Chest pain and EKG Flashcards

1
Q

EKG should be completed within __ minutes

EKG should be read by physician within __ minutes

A

6

10

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2
Q

Door to biomarker less than __ minutes or TAT (Troponin turnaround time)
Door to device less than __ minutes
Serial Troponin strategy will be __, __, and __ hours.

A

60
70
0, 3, 6

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3
Q

The hallmark of the Third Universal Definition of MI is the detection of a rise and fall of cardiac biomarker values, with at least one of the values being elevated. In addition to the highly sensitive and specific cardiac biomarker of necrosis, Troponin, at least one of the following five diagnostic criteria should be met. What are they?

A

Symptoms of ischemia
New significant ST/T wave changes or left BBB
Development of pathological Q waves on ECG
Imaging evidence of new loss of viable myocardium or regional wall motion abnormality
Identification of intracoronary thrombus by angiography or autopsy

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4
Q

If a patient cannot tolerate a treadmill stress test then a pharmacological test using ______, _______ or ______ infusion can be used.

A

Adenosine
dobutamine
persantine

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5
Q

Telemetry is “______” quality; determine the rate and rhythm only
- 12 lead ECG is “_______” quality; determination of disease, infarction, infection

A

monitor

diagnostic

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6
Q

ST segment elevation or depression are significant if greater than __mm (__ small block)

A

1

one

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7
Q

The goal is to have any patient who meets EKG guidelines to have a door to EKG time of less than __ minutes

A

5

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8
Q

Each individual EKG must have its own order, even if they are for the same patient
true or false

A

True

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9
Q

Anything outside the guidelines requires an order from the physician before completing the EKG, what are the guidelines (symptoms)? (7)

A
Pt with CP ESI level less than 3 
Rapid heart rate >100 
Slow heart rate; bradycardia 
Syncope (LOC not dizziness) 
Palpitations 
Drug overdoses 
SOB
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10
Q

Inferior Wall MI
The inferior wall is supplied by the ____ ____ ____ or ___.
ST elevations can be seen in leads __, __, and ___
Also be aware of possible right ventricular infarct, can be determined with a right sided 12- lead

A

right coronary artery
RCA
II, III, and aVF

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11
Q

The anterior wall MI (slide saved)
The anterior wall is supplied by the ____ ____ ____ or ___
This is known as the ____ ____

A

left coronary artery
LCA
widow maker

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12
Q

Septal Wall MI
Supplied by the left ____ ____ ____ or ___
Look for the lack of an _ wave in __

A

anterior descending artery
LAD
R wave in V2

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13
Q

Lateral wall MI
The lateral wall is supplied mostly by the ____ ____ ____ or ___
__% of the population has their inferior wall supplied by the ___

A

left circumflex artery
LCX
10
LCX

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14
Q

Posterior wall MI
The lateral wall is supplied by either the ___ or the ___
ST depression will be seen in leads V_, V_, V_, and V_
Reposition leads and obtain a posterior 12 lead containing leads V7, V8, and V9 for the ST elevations

A

LCA or the RCA

V1, V2, V3, and V4

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15
Q

Right sided infarction / Right sided EKG

A mirror image right sided ECG may be helpful in detecting STE associated with what?

A

right ventricular infarction.

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16
Q

Right sided EKG can be done using only the right side V_ lead in the right mid axillary line

A

4

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17
Q

Remember when doing a right sided EKG to label it a what?

A

right sided EKG

Duuuuh!

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18
Q

Posterior EKG
Posterior leads are used to evaluate for posterior wall MI. In a traditional EKG, posterior MI is demonstrated in leads V_-V_
Posterior leads V_, V_, V_ are placed below the left ____

A

V1-V4
7, 8, 9
scapula

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19
Q

Sinus arrest; arrest with slow heart rates is the same as ____ ____ ____
Management of prolonged sinus arrest where junctional or ventricular escape does not take over (ventricular asystole occurs) requires immediate attention
what are 9 possible causes?

A

symptomatic sinus bradycardia
Etiology; hypoxia, hyperkalemia, excessive digitalis or propranolol, quinidine toxicity, damage to SA node from AMI, acute myocarditis, degenerative fibrosis

20
Q

Some clinical signs of atrial fibrillation are (5)

A

SOB and pulmonary edema, drop in cardiac output and decreased cardiac output, irregular rhythm may be perceived as palpitations

21
Q

Etiology of atrial fibrillation include what? (7)

A

acute coronary syndromes, CAD, CHF, disease at mitral or tricuspid valve, hypoxia, acute pulmonary embolism

22
Q

1st Degree AV Block; Clinical signs; usually ___

Etiologies; (3)

A

asymptomatic
; AV nodal blockers
Condition that stimulates the parasympathetic nervous system
AMI that affects circulation to the AV node (right coronary artery), most often inferior AMI

23
Q

Which cardiac condition is nicknamed Wenckebach?

A

2nd Degree AV Block (Mobitz Type 1, Wenckebach)

24
Q

2nd Degree AV Block (Mobitz Type 1, Wenckebach)

what are the signs (symptoms on another card)

A

Signs; hypotension, shock, pulmonary congestion, CHF, angina

25
Q

2nd Degree AV Block (Mobitz Type 1, Wenckebach)

what are the symptoms (signs on another card)

A

chest pain, SOB, decreased level of consciousness

26
Q

2nd Degree AV Block (Mobitz Type 1, Wenckebach)

etiologies

A

AV nodal blocking agents; B-blockers, non-dihydropyridine calcium channel blockers, digoxin
Conditions that stimulate the parasympathetic nervous system
Acute coronary syndrome that involves right coronary artery

27
Q

2nd Degree AV Block (Mobitz Type II)

Clinical signs; (due to bradycardia)

A

Signs; hypotension, shock, pulmonary congestion, CHF, AMI

28
Q

2nd Degree AV Block (Mobitz Type II)

Clinical symptoms; (due to bradycardia)

A

Symptoms; chest pain, SOB, decreased level of consciousness

29
Q

2nd Degree AV Block (Mobitz Type II)

Etiologies

A

Acute coronary syndrome that involves branches of left coronary artery
3rd degree heart block- involved left anterior descending (LAD) artery and branches to interventricular septum which supplies the bundle branches

30
Q

3rd Degree AV Block (complete AV Block) clinical symptoms (due to bradycardia)

A

Symptoms; chest pain, SOB, decreased level of consciousness

31
Q

3rd Degree AV Block (complete AV Block) clinical signs (due to bradycardia)

A

Signs; hypotension, shock, pulmonary congestion, CHF, AMI

32
Q

3rd Degree AV Block (complete AV Block) etiologies

A

Acute coronary syndrome that involves branches of the left coronary artery
Involved left anterior descending (LAD) artery and branches to interventricular septum which supplies the bundle branches

33
Q

What are some of the causes of Supraventricular Tachycardia

A
Normal exercise 
Hypoxemia 
Fever
Hypovolemia
Adrenergic stimulation, anxiety
Hyperthyroidism
Anemia
Pain
34
Q

What are the clinical signs of Ventricular Tachycardia (Monomorphic)

A

Typical signs of decreased cardiac output (orthostasis, hypotension, syncope, exercise limitations, ect) do develop; can be asymptomatic; untreated and unsustained VT will deteriorate to unstable VT, often VF

35
Q

What are some of the signs of Ventricular Tachycardia (Monomorphic)

A

Ventricular irritability
R on T phenomenon
Drug induced prolonged QT interval
Low ejection fraction due to chronic systolic heart failure

36
Q

What is R-on-T phenomenon

A

It is a ventricular extrasystole caused by a ventricular depolarization superimposing on the previous beat’s repolarization. Although rare, this can result in ventricular arrhythmias, which can lead to cardiac arrest

37
Q

What is another name for Ventricular Tachycardia (Polymorphic)

A

“Torsade de Pointes”

38
Q

Ventricular Tachycardia (Polymorphic) “Torsade de Pointes”, what are the Clinical Signs

A

Typically will rapidly deteriorate to pulseless VT or VF

Symptoms of decreased cardiac output (orthostasis, hypotension, syncope) before pulseless arrest; seldom sustained VT

39
Q

What are the etiologies of Ventricular Tachycardia (Polymorphic) “Torsade de Pointes”

A

Ventricular irritability
R on T phenomenon
Hereditary long QT interval syndromes
Prolonged QT interval due to tricyclic antidepressants, procainamide, sotalol, amiodarone, ibutilide, some antipsychotics, digoxin, some long-acting antihistamines
Electrolytes and metabolic alterations (hypomagnesemia)

40
Q

What are the clinical signs of Ventricular Fibrillation / Pulseless V Tach?

A

Collapse; unresponsive; no pulse; agonal gasps or apnea; sudden death

41
Q

What are the etiologies of Ventricular Fibrillation / Pulseless V Tach?

A
Acute coronary syndromes
Unstable VT untreated 
R-on-T phenomenon
Drug, electrolyte, acid-base abnormalities 
QT prolongation 
Electrocution 
Hypoxia 
Amiodarone or Lidocaine 
Identification and treatment of the underlying causes (H’s and T’S)
42
Q

What are the clinical signs of Pulseless Electrical Activity (PEA)

A

Collapse, unresponsiveness, agonal gasps or apnea, no pulse detectable by palpation, the rhythm seen with PEA may assist in identifying PEA etiology

43
Q

What are the etiologies of Pulseless Electrical Activity (PEA)

A
Use the H’s and T’s mnemonic to recall possible causes of PEA
H’s 
Hypovolemia
Hypoxia
Hydrogen ion (acidosis) 
Hypo/hyperkalemia
Hypothermia 
T’s
Toxins (drug overdose, ingestion)
Tamponade (cardiac) 
Tension pneumothorax 
Thrombosis, coronary ACS
Thrombosis, pulmonary embolism
44
Q

As per the CPC chest pain center guidelines, what is the third universal definition of myocardial infarction?

A

Detection of a rise and/or fall of cardiac biomarker values, with at least one of the values being elevated.

45
Q

The Third universal definition of myocardial infarction
Detection is a rise and/or fall of cardiac biomarker values, with at least one of the values being elevated.
In addition, at least one of the five following criteria should be met. What are they?

A

Symptoms of ischemia
New or presumably new significant ST/T wave changes, or LBBB
Development of pathological Q waves on ECG
Imaging evidence of new loss of viable regional wall abnormality
Identification of intracoronary thrombus by angiography or autopsy

46
Q

Acute coronary syndrome is applied to patients in whom there is a suspicion or confirmation of acute MI ischemia or infarction.
Three types of ACS are

A

NSTEMI 40%
Unstable angina 40%
STEMI 20%

47
Q

What are the times for
arrival EKG?
read by provider?
Troponin turnaround time or first result?
Troponin intervals?
What should be done with each subsequent troponin?

A

arrival EKG? 6 minutes
read by provider? 10 minutes
Troponin turnaround time or first result? 60 minutes
Troponin intervals? 3 and 6 hours
What should be done with each subsequent troponin?