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Emergency Medicine > Chest Pain and EKG > Flashcards

Chest Pain and EKG Flashcards

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1
Q

what is a PCI

A

percutaneous coronary intervention

  • preferred to thrombolytics
  • should be done 90-120 min
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2
Q

when and how is nitrate used

A
  • sublingual NTG every 5 min x3

- contraindicated if hypotensive or RV infarct- no NTG if BP less than 90, HR less than 50

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3
Q

what are the anterior leads

A

V3, V4

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4
Q

Atypical symptoms of an MI / aka Anginal equivalent is most common in who and how does it present

A

-women and elderly and diabetic

  • palpitations, nausea, SOB, epigastric pain, weakness, fatigue
  • normal MI
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5
Q

Cardiac causes of chest pain

A
  1. Angina/MI
  2. Aortic Dissection
  3. Pericarditis/ Tamponade
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6
Q

what artery causes a septal MI and what are complications

A
  • LCA: LAD-septal branch

- complications: infranodal and BBB

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7
Q

what is a t wave

A

ventricular repolarization

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8
Q

what is acute coronary syndrome

A

Spectrum of clinical presentation from Unstable Angina to STEMI

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9
Q

how do you determine rhythm on an EKG

A

is there a p wave for every QRS?

-is the PR interval consistent

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10
Q

what arteries do posterior infarcts typically occur in

A
  • Usually accompanies inferior or lateral infarct

- LCA: circumflex ; RCA: Posterior Descending

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11
Q

GI causes of chest pain

A
  1. PUD/gastritis
  2. Cholecystitis**
  3. Pancreatitis-L epigastric pain that radiates to the back 4. Peritonitis
  4. GERD/spasm
  5. Esophageal ruptur
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12
Q

each tiny box on an EKG is __

each big box is ___

A

0.04 second

5 small boxes or 0.2 sec

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13
Q

what is a significant Q wave?

A
  • greater than 0.04 sec wide (1 small box)
  • greater than 1/3 the size of the QRS complex

*significant for MI

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14
Q

what is a normal QRS

A

duration less than 0.12 sec or less than 3 boxes

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15
Q

what are non-modifiable risk factors for cardiac disease

A
  1. family history
  2. gender
  3. age: men over 45, female over 55
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16
Q

classes of meds used with (N)STEMIs

A
  • anticoagulant
  • anti-platelet
  • beta blocker
  • GIIb/IIIa inhibitors
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17
Q

what is PR interval

A

delay of AV node to allow filling of ventricles

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18
Q

when should an EKG be done when someone presents to the ER with chest pain

A

first 10 minutes of arrival

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19
Q

Left axis deviation is what degrees

A

-30- -90

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20
Q

what is the treatment goal for N/STEMIs

A

-PCI within 90-120 min of ED arrival
OR
-trhombolysis (-“Ases”) within 30 min (if not PCI center)

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21
Q

New data shows that ___ is more likely to cause your MI than ____

A

acute plaque rupture

stenosis

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22
Q

4 things that are specific for acute coronary syndrome

A

Cp w/

  1. diaphoresis
  2. vomiting
  3. exertion
  4. radiation
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23
Q

pulmonary causes of chest pain

A
  1. Pneumonia/bronchitis
  2. Pulmonary embolism
  3. Pleurisy
  4. Pneumothorax/pneumomediastinum
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24
Q

what leads would EKG changes be present for a septal MI?

A

Leads V1, V2 (septal leads)

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25
Q

what is a normal PR interval

A

0.12-0.20 sec (3-5 small boxes)

-beginning of p wave to beginning of QRS complex

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26
Q

describe the pathway of cardiac conduction

A

SA node–> AV node–> AV bundle–> LBB and RBB–> purkinje fibers

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27
Q

Once you have decided to send a troponin, you have opened the door to potential cardiac disease.
Need to initiate:

A
  • provactive testing w/in 72 hrs

- stress test

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28
Q

what is the rate of success for thromolytics and what are main complications

A

-Successful reperfusion rates between 60-80%

  • Main complication is bleeding
  • ICH occurs in less than 1% of patients but carries a 55-65% mortality
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29
Q

STEMI EKG Findings

A

more than 1 mm ST segment elevation in two or more contiguous leads
+/- reciprocal ST depression

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30
Q

PE components when assessing chest pain

A
  1. chest wall tenderness (15% of MIs have CW tenderness)
  2. heart tones (Hamman’s crunch?)
  3. pulmonary exam– rales= CHF or LV dysfunction
  4. abdominal mass/tenderness
  5. vascular- pulses, bruits
  6. neuro- AMS, focal deficits
  7. derm-herpes
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31
Q

what leads would EKG changes be present for a posterior MI?

A

V1 to V4 ST depression

  • Tall R waves in these leads
  • flip the EKG

-V7-V9 on back–same horizontal plane as 6

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32
Q

cardiac risk factors are predictive of CAD in _____ patients

A

in asymptomatic patients, But poor predictors for AMI in the ED

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33
Q

Musculoskeletal causes of chest pain

A
  1. Costochondritis
  2. Rib trauma
  3. Rib Strain/ coughing
  4. Nonspecific
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34
Q

what is p wave

A

depolarization of atria in response to SA node triggering

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35
Q

what artery causes an inferior MI and what are complications

A
  • RV infarction. Can have issues w/ Hypotension, Increased N/V
  • RCA occlusion
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36
Q

___ are to assess AMI

___ are to assess CAD

A

troponins

stress tests

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37
Q

hamman’s crunch (a crunching, rasping sound, synchronous with heart beat, heard over the precordium and sometimes at a distance from the chest) is indicative of what?

A

Pneumediastinum/Pneumopericardium or Esophageal Rupture

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38
Q

what artery causes an anterior MI

A

LAD

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39
Q

when does troponin rise

A

within 1.5-3 hrs of injury

*usually a 3 hr repeat troponin to r/o AMI

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40
Q

Normal axis P waves should be upright in leads __, inverted in ___

A

I and II

AvR

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41
Q

what are modifiable risk factors for cardiac disease

A
  1. HTN
  2. Smoking
  3. Hyperlipidemia
  4. Diabetes
  5. Obesity
  6. (cocaine)
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42
Q

how to determine normal axis, LAD, RAD or extreme RAD/LAD

A
  • Normal: Lead I +, avF + (LLQ)
  • LAD: Lead I +, aVF - (LUQ)
  • RAD: Lead I -, aVF + (RLQ)
  • Extreme: Lead I -, aVF - (RUQ)
  • hand motion trick
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43
Q

what is J point

A

point where ST takes off from QRS

*can have J point elevation

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44
Q

describe the movement of charge from the of the limb leads

A

Lead I: RA (-)–> LA (+)
Lead II: RA (-)–> LL (+)
Lead III: LA (-) –> LL (+)

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45
Q

what artery causes a lateral MI and what are complications

A

LCA: circumflex

Complications: LV dysfunction

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46
Q

general EKG findings suggestive of acute MI

A
  1. Normal EKG
  2. New LBBB
  3. Hyperacute T waves (over 50% of preceding R wave)
  4. T wave inversion
  5. greater than 1mm ST elevation in at least two contiguous leads (more than 2mm if V2-V3)
  6. ST depression in Lead V1, V2 for posterior MI
  7. Q waves (necrosis)
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47
Q

how do you interpret TIMI score

A
  • If patient has TIMI score of 0-1, can be considered Low Risk
  • Low Risk: 5% risk at 14 days of: all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization.
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48
Q

what is an abnormal QTc

A

less than 0.44 sec or if over 0.5 (500)

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49
Q

inversion of T wave usually due to

A

AMI
BBB
hypertrophy

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50
Q

thrombolytics for acute MI

A
  • The Clotbusters; The “-ases”

- tPA, Streptokinase (SK) , Tenecteplase(TNKase), Reteplase (rPA)

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51
Q

what leads are associated with LAD

A

V1-4

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52
Q

what is stable angina

A

a predictable pattern of chest pain/pressure/squeezing that occurs with exertion and relieved with rest or Nitroglycerin. Lasts 5-15 min.

*PE, labs, CXR, EKG all normal in Angina and UA

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53
Q

what are the inferior leads

A

II, III, avF

*show problem w/ RCA or LCx

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54
Q

what is QRS complex

A

depolarization of ventricles, triggers main pumping contractions

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55
Q

what are the septal leads

A

V1, V2

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56
Q

what is ST segment

A

beginning of ventricle repolarization, should be flat

Time between completion of depolarization and onset of repolarization

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57
Q

what are causes of short PR interval

A
  • WPW (pre excitation of ventricle)

- LGL

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58
Q

what is the HEART score

A
  • More appropriate for ED patients
  • assesses risk for adverse cardiac event in next 6 weeks
  • Takes into account:
    1. History
    2. EKG
    3. Age
    4. Cardiac Risk Factors
    5. Troponin

*Score of 0-3: discharge home, for outpatient follow up

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59
Q

initial tx and management for chest pain

A
  1. O2 (if less than 90% sat), IV, pulse ox, monitor; EKG within ten minutes
  2. ASA (160-325mg po/pr)
  3. pain control (morphine or fentanyl)
  4. nitrates
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60
Q

what are the lateral leads

A

I, aVL, V5, V6

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61
Q

life threatening causes of chest pain

A
  1. Ischemia/ MI
  2. Pulmonary Embolism
  3. Esophageal Rupture
  4. Aortic Dissection
  5. Pericardial Tamponade
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62
Q

what is unstable angina

A

New onset, change in severity, duration, frequency of the normal angina

*PE, labs, CXR, EKG all normal in Angina and UA

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63
Q

why is ASA important to give for chest pain

A

reduces mortality, decreases rate of infarction

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64
Q

why is morphine often used for chest pain

A

pre load and afterload, and myocardial oxygen demand

-association with increased mortality. Also anxiolitic

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65
Q

what are different types of stress tests

A
  1. Treadmill: least expensive, most available, but lowest sensitivity (68%)
  2. Stress echo: no radiation, better sensitivity (80%)
  3. Nuclear Stress Testing: (myocardial perfusion imaging) highly accurate, but radiation, takes longer
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66
Q

EKG may suggest non-cardiac causes of CP including

A

tamponade

pericarditis

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67
Q

Concerning plaque growth occurs into

A

the vessel wall, rather than into the lumen

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68
Q

how to approach reading EKGs

A 
Rate
Rhythm
Axis
Intervals
Ischemia/infarct
Hypertrophy
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69
Q

what is a normal P wave interval

A
  • less than 0.12 sec (3 small boxes) and

- less than 2.5 m high

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70
Q

what is TIMI scoring

A
  • Age older than65
  • more than 3 CAD risk factors
  • Known CAD (50% stenosis or more)
  • ST elevation more than 0.5mm
  • ASA use in past 7 days
  • At least 2 anginal events in past 24 hrs.
  • Positive cardiac marker
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71
Q

Up to ___% of patients with unstable angina may have atypical symptoms - and no chest pain!

A

50%

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72
Q

low risk patients with chest pain can go home if:

A
  • Low HEART score
  • Two negative troponins, 3 hours apart
  • OR – single lab troponin negative 6 hours from onset of sx with constant pain
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73
Q

what leads would EKG changes be present for an inferior MI?

A

ST elevation in leads II, III, aVF (inferior leads)

-reciprocal changes in anterior leads

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74
Q

NSTEMI EKG findings

A

may see strain, ST depression, or normal EKG with elevated cardiac markers. BUT – if positive trop and history suggestive = NSTEMI

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75
Q

what leads are associated with RCA or LCx

A

Lead II, III, aVF

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76
Q

what is the difference between a STEMI and NSTEMI

A

NSTEMI- worsening or changing symptoms, with myocardial damage (troponin elevation), but not EKG changes

STEMI-as above plus EKG changes

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77
Q

causes of LAD

A
  • LVH (caused by chronic untx HTN)
  • LAFB
  • Inferior MI
  • Pacemaker rhythm
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78
Q

causes of RAD

A 
-RVH (PHTN, PE, pulmonary obstruction things
LPFB)
-Lateral wall MI
-Chronic Lung Dz  (COPD)
-Acute Lung Dz (PE)
-Normal:  thin adults, kids  
-Dextrocardia
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79
Q

what leads would EKG changes be present for an anterior MI?

A
  • ST elevation in V2, V3, V4
  • loss of R wave progression
  • reciprocal depression in inferior leads
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80
Q

what leads would EKG changes be present for a lateral MI?

A

ST elevation in V5, V6, aVL

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81
Q

other studies beside EKG used to assess chest pain

A
  • chest xray (heart size, pneumomediastinum, pulmonary congestive, free air)
  • labs (troponins, LFTs/lipase-pancreatitis, D dimer, CBC, BMP)
  • Chest CT or VQ scan to r/o PE
  • CTA C/A/P to r/o aortic dissection
  • echocardiogram- heart failure
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82
Q

what leads are associated with LCx or diagonal branch of LAD

A

Lead I
aVL
V5
V6

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83
Q

normal axis is what degrees

A

-30-90+

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84
Q

Neuro/psych causes of chest pain

A
  1. Thoracic outlet syndrome
  2. Herpes Zoster
  3. Anxiety
  4. Radiculopathy
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85
Q

what is a normal QT interval

A

less than ½ of R-R interval ( or 0.36-0.44 sec)

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86
Q

how to determine rate on an EKG

A

300, 150, 100

75, 60, 50

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87
Q

Classical symptoms of an MI

A
  • substernal CP/pressure
  • diaphoresis
  • nausea
  • dyspnea
  • radiation to arm/jaw
  • exertional
  • *Lasting less than 2min or more 24 hours is less likely to be ischemic
88
Q

describe the limb lead placements and their charge

A

RA(-/-)
LA (+/-)
LL (+/+)

Lead I: RA(-)—>LA(+)
Lead II: RA (-) —> LL (+)
Lead III: LA (-) –> LL (+)

89
Q

How do you identify junctional rhythm

A

P waves are inverted, absent or after QRS

-rate 60-100

90
Q

How do you identify idioventricular rhythm

A

rate 20-40
P waves absent or not related
-PR interval: N/A

91
Q

what is the difference between ventricular tachycardia and v. fib

A

VT: rhythm is regular

VF: extremely irregular

92
Q

what rhythm?
-one spike followed by an abnormal p (atrial capture) followed by a second spike producing a wide QRS (ventricular complex)

A

AV sequential pacemaker (dual chamber)

93
Q

describe the P-P interval in AV blocks

A

CONSTANT in all

94
Q

in AV blocks, where is the blockage

A

in the QRS response to the atrial impulse

95
Q

what is the difference between 1st, 2nd, and 3rd degree AV blocks?

A

1st degree – prolonged PR interval (greater than 0.20sec or 1 big box)

3rd degree – RANDOM* PR, no relationship between QRS and P waves (constantly changing). R to R and P to P are constant and independent. QRS wide or narrow

2nd degree Type I – prolonging PR interval, dropped QRS (lone P), reset
Aka Wenckebach

2nd degree type II – FIXED* PR, many dropped QRS complexes (too many p waves)

96
Q

describe the difference between type I and type II second degree AV blocks

A

2nd degree Type I – prolonging PR interval, dropped QRS (lone P), reset
Aka Wenckebach

2nd degree type II – FIXED* PR, many dropped QRS complexes (too many p waves)

97
Q 
what rhythm?
P waves march out
QRSs march out
Completely dissociated
Always slow and usually regular
QRS wide or narrow
PR interval generally constantly changing
R-R interval is constant
A

complete heart block

98
Q

why does one use a 12 lead tracing?

A
  • A single lead strip gives a “snapshot” of the electrical activity in the heart.
  • Multiple lead monitoring provides a three dimensional view of the heart.
  • 12 leads gives the provider more detailed information about the electrical pathway, allowing one to “see” different parts of the myocardium.
99
Q

what are the frontal plane leads?

A

I, II, III, aVR, aVL, aVF

100
Q

wht are the precordial leads

A

V1-V6

101
Q

what is axis determination?

A
  • It is simply a determination of the mean vectorial depolarization in the heart.
  • Axis deviation in isolation may be preexisting. New axis change is usually pathologic.
102
Q

where do you look to determine axis?

A

frontal leads

I, II, III, aVR, aVL, aVF

103
Q

Under certain circumstances, the branches to the ventricles may be blocked by

A

drugs
electrolyte abnormalities
trauma
previous surgeries, etc

104
Q

what does a bundle branch block appears as and why?

A

This appears as a widened QRS because one branch depolarizes quickly, and the “wave” then reaches the area served by the blocked branch and depolarizes through myocardium (slowly), prolonging the time for each cycle

105
Q

how do you determine a BBB?

A
  1. To determine which branch is blocked, look at V1
  2. Is the majority of the deflection up or down?
  3. which way do you move your turn signal? (Up is right, left is down)

LBBB-wide, downward QRS
RBBB- wide, upward, QRS

106
Q

causes of LBBB

A
  1. Aortic stenosis*
  2. Ischemic heart disease (as w/ RBBB)
  3. Hypertension*
  4. Dilated cardiomyopathy
  5. Anterior MI
  6. Primary degenerative disease (fibrosis) of the conducting system
  7. Hyperkalemia
  8. Digoxin toxicity
107
Q

causes of RBBB

A
  1. Right ventricular hypertrophy / cor pulmonale
  2. Pulmonary embolus
  3. Ischemic heart disease (as w/ LBBB)
  4. Rheumatic heart disease
  5. Myocarditis or cardiomyopathy
  6. Degenerative disease of the conduction system
  7. Congenital heart disease (e.g. atrial septal defect)
108
Q

___ makes it difficult to interpret infarction patterns - abnormally conducted impulses through the LV mask infarction

A

LBBB

109
Q

what is the significance of a new RBBB

A

rarely associated with acute pathology

110
Q

BBB can disguise WBTs (wide beat tachycardias), creating difficulty in differentiating __ from ___

A

SVT w/ aberrancy from VT

111
Q

what are hemiblocks?

A
  • The left bundle has two fascicles - an anterior and posterior fascicle.
  • Each fascicle can be blocked and they have different manifestations on the 12 lead ECG.
112
Q

How does a LAFB (Left anterior fascicular block) hemiblock look?

A

Left Axis deviation required!!!
LA = LA

Small Q in lead I, Small R in lead III (opposite of LPFB)

113
Q

how does a LPFB (left posterior fascicular block) hemiblock look?

A

RAD is required!

Small R in lead I, Small Q in lead III (opposite of LAFB)

114
Q

what is it called when RBBB and LAFB or RBBB and LPFB coexist?

A

bifasicular block

115
Q

what is it called when LPFB and LAFB coexists

A

LBBB

116
Q

is there a trifasciucular block?

A

NO! called complete heart block

117
Q

what causes LVH

A

pressure overload secondary to conditions such as aortic stenosis and HTN (long standing disease)

-The thickened LV wall leads to prolonged depolarization (increased R wave peak time) and delayed repolarization (ST and T-wave abnormalities) in the lateral leads.

118
Q

what does LVH look like on EKG?

A
  • increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6) and
  • increased S wave depth in the right-sided leads (III, aVR, V1-3)

-ST segment depression and T wave inversion in the left-sided leads:AKA the left ventricular ‘strain’ pattern

119
Q

what can cause an ventricular “strain pattern”

A

ST depression (seen in V5, V6

  • LVH (in left sided leads)
  • RVH (righ precordial V1-4, and inferior II, III, aVF)
  • acute MI
  • Digitalis
120
Q

Diagnostic criteria for RVH and

supporting criteria

A

Diagnostic Criteria:

  1. Right axis deviation of +110° or more.
  2. Dominant R wave in V1 (greater than 7mm tall or R/S ratio greater than 1).
  3. Dominant S wave in V5 or V6 (greater than 7mm deep or R/S ratio less than 1).
  4. QRS duration less than 120ms (i.e. changes not due to RBBB).

Supporting criteria:

  1. Right atrial enlargement (P pulmonale).
  2. Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
  3. S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III.
  4. Deep S waves in the lateral leads (I, aVL, V5-V6).
121
Q

what is hypertrophic cardiomyopathy (HCM)

A

a genetic disorder that has a variable presentation and carries a high incidence of sudden death (in kids). Its hallmark is myocardial hypertrophy that is inappropriate and often asymmetrical and that occurs in the absence of an obvious inciting hypertrophic stimulus.

*hear murmur on exam (esp. w/ valsalva)

122
Q

signs and sx of hypertrophic cardiomyopathy (HCM)

A
  1. Sudden cardiac death (the most devastating presenting manifestation)
  2. Dyspnea (the most common presenting symptom)
  3. Syncope and presyncope
  4. Angina
  5. Palpitations
  6. Orthopnea and paroxysmal nocturnal dyspnea (early signs of congestive heart failure [CHF])
  7. CHF (relatively uncommon but sometimes seen)
  8. Dizziness
123
Q

PE findings of hypertrophic cardiomyopathy

A
  1. Double apical impulse or triple apical impulse (less common)
  2. Normal S1; S2 usually is normally split but is paradoxically split in some patients with severe outflow gradients; S3 gallop is common in children but signifies decompensated CHF in adults; S4 is frequently heard
  3. Jugular venous pulse revealing a prominent a wave
  4. Double carotid arterial pulse
  5. Apical precordial impulse that is displaced laterally and usually is abnormally forceful and enlarged
  6. Systolic ejection crescendo-decrescendo murmur
  7. Holosystolic murmur at the apex and axilla of mitral regurgitation
  8. Diastolic decrescendo murmur of aortic regurgitation (10% of patients)
124
Q

describe the heart sounds in HCM

A
  • Normal S1
  • S2 usually is normally split but is paradoxically split in some patients with severe outflow gradients
  • S3 gallop is common in children but signifies decompensated CHF in adults
  • S4 is frequently heard
125
Q

describe the murmur heard w/ HCM

A
  • Systolic ejection crescendo-decrescendo murmur
  • Holosystolic murmur at the apex and axilla of mitral regurgitation
  • Diastolic decrescendo murmur of aortic regurgitation (10% of patients)
126
Q

dangers on EKG to look out for

A
  1. QT prolongation (Beginning of QRS to end of T wave, be worried anything over QTc 500)
  2. Electrolyte disturbances (esp. w/ potassium)
  3. Inherent conduction abnormalities
    - WPW, LGL
    - Brugada Syndrome
    - Wellens syndrome
127
Q

what classes of drugs often cause QT prolongation

A
  • antiarrhytmics (sotalol, amiodarone)
  • antimicrobials (levofloxacin, ciprofloxacin, erythromyocin)
  • antidepressants
  • antipsychotics
128
Q

how does hyperkalemia appear on EKG

A

Peaked t waves (symmetrically peaked)

**often seen in dialysis patients

129
Q

how does hypokalemia appear on EKG

A

Flattened T waves

May see U waves

130
Q

what is WPW (wolff parkinson white)

A
  • accessory pathway disorder
  • Narrow QRS
  • “short PRI”
  • Delta Wave (“slurred” beginning of QRS–> gives illusion of short PR interval)
  • Can lead to PMVT
131
Q

what is brugada syndrome

A
  • Inhereted sodium channelopathy
  • Mostly men in their 40s

*dangerous arrhythmia

132
Q

diagnostic criteria for brugada syndrome

A
  • ecg abnormality in more than one precordial lead (bumpish area on the QRS-T) and:
    2. Data from the family history:SCD in a family member younger than 45 years.ECG type 1 in family members
    3. Arrhythmia-related symptoms: Syncope.Seizures.Nocturnal agonal respiration.
    4. Documented ventricular arrhythmias:Polymorphic ventricular tachycardia (PVT). Ventricular fibrillation (VF).
133
Q

How does Wellen’s syndrome appear on EKG

A

-DEEP inverted T waves during a pain-free period in a pt w/ intermittent CP

134
Q

Wellen’s syndrome finding suggests:

A

-high degree stenosis of LAD that will soon result in acute anterior MI if the patient is not urgently catheterized and the occlusion opened

135
Q

where should the T wave always be inverted?

A

aVR

136
Q
  • Prior history of chest pain
  • During chest pain: EKG is normal or with mild ST elevation or depression, or with terminal negative deflection of the T wave in V1and V2
  • Cardiac enzymes are normal or mildly elevated
  • No pathologic precordial Q-waves or loss of precordial R waves
A

Wellen’s syndrome

137
Q

Deeply inverted or biphasic T-waves in V2 and V3, possibly V1, V4, V5 and/or V6 when pain free

A

Wellen’s syndrome

138
Q

what is pericarditis and what is it associated w/

A
  • Acute inflammation of the pericardium can occur in a vast array of systemic illnesses and is commonly associated with:
  • viral infection
  • autoimmune disorders,
  • uremia, and
  • myocardial infarction.
139
Q

how does pericarditis appear on EKG

A

GLOBAL ST elevation

PR depression

140
Q

DDX of ST elevation on the ECG

A
  1. acute MI
  2. LVH
  3. ventricular paced rhythm
  4. normal variant
  5. hyperkalemia
  6. PE
  7. Prinzmetal’s angina
  8. acute pericarditis
  9. LV aneurysm
  10. benign early repolarization
  11. Osborn wave of hypothermia
  12. brugada’s syndrome
  13. acute cerebral hemorrhage
  14. postelectrical cardioversion
141
Q

what reciprocal changes do you see w/ MI on EKG

A

ST depression is a “mirror image” of ST elevation. If you see ST depression, that means that there is ST elevation in the OPPOSITE side of the heart. Anterior ST depression would indicate a posterior MI.

142
Q

what MI do you need to be careful about before you give them nitro?

A

If you see an inferior MI look for RV extension before you give them nitro or else you won’t be able to get the blood pressure back up

143
Q

presents w/:
Tachycardia
Hypertensive
ST elevation in V2-V4

A

anterior MI

*high morbidity and mortality

144
Q 
presents w/
bradycardia
hypotensive
very ill-appearing
ST elevation in II, III, aVF
A

inferior MI

145
Q

presents w/:

  • Horizontal ST depression
  • Tall, broad R waves (greater than 30ms)
  • Upright T waves
  • Dominant R wave (R/S ratio greater than 1)

*classicaly in V1-3

A

posterior MI

  • typically uncommon
  • *need LOTS of fluid
146
Q

in the setting of LBBB, electricity is already flowing abnormally through the heart. This can obscure subtle changes in the setting of acs/stemi.
-Therefore how can you determine if there is true ST elevation w/ LBBB

A

use Sgarbossa’s criteria

147
Q 
what are the degrees for:
LAD
RAD
Extreme RAD or LAD
normal
A

LAD: -30- (-90)
RAD +90 - 180
Extreme RAD or LAD: -90 - 180
normal: 0 - +90 or -30- +90

148
Q

when assessing CP and you listen to their heart, what are you assessing for?

A

new murmur–paillary muscle dysfunction, valve regurgitation, chordae rupture (in cardiogenic shock)

rales– CHF, LV dysfunction

149
Q

what is the leading cause of death in the US?

A

heart disease

150
Q

CP is less likely to be a ischemic if it meets what time requirements?

A

Lasting less than 2min
OR
Lasting GREATER than 24 hours

151
Q

what studies can R/O PE

A
  • D-dimer
  • chest CT
  • V/Q scan
152
Q

what studies can R/O aortic dissection

A
  1. CTA C/A/P

2. xray

153
Q

what studies can R/O CHF

A
  1. echo
154
Q

What me is the only thing that is actually shown to reduce morality

A

Aspirin

155
Q

when are beta blockers contraindicated in (N)STEMI

A
  1. hypotensive,
  2. bradycardia,
  3. cocaine**- leads to unopposed alpha agonist effect leading to worsening vasoconstriction
  4. AV block
  5. asthma

CABHA

156
Q

what CP patients just need Telemetry?

A
  1. no ST elevation, pain free, normal troponin

2. (Hx concerning but w/u nl- usually get stress test in later)

157
Q

what CP patients need to go to CICU

A

acute MI, ongoing pain, elevated troponin, on NTG drip

158
Q

describe what different HEART score mean

A

0-3: D/c home, for outpatient F/u
4-6: 20% chance of adverse event, consider admission
7-10: 73% chance of adverse cardiac outcome, admit, early dx

159
Q

Cocaine use leads to

A
  1. Vasoconstriction
  2. increased platelet aggregation
  3. increased myocardial O2 demand
  4. increased atherosclerosis
160
Q

how do you tx cocaine chest pain

A

benzo and then standard thearpy

  • do not use BB!!
  • MI occurs in 6% of abusers w/ CP
161
Q

MI complications

A
  1. cardiogenic shock

2. LHF

162
Q

Occurs when there is insufficient cardiac output to meet metabolic demands of the tissues

A

cardiogenic shock

163
Q

sx of cardiogenic shock

A
  1. Hallmark is HYPOPERFUSION
  2. hypotension,
  3. tachy- or bradycardia,
  4. cool mottled skin,
  5. altered mental status,
  6. oliguria- decreased urine output
  7. median onset, 8hrs after AMI
164
Q

tx of cardiogenic shock

A

Get cardiology and CV surgery on board early for interventions

*no single dx test

165
Q

what is the difference between systolic and diastolic dysfunction

A

Systolic: EF less than 40% (often from AMI)

Diastolic: impaired relaxation w/ preserved EF (often from chronic HTN)

166
Q 
Pulmonary Edema / Crackles
Frothy Sputum
Cardinal symptoms:
DOE
PND
Orthopnea**
Fatigue
S3
A

LHF

167
Q

Dependent edema
Hepatic enlargement
JVD- extended neck veins w/ pulsation

A

RHF

*usually the result of Left sided HF

168
Q

Imaging: CXR
Cephalization***-dilated upper lung vessels
Kerley B lines- horizontal lines of congestion at the bases
Pleural effusion
Pulmonary Vascular Congestion

A

CHF

169
Q

labs for CHF

A 
CBC, BMP
Troponin 
BNP***
less than 100= nl
over 500 is diagnostic
170
Q

xray: dilated upper lung vessels; more prominent than in the lower lung fields

A

Cephalization

**most sensitive CXR finding of acute HF

171
Q

Acute Tx for HF (both R and L)

A
  1. Sit patient up
  2. High Flow Oxygen
    - Titrate to greater than 95%
  3. BiPAP prn
  4. Nitroglycerin
    - vasodilate
    - Preload and afterload reducer
172
Q

PE occurs when

A

a portion of venous clot breaks off, traverse the right ventricle, and lodges in a pulmonary artery

173
Q

VIRCHOWS triad

A
  1. Hypercoagulable state
  2. Venous stasis
  3. Endothelial injury
174
Q

classic triad of pain, dyspnea, hemoptysis present less than 25% of time

A

PE

175
Q 
Dyspnea (75%)
 CP  (50%) 
classically pleuritic
Anxiety
Cough 
Hemoptysis
Diaphoresis
Tachypnea
Hypoxemia less than 95%
Rales 
Tachycardia
Fever greater than 38 C
thrombophlebitis
Unilateral Lower extremity edema
A

PE

176
Q 
clinical findings
Homans sign
Palpable cords
Calf asymmetry
Phlegmasi cerulea dolens- massively swollen cyanotic limb
A

DVT

177
Q

PE/DVT workup

A 
History
PEX
EKG
CXR
D Dimer*
-Unless low clinical suspicion 
Chest CT
-May or may not give info about PE
Ultrasound
V/Q scan
178
Q

describe the significance of a Ddimer

A
  • Negative result is highly predictive
  • High Sensitivity
  • Poor specificity – lots of false positives
  • False positives in liver failure, recent surgery, malignancy, pregnancy, elderly

-Frequently falsely positive- still requires Chest CT and further workup

179
Q

work up for PE

A
  1. start w PERC rule (score that does not require blood testing)
  2. go on to use Wells, with D-Dimer, if you “PERC out”
  3. Chest CT is diagnostic
    - Or VQ scan, if can’t get CT - elevated creatinine, etc.
  • Wells= use with + d dimer
  • PERC= dont need d dimer
180
Q

when can you not use PERC

A

if on OCP

*does not require d-dimer

181
Q

Wells score

A

less than 2= low prob
2-6= mod
greater than 6= high

182
Q

non thrombic PE

A

Amniotic fluid embolism
Fat embolism
Pulmonary air embolism

183
Q

PE EKG changes

A
  1. inverted T waves in V1-V3
  2. new RBBB
  3. sinus tachy
  4. S1-Q3-T3 (s wave in lead I, prominent Q in lead III, T wave inversion in III)
  5. RAD

SR SIN

184
Q

what shows S1-Q3-T3

S wave in lead I
Prominent Q wave in lead 3
T wave inversion in lead 3

A
  1. PE
185
Q 
xray:
Hampton’s hump- wedge shaped opacification 
Westermarks sign
Atelectasis
Infiltrates
Pleural effusion
Elevated hemidiaphragm
A

PE

186
Q

what dx can you get for PE?

A

CTA

or if abnormal Cr= VQ scan

187
Q

tx of PE

A
  1. Heparin or LMWH x 3-6 months AND Coumadin (warfarin)
    - 5 mg qd for 5d
    - target INR 2-3
  2. Thrombolysis if unstable
  3. IVC filter if recurrent
188
Q

tx of DVT

A

Upper leg clot:

  1. LMWH and Coumadin
    - Pradaxa/ Xarelto
  2. Large clot burden - thrombolysis

Lower leg/Calf vein DVT:
1. recheck US in 1 week w/ primary, vs treating acutely

189
Q

If positive DVT on doppler US with pulmonary symptoms, then proceed w/ __

A

tx for PE

*consider this for ppl you don’t want to CT scan (preg, RI)

190
Q

Blood creates a false lumen between intimal and adventitial layers

A

aoritc dissection

191
Q 
sx: 
Sudden onset
Pain Above AND Below the diaphragm
Pain migrates as dissection propagates
Syncope in 10%
Can have leg ischemia
N/V/Diaphoresis
Tearing or ripping chest pain that radiates to back
A

aortic dissection

192
Q

risk factors or aortic dissection

A
  1. Bimodal age distribution
    - Older w/ HTN
    - Younger w/ connective tissues disease
  2. Chronic HTN: most common predisposing factor
    - occurs in 80% of patients
  3. Connective tissue disorders- Marfans and Ehlers-Danlos
  4. Congenital heart disease
  5. Pregnancy

BCHCP

193
Q

hallmark finding of aortic dissection

A

unequal or absent pulses

194
Q

Standford classifications of aortic dissections

A
  1. Stanford Type A: Any involvement of Ascending Aorta (I and II DeBakey)
  2. Stanford Type B: Beyond the Brachiocephalic trunk (III DeBakey)
195
Q

Debakey classification of aortic dissections

A
  • Type I: ascending aorta and part of aortic arch (most common)
  • Type II: ascending aorta only
  • Type III: descending aorta only
196
Q

xray:

  • Aortic shadow extends over 5 mm from calcified wall
  • Blurred aortic knob
  • Left pleural effusion
  • Deviation of trachea or mainstem bronchi
  • Widened mediastinum**
A

aortic dissection

197
Q

what test can confirm diagnosis of aortic dissection and distinguish between different types

*shows intimal flap with true lumen anteriorly, false lumen posteriorly

A

chest CTA

198
Q

tx of aortic dissection

A

Immediate surgical consultation

Types A
require surgical repair

Type B

  • may be managed medically (control HR and BP w/ beta blockers)
  • Surgery may be recommended by vascular
199
Q

sx:
*CP Worse when supine, relieved learning forward
Sharp or stabbing CP
Pleuritic
Radiates to left trapezial ridge, and/or back,neck
Due to diaphragmatic pleural inflammation
Recent URI
low grade temp
Friction rub

A

pericarditis

200
Q

what is Dresslers syndrome

A
  • A type of pericarditis Post MI, post surgery, post trauma
  • Most common in first week after MI
  • Thought to be an immune system response after damage to heart
201
Q

EKG changes in pericarditis

A

Stage I: most common, diffuse CONCAVE upward ST elevation and PR depression (0-2 weeks)
Stage II: ST changes normalize; T wave flattening (1-3 weeks)
Stage III: flattened T waves become inverted
Stage IV: normalization

202
Q

labs for pericarditis

A 
Troponin (myocarditis)
CBC (look for elevated WBC)
BUN
Blood cultures- if looks sick/viral
Thyroid
ESR
203
Q

tx of complicated pericarditis

A

ADMIT

  • Immunocomprised
  • Elevated troponin
  • Large pericardial effusion
  • Anticoagulation
204
Q

tx of uncomplicated, presumed viral pericarditis

A

HOME
-anti-inflammatory 7-21 days (motrin 600mg TID)
NSAIDS
-outpatient follow up, and serial EKGs

205
Q

complications of percarditis

A

pericardial effusion leading to cardiac tamponade

206
Q

becks triad

A
  • Distant heart sounds,
  • hypotension
  • JVD
207
Q
  • c/o SOB, DOE
  • -Distant heart sounds,
  • hypotension
  • JVD
  • Pulsus Paradoxus- no pulse but can hear the heart
A

cardiac tamponade

208
Q

dx cardiac tamponade

A

cxr

echo

209
Q

tx of cardiac tamponade

A

Emergent pericardiocentesis

210
Q

ekg: Electrical Alternans (alternating QRS complex axis)

A

cardiac tamponade

211
Q

Spontaneous
Classically tall, thin males, Marfans
Pleuritic CP and dyspnea
Decreased breath sounds and hyper-resonant percussion on affected side

A

pneumothorax

212
Q

tx of pneumothorax

A
  1. Supplemental O2
    - help resorb pleural air
  2. Some PTX may be able to be observed
    - No trauma
    - less than20 %
    - stable VS
  3. repeat CXR in 6 hours if stable
213
Q

Lots of puking followed by CP

A

ESOPHAGEAL RUPTURE(BOORHAAVE’S SYNDROME)

214
Q 
Subcutaneous emphysema
Hamman’s crunch
air in the mediastinum ,moved by beating heart
Left pneumothorax and or effusion
\+/- Epigastric tenderness
A

ESOPHAGEAL RUPTURE(BOORHAAVE’S SYNDROME)

215
Q

how to dx ESOPHAGEAL RUPTURE(BOORHAAVE’S SYNDROME)

A
  • CT study of choice

- If unstable CXR- Can show PTX or Mediastinal air

216
Q

tx of ESOPHAGEAL RUPTURE(BOORHAAVE’S SYNDROME)

A
  1. Abx

2. OR for surgical repair

Emergency Medicine (22 decks)

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