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Cardiovascular II Final Exam > MI--STEMI, nonSTEMI, pharm of MI (Johnston) > Flashcards

MI--STEMI, nonSTEMI, pharm of MI (Johnston) Flashcards

1
Q

Cardinal symptoms of cardiovascular disease

A
  • Chest pain or discomfort
  • Dyspnea, orthopnea, paroxysmal, nocturnal dyspnea, wheezing
  • Cough, hemoptysis
  • Pain in extremities with exertion (claudication)
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2
Q

ST elevation AMI ECG changes and characteristics of AMI

A
  • ST segment elevation
  • “transmural”
  • Complete interruption of blood flow (coronary occlusion usually due to thrombus)
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3
Q

Pathobiology of AMI

A
  • Erosion, fissuring or rupture of plaque; thrombus (platelet, fibrin rich thrombus is generated)
  • If coronary flow is occluded–STEMI
  • If partial occlusion- Unstable angina or NSTEMI
  • Most MI caused by atherosclerosis; other causes include vasospasm, vasculitis, dissection, genetics
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4
Q

Typical history of patient with MI

A
  • Chest discomfort (more severe than angina)
  • Heavy, pressure, crushing, etc
  • Retrosternal, left, across chest; neck, jaw, left arm, epigastrium
  • Nausea, vomiting, diaphoresis, dyspnea
  • Not reliably relieved by Nitro or rest
  • 20% AMI are painless (silent); diabetics elderly woman
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5
Q

Physical Exam findings

A
  • Normal
  • S4 gallop–atria contracting forcefully against less compliant, stiff ventricle
  • BP variable
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6
Q 
Sympathetic hyperactivity (increased HR, increased BP) seen in?
Parasympathetic hyperactivity (Bradycardia, decreased BP) seen in?
A
  • Sympathetic=ANTERIOR MI

- Parasympathetic= INFERIOR MI

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7
Q

Heart Failure PE findings

A
  • S3!!!
  • Crackles
  • Increased JVD
  • New murmur
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8
Q

ECG role in MI

A

-Critical role in stratification, triage, management

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9
Q

STEMI in men vs women

A
  • men: ST elevation of 2mm or more at J point in V2-V3

- women: ST elevation of 1.5 mm or more in absence of LVH or 1 mm or more or in 2 or more contiguous chest or limb leads

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10
Q

Also see what in STEMI ECG?

A

-New LBBB (obscures ST elevation analysis)

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11
Q

NSTEMI vs Unstable Angina (NSTE ACS) on ECG

A

-NSTEMI: ST segment depression, T wave inversion
-NSTE ACS: ST segment depression, T wave inversion
so doesn’t help distinguish; key is cardiac enzymes!!

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12
Q

NSTEMI vs Unstable Angina (NSTE ACS) symptoms and cardiac enzymes

A
  • NSTEMI: Chest pain, elevated cardiac enzymes

- NSTE ACS: Chest pain, normal cardiac enzymes

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13
Q

ECG evolution of MI–Early acute phase

A
  • T wave increase amplitude
  • Hyper-acute pattern
  • Convex upward ST pattern
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14
Q

What are other causes of ST segment elevation?

A
  • Pericarditis–but you will see ST elevation in multiple leads and you won’t see reciprocal depression
  • LV aneurysms with J point elevation–ST elevation that does not resolve for weeks–often associated with ANTERIOR WALL infarction
  • African Americans have normally elevated ST segments indicating early ventricular depolarizations–this is normal
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15
Q

ECG evolution of MI: Elevated Acute phase–Chronic phase

A
  • Resolution of ST elevation is variable (2 weeks inferior wall; later anterior wall)
  • Persistent ST elevation (after 2 weeks) think ventricular aneurysm!!!
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16
Q

QRS complex indicates what? Normal duration? Normal width?

A
  • Ventricular depolarization
  • 0.05-0.10 sec duration
  • Q waves should not be found more than 0.03 sec in width
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17
Q

Narrow small q waves (1-2 mm) is normal in what leads?

A

-1, AVL, AVF, V5 and V6

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18
Q

Normal and abnormal morphology of the ST segment

A
  • Observe the level relative to baseline (elevated or depressed) and shape
  • Normally ISOELECTRIC
  • Sometimes normally elevated not more than 1 mm in standard chest leads
  • NEVER normally depressed more than 0.5 mm
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19
Q

ST depression indicates

ST elevation indicates

A
  • depression=Sub endocardial

- ST elevation=sub epicardial or transmural injury or ischemia

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20
Q

T wave is a marker for

A

ischemia

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21
Q

Normal T wave indicates? Upright in what leads? inverted in which leads? normal morphology/shape?

A
  • indicates ventricular Repolarization
  • Upright in 1, 2, V3-V6
  • Inverted in AVR
  • Variable in 3, AVL, AVF, V1-V2
  • Shape: slightly rounded and asymmetrical/height–not greater than 5 mm in standard leads not greater than 10 mm in precordial leads
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22
Q

QT duration reflects

A

-Ventricular systole!

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23
Q

Ischemia–T wave pattern

A

-inverted T waves and tall, peaked T waves

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24
Q

Pattern of injury is determined by?

Pattern of necrosis is determined by?

A
  • Pattern of injury determined by ST elevation

- Pattern of necrosis or infarction determined by Q wave or QS complex

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25
Q

In precordial leads V1-V3 what happens to the R wave?

A
  • normally should get larger until it reaches an isoelectric point where positive deflection equals negative deflection
  • called transition zone ( between V3 and V4?)
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26
Q

Infarction is? Indicated by what on ECG

A
  • Dead tissue
  • Lacks depolarization
  • Seen by changes in Q WAVES!
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27
Q

Myocardial injury is? indicated by what on ECG?

A
  • Deficient blood supply
  • Inability to fully polarize
  • ST segment shifts
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28
Q

Ischemia is? Indicated by what on ECG?

A
  • Deficient blood supply
  • Impaired repolarization
  • T wave changes!
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29
Q

LAD associated with

A
  • ANterior wall infarction

- Leads V1-V7

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30
Q

RCA associated with

A
  • Inferior wall infarction (RV infarction)
  • II, III and AVF
  • V3R-V6R
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31
Q

Circumflex artery associated with

A

Lateral wall
-I, AVL
V5-V6

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32
Q

Posterior descending artery

A
  • Posterior wall infarction

- V1-V3

33
Q

Indicative vs reciprocal changes

A
  • Indicative changes happens on the side where changes are taking place (example LV)
  • Reciprocal changes happens on the opposite side of where change is taking place (RV)
34
Q

Ischemia changes

A
  • Inversion of T wave due to altered repolarization
  • reciprocal changes on opposite side (upright T waves)
  • Muscle injury causes elevation of ST segment; on opposite side see ST depression
  • Death (infarction) of muscle causes Q or QS waves due to absence of depolarization current from dead tissue and opposite currents from other parts of heart
35
Q

During recovery from ischemia (subacute and chronic stages)–what ECG changes are seen?

A

-S-T segment often is first to return normal, then T wave, due to disappearance of zones of injury and ischemia

36
Q

Typically the q wave/ qs complex should not be greater than

A

1/3 of the whole qrs complex

-if its greater, its pathological

37
Q

Chronic ischemia (from Old MI) indicated by

A

-DEEP QS complexes

38
Q

Onset and first several hours of transmural infarction

A
  • Subendocardial injury and myocardial ischemia
  • No cell death yet
  • R wave is normal or nearly normal
  • Peaked T wave
  • ST segment elevated
39
Q

First day after transmural infarction

A
  • Ischemia and injury extend to epicardial surface; subendocardial muscle dying in area of most severe injury
  • R wave amplitude diminishing
  • ST elevation more marked
40
Q

First and second days of transmural infarction

A
  • Transmural infarction nearly complete
  • Some ischemia and injury may be present at borders
  • R wave gone or nearly gone
  • Significant Q wave
  • ST elevation may decrease
  • T wave inversion beginning
41
Q

After 2-3 days of transmural infarction

A
  • Transmural infarction complete
  • No R wave
  • Marked Q wave
  • ST may be at baseline
  • Deep T wave inversion
42
Q

After several weeks or months of transmural infarction

A
  • Infarcted tissue replaced by fibrous scar, sometimes bulging (ventricular aneurysm)
  • Some R wave may return
  • Significant Q wave usually persists
  • T wave often less inverted
  • ST elevation may persist if aneurysm develops
43
Q

With inferior infarction (leads II, III, AVF) you see reciprocal changes in which leads?

A
  • Laterally

- I, AVL

44
Q

Tall, broad, peaked T waves in precordial leads indicates

A
  • ischemic pattern
  • Most likely LAD (V1-V6)
  • Marker for person ready to have STEMI
  • Anterior wall infarction
45
Q

Lost r wave voltage, and Large QS voltage and inverted T waves

A

-Progression into myocardial necrosis

46
Q

Persistent ST segment elevation after weeks after having MI think_____

A

-ventricular aneurysm

47
Q

Posterior wall infarction

A
  • IF we know posterior wall is infarcted inscribing a q wave in that area, the reciprocal change of a q wave (which is down) will be a positive strong R wave (which will be up) and see these in V1 and V2
  • Reciprocal changes of ST segments that shows current of injury posteriorly, we would see anteriorly as ST segment depression
  • must really have index of suspicion for posterior wall infarction
48
Q

To diagnose posterior wall infarction, need to look at what leads?

A
  • V1 and V2 and look for reciprocal changes
  • Since no leads reflect posterior electrical faces, changes are reciprocal of those in anterior leads
  • V1 shows unusually large R wave (reciprocal of posterior Q wave) and upright T wave (reciprocal of posterior T wave inversion)
49
Q

First few hours after SUBendocardial infarction (NONSTEMI)

A
  • subendocaridal muscle ischemic and injured but not dead
  • ST depressed or elevated
  • T wave inversion
50
Q

Lab findings associated with MI

A
  • Increased WBC
  • Increased CRP
  • BNP is increased in ventricular wall stress and fluid overload
51
Q

Cardiac biomarkers of necrosis–when detected and when peak?

A
  • Troponin I (cTnI) or T(cTnT)
  • 1-4 hours detectable after onset AMI
  • 10-24 hours peak
  • Persist 5-14 days
52
Q

What can cause false positive cTnT?

A

-Renal failure

53
Q

What are non-myocardial infarction causes and elevated troponin levels? Heart causes:

A
  • Myocardial injury: cardiac contusion, surgery, ablation, shocks
  • Myocardial inflammation: myocarditis, pericarditis
  • Heart failure
  • Cardiomyopathies: infiltrative, stress, hypertensive, hypertrophic
  • Aortic dissection
  • Severe aortic stenosis
  • Tachycardia
54
Q

elevated troponin levels–pulmonary causes

A
  • Pulmonary Embolism
  • Pulmonary hypertension
  • Respiratory failure
55
Q

Neurologic causes of elevated troponin levels

Other causes

A
  • Stroke
  • Intracranial hemorrhage

-Other causes: shock (septic, hypovolemic, cardiogeninc), Renal failure

56
Q

Majority of deaths from AMI happen when and how?

A
  • occur within 1 hour of onset of symptoms
  • Most deaths related to V. Fib
  • Greatest time lag to repercussion therapy is patients delay in calling for help
57
Q

E.D standard of care–STEMI

A
  • 12 lead ECG with continuous cardiac monitoring
  • IV lines inserted
  • Cardiac enzymes (cTnI), CBC, CMP, PT, PTT
58
Q

Repercussion strategy choices

A
  • Primary percutaneous coronary intervention with angioplasty and stunting
  • Cath lab within 90 minutes (goal)
  • Fibrinolysis: fibrinolytic or thrombolytic
  • Begun in ED within 30 min
59
Q

Dangers of fibrinolytic agents

A

-Bleeding

60
Q

Reperfusion therapy

A
  • Accelerates changes over minutes to hours
  • Failure of ST elevation to resolve by >50-70% within 1-2 hours, suggests failure of fibrinolysis
  • If hospital doesn’t have cath lab (non PCI capable), transfer within 120 min
61
Q

Primary PCI preferred for

A
  • STEMI with symptoms <12 hours

- Lower mortality and ICH (intracerebral hemorrhage)

62
Q

Fibrinolytic therapy useful for

A
  • Useful for STEM or new left BBB within 12 hours of onset of symptoms
  • Major risk is ICH (0.5-1.0%)
63
Q

Absolute contraindication for fibrinolytic therapy

A
  • Active bleeding or bleeding diathesis (menses EXcluded)
  • Prior hemorrhagic stroke, ischemic stroke within 3 months, except acute ischemic stroke within 3-4.5 hours
  • Intracranial or spinal cord neoplasm or AV malformation
  • Suspected or known aortic dissection
  • Closed head or facial trauma within 3 months
64
Q

Initial medical management STEMI

A

-ASA (162-325mg) po–given on presentation unless contraindicated

65
Q

IV heparin or exoxaparin

A
  • Adenosine diphosphate receptor (p2Y12) inhibitor
  • Antiplatelet agent (clopidogrel prasugrel or ticagrelor)
  • Use for 1 year after PC1 for STEMI with stenting to prevent stent stenosis
66
Q

Treatment for STEMI–meds and uses

A
  • Nitro: relieve vasoconstriction, relieve pain, reduce pre and after load
  • Morphine: persistent pain
  • Beta blocker: esp if BP increase or HR increases; DONT use in decompensated HF, decreased HR, decreased BP or MCO2
  • Oxygen
  • Stool softener
  • ACEI helpful in EF is reduced, increased BP; prevent remodeling statin
  • Coronary ICU–AHA diet
67
Q

Beta blocker contraindicated in which kind of heart block?

A

-greater than 1st degree

68
Q

Complications of MI and treatment

A
  • Recurrent chest pain after MI
  • Acute pericarditis–2 to 4 days post MI
  • 2-10 weeks after MI could be Dressler syndrome (immune mediated)–hurts to breathe, feels better learning forward
  • Tx: ASA and NSAID
69
Q

rhythm disturbances associated with MI

A

-Ventricular: occur early–
-VF (3-5% in 1st 4 hours)–Tx is elective cardioversion
-VT
-VT (polymorphic VT)—some are going up and some down on ECG bc coming from different foci
VF
-Afib– 5-10% in 1st 24 hrs
-Sinus bradycardia–inferior MI
-2nd degree AV block (Wenkebach)–inferior MI

70
Q

Accelerated idioventricular rhythm (AIVR)–rate and see when?

A
  • Show VT (60-100 BPM)
  • After fibrinolytic therapy
  • Benign
71
Q

Leading cause of in hospital death from AMI

A

-Heart failure

72
Q

Heart failure PE findings

A
  • LV dysfunction–S3 and S4, crackles
  • RV infarction–10-15% of inferior STEMI–decreased BP, clear lungs, increased JVP, Kussmaul sign, treat with IV fluids
  • Cardiogenic shock–decreased BP, decreased CI
  • Increased PCWP>18 mm Hq
  • Mortality 70-80
73
Q

Mechanical complications associated with MI

A
  • Acute mitral valve regurg–infarction related rupture or dysfunction of papillary muscle
  • New holosystolic murmur associated with inferior wall MI
  • Rx=surgery
74
Q

Septal rupture with VSD associated with

A
  • ANterior wall infarction
  • LV free wall rupture causes tamponade

LV aneurysm associated with Anterior MI
-Rx=surgery

75
Q

Thromboembolic complications with AMI

A
  • Arterial emboli from LV aneurysm

- Cause stroke, ischemic bowel

76
Q

RV infarction

A
  • Proximal occlusion of RCa before acute marginal branch; can cause acute inferior wall MI in 30% of cases
  • Use R precordial chest leads
  • ST elevation or 1mm or more in V40V6
  • Pericarditis, myocarditis, stress induced (takotsubo) syndrome, early depolarization
77
Q

Differential diagnosis of a STEMI

A
  • Pericarditis
  • Myocarditis
  • Stress induced (takotsubo) syndrome–broken heart syndrome
  • Early repolarization
78
Q

Uses for echocardiogram

A
  • Global and RWM abnormalities
  • Murmur
  • Papillary muscle dysfunction
  • VSD
  • LV free wall rupture
  • LV aneurysm
  • Mural thrombosis

Cardiovascular II Final Exam (13 decks)

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