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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
Lateral MI
26
Anterolateral Infarct
27
Inferior MI
28
Posterior MI
29
Serum Markers of MI (2)
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
30
Troponin
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
31
Overview: Troponin vs CK-MB
32
LDH
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
Labs overview (dont need to know times)
34
Axis and Vectors
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
Standard Limb Leads
I, II, III, aVL, aVR, aVF
36
Determining Electrical Axis in the Frontal Plane
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
Axis Deviation (3)
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
Factors That Alter the Normal Axis: obesity and ventricular hypertrophy
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
Other factors that alter the normal axis: (3)
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
last factor that alters normal axis...
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
Cardiac Conduction System
SA node: Anterior, middle, and posterior internodal system AV node Bundle of His Right and Left bundle branches Purkinje system
42
Excitation-Contraction Coupling
Depolarization of muscle cell Entry of calcium Release of calcium stored in the SR Calcium binds troponin Interaction of actin myosin Contraction
43
Waveforms for conduction system parts
44
Ion Channels in Ventricular Muscle
45
Phases
46
Mechanisms of Dysrhythmias
47
Mechanisms of Dysrhythmias: Automaticity
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
Decreased Automaticity
--> sinus brady
49
Increase Automaticity
--> tachy
50
Early Afterdepolarization:
Triggered activity... @ late phase 2-3 --> long action potential --> VF - can be caused by Lidocaine or Calcium channel blockers
51
Delayed Afterdepolarizations (DAD)
@Phase 4 -- near or fully repolarized - long QT syndrome --> Torsades and VF or tachyarrhythmias - occurs with Dig toxicity and excess catecholamines
52
Mechanisms of Dysrhythmias: Impulse Conduction
Abnormal impulse conduction AV block Re-entry Unidirectional conduction block Establishment of new loop of excitation Conduction time that outlast refractory period
53
Normal Action Potential Conduction
54
Ischemia and Re-entry Arrhythmia
55
Re-Entry EAD / DAD
56
AFLUTTER
57
AFIB
58
WPW
59
PVC with morphology
60
Bigeminy -- 1st check O2 and increase, if not resolved, workup other causes
61
VTACH
62
VFIB - no visible P waves or QRS complex - irreg electrical activity - rate 150 - 500
63
TORSADES -- ribbon LOW Mag** pulselss & lethal
64
Types of AV Block
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
1st degree
66
2nd degree type 1 (Wenchbach / Mobitz 1)
67
Complete heart block -- constant PR interval with intermittent failure to conduct no relationship b/w P and QRS
68
Questions to answer in order to identify an unknown Dysrhythmia:
1. Rate 2. Rhythm 3. QRS complex 4. P waves 5. P and QRS relationship 6. onset/termination
69
1. Rate
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
2. Rhythm
Is the rhythm irregular? Irregular --> Suggests atrial fibrillation, 2nd degree AV block, multifocal atrial tachycardia, or atrial flutter with variable AV block
71
3. QRS complex
3. Is the QRS complex narrow or wide? Narrow --> Rhythm must originate from the AV node or above Wide --> Rhythm may originate from anywhere
72
4. P waves
4. Are there P waves? Absent P waves --> Suggests atrial fibrillation, ventricular tachycardia, or rhythms originating from the AV node
73
5. P and QRS relationship
5. 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
6. Onset/Termination
6. Is the onset/termination of the rhythm abrupt or gradual? Abrupt: Suggests reentrant rhythm Gradual: Suggests altered automaticity
75
Systematic Interpretation
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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