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Cardiology > ACS 1 > Flashcards

ACS 1 Flashcards

1
Q

What are some of the endogenous anti-thrombotics that prevent spontaneous thrombosis and arterial occlusion?

A
  • Antithrombin 3: Plasma protein that binds irreversible to thrombin and other clotting factors; increased effectiveness with heparin
  • Protein C and S- Degrades factors Va and VIIIa
  • Tissue factor pathway inhibitor: Plasma serine protease inhibitor activated by factor Xa; inhibits coagulation via the extrinsic pathway
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2
Q

What are other endogenous factors involved in ACS?

A
  • TPA: Secreted by endothelial cells; cleaves plasminogen to form plasmin, which degrades fibrin clots
  • Prostacyclin: Secreted by endothelial cells; increases platelet levels of cAMP and thus inhibits platelet activation/aggregation; also a vasodilator
  • Nitric oxide- Secreted by endothelial cells; acts locally to inhibit platelet activation; potent vasodilator
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3
Q

What are some characteristics of Acute MI?

A
  • Discrete focus of ischemic necrosis in the heart
  • Development related to duration of ischemia and metabolic rate of ischemic tissue
  • 20-30 minutes of ischemia can cause infarct
  • Frequently result of acute plaque change with coronary artery thrombosis
  • Dissolution of thrombus frequent within 12-24 hrs
  • Infarcts involve LV more commonly and extensively than RV
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4
Q

What is a transmural infarct?

A

Spans the entire thckness of myocardium; due to prolonged, total occlusion of an epicardial coronary artery (LAD, LCx, RCA or one of the major branches)

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5
Q

What is a subendocardial infarct?

A

Involves only the innermost layers of the myocardium (most susceptible to ischemia due to poor collateral flow, adjacent to high pressure ventricle, furthest from epicardial coronaries)

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6
Q

The amount of tissue that succumbs to infarction depends on?

A
  • Mass of myocardium perfused by coronary artery
  • Magnitude and duration of ischemia
  • Oxygen demand of affected area
  • Adequacy of collateral coronary flow (collateral flow is supplied by other coronaries)
  • Degree of reperfusion and inflammatory response
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7
Q

The LAD supplies which portions of the heart?

A
  • Anterior LV
  • Anterior 2/3 septum
  • Apical LV
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8
Q

The LCx supplies which portions of the heart?

A
  • Lateral LV

- Posterolateral LV

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9
Q

The RCA supplies which portions of the heart?

A
  • Posterior LV
  • Posterior 1/3 septum
  • Posterior papillary muscle
  • Inferior or diaphragmatic
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10
Q

What are some of the early changes that occur during an MI?

A
  • Rapid shift from aerobic to anaerobic metabolism (lactic acid accumulates)
  • Reduction in ATP
  • Rising Na+ leading to cellular edema
  • Abnormal electrolyte/ion shifts increasing arrhythmia risk (Vtach, vfib)

Irreversible cell injury ensures in 20 min

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11
Q

What are the macroscopic features that occur less than 4 hours after infarction?

A

No abnormalities

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12
Q

What are the macroscopic features that occur at 4-12 hours after infarction?

A

Occasional dark mottling

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13
Q

What are the macroscopic features that occur at 12-24hours after infarction?

A

Dark mottling

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14
Q

What are the macroscopic features that occur at 1-3 days after infarction?

A

Mottling with developing yellow-tan necrotic center

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15
Q

What are the macroscopic features that occur at 3-14 days after infarction?

A

Maximally yellow-tan and soft, depressed red-tan borders

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16
Q

What are the macroscopic features that occur at 2-8 weeks after infarction?

A

Gray-white scar, progressive from border to core of infarct

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17
Q

What are the macroscopic features that occur at greater than 2 months after infarction?

A

Mature scar

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18
Q

What are the MICROroscopic features that occur less than 4 hours after infarction?

A

None, variable wavy fibers at border

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19
Q

What are the MICROroscopic features that occur at 4-12 hours after infarction?

A

Early coagulative necrosis, edema, hemorrhage, wavy fibers

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20
Q

What are the MICROroscopic features that occur at 12-24 hours after infarction?

A

Coagulative necrosis, nuclear pyknosis, hypereosinophilia, contraction band necrosis, early PMNs

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21
Q

What are the MICROroscopic features that occur at 1-3 days after infarction?

A

Extensive coagulative necrosis with loss of nuclei and striations, interstitial PMNs

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22
Q

What are the MICROroscopic features that occur at 3-14 days after infarction?

A

Early disintegration of dead myocytes, dying PMNs, macrophages and granulation tissue at border

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23
Q

What are the MICROroscopic features that occur at 2-8 weeks after infarction?

A

Gradual loss of cellularity, increasing collagen

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24
Q

What are the MICROroscopic features that occur greater than 2 months after infarction?

A

Dense collagenous scar

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25
Q

What are some of the impaired systolic changes that occur with MI?

A

Hypokinesis: Local region with reduced contraction
Akinesis: Local region with no contraction
Dyskinesis: Local region that bulges outward with contraction

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26
Q

What are some of the impaired relaxation/diastolic changes that occur with MI?

A

Reduced compliance and elevated ventricular filling pressures

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27
Q

What is stunned myocardium?

A

A functional change from an MI where there is a reversible period of contractile dysfunction. This takes days to weeks to recover

28
Q

What is ischemic preconditioning?

A

Brief ischemia that renders tissue perhaps more resistant to future episodes of ischemia. MI following recent anginal episodes- less morbidity and mortality?

29
Q

What are some of the ventricular remodeling changes that occur after MI?

A
  • Changes to the geometry of the infarcted AND noninfarcted myocardium; ventricular dilatation
  • Infarct expansion, myocyte side-to-side slippage
  • Mechanically disadvantageous
  • Increased wall stress
30
Q

What are some MI complications?

A
  • Arrythmias (account for 50% of deaths)
  • LV failure, cardiogenic shock (infarct involves>40% LV, up to 90% mortality, high grade stenosis of coronary vessels)
  • Extension of infarct (apparent in up to 10 of patients during 1st 2 weeks, significant extension twofold increased mortality)
  • Myocardial free wall rupture
  • Septal perforation (left to right shunt)
  • Paillary muscle rupture (Mitral regurg, Massive MV incompetence)
  • Aneurysm
  • Mural thrombosis
31
Q

What are some characteristics of Myocardial free wall rupture?

A
  • occurs during first 3 weeks
  • Most common days 1-4 when wall is weakest
  • Complication of large infarcts (>20% of LV)
  • Occur at junction of infarct and normal muscle
  • Hemoperricardium and death from tamponade
  • 10% deaths from AMI in hospitalized patients
32
Q

What are some characteristics of aneurysm after MI?

A
  • After transmural AMI, wall bulges outward during systole
  • As infarct matures, fibrous scar progressively stretches
  • Increased risk for myocardial rupture
  • predisposes to mural thrombosis
  • Increases workload
33
Q

What are some characteristics of mural thrombosis?

A
  • Seen in almost 50% of fatal AMI
  • Especially after apical infarcts
  • Predisposes to systemic embolization
34
Q

What are MI symptoms?

A
  • Chest pain-persistent, substernal
  • nausea, vomitting, weakness (parasympathetic vagal effect)
  • Diaphoresis, cool/clammy skin (sympathetic)
  • Fever (inflammatory response)
  • SOB
35
Q

What are symptoms of MI during “typical chest pain” (increases liklihood

A
  • radiation to arm or shoulder
  • radiation to both arms or shoulders
  • associated with exertion
  • associated with diaphoresis
  • associated with nausea or vomitting
  • Worse than previous angina or similar to previous MI
  • Described as pressure
36
Q

What are symptoms of MI during “atypical chest pain” (decreases liklihood of AMI)

A
  • Described as pleuritic
  • Described as positional
  • Described as sharp
  • Reproducible with palpation
  • Inframammary location
  • Not associated with exertion
37
Q

DDX for chest pain?

A

Cardiac: ischemia, pericarditis
Pulmonary: Pneumonia, Pleurisy, PE
MSK: COstochondritis, cervical radiculitis
GI: GERD, esophageal spasm, peptic ulcer disease, biliary colic

38
Q

What is included in the physical exam for an MI?

A
  • Airway, breathing, circulation
  • Evidence of systemic hypoperfusion (hypotension, tachycardia, impaired cognition, cool extremities, end-organ injury)
  • Evidence of heart failure (Elevated JVP, pulmonary crackles, Gallops-S3, S4, New murmurs)
39
Q

What are EKG abnormalities in in myocardial schemia?

A
  • New ST Segment elevation >/= 1mm (in setting of chest pain)
  • New ST-segment depression
  • New T-wave inversion
40
Q

What are high risk MI features?

A
  • Increased age
  • Low BP
  • Elevated HR
  • HF
  • Anterior location
41
Q

Defining an MI includes what criteria?

A
  • Detection of a rise/and/or fall of hs cardiac troponin with at least one value above the 99th upper reference limit
    AND ONE OF THE FOLLOWING:
  • Symptoms of acute ischemia
  • ECG: New (or presumed new) ST-T changes or LBBB; pathological Q waves
  • Imaging: New loss of viable myocardium or regional wall motion abnormality
  • Angiography or autopsy: Identification of an intracoronary thrombus
42
Q

94-97% of troponins are located where?

A

Myofibrils

43
Q

6-8% of troponins are?

A

cTNT

44
Q

3-4% of troponins are?

A

cTnI in cytosol

45
Q

Troponins are released during?

A

Cell death (necrosis or injury)

46
Q

What is the criteria for diagnosis of MI using CK-MB (NOTE: CK-MB no longer used clinically for diagnosis but might appear on step 1)

A

CK-MB>upper limit of normal and >2.5% of total CK

47
Q

where is CK-MM (CK-3) located?

A

skeletal muscle, cardiac, thyroid, and lung

48
Q

Where is CK-MB (CK-2) located?

A

Cardiac tissue, skeletal muscle, stomach, small intestine, prostate, uterus (Non-cardiac increases: CO poisoning, malignant hyperthermia, muscular dystrophies, some malignancies)

49
Q

Where is CK-BB (CK-1) located?

A

Brain, colon, intestine, stomach, uterus, thyroid

50
Q

What are some noncardiac causes of Tn elevation?

A
  • Acute heart failure
  • PE
  • Shock
  • Aortic dissection
  • Myocarditis
  • Trauma
  • ICD Discharge
51
Q

Criteria for ST-elevation MI

A
  • Presence of >1mm ST-segment elevation in at least 2 anatomically contiguous leads, or >2mm ST-segment elevation in 2 contiguous precordial leads
    OR
  • New left bundle branch block
52
Q

Contiguous leads II, III, aVF correspond to what anatomic location and coronary artery?

A

Inferior; RCA»LCx

53
Q

Contiguous leads V2-V4 correspond to what anatomic location and coronary artery?

A

Anterior; LAD

54
Q

Contiguous leads V1-V4 correspond to what anatomic location and coronary artery?

A

Anteroseptal; LAD

55
Q

Contiguous leads 1, aVL, V5, V6 correspond to what anatomic location and coronary artery?

A

LCx>LAD

56
Q

LBBB corresponds to what anatomic location and what coronary artery?

A

Anterior; LAD

57
Q

Lead V4R corresponds to what anatomic location and what coronary artery?

A

Right ventricle; RCA

58
Q

Leads V1, V2 with ST depressions correspond to what anatomic location and what coronary artery?

A

RCA»LCx

59
Q

Electrically silent leads correspond to what coronary artery??

A

LCx

60
Q

Pathologic Q waves are indicative of?

A

Prior transmural (ST elevation) MI

61
Q

What are the diagnostic criteria for pathologic Q waves?

A
  • Q wave should be >/= 1mm wide
  • Q wave should be >25% of overall amplitude of QRS complex
  • Pathologic Q wave should be present in >/= 2 contiguous leads
62
Q

What is variant (prinzmetal) angina?

A

A focal coronary artery spasm in the absence of atherosclerotic lesions, that presents with CP and transient ST elevations >5-15 min in duration. Smooth muscle hyperractivity and endothelial dysfunction. Smoking increases risk

63
Q

How do you diagnose variant (prinzmetal) angina?

A

Intracoronary acetylcholine provokes spasm (cardiac cath required)

64
Q

How do you treat variant (prinzmetal) angina?

A

nitrates, CCBs

65
Q

Who tend to have higher mortality, pts with ST elevation or NSTEMI?

A

NSTEMI

66
Q

What are the risk stratification criteria in NSTEMI and UA (TIMI RISK SCORE 1 pt each?)

A
  • Age>/= 65 years
  • Known CAD (coronary stenosis >/=50%)
  • > /= 3 risk factors for CAD
  • ASA use within the past 7 days
  • > /= 2 episodes of angina within the past 24 hours
  • ST changes >/= 0.5mm
  • Elevated cardiac markers
67
Q

Other causes of ACS?

A
  • Decreased myocardial oxygen supply (Decreased perfusion pressure due to hypotension i.e. septic shock. Severely decreased blood oxygen content such as marked anemia. Coronary artery dissection or emboli
  • Increase in myocardial oxygen demand (rapid rachhyarrhythmias, acute hypertension, severe aortic stenosis)

Cardiology (18 decks)

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