Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology > Ischemic Heart Disease (CM) > Flashcards

Ischemic Heart Disease (CM) Flashcards

1
Q

The leading cause of death in the US

A

Ischemic Heart Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Definition of myocardial ischemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Definition of myocardial injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Definition of myocardial infarction

A

Irreversible cell death leading to impairment of electrical activity and contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cause of IHD

A

atherosclerotic obstruction of coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Modifiable risk factors for IHD

A

smoking HTN hypercholesterolemia diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Non-modifiable risk factors for IHD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

3 basic presentations of IHD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Typical mechanism of unstable angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cardiac enzyme findings of unstable angina

A

Possibly normal elevations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prognosis of unstable angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Acute MI

A

Irreversible cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acute MI EKG findings

A

ST elevation with evolving Q waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acute MI EKG cardiac enzymes

A

elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute Coronary Syndrome

A

encompasses the spectrum of presentations between unstable angina and acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Components necessary to Dx IHD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

History

A

Single most important tool of chest pain evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Associated symptoms of angina/MI CP

A

Anginal equivalents: SOB Diaphoresis Nausea Sometimes: dizziness, palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Populations that present atypically CP silent or atypical

A

Women Elderly Diabetics

26
Q

IHD presentation in women

A

Less likely to have CP, more likely to have: Pain in back, neck or jaw Diaphoresis Nausea

27
Q

Physical exam findings of MI

A

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
Q

Does a normal EKG rule out MI?

A

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
Q

EKG changes in AMI

A

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
Q

Reciprocal changes in EKG

A

mirror image ST-T changes (usually ST depression) in leads distant to primary ST elevations

31
Q

Classic EKG evolution in MI

A

Hyperacute T waves Giant R waves ST elevation Q waves

32
Q

Hyperacute T waves

A

Tall, broad T waves that are transient and occur within minutes of interruption of blood flow

33
Q

Giant R-waves

A

Form when R wave merges with elevating ST segment Last only minutes

34
Q

ST elevation

A

classic sign of AMI-significant when >1mm may persist hour to days before returning; occasionally indefinitely

35
Q

Q waves

A

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
Q

Cardiac enzymes in MI

A

Rate of rise and peak is proportional to severity Normal serial enzymes r/o possibility of MI, but not underlying IHD

37
Q

Myoglobin

A

Not specific because also in skeletal muscle Rises early: 1-2 hrs Normalize 1st day

38
Q

CK-MB

A

Specific to cardiac muscle, not as widely used Earliest risk: 3-4 hrs Normalize 2nd day

39
Q

Troponin

A

Sensitive and specific (most useful) Rise 3-6 hrs Normalize 7th day

40
Q

Anterior leads

A

V1-V4

41
Q

Inferior leads

A

II, III, aVF

42
Q

Lateral leads

A

I, aVL, V5, V6

43
Q

Artery obstructed in anterior MI

A

LAD

44
Q

Artery obstructed in lateral MI

A

left circumflex

45
Q

Artery obstructed in anterolateral MI

A

Main left coronary artery Widowmaker

46
Q

Artery obstructed in inferior MI

A

90% right coronary 10% left circumflex

47
Q

Artery obstructed in inferiolateral MI

A

Right coronary

48
Q
A

Lateral MI

49
Q
A

Anterior MI

50
Q
A

Inferior MI

51
Q

Complications of Acute MI

A
  • Dysrhythmia
  • LV pump failure/cardiogenic shock
  • Papillary muscle insufficnecy
  • Ventricular septal rupture
  • cardiac rupture
  • thromboembolism
  • pericarditis
  • ventricular aneurysm
  • right ventricular infarction
52
Q

Major cause of out of hospital mortality in context of MI

A

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
Q

LV pump failure cause

A

Large anterior or anterolateral infarctions cause death of tissue

54
Q

Signs of LV pump failure

A

dyspnea

rales in lung bases

hypoxemia

hypotension

55
Q

Cause of cardiogenic shock

A

massive anterior or anterolateral infarction that results in >50% loss of myocardium

56
Q

Clinical signs of cardiogenic shock

A

hypotension, tachycardia

reduced urine output

confusion

cold extremities

Mortality >65%

57
Q

Papillary muscle insufficiency

A

muscle becomes ischemic/infarcted and may rupture

leads to mitral regurgitation (apical systolic murmur)

Most commonly seen with inferior MI

Dx with echocardiogram

58
Q

Cardiac Rupture

A

Infarcted wall of heart ruptures, usually within 14 days of MI

Sudden hypotension, pericardial tamponade, cardiac arrest

95% mortality

59
Q

Thromboembolism

A

Decreased motion of myocardium may lead to thrombus formation that may embolize

MC in large anterior MI

Dx: echo

60
Q

Pericarditis

A

inflammation adjacent ot area of infarction with classic friction rub

61
Q

Ventricular aneurysm

A

May lead to arrhythmias or thrombus/embolus

Cardiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions