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Ischemic Heart Disease (CM) Flashcards

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1
Q

The leading cause of death in the US

A

Ischemic Heart Disease

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2
Q

Definition of myocardial ischemia

A

Angina Decreased coronary artery perfusion leading to demand of oxygen>supply

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3
Q

Definition of myocardial injury

A

Occurs with ongoing ischemia, may either reverse to myocardial ischemia, or progress to myocardial infarction

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4
Q

Definition of myocardial infarction

A

Irreversible cell death leading to impairment of electrical activity and contraction

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5
Q

Cause of IHD

A

atherosclerotic obstruction of coronary arteries

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6
Q

Modifiable risk factors for IHD

A

smoking HTN hypercholesterolemia diabetes

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7
Q

Non-modifiable risk factors for IHD

A

age FHx (first degree relatives) gender–being a male (females not until post-menopausal)

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8
Q

3 basic presentations of IHD

A

Stable angina (typical or Prinzmetal’s) Unstable angina Acute MI

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9
Q

Stable Angina characteristics

A

episodic chest pain, lasting minutes (5-15) that is often provoked by exertion/stress Relieved by rest/NTG Reversible ischemia

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10
Q

EKG and cardiac enzymes–stable angina

A

EKG findings: ST depressions +/- T wave inversion or flattening that return to normal after attack Cardiac enzymes: normal b/c no cell death

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11
Q

Prinzmetal’s Angina

A

“Variant angina” Occurs at rest, usually at the same time of day ST elevation during attack, returns to baseline after Caused by coronary artery spasm (1/3 have normal coronary arteries) Usually relieved by NTG, give CCB prophylactically

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12
Q

Unstable Angina

A

“crescendo angina or accelerated angina” a change in prior angina pattern 1. new onset of exertional angina 2. increased severity, frequency or duration of pain 3. more NTG to relieve pain 4. pain now comes at rest

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13
Q

Typical mechanism of unstable angina

A

Rupture of coronary artery plaque, leading to platelet aggregation and thrombosis

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14
Q

EKG findings of unstable angina

A

Similar to stable angina ST depression +/- T wave inversion/flattening that may persist for several hours before returning to normal May progress to MI

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15
Q

Cardiac enzyme findings of unstable angina

A

Possibly normal elevations

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16
Q

Prognosis of unstable angina

A

Can greatly improve chances of avoid MI and death by hospitalizing and treating agressively!!

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17
Q

Acute MI

A

Irreversible cell death

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18
Q

Acute MI EKG findings

A

ST elevation with evolving Q waves

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19
Q

Acute MI EKG cardiac enzymes

A

elevated

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20
Q

Acute Coronary Syndrome

A

encompasses the spectrum of presentations between unstable angina and acute MI

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21
Q

Components necessary to Dx IHD

A

History Physical exam EKG Cardiac Enzymes CXR Echo Radionuclide scan Coronary angiography

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22
Q

History

A

Single most important tool of chest pain evaluation

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23
Q

Typical CP in Angina/MI

A

Location: substernal or left sided Radiation: to neck, jaw, left or both arms Quality: heaviness, pressure, tightness, squeezing Not positional or pleuritic Often brought on by physical exertion/stress Relieved by rest/NTG

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24
Q

Associated symptoms of angina/MI CP

A

Anginal equivalents: SOB Diaphoresis Nausea Sometimes: dizziness, palpitations

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25
Populations that present atypically CP silent or atypical
Women Elderly Diabetics
26
IHD presentation in women
Less likely to have CP, more likely to have: Pain in back, neck or jaw Diaphoresis Nausea
27
Physical exam findings of MI
Can often be deceptively normal OR: Anxious, pale and diaphoretic May have inc'd HR and BP by inc'd sympathetic stimulation May have dec'd HR in inferior MI May have dec'd BP because myocardial damage New murmur may suggest papillary muscle rupture, ventricular septal rupture, or mitral regurgitation May see signs of congestive heart failure
28
Does a normal EKG rule out MI?
NO! Only 50% of MI's initially have class ST elevation Use in conjunction with H&P and serial cardiac enzymes to r/o
29
EKG changes in AMI
ST elevation Variable T wave changes Followed hours later by permanent Q waves Possible new bundle branch block Reciprocal changes (help r/o pericarditis)
30
Reciprocal changes in EKG
mirror image ST-T changes (usually ST depression) in leads distant to primary ST elevations
31
Classic EKG evolution in MI
Hyperacute T waves Giant R waves ST elevation Q waves
32
Hyperacute T waves
Tall, broad T waves that are transient and occur within minutes of interruption of blood flow
33
Giant R-waves
Form when R wave merges with elevating ST segment Last only minutes
34
ST elevation
classic sign of AMI-significant when \>1mm may persist hour to days before returning; occasionally indefinitely
35
Q waves
Significant when wider than one box, 1/3 the height of the QRS Develop 8-12 hrs after MI Can be normal in inferior leads in young men
36
Cardiac enzymes in MI
Rate of rise and peak is proportional to severity Normal serial enzymes r/o possibility of MI, but not underlying IHD
37
Myoglobin
Not specific because also in skeletal muscle Rises early: 1-2 hrs Normalize 1st day
38
CK-MB
Specific to cardiac muscle, not as widely used Earliest risk: 3-4 hrs Normalize 2nd day
39
Troponin
Sensitive and specific (most useful) Rise 3-6 hrs Normalize 7th day
40
Anterior leads
V1-V4
41
Inferior leads
II, III, aVF
42
Lateral leads
I, aVL, V5, V6
43
Artery obstructed in anterior MI
LAD
44
Artery obstructed in lateral MI
left circumflex
45
Artery obstructed in anterolateral MI
Main left coronary artery Widowmaker
46
Artery obstructed in inferior MI
90% right coronary 10% left circumflex
47
Artery obstructed in inferiolateral MI
Right coronary
48
Lateral MI
49
Anterior MI
50
Inferior MI
51
Complications of Acute MI
* Dysrhythmia * LV pump failure/cardiogenic shock * Papillary muscle insufficnecy * Ventricular septal rupture * cardiac rupture * thromboembolism * pericarditis * ventricular aneurysm * right ventricular infarction
52
Major cause of out of hospital mortality in context of MI
Dysrhythmia * Occurs in \>90% of AMI * Any arrhythmia possible * Sinus brady/tach * PVC's (Very common) * AV block * V. tach/V.fib (most lethal)
53
LV pump failure cause
Large anterior or anterolateral infarctions cause death of tissue
54
Signs of LV pump failure
dyspnea rales in lung bases hypoxemia hypotension
55
Cause of cardiogenic shock
massive anterior or anterolateral infarction that results in \>50% loss of myocardium
56
Clinical signs of cardiogenic shock
hypotension, tachycardia reduced urine output confusion cold extremities Mortality \>65%
57
Papillary muscle insufficiency
muscle becomes ischemic/infarcted and may rupture leads to mitral regurgitation (apical systolic murmur) Most commonly seen with inferior MI Dx with echocardiogram
58
Cardiac Rupture
Infarcted wall of heart ruptures, usually within 14 days of MI Sudden hypotension, pericardial tamponade, cardiac arrest 95% mortality
59
Thromboembolism
Decreased motion of myocardium may lead to thrombus formation that may embolize MC in large anterior MI Dx: echo
60
Pericarditis
inflammation adjacent ot area of infarction with classic friction rub
61
Ventricular aneurysm
May lead to arrhythmias or thrombus/embolus

Cardiology (12 decks)

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