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CRAAB- Golijan Heart Disorders > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What is ischemic heart disease?

A

Imbalance in demand of 02 and supply

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2
Q

How does tachycardia lead to ischemia?

A

Tachycardia (>180bpm)>decreased filling time of coronary arteries>ischemia

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3
Q

What does the LAD supply?

A

Anterior portion of LVAnterrior 2/3 IVSApex

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4
Q

What is the most common site for coronary artery thrombosis?

A

LAD

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5
Q

What does the RCA supply?

A

Posterior LVposterior 1/3 IVSRVposteromedial papillary muscleSA/AV nodes

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6
Q

What percent of coronary artery thromboses occur in the RCA?

A

30-40%

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7
Q

What does the LCA supply?

A

Lateral wall of the left ventricle15-20% coroanry thrmboses

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8
Q

What is the most common cause of death in the US?

A

IHDIncidence peaks in mean after 60 and women after 70

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9
Q

What are the risk factors for IHD?

A

Age (M>45, W >55)Family hx of premature CAD or strokeLipid abnormatlitiesSmokingHTNDiabetes

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10
Q

Angina pectoris is most commonly observed in what population?

A

Middle aged/elderly malesWomen after menopause

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11
Q

What is stable angina? Common Sxs? EKG? Tx?

A
  1. Exercise induces substernal chest pain lasting >30 mins2. SOB, diaphoresis, numbness, pain in arm/shoulder/jaw3. Subendocardial ischemia> ST segment DEPRESSION> 1 mm4. Nitroglycerin
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12
Q

What causes stable angina?

A

Atherosclerosis of coronary artery >70%>subendocardial ischmeia d/t decreased coronary blood flow (concentric hypertrophy)

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13
Q

What is prinzmetal varian angina?

A

Vasospasm with TRANSMURAL ischemia > ST ELEVATION

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14
Q

What is unstable angina?

A

Angina at RESTMultivessel atherosclerosis>Disrupted plaques>Frequent bouts of chest pain w/ minimal exertion

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15
Q

What is worrisome about unstable angina?

A

It can progress to MI

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16
Q

What diagnostic tests can be done to work up chest pain?

A
  1. Resting EKG2. Exercise test with ECG monitoring3. Stress echocardiography4. Coronary angiography
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17
Q

How do you commonly treat Prinzmetal angina?

A

Ca channel blockers> vasodilate arteries

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18
Q

What is the common pharmacological therapy for angina?

A
  1. Nitrates (decrease preload and afterload through vaso/venodilation)2. B blockers (decrease O2 consumption, decrease HR)3. Aspirin- decreases platelet aggregation/thrombus4. Clopidogrel- used if pt allergic to aspirin
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19
Q

What treatment is often used for pts with unstable angina?

A

Heparin plus aspirin–> decreases risk of developing MI

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20
Q

What is chronic IHD?

A

long term ischemid damge to myocardium>Muscle replaced by noncontractile fibrous tissue>progressive CHF

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21
Q

What is Sudden Cardiac death?

A

Unexpected death from cardiac cause in persons w/out symptomatic heart disease or w/in 1 hour of onset of sxs

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22
Q

What are the risk factors for SCD?

A
  1. IHD**2. Obesity diabeties, hyperlipidemia, LVH, HTN, smoking, recent NSTEMI
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23
Q

What does SCD most commonly occure?

A

morning hrs 8-11 am and late afternoon 4-7 pm

24
Q

What are non coronary artery causes of SCD syndrome?

A
  1. Cardiomyopathy2. AV stenosis3. Mitral valve prolapse, cocaine, myocarditis, WPW
25
Q

What are causes of SCD in children?

A

AV stenosisCardiomyopathiesWPW

26
Q

What is the most common cause of death in adults in the US?

27
Q

What is the pathogenesis of MI?

A

Rupture of disrupted plaque>exposure subendothelial collagen>platelet thrombosis>MI

28
Q

What are less common causes of MI?

A
  1. Vasculatis (polyarteris nodosa, kawasaki disease)2. Cocain use3. Embolization of plaque from aorta or CA4. Thrombosis syndromes5. Dissection of blood into into wall of CA
29
Q

What are the two types of MI?

A

STEMINSTEMI

30
Q

What is a STEMI? Depth of heart involved? What is seen on EKG?

A

ST segment elevation MIFULL thickness myocardium involvedNew Q waves on ECG

31
Q

What is a NSTEMI? Depth of heart involved? ECG?

A

Inner third of myocardium (subendocardium) involvedQ waves are absent

32
Q

What are the benefits of reperfusion following MI?

A

Previously ischemic cells are salvagedCells irreversibly damaged are destroyedLIMITS the size of infarction

33
Q

What is reperfusion injury following MI?

A

Ischemic myocardial cells not already irreversibly damaged become so after reperfusion

34
Q

How does the timing of reperfusion affect the extent of myocardial damage?

A

cell death> contraction bands>3 hrsGreater chance of reperfusion injury (previously ischemic cells are irreversibly damaged)

35
Q

What is the mechanism of irreversible myocardial injury?

A
  1. Superoxide free radicals FRs2. Neutrophils (occlude BVs and decrease blood flow, and increase production of ROS)
36
Q

What type of necrosis is seen in the heart within 24 horus?

A

Coagulation necrosis

37
Q

Following MI, when is the heart the softest and most in danger of rupturing?

A

3-7 days after MI

38
Q

A pt presents with retrosternal pain >30 mins, radiating to the left arm/shoulder and is diaphoretic. What do you expect?

39
Q

What nerves supply the heart?

40
Q

Inner arm pain is associated with what nerve?

41
Q

Epigastrum (upper/central region of abdomen) radiation is associated with what nerves?

42
Q

When do silent MIs occur?

A

20% of casesUsually in elderly and individulas with diabetes who frequently have neuropathies and can’t feel pain.

43
Q

Do STEMI or NSTEMI have increased early mortality rate?

44
Q

What complications commonly follow STEMIS?

A
  1. Cardiogenic shock2. Arrythmias (PVS or v. fib> death)3. CHF (w/in 24 hrs)4. Rupture (3-7 days)5. Mural thrombosis6. Fibrous pericarditis7. Ventricular aneurysm8. Right ventricular AMI
45
Q

What is associated with mural thrombosis?

A

Danger of embolization

46
Q

What is fibrinous pericarditis?

A

Occurs w/in 1-7 days of a STEMI-Substernal chest pain that is relieved when pt leans forward-Precordial friction rub present on asucultation

47
Q

What is autoimmune pericarditis (Dressler syndrome)?

A

Occurs 1-8 wks after a STEMIAutoantibodies are directed against the damaged pericardial antigens (type II hypersensitivityFever and precordial friction rub present

48
Q

When is a ventricular aneurysm recognized after a STEMI?

A

4-8 weeks after, but begins to develop during the first 48 hrs

49
Q

What is a ventricular aneurysm?

A

Precordial bulge during systole

50
Q

What is the gold standard for diagnosing Acute MI?

A

Troponinappear within 3-12 hrs and peak at 24 dissappear within

51
Q

What is CK-MB used for?

A

Detect reinfarction

52
Q

What ECG findings do you expect to see on a STEMI?

A

Inverted T waves (areas of ischemia at periphery of infarct)Elevated ST waves (injured myocardial cells around areas of necrosis)New Q waves (coagulation necrosis)

53
Q

Q waves in V1-V2

A

LAD anterior wall infarctionAnterioseptal infarction

54
Q

Q waves in leads V4-V6, I, aVL

A

Anterolateral infarction d/t mid LAD or circumflex artery occlusion

55
Q

Q waves in I, aVL

A

Lateral wall infarction d/t left circumflex

56
Q

Q waves in II, III, aVR

A

Inferior wall infarction d/t RCA occlusion

CRAAB- Golijan Heart Disorders (9 decks)

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