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Concepts 2 > MI and ECG > Flashcards

MI and ECG Flashcards

1
Q

MI Risk Factors

A

Hypertension.
Tobacco use.
Diabetes mellitus.
Hyperlipidemia.
Gender = males
African American (HTN)
Hereditary: More common in the case of family history
Obesity
Stress
Unhealthy habits

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2
Q

MI Symptoms

A

Chest pain in the mid-thorax,
Crushing substernal pain.
Pain may radiate to teeth or jaw,or shoulder, or arm, or back.
Dyspnea or shortness of breath.
Diaphoresis
Impending Doom
Epigastric discomfort, +/- nausea vomiting.
Preceded by angina pectoris (50%).
Pain not relieved by nitroglycerin or rest

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3
Q

World Health Organization MI Criteria

A

Dx of MI Requires ≥ 2 of the Following:
1. Prolonged ischemic-type chest discomfort
- Stable vs Unstable Angina

  1. Serial electrocardiogram (ECG) changes
    - ST Elevation MI (STEMI)
    - Non-ST Elevation MI (NSTEMI)
  2. Rise and fall of serum cardiac markers
    - CK, CK-MB
    - Troponin
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4
Q

Stable Angina

A

Normal ECG and Troponin
- angina pain d/t increased demand in the setting of a stable atherosclerotic plaque. vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand

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5
Q

Unstable Angina

A

ECG: normal, inverted T waves, or ST depressing
Troponins: normal

plaque rupture –> thrombus around –> partial occlusion
- @ rest or progresses rapidly over short period of time
- ISCHEMIA WITHOUT NECROSIS
- partially or transiently obstructive thrombosis
- S&S: chest pain, severe angina
- TX: non-invasive/conservative

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6
Q

NSTEMI (ECG and Troponin)

A

ECG: normal, inverted T waves, or ST depressing
Troponins: Elevated *

plaque rupture and thrombus formation –> partial occlusion –> infarct to the subendocardial myocardium

  • ischemia with necrosis
  • partial or transiently obstructive thrombus
  • Chest pain that’s prolonged and “crushing”
  • Tx: early invasive
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7
Q

STEMI

A

ECG: Hyperacute T waves or ST ELEVATION, new LBB
Troponins: Elevated*

COMPLETE occlusion of blood vessel –> transmural injury and infarct to myocardium

  • ischemia with necrosis
  • COMPLETE obstruction by intracoronary thrombus
  • Tx: immediate reperfusion
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8
Q

Stable Angina

A

Trigger = Physical activity
Predictable
<15min
Relieved with REST

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9
Q

Unstable Angina

A

Not triggered by physical activity, not predictable, >30min, and not relieved with rest

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10
Q

Variant Angina

A

Sometimes triggered by physical activity, not predictable, worsens with time, and not relived with rest

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11
Q

Three Types of Angina

A

Printzmetal’s Variant Angina
Chronic Stable Angina
Unstable Angina

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12
Q

Printzmetal’s Variant Angina

A

Vasospasm – supply ischemia

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13
Q

Chronic Stable Angina

A

Demand ischemia and FIXED stenosis

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14
Q

Unstable angina

A

THROMBUS and supply ischemia

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15
Q

NSTEMI

A

Partial or Temporary Blockage
No ST segment elevation:
- ST-segment depression
- T-wave inversion
- non-specific ST-T wave changes
- Normal ECG
Interpretation of subtle ECG changes can be difficult
Baseline for comparison
Left bundle branch block (LBBB) – largely precludes further analysis
- Abnormal Depolarization/repolarization
- ST/wave Abnormality

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16
Q

ST-Segment Elevation

A

Intervalbetween ventricular depolarization and repolarization.
ST elevation (with compatible history)
- Specificity = 91% & Sensitivity = 46%

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17
Q

STEMI Defined by ECG changes

A
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18
Q

ECG Leads and Areas of Myocardial Necrosis

A
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19
Q

Evolution of Acute MI

A
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20
Q

ST segment variation during stress testing

A
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21
Q

Evolving MI: Hyperacute/Acute Phases

A

Tombstone

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22
Q

Q Wave

A

Evidence of infarction
One third the height of the QRS complex
Necrotic tissue no longer contributes positive vectors to the wave of depolarization

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23
Q

Cardiac Vessels and ECG Leads

A
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24
Q

Anterior MI

A
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25
Q

Lateral MI

A
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26
Q

Anterolateral Infarct

A
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27
Q

Inferior MI

A
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28
Q

Posterior MI

A
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29
Q

Serum Markers of MI (2)

A

CPK:
3-4 hours, peaks in 8-24 hours, lasts for 3-4 days
Skeletal, smooth muscle injury & CNS injury
Peak value commonly used as a index of MI size

CKMB:
4-6 hours, peaks at 12-24 hours, lasts for 2-3 days
More specific for cardiac muscle
Rises and falls slightly earlier than total CK

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30
Q

Troponin

A

Troponins: T And I

Protein Complex In Skeletal And Cardiac Muscle
Calcium-mediated Contraction Through Action With Actin & Myosin
Highly Concentrated In Myocytes
- Sensitive (100% 12 Hrs – 5 Days)
- Specific (Myocytes 94-97%)
- More Specific That CK MB
Elevated In (2-4 Hrs) Elevated Longer (T- 10-14 Days & I 7-10 Days)
- Identifies Patients Presenting Late After MI
May Be Mildly Elevated In Unstable Angina: Worse Prognosis

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31
Q

Overview: Troponin vs CK-MB

A
32
Q

LDH

A

LDH = (Lactate Dehydrogenase Enzyme)
High LDH1 isoenzyme more specific
LD-1(17 to 27%) highest concentration is found in the heart
Also found in RBC’s and kidneys.
Rises late and stays elevated after 4-5 days

33
Q

Labs overview (dont need to know times)

A
34
Q

Axis and Vectors

A

Axis:
Refers to the direction of depolarization as it spreads throughout the heart

Vectors:
Vectors indicate, through the use of an arrow, the direction of depolarization
Vectors vary in size according to the magnitude of the electrical stimulus to which the vectors refer

35
Q

Standard Limb Leads

A

I, II, III, aVL, aVR, aVF

36
Q

Determining Electrical Axis in the Frontal Plane

A

Normal Axis
QRS is upright in Leads I and AVF
Check Leads I & AVF
- If QRS is positive in Lead I, then Mean QRS Vector points to the patient’s left side
- If QRS is positive in AVF, then Mean QRS Vector points to 0’- 90’ quadrant

37
Q

Axis Deviation (3)

A

Left Axis Deviation
Lead I: positive QRS; AVF: negative QRS
Right Axis Deviation
Lead I: negative QRS; AVF : positive QRS
Extreme Right Axis Deviation:
Lead I: negative QRS; AVF: negative QRS

38
Q

Factors That Alter the Normal Axis: obesity and ventricular hypertrophy

A

Obesity:
May cause axis to be pointed directly to the patient’s left due to the heart being pushed up by the diaphragm

Ventricular Hypertrophy:
Greater electrical activity in the hypertrophied ventricle; therefore the axis is deviated toward the hypertrophied ventricle

39
Q

Other factors that alter the normal axis: (3)

A

HTN: Can lead to LVH as well as Hemiblocks or Bundle Branch Blocks, all of which result in axis deviation

Pulmonary HTN: Can lead to RVH as well as Right Bundle Branch Block

Bundle Branch Blocks:
Depolarization in one of the Bundle Branches is blocked, resulting in a RSR’ complex
RSR’ makes identification of axis deviation difficult
RSR’ makes identification of ventricular hypertrophy difficult

40
Q

last factor that alters normal axis…

A

MI!!!!
MI results in an area of dead myocardium which does not conduct electrical impulses and, thus, has no vectors

Axis points in opposite direction of the area of infarction

41
Q

Cardiac Conduction System

A

SA node: Anterior, middle, and posterior internodal system
AV node
Bundle of His
Right and Left bundle branches
Purkinje system

42
Q

Excitation-Contraction Coupling

A

Depolarization of muscle cell
Entry of calcium
Release of calcium stored in the SR
Calcium binds troponin
Interaction of actin myosin
Contraction

43
Q

Waveforms for conduction system parts

A
44
Q

Ion Channels in Ventricular Muscle

A
45
Q

Phases

A
46
Q

Mechanisms of Dysrhythmias

A
47
Q

Mechanisms of Dysrhythmias: Automaticity

A

Abnormal Impulse Generation (Automaticity)
Automaticity of normally automatic cells
SA - AV – His

Generation Of Impulses In Non-automatic Cells
Development of phase 4 depolarization
Triggered activity due to afterdepolarizations
Early afterdepolarizations - Late afterdepolarizations

48
Q

Decreased Automaticity

A

–> sinus brady

49
Q

Increase Automaticity

A

–> tachy

50
Q

Early Afterdepolarization:

A

Triggered activity… @ late phase 2-3 –> long action potential –> VF
- can be caused by Lidocaine or Calcium channel blockers

51
Q

Delayed Afterdepolarizations (DAD)

A

@Phase 4 – near or fully repolarized
- long QT syndrome –> Torsades and VF or tachyarrhythmias
- occurs with Dig toxicity and excess catecholamines

52
Q

Mechanisms of Dysrhythmias: Impulse Conduction

A

Abnormal impulse conduction
AV block
Re-entry
Unidirectional conduction block
Establishment of new loop of excitation
Conduction time that outlast refractory period

53
Q

Normal Action Potential Conduction

A
54
Q

Ischemia and Re-entry Arrhythmia

A
55
Q

Re-Entry EAD / DAD

A
56
Q
A

AFLUTTER

57
Q
A

AFIB

58
Q
A

WPW

59
Q
A

PVC with morphology

60
Q
A

Bigeminy – 1st check O2 and increase, if not resolved, workup other causes

61
Q
A

VTACH

62
Q
A

VFIB
- no visible P waves or QRS complex
- irreg electrical activity
- rate 150 - 500

63
Q
A

TORSADES – ribbon
LOW Mag**
pulselss & lethal

64
Q

Types of AV Block

A

AV Block (relatively common)
1st degree AV block
Type 1 2nd degree AV block
Type 2 2nd degree AV block
3rd degree AV block

65
Q
A

1st degree

66
Q
A

2nd degree type 1 (Wenchbach / Mobitz 1)

67
Q
A

Complete heart block – constant PR interval with intermittent failure to conduct
no relationship b/w P and QRS

68
Q

Questions to answer in order to identify an unknown Dysrhythmia:

A
  1. Rate
  2. Rhythm
  3. QRS complex
  4. P waves
  5. P and QRS relationship
  6. onset/termination
69
Q
  1. Rate
A

Is the rate slow (<60 bpm) or fast (>100 bpm)?
Slow –> Suggests sinus bradycardia, sinus arrest, or conduction block
Fast –> Suggests increased/abnormal automaticity or reentry

70
Q
  1. Rhythm
A

Is the rhythm irregular?
Irregular –> Suggests atrial fibrillation, 2nd degree AV block, multifocal atrial tachycardia, or atrial flutter with variable AV block

71
Q
  1. QRS complex
A
  1. Is the QRS complex narrow or wide?
    Narrow –> Rhythm must originate from the AV node or above
    Wide –> Rhythm may originate from anywhere
72
Q
  1. P waves
A
  1. Are there P waves?
    Absent P waves –> Suggests atrial fibrillation, ventricular tachycardia, or rhythms originating from the AV node
73
Q
  1. P and QRS relationship
A
  1. What is the relationship between the P waves and QRS complexes?
    More P waves than QRS complexes –> Suggests 2nd or 3rd degree AV block
    More QRS complexes than P waves  Suggests an accelerated junctional or ventricular rhythm
74
Q
  1. Onset/Termination
A
  1. Is the onset/termination of the rhythm abrupt or gradual?
    Abrupt: Suggests reentrant rhythm
    Gradual: Suggests altered automaticity
75
Q

Systematic Interpretation

A
  1. First Impression
  2. Rate
  3. Rhythm
  4. PQRST Evaluation
  5. Ischemia and Infarction
  6. Other Abnormalities
    - Axis Deviation
    - Hypertrophy

Concepts 2 (11 decks)

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