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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
When should you not give a B-blocker in heart attack?
do not give if there is significant LV dysfunction this could cause bradycardia / heart block
25
What happens to HR in heart failure?
CO = HR * SV since SV decreases, HR will increase to try to stabilize CO
26
Reciprocal ST-depression
small depressions that occur in reciprocal leads when there are ST-elevations in other leads
27
What is main concern when giving a thrombolytic to treat MI?
intracranial hemorrhage / bleeding
28
What time should you be doing PCI by?
3 hours
29
What is a hard stop for giving thrombolytics?
high BP
30
When you have inferior lead ST-elevation, what else should you check for?
st-depressions in leads V1-V4 with tall R waves
31
What are other causes of ST-inversion besides MI?
pericarditis, BBB, LVH/RVH
32
What type of MI represents transmural infarction?
STEMI
33
What is common in the first 4 days after infarction?
ventricular tachycardia or arrthymia
34
5-10 days after MI what can happen?
papillary muscle rupture interventricular septal rupture
35
Signs of papillary muscle rupture
Inferior MI holosystolic murmur heart failure / shock *acute pulm. edema from fluid backing up in LA*
36
Signs of interventricular rupture
Hypotension right heart failure comes before left sided can also hear a systolic murmu
37
Difference between fibrinous pericarditis and Dressler
Dressler is an autoimmune reaction that can occur weeks after MI Fibrinous pericarditis can occur as early as 2-4 days later
38
For 1 year after stent, what do you use?
aspirin and clopidogrel antiplatelets
39
What does clopidogrel work on?
prevents ADP platelet activation works on the P2RY12 receptor
40
What 4 drugs do you give in hospital when someone is having an MI? Why?
B-blocker (reduce O2 consumption) Nitrate (reduce O2 consumption) aspirin (anti-platelet) heparin (anti-coagulant)
41
How does heparin work?
Heparin increases activity of antithrombin III which prevents thrombin from forming clots
42
What can happen in an inferior MI to autonomics? What should you be wary of?
inferior MI can stimulate vagal nerve and cause decreased heart rate in this case, do not want to give beta blockers
43
When should you be wary of giving nitrates? Why?
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
Should you give thrombolytics when someone is having a supply-demand (stenosis) heart attack / angina?
No! You do not have a thrombus
45
Why do we often give nitrates and B-blocker together?
Decrease preload = decreased SV with nitrates Decreased SV = increased HR to maintain CO Increased HR = give beta blocker
46
How do B-blockers work?
they decrease heart rate and contractility by blocking sympathetic simulation of B1 receptors
47
What class of drugs is an example of a negative inotrope?
Ca2+ channel blockers (verapamil + diltiazem) they will decrease heart rate and contractility also b-blocker
48
Why might you not want to give a Ca2+ channel blocker?
they also increase preload this could worsen heart failure diltiazem and verapamil should be discontinued in HF
49
Why does QT prolongation occur?
due to delayed repolarization (phase 3) of the myocyte action potential K+ channels are blocked
50
Why does PR prolongation occur?
delayed conduction through AV node
51
Ranolazine
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
Ranolazine effect at high dose
can cause QT prolongation since it blocks repolarization at high doses
53
Beta blockers effect on SA node
Less beta stimulation = less cAMP less cAMP = less calcium less calcium = phase 0 of SA node potential delayed
54
Which cardiac action potential uses Ca2+ in depolarization?
the SA node
55
Which cardiac action potential uses Na+ in depolarization?
the myocyte
56
Adenosine
direct negative inotropic effect useful for treating supraventricular tachycardia (PSVT)
57
What is an example of cardiac glycoside?
digoxin
58
Digoxin MOA (2)
1) positive ionotropic 2) AV node inhibition: stimulates the parasympathetic nervous system
59
Lisinopril MOA
ACE inhibitor ACE normally makes angiotensin which is a vasoconstrictor By inhibiting ACE, you lower angiotension / vasoconstriction which helps to lower BP
60
2 examples of positive iontropes
Cardiac glycosides (digoxin) Beta agonists (dobutamine, epi, norepi)
61
Which beta agonist has lowest risk of tachycardia?
norepinephrine
62
when do you use a Swan cath?
if you suspect papillary muscle rupture or intraventricular rupture after an MI
63
How does an intraventricular defect lead to hypotensive and pulmonary edema?
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
What are signs of the neurocardiac reflex?
Bradycardia Good perfusion Post-MI (inferior)
65
What drug blocks a parasympathetic response?
atropine *use for the neurocardiac reflex*
66
What is the neurocardiac reflex?
LV stretch makes it seem like there is an increased SV so you want to decrease HR causes bradycardia
67
Kussmaul sign PE
upon inspiration JVP increases (JVP should normally fall when you inhale because you are pulling blood into the RA)
68
What does Kussmaul's sign indicate?
right heart dysfunction / limited right ventricle filling paradoxically, right atrial pressure is rising during inspiration
69
If you have an inferior infarct, what are you worried about electrically?
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
If you have a anterior infarct, what are you worried about electrically?
LAD supplies bundles of HIS, BBB, etc. so you are worried about a AV block (Mobitz II or 3rd degree block)
71
What is heart rate response to heart failure normally?
tachycardia to try to make up for decrease in SV CO= HR * SV
72
PVC vs. PAC on EKG
PVC looks like wide, random, big QRS complex PAC looks like normal beat just thrown too early
73
Why can you see PVCs after a MI?
acute MI can cause an electrical storm and lead to electrical problems
74
What are some features of HPI that can tell you someone has unstable angina due to thrombus not stenosis?
new onset angina angina in a crescendo pattern angina at rest
75
What is frontline treatment for preventing MI in outpatient setting?
aspirin (prevent clot) statin (manage LDL) B-blocker (reduce O2 consumption)
76
What is a Q-wave?
a pathological Q-wave is when the Q part of the QRS complex really dips below normal Q wave is stretched downward
77
If a MI is not totally occlusive what does it have to be?
an NSTEMI
78
What are the pre-cordial leads?
V1-V6
79
What does pulmonary edema indicate?
indicates left sided volume overload since you are backing up into the pulmonary vein
80
What does elevated JVP indicate?
right side volume overload since you are backing up into the vena cava
81
Mild bradycardia following an MI can indicate ...
neurocardiac reflex
82
Should you give patients B-blockers if they have asthma?
No! They need vasodilation from B2 receptors in the chest
83
When you have an inferior wall block what is normally the culprit?
RCA!
84
What drug do you give for pulmonary edema?
diuretic
85
Major risk factors for ruptures following MI
Age, gender (female), and history of HTN
86
What is upper normal for JVP?
6-8cm
87
What medications should you avoid with the neurocardiac reflex?
anything that decreases preload and inotropy
88
What happens with mechanical dysfunction of right ventricle?
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
What 3 things is cardiogenic shock characterized by?
1) hypotension 2) reduced CO 3) elevated filling pressures
90
How do you treat cardiogenic shock?
need reperfusion
91
More fluid normally means what for pressure ...
higher pressure!
92
What happens to pressures when volume depleted?
pressures drop
93
What can you use to treat PVCs?
beta blockers
94
Why do atrial flutter and Afib occur after MI?
increased intracardiac pressures and increased left atrial stretch
95
Rate control drugs for Afib
Beta blockers, Ca2+ channel blockers, digoxin
96
What other drug do you need to give with afib?
anticoagulation!
97
How can you tell VT versus SVT?
VT has wide-complexes and AV dissociation
98
How can you treat VT?
electrical or medical cardioversion
99
How can you determine if VT is driven by acute MI or actual damage?
< 48 hrs after MI = post-MI irritability > 48 hrs after MI = damage / re-entrant pathways
100
Why is adding visualization of perfusion good in stress testing?
Perfusion is an early sign of ischemia can detect things sooner

Cardio (8 decks)

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