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MED233 Cardiovascular > PMT, Johnstons - MI (STEMI, NSTEMI) > Flashcards

PMT, Johnstons - MI (STEMI, NSTEMI) Flashcards

1
Q

What are the cardinal symptoms of CVDisease?

A
  1. Chest pain/discomfort
  2. Dyspnea, orthopnea, paroxysmal, nocturnal dyspnea, wheezing
  3. Cough, hemoptysis
  4. Fatigue, weakness
  5. Pain in extremities with exertion (claudication)
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2
Q

STEMI means what?

A

ST segment Elevation

“Transmural” - involves entire wall with complete interruption of blood flow.

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3
Q

CHD occurs in how many adults?

A

1/6

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4
Q

Pathobiology of MI

A

Most MIs are caused by atherosclerosis and rupturing of the plaque.

  • STEMI = coronary flow occluded
  • NSTEMI or UA = partial coronary occlusion
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5
Q

S/S of MI

A
  1. Chest discomfort (more severe than angina)&raquo_space; “heavy, crushing”
  2. Retrosternal, left, across chest, neck, jaw, left arm, epigastrum
  3. N/V. Diaphoresis, dyspnea.
  4. Cannot be relieved by nitro or rest
  5. 20% are painless&raquo_space; diabetics and elderly!
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6
Q

PE of MI

A
  • May be normal
  • S4
  • S/S of HF = (S3, crackle, JVD, new murmur)
  • BP and HR dependent on location of infarct**
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7
Q

BP and HR in anterior wall infarct v. inferior wall infarct.

A

Anterior wall infarct (LAD) results in increased sympathetic tone = inc. BP/HR
Inferior wall infarct (RCA) results in decreased vagal/PS tone = dec. BP/HR

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8
Q

What is J point?

A

Where QRS stops and ST begins.

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9
Q

STEMI on ECG

A

**ST elevation of 2mm or more in 2 or more contiguous chest or limb leads.
(May be obscured in LBBB.)

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10
Q

Difference in ECG and s/s of NSTEMI v. NSTEMI ACS

A

Both have: ST depression, T inversion, and chest pain.
NSTEMI has elevated cardiac enzymes, meaning YES, MI.
NSTEMI ACS does NOT have elevated cardiac enzymes, meaning NO MI.

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11
Q

Other than MI, what are causes of ST elevation?

A
  • Pericarditis
  • LVH with J point elevation
  • Normal variant early repolarization (i.e. young, healthy athlete or young blacks)
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12
Q

Describe ECG evolution in STEMI

A

Early Acute Phase - T wave amplitude increases; hyperacute pattern; convex upward ST pattern.
Evolved Acute Phase (Chronic Phase) - Resolution of ST elevation variable.

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13
Q

In Evolved Acute Phase (Chronic Phase), resolution of ST elevation variable - this is dependent upon what?
If after two weeks there is still persistent elevation, think what?

A
  • Dependent upon location - 2 weeks for inferior wall infarct. Later for anterior wall.
  • Ventricular aneurysm
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14
Q 
Normal QRS duration.
Normal Q wave duration.
Normal QT* duration.
Normal ST 
Normal T
A
  • QRS is 0.05-0.10 sec
  • Q wave is less than 0.03 sec
  • ST is NEVER normally depressed (, but can be elevated in standard (1mm) and chest (2mm) leads
  • Normal QT is 0.40sec (Fatal if prolonged)
  • T is postive in L1, L2, V3-V6 (not greater than 5mm in standard, 10mm in chest). Is inverted in AVR.
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15
Q

ST depression means what?

A

Subendocardial injury. No Q wave.

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16
Q

ST elevation means what?

A

Subepicardial or transmural injury.

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17
Q

Myocardial ischemia to injury to infarction is indicated by what zones of infarction on ECG?

A

1) Ischemia - T wave inversion - due to deficient blood supply affecting repolarization
2) Injury - ST segment elevation - shifts (deficient blood supply)
3) Infarction - large Q waves - due to dead tissue causing absence of deloparization current. T waves inverted

18
Q

Localization of MI/Myocardial ischemia

A
  • LAD is anterior wall ischemia, seen on V1-V6
  • RCA is inferior wall ischemia, seen on L2, L3, AVF
  • LCX is lateral wall ischemia, seen on L1, AVL
19
Q

Tombstone T waves indicate what?

A

Infarction

20
Q

What do you see on an ECG in a posterior wall infarction?

A

Reciprocal of anterior wall:

V’s: unusually large R and upright T

21
Q

Labs in MI

A
  • Inc. WBC 12k-15k (hrs to 2-4 days)
  • Inc. CRP
  • Inc. BNP
22
Q

Cardiac biomarkers of necrosis.

What can cause false positives?

A

Troponin.

Renal failure.

23
Q

What are non-MI causes of elevated troponin?

A

CV, pulmonary (pulm embolism, HTN) , neurological (IC-hemorrhage, stroke), shock, renal

24
Q

Most deaths from aMI are due to what?

A

VFib

25
Q

Tx of STEMI and time frame.

What is DIDO and time frame?

A
  1. Reperfusion with PCI in Cath Lab within 90 minutes (transfer within 120min if hospital does not have cath lab)
  2. Fibrinolysis within 30 minutes
    - “Door In, Door Out” within 30 min if non-PCI-capable hospital
26
Q

Failure of ST elevation to resolve by __% in __hrs suggests failure of fibrinolysis.

A

50% in 1-2hrs

27
Q

When is PCI preferred and what are its advantages?

A
  • Preferred with STEMI within 12 hours of s/s onset.

- Lowers mortality rate and ICH

28
Q

What two things are PCI useful for and what is its major disadvantage?

A
  • Useful for STEMI, new LBBB, within 12 hours of s/s onset.

- Major risk of ICH

29
Q

Contraindications of fibrinolytic therapy.

Are menses contraindicated?

A
  • Active bleed or bleed tendency. (**Menses excluded!)
  • Prior hemorrhagic stroke, ischemic stroke within 3 months, except acute ischemic stroke within 3-4.5hrs
  • Intracranial or spinal cord neoplasm or AV malformation
  • Suspected or known aortic dissection
  • Closed head or facial trauma within 3 months
30
Q

What is the initial pharmacological management of a STEMI

A
  • **ASA - given upon presentation
  • **IV Heparin or Enoxaprin (ADP-receptor inhibitor or Antiplatelet agent - clopidogrel; use for once year after PC1 for STEMI with stenting to prevent stent stenosis)
  • **Nitroglycerin
  • **Morphine
  • BB
  • Oxygen
  • Stool Softener
  • ACE
31
Q

When do you NOT give BB to a STEMI?

A

When the patient is decompensated&raquo_space; dec. HR, BP, MVO2.

Don’t use anything higher than 1st degree AVB.

32
Q

“hurts to breath, but feels better leaning forward” is what? A complication, post-MI, is what and tx?

A

Acute pericarditis 2-4 days post MI. If 2-10 weeks after MI could be Dressler.
Rx - ASA and NSAID

33
Q

What rhythm disturbances do you get post MI?

A
  • VT, VF
  • Accelerated Idioventricular Rhythm (AIVR)
  • AFib (5-10% of aMI)
  • Sinus brady - inferior MI
  • Wenckebach - inferior MI
34
Q

What is AIVR and when does it occur?

A
  • After fibrinolytic therapy as reperfusion occurs.
  • SLOW, but looks like vtach (60-100BPM)
  • BENIGN
35
Q

What is the leading cause of death in hospital from aMI?

A

HF due to LV dysfunction (S3, S4 crackles), RV infarct (inferior STEMI), cardiogenic shock

36
Q

Kaussmaul sign indicates what?

A

JVD - RV infarct.

37
Q

What mechanical complications can occur after an inferior wall-MI? What indicates this? Tx?

A
  • MR due to Infarction of papillary muscles
  • NEW holosystolic murmur associated with inferior wall MI
  • Sinus brady
  • Wenckebach
    Tx - surgery
38
Q

What mechanical complications can occur after an anterior wall-MI? What indicates this? Tx?

A
  • Septal rupture with VSD.
  • LV free wall rupture - causes tamponade
  • LV aneurysm - associated with anterior MI
    Rx - surgery
39
Q

What leads can dx RV infarction due to proximal occlusion of RCA before acute marginal branch?

A

R precordial, ST elevation of 1+mm in V4-V6R

Pericarditis, myocarditis, Takotsubo, Early repolarization

40
Q

**DDx of STEMI?

A
  • Pericarditis
  • Myocarditis
  • Takutsubo (ST elevation, coronaries normal)
  • Early ventricular repolarization (blacks)
41
Q

Anterior MI:

  • LV free wall rupture - causes what?
  • LV aneurysm - associated with what?
A

Tamponade

anterior MI

MED233 Cardiovascular (18 decks)

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