cardiac tamponade and immediate death

Rupture of ventricular septum causes acute VSD and left to right shunts

37
Q

IHD: MI - Consequences and complications - 4. Pericarditis

A

Fibrinous deposition due to inflammation

Known as Dressler’s Syndrome - Post MI pericarditis (etiology thought to be immune mediated)

38
Q

IHD: MI - Consequences and complications - 5. Right Ventricular Infarction

A

Ventricular septal infarcts and infarction of the posterior part of left ventricles

Causes acute right sided heart failure

39
Q

IHD: MI - Consequences and complications - 6. Extension of Infarct

A

New infarcts develop around existing infarcts

40
Q

IHD: MI - Consequences and complications - 7. Expansion of infarct

A

Depends on severity of obstruction

Associated with anteroseptal infarcts. Due to necrosis, myocardium shows thinning, dilation and stretching

41
Q

IHD: MI - Consequences and complications - 8. Mural Thrombus

A

Formation leads to thromboembolic complications

MI Apex of LV

6 months later ventricular bulge not contracting during systole, suffers massive STROKE and expires

42
Q

IHD: MI - Consequences and complications - 9. Ventricular aneurysms

A

After 3 months

Scarred myocardium gives rise to true aneurysms

Once scar is formed. Terminal portion of infarction will dilate. Not in harmony with cardiac muscle  dilation of ventricle (ventricular aneurysms

43
Q

IHD: MI - Consequences and complications - 9. Ventricular aneurysms

A

After 3 months

Scarred myocardium gives rise to true aneurysms

Once scar is formed. Terminal portion of infarction will dilate. Not in harmony with cardiac muscle  dilation of ventricle (ventricular aneurysms

44
Q

IHD: MI - Consequences and complications - 10. Papillary muscle dysfunction and ruptures causes?

A

Mitral regurge

secondary and functional

45
Q

IHD: MI - Consequences and complications - 11. Progressive Heart Failure

A

AKA Chronic IHD

46
Q

Mnemonic to remember complications of MI is?

A

“APPEAR”

A- Arrhythmias
P- Pump failure
P- Pericarditis
E- Embolisation
A-Aneurysm of the ventricle 
R- Rupture ( cardiac wall or papillary muscle )
47
Q

High Yield Fact: Common cause of death in MI is?

A

Arrhythmias ( Ventricular tachycardia and ventricular fibrillation ) - within 2 hrs.

48
Q

High Yield Fact: Delayed complication dramatic and sudden rupture of myocardium can occur when?

A

4-8 days post MI