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Cardiology (Fall 2023) > Lecture 10: Ischemic Heart Disease Part 2 > Flashcards

Lecture 10: Ischemic Heart Disease Part 2 Flashcards

1
Q

What is always the initial test for anyone presenting with chest pain?

A

EKG

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2
Q

How fast should an EKG be done if someone presents with ACS symptoms to the ER?

A

10 minutes!

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3
Q

if the initial EKG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, what should be done?

A

serial EKGs (15-30 min intervals in the first 1-2 hours) should be performed to detect ischemic changes

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4
Q

what is the earliest presentation of ACS that can be seen on EKGs

A

Hyperacute T waves

Only exists 20-30 minutes after MI so rarely seen in clinical practice

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5
Q

what do hyperacute T waves have to be distinguished from

A

peaked T - waves assocaited with hyperkalemia

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6
Q

what are the findings indicating suspicion for NSTEMI and STEMI

A

i think its not a bad idea to know this chart

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7
Q

this chart would not be bad to memorize either

chart defining evolution of STEMI in EKG

A
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8
Q

after ordering an EKG, what is step two in evaluating a pt with s/s of ACS

A

order cardiac biomarkers!

aka cardiac enzymes

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9
Q

What are the 3 types of cardiac enzymes we can order?

A
  • Myoglobin
  • CK-MB
  • Troponin I, T (the best)

This comes AFTER EKG.

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10
Q

what is troponin

A

a contractile protein that is NOT normally found in the serum

only relesed when myocardial infarction occurs!!

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11
Q

Why are troponins the preferred marker for myocardial study?

A
  • highly sensitive AND specific for even small amounts of cardiac damage
  • ONLY RELEASED when myocardial necrosis occurs.
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12
Q

when do troponin serum levels increase, peak and return to baseline?

A
  • Increases within 3-6 hours
  • Peaks within 24-48 hrs
  • Takes 5-14 days to recover.
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13
Q

How often should we repeat troponin?

A
  1. Initial presentation
  2. 90 Minutes
  3. 6-8 hrs after x3 or unil trending down.
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14
Q

What are we specifically looking for in serial troponin readings?

A

A trend, trends have more weight than a single reading!

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15
Q

what are other potential causes of elevated troponin?

A
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16
Q

How long does it take serum CK-MB levels to increase, peak and return to baseline

A

Increase 4-8 hrs after injury
Peak around 24 hrs
Return to normal by 48-72 hrs

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17
Q

What is considered a positive CK-MB?

A

if CK-MB > 5% of total CK

Not preferred test (less sensitive and specific than troponin)

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18
Q

What might cause a false positive of CK-MB?

A
  • Exercise
  • Trauma
  • Muscle disease
  • DM
  • PE
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19
Q

What cardiac biomarker is the earliest marker for MI?

A

Myoglobin

Highly sensitive, but poor specificity.

Could appear within 2 hrs.

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20
Q

what is myoglobin

A

found in cardiac and skeletal muscle

most sensitive early marker for myocardial infarction

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21
Q

what is lactate dehydrogenase (LDH)

A

found in many tissues (kidneys, skeletal muscles, brain, blood cells, lungs, liver) so it is very non-specific!

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22
Q

How long does it take LDH to increase, peak and return to baseline

A

Rises within 24 - 72 hrs after MI
Peaks in 3 - 4 days
Returns to normal in ~14 days

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23
Q

What is the order of enzyme elevation in ACS?

A
  1. Myoglobin
  2. CK-MB
  3. Troponin
  4. LDH

Trop takes longer to elevate.

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24
Q

What 3 lab levels may elevate as a result of ACS? how long do these take to rise/fall?

A
  • Leukocytosis (within several hours, peaks at 2-4 days, falls within a week)
  • ESR (rises within 3 days, may be elevated for weeks)
  • CRP ( no timeline specified)
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25
Q

patients w/o biochemical evidence of myocardial necrosis but with elevated _____(what lab)_____ are at risk of subsequent ischemic events

A

Elevated CRP

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26
Q

what are stress tests used to evaluate?

A

inducible ischemia in patients with angina

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27
Q

what are the 2 ways stress tests can be done

A
  • via exercise (PREFERRED)
  • via pharmacologic measures
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28
Q

What is the general minimum for doing an exercise stress test?

A
  • Walk 5 minutes on flat ground
  • 1-2 flights without stopping
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29
Q

What are the indications for a stress test?

A
  • Confirm angina
  • Determine severity of limitation due to angina
  • Assess prognosis of known CAD and MI recovery
  • Evaluate response to therapy
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30
Q

Who is an exercise stress test most useful for?

A
  • Low pretest likelihood and normal baseline EKGs
  • Best in young, females with atypical symptoms.
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31
Q

what are limitations to exercise (only) stress testing

A
  • More false-positives than true-positives
  • Not a screening tool in asymptomatic patients
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32
Q

What is the max HR for a stress test and the finding that makes it positive?

A
  • 85% of max HR (220-age)
  • ST depression of 1mm = positive
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33
Q

what is the MC protocol used in exercise stress testing

A

Bruce treadmill protocol

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34
Q

The intensity of exercise is periodically increased, continuing until what occurs

A
  • The patient reaches maximum HR
  • Changes in heart function are detected on the EKG
  • Patient is symptomatic
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35
Q

what is the equation for HR max

A

220 - age

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36
Q

When do you absolutely need to terminate a stress test?

A
  • SBP drop of 10mm Hg from baseline BP despite increasing workload, when accompanied by other evidence of ischemia or hypoperfusion
  • Mod-severe angina
  • Nervous system symptoms (ataxia, dizziness, enar-syncope)
  • Poor perfusion (cyanosis, pallor)
  • Subject wants to stop
  • Sustained Vtach
  • ST elevation >1mm without Q-waves
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37
Q

What are the absolute contraindications to TMSTs? (treadmill stress tests)

A
  • Acute MI within 2d
  • High-risk, unstable angina
  • Uncontrolled arrhythmias resulting in hemodynamic instability
  • Severe, symptomatic AS
  • Uncontrolled symptomatic HF
  • Acute PE
  • Acute myocarditis or pericarditis
  • Acute aortic dissection
  • preexcitation syndrome (WPW syndrome)
  • electronically paced ventricular rhythm
  • greater than 1mm of resting ST depression
  • complete LBBB
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38
Q

When do we add imaging to an exercise stress test?

A
  • Resting EKG is difficult to interpret (LBBB, baseline changes, low voltage)
  • confirm a positive test in a asymptomatic pt
  • localize the region of ischemia
  • distinguish ischemic from infarcted myocardium
  • assess completeness of revascularization following bypass surgery or coronary angioplasty
  • as a prognostic ingicator in patients with known coronary disease
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39
Q

What scan is associated with a nuclear stress test?

A

SPECT (single photon emission CT)

this provides perfusion data following injection of a radioactive material prior to stress test and then compared after stress test.

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40
Q

when would you add a stress Echo to an exercise stress test

A
  • in attempt to increase specificity and sensitivity of test
  • determine extent of myocardium at risk for ischemia
  • looking for regional wall motion abnormalities or LV dilation in response to exercise
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41
Q

when is a pharmacologic stress test used

A

Used when a patient is unable to exercise to a sufficient cardiac workload or has a contraindication to or a clinical reason not to perform an exercise stress test

Ex. LBBB, V paced rhythm, beta blocker or CCB therapy, large AAA

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42
Q

Why does a pharmacological stress test require imaging?

A

Sensitivity of a pharmacologic stress EKG is very low, so these tests are always combined with an imaging modality

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43
Q

what are the preferred pharmacologic stress agents

A

vasodilators

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44
Q

What are the 3 vasodilators used for pharmacological stress tests? what do these do?

A
  • Adenosine
  • Dipyridamole
  • Regadenoson

cause direct CORONARY ARTERY VASODILATION

Preferred agents.

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45
Q

what are common SE of vasodilators in pharm stress test

A
46
Q

What is the primary contraindication to pharmacological stress agents?

A

Bronchospasms

also see:

47
Q

What are the 2nd line stress agents used in pharmacological stress tests? what do they do?

A
  • Dobutamine
  • atropine is added to dobutamine in paients who do not achieve target HR

Adrenergic stimulants

synthetic catecholamines that cause B1 and B2 stimulation.
Only used if you can’t use a vasodilator (i.e. asthma)

48
Q

what are the SE for adrenergic stimulating agents

A
49
Q

what are the CI for adrengergic stimulating agents

A
50
Q

What is the definitive diagnostic procedure to evaluate CAD and heart muscle function?

A

Coronary angiogram/cardiac catheterization

51
Q

what is a coronary angiogram/cardiac catheterization and what is it used for?

A

An invasive imaging procedure that allows for evaluation of heart function
used for:
- evaluation or confirmation of presence of CAD, valve disease, or aortic disease
- evaluate heart muscle function
- determine need for further tx (PCI or CABG)

52
Q

what side of the heart is used in a standard Coronary angiography?

A

LEFT (through aorta)

right can be assessed if looking for pulm HTN or hemodynamic monitoring (through pulm artery)

53
Q

What common medication MUST BE HELD for 48 hours prior to cath?

A

Metformin!!!!

Contrast = nephrotoxic

54
Q

What is the prep required for a coronary angiogram?

A
  • NPO 4-6 hrs
  • Written consent
  • IV NS to flush contrast
  • Hold metformin for 48hrs to avoid contrast induced nephropathy
55
Q

When is coronary angiography indicated?

A
  • Life limiting stable angina
  • High pretest likelihood
  • Aortic valve disease
  • Valve surgery
  • Survivors of sudden death
  • Chest pain of unknown etiology or idiopathic cardiomyopathy
  • STEMI patients requiring immediate revascularization
56
Q

what are the risks for coronary angiogram

A
  • low mortality risk (.1%)
  • CVA, Coronary atrery dissection
  • performed under moderate sedation = risky
57
Q

when is coronary angiogram first line and what are the relative CI to coronary angiograms

A
  • Invasive and costly, so it is not first-line unless high pre-test likelihood
  • Relative CI: severe renal disease, anaphylactic allergy to contrast
58
Q

If a patient has a contrast allergy, can we still perform coronary angiography?

A

If it is a life-threatening emergency, yes.

Add benadryl and steroids prophylactically.

59
Q

What is a CXR mainly used for in chest pain?

A

R/o pulmonary causes or widened mediastinum aortic dissection

60
Q

when is Chest CT with IV contrast used in Chest pain CC

A

Can help exclude PE and aortic dissection

61
Q

why would a transthoracic echo be used in a chest pain CC

A
  • Can identify a pericardial effusion and tamponade physiology
  • May be useful to detect regional wall motion abnormalities
  • Can identify a proximal aortic dissection
62
Q

What must HR be for a CT of the coronary arteries?

A

Under 50 to prevent artifact.

63
Q

What is the most sensitive and specific NON-invasive imaging modality for CAD?

A

CT Angiography

64
Q

for outpatient workup of stable angina, what are the diagnostic tests that should be ordered

A
  • EKG
  • CBC (r/o anemia), possible trops, CK-MB
  • Low- intermediate probability = noninvasive stress test (if abnormal reer to cardio for possible cath)
  • high probability = refer to cath
65
Q

For inpatient workup of unstable angina, what are the diagnostic tests we should order?

A
  • EKG
  • Trops +/- CK-MB
  • Low prob = no testing
  • intermediate prob = consider stress test w nuclear imaging
  • high = refer to cardio for cath
66
Q

for inpatient wrkup of NSTEMI, what diagnostic studies should be ordered

A
  • EKG
  • Trops +/- CK-MB
  • Low- intermediate probability = noninvasive stress test (if abnormal reer to cardio for possible cath)
  • high probability = refer to cath
67
Q

What is the primary difference between unstable angina and NSTEMI?

A

Troponin is negative in unstable angina.

EKG is the same usually.

68
Q

If we have ST elevation >= 1mm in two contiguous leads, what is the workup?

A

No labs, straight to cath lab!

69
Q

What are the drug classes indicated for stable angina managment?

A
  • NTG
  • BB
  • CCB
  • Ranexa (Metabolic modulator)

goal of therapy is to manage symptoms and prevent CV events!

70
Q

What are the first-line therapies for unstable angina/NSTEMI/STEMI?

A
  • Admission to hospital
  • placed on telemetry/cardiac monitoring
  • strict bedrest
  • Supplemental O2 (only if hypoxemic)
  • Nitrates
  • ASA (162-324mg chewable) give even if the patient already is taking aspirin

ASA is given regardless of fibrinolytic therapy.

71
Q

If a patient has an ASA allergy, what is the alternative for them in ACS?

A
  • P2Y12 inhibitors:
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
72
Q

After the first-line therapies for ACS management, what are the next meds?

A
  • Morphine for pain refractory to nitro and ASA, benzo may be used for sedation
  • Oral BB within 24 hrs unless CHF, brady, or AVB
  • ACEI within 24 hrs (ARB if ACE not tolerated)
  • Statin within 48 hrs

Consider: CCB for persistent ischemia

73
Q

What are the reperfusion goals?

A
  • Door to balloon in 90 minutes
  • Door to needle in 30 minutes

Preferred is PCI, but if not available, then we use tPA for thrombolysis.

74
Q

What does NTG do?

A
  • enters vascular smooth muscle and is converted to nitric oxide, leading to activation of cGMP and vasodilation
  • dilates coronary vessels, increasing blood flow
  • decreases SVR and preload
  • This is FIRST LINE thereapy for pts with ACS EXCEPT in patients with IWMI

IWMI involves the RV, which will affect preload too much if treated.

75
Q

When should NTG be used in caution?

A
  • Hypotension < 100
  • Brady
  • Tachy
  • RV infarction

RV infarction already presents with decreased preload, and decreasing it further will bottom out a patient.

76
Q

what are SE of NTG

A

SE: most commonly causes reflex tachycardia, but can cause paradoxical bradycardia
MC adverse Affect = headache. but can also see postural hypotension and tolerance developement

77
Q

what are non-parental options for NTG? if pain persists with the use of these, what should you do?

A
  • SL, oral, ointment, spray
  • If pain persists or recurs, start IV NTG until angina disappears or MAP drops by 10%.

Continuous BP monitoring is required with IV NTG

78
Q

how does tolerance occur to NTG? how do you fix it?

A
  • Prolonged treatment with nitrates may not only induce a loss of response to nitrates, but also actually decrease angina threshold in the interval
  • High doses should be avoided and therapy interrupted for 8–12 h daily (treatment “holiday”)
79
Q

What should you never give a nitrate with?

A

PDE-5 inhibitors!!!!!!!!!!!!!!!!!!!!!!!

Works on cGMP the same way. causes dramatic reduction in BP

80
Q

What does morphine do in terms of the heart?

A
  • Decreases sympathetic tone
  • Decreases SVR
  • O2 demand

all of this = Reduction of afterload.

Often used for refractory angina during ACS.

81
Q

what are SE of morphine and when should they be cautioned?

A
  • SE: bradycardia, diaphoresis, nausea, constipation, drowsiness, dizziness, confusion
  • Use with caution in hypotension, hypovolemia, respiratory depression
82
Q

Why do we give chewable asa for ACS?

A
  • Antiplatelet aggregation
  • Stabilize plaque and prevent it from forming a big thrombus.
  • Chewable ASA absorbs much more quickly.
83
Q

What are the main concerns with ASA?

A
  • PUD
  • Allergy
  • Bleeding disorders

Often treated with PPI.

84
Q

What drug is bolused prior to a cardiac cath?

A

600mg of plavix

but you must POSTPONE plavix for 5 days prior to CABG.

must postpone CABG for 7 days after last dose of ticagrelor

85
Q

What do glycoprotein 2b/3a inhibitors do?

A
  • Inhibition of platelet aggregation
  • Supports PCI
  • High risk patients only

Aggrastat
Integrilin
Reopro

86
Q

What 3 situations might glycoprotein 2b/3a inhibitors be used?

A
  • Ongoing ischemia despite ASA and P2Y12 inhibitor use
  • Large thrombus during angiography
  • Stabilize urgent CABG patients in place of using a P2Y12.
87
Q

When are anticoagulants (UFH, LMWH, DTIs) used in ACS?

A
  • Adjunct to surgical revascularization and thrombolytic / PCI reperfusion
  • Used in combo with ASA and/or other platelet inhibitors
  • UFH, LMWH (lovenox, arixtra, fragmin) and direct thrombin inhibitors (Angiomax)
88
Q

When are BBs indicated in regards to ACS?

A
  • Added 24-48 hrs to post-MI patients that are STABLE
  • Reduction in infarct size, rate, and life-threatening tachyarrhythmias
  • Reduction in cardiac remodeling and enlargement
  • 14% reduction in mortality risk at 7 days and 23% reduction long term.
89
Q

When are BBs contraindicated?

A
  • Acute CHF
  • Heart Block
  • Hypotension
90
Q

What BBs are typically used in post-MI patients?

A
  • Metoprolol tartrate
  • Carvedilol
91
Q

What is ranolazine?
(MOA, indication, danger, advantages)

A
  • MOA: late Na channel blocker.
  • Indication: Chronic, stable angina
  • Danger: QT prolongation
  • advantages: no effect on HR or BP, safe with ED drugs.

500mg PO BID, difficult to get insruance to cover, costly.

92
Q

What is the role of ACEis and ARBs post MI?

A
  • Reduction in fibrosis and remodeling
  • Preserve myocardium in setting of a MI
93
Q

What other medications are indicated for post MI patients?

A
  • Statins post ACS (start within days following MI)
  • Warfarin for intracardiac thrombus or embolic events
  • Aldosterone antagonists for LV dysfunction pts
  • CCBs NOT usually used, 3rd line therapy in pts with continuing s/s on BB and nitrates or those who are not candidates for those drugs
94
Q

What are the two formulations of fibrinolytics? Who is fibrinolytic therapy used in?

A
  • Alteplase (Recombinant)
  • Tenecteplase (genetically engineered)
  • USED IN STEMI TX ONLY
95
Q

What is the life-threatening complication that can occur due to tPA administration?

A

ICH

can see major bleeding complications!!!

96
Q

What must be done post-tPA?

A
  • ASA
  • AC with LMWH
97
Q

How quickly does tPA needed to be administered for STEMI?

A
  • Ideal: 30 minutes to ED arrival
  • Reducion in mortality within first 3 hours of presentation.

CATH IS PREFERRED

only use tPA isf cardiac cath cant be done within a few hours of event

98
Q

If a patient requires fibrinolytics for a STEMI, what two medications must they be started on after?

A
  • PPIs
  • Alternate options: antacids and H2 Blockers while hospitalized
99
Q

What are the absolute CIs to fibrinolytics?

A
  • Prior ICH
  • Known AVM
  • Known malignancy
  • Ischemic stroke within past 3 months (unless within past 3 hrs)
  • Active internal bleeding
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis
  • Significant closed head or facial trauma within 3 mo.
100
Q

When is PCI indicated?

A

Unstable disease

GOLD STANDARD

no benefit over taking appropriate meds for those with stable CAD

101
Q

What therapy follows PCI?

A
  • Dual antiplatelet therapy (DAPT)
  • P2Y12 receptor blocker + ASA for 3-12 months.
102
Q

What exactly is a stent?

A
  • Thin-wire mesh used to keep an artery open.
  • Can contain drugs
  • Supports the artery.
103
Q

what is a bare metal stent

A
  • vascular stent without a coating
  • rate of restenosis is high with these (20-30%)
104
Q

What is the caveat to a drug-eluting stent?

A
  • Longer period of DAPT
  • However, it is the preferred stent in PCI.

Drug-eluting gives off a drug slowly to help prevent cell proliferaiton.

105
Q

What is atherectomy?

A
  • Specialized catheter that removes plaque
  • Requires DAPT post-procedure
106
Q

what is CABG

A

Procedure in which arteries or veins are harvested from elsewhere in the body and are grafted to the coronary arteries to bypass atherosclerotic narrowing and improve blood supply to the myocardium

107
Q

When is CABG preferred for revascularization?

A
  • Left main trunk artery stenosis
  • Poor LV function
  • Significant 3-vessel CAD or 2-vessel disease involving proximal LAD
  • DM with focal stenosis in more than 1 vesse;
  • Concomitant severe valvular disease that necessitates open heart surgery
  • Diffuse disease not amenable to treatment with PCI
108
Q

what is used during CABG

A

cardiac bypass, because the procedure is usually done with the heart stopped!! so cool

109
Q

what is enhanced external counterpulsation

A
  • non-invasive procedure performed on pts with angina, HR, or cardiomyopathy in order to diminish symptoms of ischemia and incease QOL
  • cufs placed on lower extremities and they inflate/deflate to increase blood flor to the heart and decrease cardiac workload
110
Q

yayyyyy all done

A

Cardiology (Fall 2023) (45 decks)

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