Ischemic Heart Disease Flashcards

(49 cards)

1
Q

Three ways a heart might have inadequate O2 delivery (broad)

A

Decreased Perfusion
Other oxygenation causes
Inadequate O2 secondary to increased demand

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2
Q

Causes of decreased perfusion of the heart (5)

A
Progressive stenosis
Thromboembolus
Vasospasm
Vasculitis
Hypovolemia
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3
Q

Non-perfusion oxygenation issues (5)

A
Anemia
CO
Congenital Heart Disease
Asphyxia
Lung Disease
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4
Q

Once stenosis reaches _____%, there is a decreased ability to meet the demand

A

75%

severe/fatal usually requires a 70% reduction in diameter

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5
Q

Where is the most severe narrowing typically?

A

The proximal 2cm

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6
Q

Thrombus formation usually results from

A

rupture or fissure of plaque with platelet aggregation, release of thromboxane

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7
Q

Vasospasm is associated with…

A

Adrenergic stimulation, local factors (NO, endothelin, platelet factors), HTN/Platelet Activity

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8
Q

Two types of coronary vessels

A

Epicardial (Conductance Vessels – get athero)

Intramyocardial (Resistance Vessels - autoregulation and flow)

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9
Q

How does hypoxia kill muscle cells

A

Switch to anerobic glycolysis, lactate buildup, lowered pH, impaired membrane fxn lets K leak and Na in

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10
Q

Injury becomes permanent after…

A

20-40 minutes

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11
Q

Irreversible Injury to the heart…whats that like

A

Necrosis and permanent loss of functional myocardium

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12
Q

What is acute ischemic heart disease

A

blockage of flow in a coronary vessel leads an entire region of myocardium to become necrotic (MI)

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13
Q

What is chronic ischemic heart disease

A

Ischemia leading to loss f individual myocytes and diffuse fibrosis, resulting in myocarfial dysfunction and eventually heart failure

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14
Q

Morphology of reversible injury

A

Stunned Myocytes

Mitochondrial swelling, Relaxation of myofibrils, distortion of cristae

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15
Q

Morphology of irreversible injury (in chronic)

A

Chronic loss of myocytes, esp. in subendocardial
Coagulative necrosis + Apoptosis
Area becomes fibrotic
Subendocardial band of infarcted myo at watershed

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16
Q

Morphology of acute ischemia (MI) - Gross

A

Early – Pallor with hyperemic border
3-7 days: hyperemic border with central, yellow-brown softening. Possibly hemorrhage.
Eventual replacement w/ red-brown, depressed, scarred area.
Eventually gray and fiber like

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17
Q

Phases of color of a post-MI heart

A

White–> Yellow Brown –> Red-Brown –> Gray

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18
Q

Morphology of acute ischemia (MI) – Microscopic

A

Necrosis of Myocytes
Inflammation, Infiltration w/ Inflamm cells
Clean up of necrotic debris
Replacement of myocardium w/ scar tissue

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19
Q

Morphology of reperfusion injury?

A

Presence of contraction bands in damaged myocytes.

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20
Q

Two main symptoms of cardiac ischemia?

A

Chest Pain + Diaphoresis

21
Q

Describe the chest pain of an MI

A

Crushing Pain over sternum
Radiates to left arm/back
NOT sharp or fluctuating

22
Q

Describe MI diaphoresis

A

Shortness of Breath, Sweating, Nausea

23
Q

Three serum enzymes associated with ischemic heart

A

Troponin I/T
Creatinine kinase (MB isoenzyme)
Lactic dehydrogenase

24
Q

Whats the deal with troponin?

A

Cardio specific/Sensitive
Increase w/ CMB, elevated up to 7 days
Most sensitive/specific

25
Whats the deal w/ CK-MB
Highly specific and sensitive Peaks at 12-24 hrs. Down quickly after. Indicator of repeat infarct
26
Whats the deal with lactic dehydrogenase
Indicator of tissue damage that rises form 24h to 3-6 days. Stays up for weeks. Nonspecific and basically useless.
27
Aside from symptoms and enzymes, how else might you diagnose an MI
EKG | Leukocytosis + Elevated ESR
28
The triad of symptoms associated with ischemic heart disease...
Systemic HTN LVH CAD
29
Most important clinical correlation with ischemic heart?
atherosclerosis
30
Difference between Stable, Unstable, and Prinzmetal's angina
S -- Relieves with rest+nitro U -- Not relieved with rest+mitro P -- Caused by vasospasm (ex. from cocaine)
31
How do chronic heart disease patients tend to present?>
History of angina/MI in last 5-10 years | Cardiac decompensation from slow myocardial atrophy
32
Pathophysiology of Chronic ischemic heart disease?
Progressive injury resulting in eventual CHF | Diffuse atherosclerosis w/ myocardial fibrosis + patchy scars
33
Most MIs are precipitated by...
Rupture of atherosclerotic plaque and thrombus formation | Sometimes from thromboemboli
34
Characteristic unique histological feature of MI
Inflammation delayed by 24-48 hours
35
MI sign at first few hours...
Acute Cell Injury --> Necrosis
36
First visual sign of inflammation?
Edema occurs at margin within first 24 hours
37
Hallmarks of coagulative necrosis
Loss of nuclei and hypereosinophilic fibers
38
In the 2-4 days following the day of MI....
Neutrophils migrate into necrotic area, cellular infiltrate becomes prominent Afterwards macrophages get in
39
What's going on with the heart 4-5 days following MI
Highest risk of rupture
40
Early complications of MI
Dysfunctional Heart Muscle Arrythmia Extensions of Infarct
41
Late complications of MI (5)
``` Aneurysm/Dilation Ventricular Rupture Mural Thrombus Pericardial effusion/Pericarditis Papillary Muscle Infarct with Mitral Insufficiency ```
42
How does ischemia show up on an EKG?
Inverted T Wave | Displacement of ST
43
Transient ST depression suggests...
subendocardial ischemia
44
Transient ST elevation suggests...
Transmural ischemia
45
Whats unique about an EKG after infarction?
Q waves/Loss of R waves ST changes Q wave, non-Q infarction
46
Angiography perfusion study indicated in...
Chronic Stable or Unstable Angina (symptoms despite therapy) Patients w/ troublesome symptoms that occlude diagnosis Patients with severe ischemia
47
Treatment of Angina
Lifestyle changes/Treat risk factors Treat underlying conditions Drugs -- Nitrates, b-blockers, calcium channel blockers Prevent thrombosis -- aspirin, platelet adhesion blockers
48
Treatment of MI
Diagnose+Increase oxygenation Aspirin Anti-arrythmics Reestablish bloodflow (Angiography, PCI, Fibrinolysis)
49
Fibrinolysis is most effective in...
the first 30 minutes