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Cardio > CAD / Acute Coronary Syndrome > Flashcards

CAD / Acute Coronary Syndrome Flashcards

1
Q

What are the 3 stages on EKG of MI?

A

1) ST-depression (represents ischemia not necessarily damage)

2) ST-elevation (represents injury not necessarily infarct)

3) Q-waves (represent infarct that is worsening)

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1
Q

What leads represent Lcx or LAD injury?

A

Lateral leads

I, aVL, V5-V6

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2
Q

What leads represents RCA injury?

A

Inferior leads

II, III, aVF

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3
Q

What leads represent LAD injury?

A

Anterior / septal leads

V1-V4

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4
Q

What do we define as an ST-elevation?

A

2 small boxes from baseline

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5
Q

What can be a problem with checking troponins?

A

you might check too early

they don’t really start to peak until about 4 hours after infarct

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6
Q

What peaks first troponin or CK-MB?

A

CK-MB peaks first (16 hours)

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7
Q

When does troponin peak?

A

24 hours

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8
Q

How long does CK-MB last?

A

48-72 hrs

useful for detecting reinfarction since troponin levels can stay elevated for 7-10 days after

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9
Q

What are markers of stable angina?

A

Exertional

No ST-elevation

No increase in biomarkers

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10
Q

What are the two pros of statins?

A

1) lower LDL

2) have anti-inflammatory effects to stabilize a plaque

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11
Q

What makes a plaque more stable?

A

a thick fibrin cap

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12
Q

How does nitroglycerin relieve chest pain?

A

1) arterial dilation decreases afterload which decreases the amount of O2 consumption needed (higher doses)

2) venous dilation decreases preload which decreases the amount of O2 consumption needed (lower doses)

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13
Q

What can be the 2 general causes of ischemic discomfort?

A

supply-demand imbalance / stenosis

acute coronary syndrome

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14
Q

What defines acute coronary syndrome?

A

there is a thrombus

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15
Q

If ST-elevation is absent but biomarkers are elevated, what do you have?

A

non-stemi

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16
Q

If ST-elevation is absent, biomarkers are absent but pain occurs at rest, what do you have?

A

unstable angina

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17
Q

Can NSTEMI be caused by either stenosis (suppply-demand) or acute coronary syndrome (thrombus) ?

A

yes!

if biomarkers are elevated, you are having cell death and an NSTEMI

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18
Q

Can STEMI be caused by either stenosis (suppply-demand) or acute coronary syndrome (thrombus) ?

A

No

STEMI is only caused by a thrombus

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19
Q

When you see Q-waves what does this indicate (specific)?

A

this indicates that you now have transmural infarction

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20
Q

What can be a lasting effect of MI?

A

heart failure

damaged areas of heart might not move as well and lead to dysfunction

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21
Q

What valve does a LAD heart attack often effect?

A

this can cause mitral regurgitation

ischemia can affect the papillary muscles and lead to mitral regurgitation

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22
Q

What can RCA infarct effect electrically?

A

can damage the vagus nerve which can then suppress the AV node through parasympathetic stimulation

also RCA gives blood to SA and AV node

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23
Q

What can PDA infarct effect eletrically?

A

PDA supplies the AV node

Infarct can lead to bradycardia or heart block

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24
Q

When should you not give a B-blocker in heart attack?

A

do not give if there is significant LV dysfunction

this could cause bradycardia / heart block

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25
Q

What happens to HR in heart failure?

A

CO = HR * SV

since SV decreases, HR will increase to try to stabilize CO

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26
Q

Reciprocal ST-depression

A

small depressions that occur in reciprocal leads when there are ST-elevations in other leads

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27
Q

What is main concern when giving a thrombolytic to treat MI?

A

intracranial hemorrhage / bleeding

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28
Q

What time should you be doing PCI by?

A

3 hours

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29
Q

What is a hard stop for giving thrombolytics?

A

high BP

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30
Q

When you have inferior lead ST-elevation, what else should you check for?

A

st-depressions in leads V1-V4 with tall R waves

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31
Q

What are other causes of ST-inversion besides MI?

A

pericarditis, BBB, LVH/RVH

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32
Q

What type of MI represents transmural infarction?

A

STEMI

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33
Q

What is common in the first 4 days after infarction?

A

ventricular tachycardia or arrthymia

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34
Q

5-10 days after MI what can happen?

A

papillary muscle rupture

interventricular septal rupture

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35
Q

Signs of papillary muscle rupture

A

Inferior MI

holosystolic murmur

heart failure / shock

acute pulm. edema from fluid backing up in LA

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36
Q

Signs of interventricular rupture

A

Hypotension

right heart failure comes before left sided

can also hear a systolic murmu

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37
Q

Difference between fibrinous pericarditis and Dressler

A

Dressler is an autoimmune reaction that can occur weeks after MI

Fibrinous pericarditis can occur as early as 2-4 days later

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38
Q

For 1 year after stent, what do you use?

A

aspirin and clopidogrel

antiplatelets

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39
Q

What does clopidogrel work on?

A

prevents ADP platelet activation

works on the P2RY12 receptor

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40
Q

What 4 drugs do you give in hospital when someone is having an MI? Why?

A

B-blocker (reduce O2 consumption)

Nitrate (reduce O2 consumption)

aspirin (anti-platelet)

heparin (anti-coagulant)

41
Q

How does heparin work?

A

Heparin increases activity of antithrombin III which prevents thrombin from forming clots

42
Q

What can happen in an inferior MI to autonomics? What should you be wary of?

A

inferior MI can stimulate vagal nerve and cause decreased heart rate

in this case, do not want to give beta blockers

43
Q

When should you be wary of giving nitrates? Why?

A

When there is an inferior / right side MI

By decreasing preload in an already compromised right EF, you might reduce cardiac output and precipitate hypotension

44
Q

Should you give thrombolytics when someone is having a supply-demand (stenosis) heart attack / angina?

A

No! You do not have a thrombus

45
Q

Why do we often give nitrates and B-blocker together?

A

Decrease preload = decreased SV with nitrates

Decreased SV = increased HR to maintain CO

Increased HR = give beta blocker

46
Q

How do B-blockers work?

A

they decrease heart rate and contractility by blocking sympathetic simulation of B1 receptors

47
Q

What class of drugs is an example of a negative inotrope?

A

Ca2+ channel blockers (verapamil + diltiazem)

they will decrease heart rate and contractility

also b-blocker

48
Q

Why might you not want to give a Ca2+ channel blocker?

A

they also increase preload

this could worsen heart failure

diltiazem and verapamil should be discontinued in HF

49
Q

Why does QT prolongation occur?

A

due to delayed repolarization (phase 3) of the myocyte action potential

K+ channels are blocked

50
Q

Why does PR prolongation occur?

A

delayed conduction through AV node

51
Q

Ranolazine

A

novel agent that has anti-angina effects with NO CHANGE on BP / HR

decrease O2 demand by preventing intracellular Ca2+ overload

inhibits late phase of the Na+ current (less Na+ = less Ca2+)

52
Q

Ranolazine effect at high dose

A

can cause QT prolongation since it blocks repolarization at high doses

53
Q

Beta blockers effect on SA node

A

Less beta stimulation = less cAMP

less cAMP = less calcium

less calcium = phase 0 of SA node potential delayed

54
Q

Which cardiac action potential uses Ca2+ in depolarization?

A

the SA node

55
Q

Which cardiac action potential uses Na+ in depolarization?

A

the myocyte

56
Q

Adenosine

A

direct negative inotropic effect

useful for treating supraventricular tachycardia (PSVT)

57
Q

What is an example of cardiac glycoside?

A

digoxin

58
Q

Digoxin MOA (2)

A

1) positive ionotropic

2) AV node inhibition: stimulates the parasympathetic nervous system

59
Q

Lisinopril MOA

A

ACE inhibitor

ACE normally makes angiotensin which is a vasoconstrictor

By inhibiting ACE, you lower angiotension / vasoconstriction which helps to lower BP

60
Q

2 examples of positive iontropes

A

Cardiac glycosides (digoxin)

Beta agonists (dobutamine, epi, norepi)

61
Q

Which beta agonist has lowest risk of tachycardia?

A

norepinephrine

62
Q

when do you use a Swan cath?

A

if you suspect papillary muscle rupture or intraventricular rupture after an MI

63
Q

How does an intraventricular defect lead to hypotensive and pulmonary edema?

A

when LV pumps, blood can go to RV and out pulmonary artery causing backup in lungs

also you’re not pumping as much to systemic circulation which causes hypotension

64
Q

What are signs of the neurocardiac reflex?

A

Bradycardia

Good perfusion

Post-MI (inferior)

65
Q

What drug blocks a parasympathetic response?

A

atropine

use for the neurocardiac reflex

66
Q

What is the neurocardiac reflex?

A

LV stretch makes it seem like there is an increased SV so you want to decrease HR

causes bradycardia

67
Q

Kussmaul sign PE

A

upon inspiration JVP increases

(JVP should normally fall when you inhale because you are pulling blood into the RA)

68
Q

What does Kussmaul’s sign indicate?

A

right heart dysfunction / limited right ventricle filling

paradoxically, right atrial pressure is rising during inspiration

69
Q

If you have an inferior infarct, what are you worried about electrically?

A

the RCA could have reduced blood to SA / AV node

also the RCA could hit vagal nerve and increase parasympathetic

all this could lead to PR prolongation / AV block (I or Mobitz II)

70
Q

If you have a anterior infarct, what are you worried about electrically?

A

LAD supplies bundles of HIS, BBB, etc. so you are worried about a AV block (Mobitz II or 3rd degree block)

71
Q

What is heart rate response to heart failure normally?

A

tachycardia to try to make up for decrease in SV

CO= HR * SV

72
Q

PVC vs. PAC on EKG

A

PVC looks like wide, random, big QRS complex

PAC looks like normal beat just thrown too early

73
Q

Why can you see PVCs after a MI?

A

acute MI can cause an electrical storm and lead to electrical problems

74
Q

What are some features of HPI that can tell you someone has unstable angina due to thrombus not stenosis?

A

new onset angina

angina in a crescendo pattern

angina at rest

75
Q

What is frontline treatment for preventing MI in outpatient setting?

A

aspirin (prevent clot)

statin (manage LDL)

B-blocker (reduce O2 consumption)

76
Q

What is a Q-wave?

A

a pathological Q-wave is when the Q part of the QRS complex really dips below normal

Q wave is stretched downward

77
Q

If a MI is not totally occlusive what does it have to be?

A

an NSTEMI

78
Q

What are the pre-cordial leads?

A

V1-V6

79
Q

What does pulmonary edema indicate?

A

indicates left sided volume overload since you are backing up into the pulmonary vein

80
Q

What does elevated JVP indicate?

A

right side volume overload since you are backing up into the vena cava

81
Q

Mild bradycardia following an MI can indicate …

A

neurocardiac reflex

82
Q

Should you give patients B-blockers if they have asthma?

A

No! They need vasodilation from B2 receptors in the chest

83
Q

When you have an inferior wall block what is normally the culprit?

A

RCA!

84
Q

What drug do you give for pulmonary edema?

A

diuretic

85
Q

Major risk factors for ruptures following MI

A

Age, gender (female), and history of HTN

86
Q

What is upper normal for JVP?

A

6-8cm

87
Q

What medications should you avoid with the neurocardiac reflex?

A

anything that decreases preload and inotropy

88
Q

What happens with mechanical dysfunction of right ventricle?

A

BP decreases

the pressure on right side rises

cardiac output to pulmonary artery (from RV) is low

peripheral resistance rises to try to raise BP

89
Q

What 3 things is cardiogenic shock characterized by?

A

1) hypotension

2) reduced CO

3) elevated filling pressures

90
Q

How do you treat cardiogenic shock?

A

need reperfusion

91
Q

More fluid normally means what for pressure …

A

higher pressure!

92
Q

What happens to pressures when volume depleted?

A

pressures drop

93
Q

What can you use to treat PVCs?

A

beta blockers

94
Q

Why do atrial flutter and Afib occur after MI?

A

increased intracardiac pressures and increased left atrial stretch

95
Q

Rate control drugs for Afib

A

Beta blockers, Ca2+ channel blockers, digoxin

96
Q

What other drug do you need to give with afib?

A

anticoagulation!

97
Q

How can you tell VT versus SVT?

A

VT has wide-complexes and AV dissociation

98
Q

How can you treat VT?

A

electrical or medical cardioversion

99
Q

How can you determine if VT is driven by acute MI or actual damage?

A

< 48 hrs after MI = post-MI irritability

> 48 hrs after MI = damage / re-entrant pathways

100
Q

Why is adding visualization of perfusion good in stress testing?

A

Perfusion is an early sign of ischemia

can detect things sooner

Cardio (8 decks)

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