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ECG 7150/7220 > 7220 Acute Coronary Syndrome > Flashcards

7220 Acute Coronary Syndrome Flashcards

1
Q

what is the main problem in ACS?

A
  1. reduced O2 supply due to atherosclerotic narrowing of coronary arteries
    - inflammatory or vasospastic
  2. Blood flow decreases = symptom of lack of O2

**vasospasm, inflammation and atherosclerosis

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2
Q

Function of the endothelium? 5

A
  1. Role of endothelial NO sinthase (eNOS)- nitric oxide synthase enzyme. Dilates. normal levels = can vasodilate coronary arteries. if there isnt then = narrowing***
  2. sellective barrier between vessel lumen and surrounding tissue
  3. Regulation of vascular tone and growth
  4. Regulation of thrombosis and fibrinolysis
  5. plays a role in immune and inflammatory reactions
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3
Q

causes of endothelial injury: 4

A
  1. elevated levels of cholesterol and triglycerides = plaques
  2. HTN - constant pressure
  3. smoking
  4. bacterial/viral infections (flu, strep, pneumocc, RSV)

risk factors to endothelium dysfunction: obese, elevated CRP, chronic systemic infection

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4
Q

what is shear stress?

A

not laminar

where there are curves, or turbulant flow.

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5
Q

what does shear stress cause?:

A
  • decreased eNOS
  • decreased endothelial repair
  • decreased alignment/direction of flow
  • increased reactive O2 species
  • increased leukocyte adhesion
  • increased lipoprotein permeability
  • increased inflammation
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6
Q

ACS:
Ischemia, injury, infarct

timing and ST/Q-wave

A

Ischemia- 10-20 min (unstable angina)
ST depress

Injury - > 20 min NSTEMI/ non Q-wave
ST depress

Infarct- > 30 min STEMI/ Q-wave

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7
Q

why might there be refered pain of angina/chest pain?

A

the same chemoreceptors/mechanoreceptors from the myocardial stretch. Dermatomes are shared to the brain

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8
Q

Classic S and S of angina/chest pain

A

classic: sweating, nausea, lightheadedness, SOB, plus referred pain

chest pain reflects = end organ perfusion CVS!!!* decreased coronary supply***

Common- silent or nonpainful

Atypical- fatigue or unwell (women, elderly and DM’s)

other: tachy, S3/S4, cardiac/femoral bruit, deficits in periph pulses, HTN, Pallor, Cold Clammy skin, Xanthomas

**pain with exercise that is relieved with rest. HX risk factor

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9
Q

Primary Assess:

NOPQRST

A 
N- normal baseline before onset
O- onset time started
P- precipitating- how started. Palliative- how it ended
Q- quality
R- region and radiation
S- severity
T- timing- how long it lasts
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10
Q

What does the RCA supply?

conduction?

A 
Right coronary artery:
Supply:
- Right atrium
- right vent
- inferior and posterior wall of left vent

Conduction:

  • SA node 55%
  • AV node 90%
  • proximal portion of bundle of his
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11
Q

What does the LAD supply?

conduction?

A

Left anterior descending:
Supply:
- portions of the anterior left and right ventricles
- interventricular septum

Conduction:
- bundle branches (vnet conducting tissue)

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12
Q

What does the Circumflex supply?

conduction?

A

Supply:

  • Left atrium
  • posterior/lateral wall of left vent

Conduction:

  • SA node 45%
  • AV node 10-15%
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13
Q

what happens if you block the RCA?

A

bradycardia

  • evaluation of the right ventricular wall involvement
  • some hemodynamic changes
  • Potential for significant dysrhythmias caused by SA and AV node dysfunction
  • CHF
  • cardiogenic shock
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14
Q

what happens if you block the LAD?

A
  • Left vent dysfunction
  • potential for hemodynamic compromise
  • HF
  • pulm edema
  • cardiogenic shock
  • intraventricular conduction disturbances
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15
Q

what happens if you block the circ?

A
  • evaluation of posterior and lateral wall involvement
  • some hemodynamic changes
  • dysrhythmias caused by SA and AV node dysfunction
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16
Q

Anteroseptal ECG evidence

A

V1-V4

Q-waves and ST segment elevation

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17
Q

Lateral Wall ECG evidence

A

I, aVL, V5-V6

Q-waves and ST segment elevation

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18
Q

Posterior Wall ECG evidence

A
  • V1-V2
  • Tall upright R waves with ST depression
  • Q-wave and ST elevation in
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19
Q

Inferior Wall ECG evidence

A

Q-wave and ST elevation in II, III, aVF

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20
Q

Right Ventricle Wall ECG evidence

A

Q-waves and ST elevations in Right precardial leads RV1-RV6

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21
Q

What is NSTEMI? what happens to the ST? Biomarkers?

A

No ST elevation or ST depression (ischemia).

cells can be saved if reperfused early

Can have + biomarkers

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22
Q

What does T-wave flattened or inversion mean?

A

ischemia or resolution phase

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23
Q

What does tall T-waves mean?

A

Tombstone T waves = early signs of infarction

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24
Q

what does ST elevation mean?

A

injury.

Cells may recover

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25
Q

what does a Right BBB look like?

where do you see it on an ECG?

A

rabbit ears

V1-3

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26
Q

What does a left BBB look like?

Where do you see it on an ECG?

A

top hat

I, V5-6

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27
Q

what happens to the QRS in BBB’s?

A

it is wide (prolonged)

> 0.12

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28
Q

what are the 3 main evolutionary stages of MI?

A
  1. Acute injury
  2. Necrosis
  3. Resolution
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29
Q

stage 1 Acute injury…

A

time between the acute blockage and the tissue death

ST elevation

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30
Q

stage 2 Necrosis…

A

“dead zone” presence of tissue death

pathological Q-waves

> than one small box or 1/3 the height of the QRS

necrotic cells dies from lack of O2 in blood

Cardiac biomarkers

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31
Q

stage 3 Resolution…

A

2 weeks after stage 2 scar tissue develops in the infarcted area

persistent Q-waves or inverted T waves*

No cardiac biomarkers

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32
Q

what kind of STEMI do you call this…

Elevated ST in… II, III, aVF

A

Inferior wall STEMI

RCA

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33
Q

what kind of STEMI do you call this…

Elevated ST in… V1 and V2

A

Septal STEMI

LAD

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34
Q

what kind of STEMI do you call this…

Elevated ST in… V3 and V4

A

anterior wall STEMI

LAD

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35
Q

what kind of STEMI do you call this…

Elevated ST in… I, aVL, V5 and V6

A

Lateral wall STEMI

Circumflex

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36
Q

what is the reciprocal of inferior?

A

anterior

V1-4

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37
Q

what is the reciprocal of lateral?

A

inferior

II, III, aVF

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38
Q

what is the reciprocal of anterior?

A

inferior

II, III, aVF

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39
Q

what is the reciprocal of Anteriolateral wall?

A

Inferior

II, III, aVF

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40
Q

If you have an ST elevation in V1-V4 then you will have reciprocal in?

A

Inferior II, III or aVF (at least 2)

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41
Q

When is ST depression significant on an ECG?

A

When there is no ST elevation**

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42
Q

what do you call paced rhythms

A

Vent paced, atrial paced or dual paced rhythm

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43
Q

What is ST fingerprinting?

ex. Primary lead II
secondary V2
If the PT has a hx of having an inferior MI are these the best leads to display?

A

you have primary and secondary lead II and V2

fingerprinting is customizing to display on monitor.

** you would want one of the leads to then be looking at the inferior wall**

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44
Q

if you have a lateral wall MI, what would you want to display on the monitor?

A

one of I, aVL, V5-V6

45
Q

Why do we ask you to do

QT analysis

A

R on T phenomenon

can cause fatal dysrhythmia

46
Q

QTc

A

corrected measurement of

47
Q

which drug prolongs QT or QTc?

A

Amiodarone

Antiphychotic- haldol, zofran, gravol

48
Q

whats the best way to document a prolonged QT?

A

Request for a 12 lead ECG to see if the QT is prolonging. Get a 12 lead to compare to the first one taken

49
Q

how often do you look at trops?

A

Q4-6 hrs

stop when the trend starts to go down

50
Q

whats the diff btwn CK and CK-MB

A

Creatinine Kinase

CK- non specific substance that would be elevated in ANY event in muscle injury

CK-MB- isoenzyme specific to heart muscles

51
Q

why do we order these labs: in context of ACS

  1. HGB, HCT
  2. Differential count
  3. Plt
  4. lytes- which ones
  5. PT and aPTT
  6. Glucose
  7. kidney function
A
  1. HGB, HCT- blood flow/ transport. For O2 to body. HCT to see if blood flow is viscus
  2. Differential count- signs of infection = increased myocardial O2 demand. percentage of blood cells
  3. Plt- bleeding
  4. lytes- K+, Ca+, Mg- for myocardial contractility
  5. PT and aPTT- heparin. need baseline if we want to start hep inf. Mostly with NSTEMI
  6. Glucose- control for long term management of ACS
  7. kidney function- for drugs you will give (lasix, ACE inhibit* post-recovery, ARBs, non-steroidal)
52
Q

We have a PT who presents with chest pain, has risks but has a normal ECG

what to do?

A
  • follow ACS pathway and request cardiac biomarkers. We need to know if it is unstable angina or NSTEMI.

If there are no biomarkers, we can call it unstable angina. if there are biomarkers we can call it NSTEMI

53
Q

what other diagnostic tests could be ordered?

A
  • CXR- size of heart, lungs
  • PET,
  • ECHO 2D- EF, vent function, valves (looks like US)
  • Coronary angio- artery function
  • MRI
  • exercise stress test- resolution phase
54
Q

Treat ACS to avoid complications of MI: 5

A
  1. Cardiogenic shock (rapid thready pulse, dyspnea, tachypnea, crackles, +JVD, oliguria, LOC changes)
  2. Mechanical complications- (vent/septal wall rupture or LV free wall rupture)
  3. Pericarditis- inflammation
  4. Thromboembolic Complications- DVT, PE’s, systemic emboli
  5. Electrical Complications- dysrhythmias, brady/tachy/SVT, other conduction disturbances
55
Q

What do we give PTs with ACS symptoms?

Imbalance of myocardial O2 supply and demand

A

MONA

Nitrates
ASA
O2/IV access/12 lead ECG
Morphine (analgesics)

56
Q

Do you always give the PT O2?

A

No only if it is under < 94%

57
Q

Why do we give nitroglycerine ***

A
  1. vasodilates coronary arteries to improve perfusion***

2. VENODILATORS= increase venous capacitance vessels = preload will decrease (decrease venous return)

58
Q

Side effect of Nitro

A

decrease BP

59
Q

What can PTs be started on for the management of UA/NSTEMI? examples

A
  • ASA
  • Clopidogel (plavix) or ticlopidine
  • IV hep or LMWH
  • GP IIb/IIIa antagonist (Gycoprotein inhibitors)
60
Q

How does ASA, Clopidogel/Ticlopidine, GP IIb/IIIa antagonist function for ACS?

A

Antiplatelet- disrupts platelet adhesion aggregation

61
Q

How does IV heparin or LMWH function for ACS?

A

Disrupts thrombin formaiton by binding with antithrombin III and thrombin to create inactive complexes

Heparin is not there to dissolve the clot but to prevent more from forming

62
Q

How does ASA work?

A

Inhibit platelet aggregation to avoid clot formation

63
Q

How does plavix (clopidogel) or ticagrelor work?

When do you use either?….

A

platelet inhibitors. Decrease Atherosclerosis

clop- inhibits binding of ATP to platelet receptor = inhibit platelet activation/aggregation 
- clop can cause brady dysrhythmias

ticagrelor- more rapid onset than plavix

64
Q

How does BB act? why used in ACS?

A

decrease HR to decrease myocardial O2 demand

will also decrease the contractility

65
Q

How do ACEI and ARBS act? why use it for ACS

A

ACE- pril. prevents the conversion of angiotension I to angiotension II to decrease afterload.

to avoid vent remodeling (will learn this later)

66
Q

What do you need to consider for myocardial reperfusion therapy?

A
  1. Length of time from onset of symptoms

2. Hospital capability

67
Q

Need to treat PT within first

A

12 hrs. Start count when they get through the doors of the hosp

68
Q

Symptom to needle

A

within 30 min for fibrinolytic therapy if you are not near a cath lab

69
Q

If they are in RCH how long for PCI therapy?

A

90 min.

Door to balloon time

70
Q

the goals for treatment of STEMI for time to reperfusion

A

90 in for primary PCI and 30 min for fibrinolysis

71
Q

Absolute contraindications for thrombolytic therapy

A
  • previous hemorrhagic stroke at any time
  • ischemic stroke within 3 months except acute ischemic stroke within 3 hrs
  • known structural cerebral vascular lesion
  • known intercranial neoplasm
  • active internal bleeding (not period)
  • suspected aortic dissection
  • significant closed head or facial trauma within 3 months
72
Q

Caution/Relative Contraindications

A
  • severe uncontrolled HTN on presentation (SBP >180 or DBP >110)
  • Hx of prior ischemic stroke > 3 months, dementia, or known intracranial pathology not covered in contraindications
  • current use of anticoagulants in theraputic doses (INR>2-3); known bleeding diathesis
  • tramatic or prolonged (>10min) CPR or major sx (3 weeks)
  • recent (2-4 weeks) internal bleeding
  • non-compressible vascular punctures
  • for streptokinase/antistreplase: prior exposure (>5 days ago) or prior allergic reaction to these agents
  • actice peptic ulcer disease
  • pregnancy
  • current use of anticoagulants: the higher the INR, the higher the risk of bleeding
73
Q

RBBB

A

> 0.12 QRS

V1-3

Small R-large S- large R

Rabbit ears

74
Q

LBBB

A

> 0.12 QRS

V1-2

tiny R (if any)- large downward S (can be rS wave) then joins T wave

75
Q

which are the fibrin selective agents that are the ‘specific clot busters’ (lysis)

A
  • alteplase
  • reteplase
  • tenecteplase (TNK)
76
Q

Non-selective thrombolytic therapy agents

A

plasminogenolysis and fibrinolysis =

stroptokinase

77
Q

nursing responsibilities for reperfusion therapy:

A
  1. Ensure 2x IV access 20g. then no venipunctures for 24 hrs
  2. ensure drug circulates systemically
  3. avoid use of auto BP cuffs
  4. No shaving and avoid brushing teeth
78
Q

Post-fibrinolytic therapy what to expect:

A
  1. evidence or reperfusion: regression of ST segment to normal
  2. Self-limiting/ non-sustainable dysrhythmias - PVC’s, brady, H blocks, VT
  3. Washout: early and marked rise in cardiac biomarkers
  4. prompt relief of chest pain
  5. Bleeding: bleeding/bruising at puncture sites, blood from any body openeings, skin changes, LOC changes, changes in VS, Hct
79
Q

What is PCI?

A

Percutaneous Intervention

Cardiac catheterization

Diagnostic - gold standard treatment procedure

80
Q

name 2 common PCI’s

A
  1. Angioplasty- single or double vessel disease. Displaces plaque and overstretches the vessel with balloon
  2. Coronary stents - wire mesh tubes as scafolding

Other: Atherectomy, laser angio, cutting balloon angio, brachytherapy

81
Q

Nursing post-PCI care

A

(post-cath lab)
- ongoing assessments
(50% of PTs report chest pain after PCI) sites and periph circulation
- telemetry
- assays for biomarkers
- early sheath removal (ART/groin access removal)
- bedrest (3 hr min) and mobility
supine, flat legs, fowlers ok, compression

82
Q

signs and symptoms of reperfusion

A

Washout

  • cardiac biomarkers rise then fall
  • normalize of ST segments
  • non-sustained arrhythmias (asymptomatic)
83
Q

medication Management of Acute STEMI: 5

A
  1. Myocardial Reperfusion Therapy - TNK
  2. Anticoagulation - Heparin
  3. Prevention of Dysrhythmia - amiodarone, sotalol, lidocaine
  4. Glucose control/ - insulin?
  5. Prevention of Ventricular Remodeling - ACEI and ARBS
84
Q

Clinical guidlines for management of Acute STEMI anticoagulation:

A

IV Heparin

also give ASA daily

85
Q

What drugs are used for the prevention of Dysrhythmias?

A
  1. Amiodarone
  2. Beta-Blockers
class 1 - Na+ channel blockers
class 2 Beta blockers
class 3 K+ channel blockers 
class 4 Ca+ channel blockers
86
Q

tobacco contributes to atherosclerosis by

A

increases LDL and decreases HDL, promotes vasoconstriction and damage to the epithelium

87
Q

Dysfunction of the Endothelium produces…

A 
Nitric Oxide (NO dilates). 
Key leukocyte, platelet inhibitors and vasodilator that help maintain vascular smooth muscle cells in a normal, nonproliferative state. Meaning more vasoconstrictor substances are released. This attracts and retains LDL, which in turn becomes fatty streak (foam cells). These cells continue to release inflammatory substances, which weaken the fibrous cap of the plaque
88
Q

what does wide QRS mean?

A

BBB

or ventricular related. When higher pacemaker sites have failed or blocked. (vent escape, vent tachy, vent fib, premature vent contractions)

89
Q

pathological Q wave

A

at least 1 small box wide and 25% the height of the R

90
Q

CK

CK-MB

A

CK creatinine kinase- enzyme found in heart and skeletal muscle. when muscle is damaged CK is released into blood

CK-MB isoenzyme specific to heart

91
Q

Trop

A

Contractile protein specific to cardiac muscle.

92
Q

BNP

A

brain natriuretic peptide- protein found in heart when having HF

93
Q

CRP

A

When there is inflammation in the body

94
Q

Differential count

A

signs of infection = increases myocardial demand

percentage of blood cells (WBC’s)

95
Q

Lytes

A

Mg, K+, Ca for cardiac function

96
Q

Kidney function

A

for which drugs to give

97
Q

how do you know if MI is acute and not older

A

if there are no Q waves then it is not in necrosis or resolution phase

If there are no biomarkers, but there are Q waves then it is older (resolution)

98
Q

when do you give plavix rather then ticagrelor with TNK?

A

when the MI is inferior due to the risk of brady

99
Q

If the PT still has nausea, why do you give more nitro?

A

because there is still an O2 imbalance. Nitro can vasodilate

100
Q

there are 4 goals to myocardial reperfusion therapy

A
  1. re-establish early patency of the coronary artery
  2. to increase “salvage” of myocardial tissue
  3. to preserve left vent function
  4. to increase survival from MI
101
Q

what are the 2 reperfusion strategies and how long do you have to start them?

A

either need to be started within 12 hours of onset

Thrombolytic- 30 min
primary PCI- 90 min

rescue PCI if fibrinolytic fails should be done within 120 min

102
Q

absolute contraindications for thrombolytic therapy

A
  1. Previous stroke at any time
  2. Ischemic stroke within 3 months except within 3 hours
  3. knows structural vascular lesion
  4. active internal bleeding
  5. suspected aortic dissection
  6. signif closed head injury or facial trauma within 3 months
  7. severe uncontrolled HTN SBP >180, DBP> 110

avoid automated BP cuffs and brushing teeth, no venipunctures within 24 hrs after heparin stops

103
Q

2 examples of PCI

A
  1. coronary artery angioplasty

2. Stents

104
Q

how do you know if you have successful thrombolysis therapy?

A
  1. reduced chest pain
  2. reperfusion dysrhythmias (vent premature contractions, vent tachy, accelerated idiovent rhythm, A.fib, vent fib)
  3. resolution of ST elevation
  4. abrupt and early rise of biomarkers
105
Q

what does vomiting induce?

A

vagal stimulation of SA and AV node triggers parasympathetic stimulation of nervous system to decrease HR and conductivity through the AV node

can worsen bradycardia

106
Q

what is atropine used for

A

a vagolytic for bradycardia with AV block

107
Q

special considerations for PCI

A
  1. the stiff wire can perf causing cardiac tamponade

2. the wire can be irritating and cause dysrhythmias

108
Q

what is loss of capture>

A

when the pacemaker fires but doesnt create depolarization

ECG 7150/7220 (6 decks)

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