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Cardiology > ischemic heart disease > Flashcards

ischemic heart disease Flashcards

1
Q

Epidemiology of CAD?

A

responsible for 1/3 of all deaths over age of 35

  • half of middle aged men will develop sxs
  • a 1/3 of middle aged women will develop sxs
  • 17.6 mill in US have CAD
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2
Q

What is stable angina?

A
  • fixed atherosclerotic plaque, increased oxygen demand from exertion, coronary vasospasm (Prinzmetal’s)
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3
Q

What is unstable angina?

A
  • plaque rupture with thrombus (inflammatory mediators and clotting proteins form clot at plaque rupture)
  • arterial dissection - tear in blood vessel and plaque ruptured and lifted up
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4
Q

What are the variety of sxs of cardiac ischemia?

A
  • substernal chest pain or discomfort
  • may radiate to jaw, shoulders, and arms (don’t have to have central chest pain)
  • dyspnea
  • nausea
  • diaphoresis
  • syncope
  • threshold for angina less after meals for in the cold
  • may be worse lying down (severe end stage angina)
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5
Q

What populations have less overwhelming sxs of angina?

A
  • elderly and diabetics
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6
Q

Sxs with stable angina?

A
  • predictable pattern
  • sxs precipitated by stress or exertion
  • relieved by rest or nitrates
  • long standing, more than 1-2 months
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7
Q

Sxs of untable angina?

A
  • CP at rest or with minimal exertion
  • new onset angina
  • worsening angina (crescendo)
  • change in pattern for those with previous hx of stable angina (getting worse) - can’t complete ADLs
  • if pt isn’t getting any relief from rest or nitrates - move status from stable to unstable angina
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8
Q

Description of cardiac chest discomfort?

A
  • tightness
  • squeezing
  • burning
  • pressure
  • choking
  • aching
  • indigestion
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9
Q

What should you ask on your hx?

A
  • precipitating and alleviating factors
  • characteristics of discomfort
  • location and radiation
  • duration: how long this has been going on, how long each episode lasts
  • effects of nitro
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10
Q

Typical angina?

A
  • substernal in location with cardiac charateristics to pain, provoked by stress or exertion
  • relieved by rest or nitro
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11
Q

Atypical angina?

A
  • CP that meets 2 or less of criteria above

- not relieved by nitro, CP not in typical location

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12
Q

New york heart association of functional status classification

A
  • class 1: asx but with RFs
  • class 2: mild limitation of exercise, sxs with ordinary exertion
  • class 3: mod limitation of exercise tolerance, sxs with minimal exertion
  • class 4: severe limitationof activities, sxs at rest
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13
Q

Diff Dx of CP

A
  • any disease in chest, musculoskeletal, GERD, stomach, pulmonary, aortic dissection, esophageal spasm
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14
Q

Work up of pt with angina?

A
  • hx
  • PE
  • lab
  • EKG
  • cardiac dx testing
  • CXR to exclude other dxs
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15
Q

What is the most impt part of the work up?

A
  • Hx!!!!

- listen

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16
Q

What should you look for on PE?

A
  • levine’s sign
  • diaphoresis
  • note vital signs (HTN?)
  • S4: (atrial contraction against decreased LV compliance)
  • S3: decreased systolic function
  • apical systolic murmur of MR
  • paradoxically split S2 (split on expiration instead b/c ventricle isn’t working)
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17
Q

Lab work up of stable angina?

A
  • update lipids if needed
  • CBC
  • TSH
  • do they have DM
  • update BMP if needed
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18
Q

Untable angina lab work up?

A
  • troponin 1
  • CBC (anemia)
  • TSH
  • uptdate lipids if needed
  • do they have DM
  • CMP
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19
Q

What would an EKG show that is suggestive of ischemia?

A
  • new BBB: new LBBB with CP is an MI until proven otherwise
  • T wave inversion, depression or flattening
  • changes from previous EKG
  • ST depression or elevation
  • Q waves (usually late presentation - muscle tissue already necrotic)
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20
Q

How would an EKG distinguish b/t stable and unstable angina?

A
  • chronic stable angina: shouldn’t have acute EKG changes
  • variable degrees of ischemia can be seen with acute sxs
  • untable angina: may have transient EKG changes,
  • NSTEMI: EKG may be persistent or evolving
  • STEMI: EKG changes persistent until revascularization
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21
Q

Further workup for stable angina once ACS ruled out?

A
  • chronic stable angina - stress testing and or cardiac cath rarely needed
  • but stress testing can confirm dx of angina, determine severity of limitation of activity, assess prognosis, and eval response to therapy (based on sxs)
  • cardiac cath/coronary angiography indicated: persistent limiting angina despite max medical therapy, stress test suggestive of high risk disease, hx of aortic valve disease to determine if CP is ischemic or due to valve disease
  • worsening sxs: failed max med therapy
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22
Q

Medical therapy for chronic stable angina?

A
  • nitrates
  • b blockers
  • CCBs
  • Na channel blockers
  • antiplatelet agents
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23
Q

Goal of medical therapy for stable angina?

A
  • prevent chest pain

- allow for normal activities with an acceptable degree of CP in terms of frequency and severity for pt

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24
Q

What medical conditions need to be controlled that may precipitate anginal attacks?

A
  • HTN (increasing O2 demand of heart)
  • HF
  • tachyarrhythmias (increasing O2 consumption)
  • emotional upset: depressed or anxious - release E or NE - increase sxs
  • anemia (decrease in O2)
  • thyroid disease
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25
Q

MOA of nitrates?

A
  • cause both coronary and peripheral vasodilation

-

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26
Q

SEs of nitrates?

A
  • HA, passing out, dizziness

long term: need to take a break, otherwise develop a tolerance

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27
Q

Short acting nitrates?

A
  • used for immediate relief of anginal sxs
  • sublingual nitro tablets or spray, 0.4 mg
  • repeat in 3-5 min (up to 3x), if sxs not better in 20 min than need to go to ED via EMS
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28
Q

What is preload? afterload?

A
  • preload: volume of blood in ventricles at end of diastole (diastolic pressure),
    increases in hypervolemia, regurg of valves, and HF
  • Afterload: resitance left ventricle must overcome to circulate blood, increased in HTN and vasoconstriction (increasing after load increases cardiac workload)
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29
Q

Which med class has the only antianginal agents that have been demonstrated to prolong life in pts with CAD post MI?

A
  • B blockers

- first line therapy for tx of angina

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30
Q

BBs MOA?

A
  • blocks beta receptors in heart causing:
    decreased HR, decreased force of contration, decreased rate of AV conduction (all of these decrease BP and myocardial O2 consumption)
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31
Q

SEs of BBs?

A
  • bradycardia
  • lethargy
  • GI disturbance
  • CHF
  • decrease in BP
  • depression
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32
Q

CIs to BBs?

A
  • bradycardia, heart block, careful in diabetics (mask sxs of severe hypoglycemia), hypotension, severe bronchospasm (in asthmatics - don’t use nonselective B blockers)
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33
Q

MOA of CCBs?

A
  • decrease myocardial O2 demand by blocking influx of Ca into cells which decreases afterload, dilates peripheral arterioles
34
Q

What is Ranolazine (Ranexa)?

A
  • unique
  • add on after other meds have failed to control sxs
  • blocks Na channel into myocyte during repolarization
  • results in decreased intracellular Ca due to Na/Ca exchange
  • decrease intracellular Ca = decrease in ventricular tension + decrease in myocardial O2 consumption
    (doesn’t lower BP or HR)
  • used as add on to std therapy in refractory angina
  • can cause QT prolong
  • monitor QT interval when first starting
  • leave cardiology to Rx, metabolized in liver ( a lot of drug interactions)
35
Q

Antiplatelets that are used?

A
  • aspirin 81-325 mg daily
    0r
  • P2Y12 inhibitor daily if aspirin intolerance or allergy
36
Q

What are tx plans are there for angina?

A
  • risk factor reduction through therapeautic lifestyle changes
  • stabilization of plaque with statin therapy
  • coronary revascularization for refractory angina (CABG, or stent): indicated when on max therapy and worsening sxs
37
Q

What is another name for coronary vasospasm?

A
  • prinzmetal’s angina or variant angina
38
Q

What is vasospastic angina? Common in what populations?

A
  • CP w/o usual precipitating factors (stress or exercise0
  • assoc with ST elevation during episodes (instead of depression)
  • often young women
  • May waken pt from sleep in early morning hours
  • may be assoc with arrhythmias or conduction defects
  • cyclical pain pattern over months
39
Q

Dx signs of vasospastic angina?

A
  • EKG evidence of ischemia during pain: ST elevation
  • normal exercise tolerance (stress test will be neg)
  • normal coronary angiogram: angiography catheter may induce vasospasm
  • should respond to intracoronary nitro or CCB
40
Q

Vasospasm triggers?

A
  • spontaneous
  • exposure to cold
  • emotional stress
  • vasoconstricting meds: cold medicine (decongestant)
  • cocaine
  • tobacco
  • B blockers may trigger (problem is with alpha receotors, if you block B receptors than alpha receptors are unopposed and more likely to cause spasm)
41
Q

What are assocd disorders of vasospastic angina?

A
  • many have concomitant coronary artery disease (up to 60%)
  • may also have:
    migraine HAs
    raynaud’s phenomenon
42
Q

Tx of coronary vasospasm?

A

rule out obstructive disease with cardiac cath

  • CCBs and long acting nitrates if needed for prevention
  • SL nitro for acute relief
  • avoid B blockers (leave alpha receptors unopposed)
43
Q

What are the 3 processes that are considered ACS?

A
  • plaque rupture

- NSTEMI, unstable angina, and STEMI

44
Q

What are high risk features of UA?

A
  • accel sxs overs last 48 hrs
  • prolonged ongoing rest pain
  • new ST depression
  • PCI w/in 6 months
  • previous CABG
  • post MI angina
  • arrhythmias (myocardium irritated)
  • recurrent sxs despite max medical therapy
  • these pts should be in the hospital!!!
45
Q

Pts with unstable angina and correlation with CABG?

A
  • the older the saphenous vein graft, the greater the likelihood that sxs result from culprit lesion within graft rather than lesion in native coronary artery
  • 92% of lesions after 10 years were result of vein graft
46
Q

Unstable angina may be the precursor to what?

A
  • to an MI
  • have to take it seriously
  • may have transient EKG changes
  • cardiac enzymes are normal
  • if not dx and tx properly - may progress to MI
47
Q

Definition of MI?

A
  • elevated CK-MB and/or troponin
  • plus at least one of the following:
    sxs of ischemia
    EKG changes consistent with new ischemia
    New Q waves
    imaging evidence of new wall motion abnormality (ischemia)
48
Q

EKG criteria for dx of NSTEMI

A
  • new horizontal or down sloping ST depression of more than 0.5 mm in 2 contiguous leads
    and/or
    T wave inversions
49
Q

EKG criteria for sx of STEMI?

A
  • ST elevation at J pt in 2 contiguous leads of greater than 1 mm
  • ST elevation of 2 mm or greater in men and 1.5 mm or greater in women in leads V2 and V3
50
Q

Tx of unstable Angina and NSTEMI goals?

A
  • relief of ischemic pain
  • correction of hemodynamic abnormalities (HTN, tachycardia)
  • est of risk (TIMI score)
  • choice of management strategy - reperfusion?
  • antithrombotic therapy
  • BB therapy
51
Q

Medical therapy for unstable angina and NSTEMI?

A
  • O2
  • nitro
  • morphine
  • BBs
    (all 4 of these relieve ischemic pain, and decrease myocardial O2 consumption)
  • antiplatelet therapy
  • anticoag
52
Q

O2 therapy?

A
  • 2 L supp O2 via nasal cannula
  • may help relieve anginal sxs
  • a must for pts who are hypoxic
  • no evidence based data to suggest that pts with O2 have better outcomes if their baseline O2 sat was normal
53
Q

Nitro?

A
  • SL nitro: 1 tab or spray at a time, repeat q 3-5 min until relief of CP or 3rd dose
  • IV drip if persisent pain after 3 tablets/spray, HTN or CHF
  • CI in RV infarction, severe aortic stenosis, recent meds for ED
54
Q

Morphine?

A
  • 2-4 mg for CP or anxiety
  • repeat q 5-15 min
  • can be given with nitro
55
Q

BBs?

A
  • metoprolol or atenolol
  • IV if ongoing CP, HTN, tachycardia
  • CI if hypotension, bradycardia, or systolic CHF exacerbation
56
Q

Antiplatelet therapy?

A 
- aspirin 325 mg chewed 
(non-enteric coated)
\+
for NSTEMI add P2Y12 receptor blocker:
clopidogrel (Plavix)
Prasugrel (effient)
ticagrelor (brilinta)
DONT give without checking with cardiologist first (irrerversible platelet inhibition)
57
Q

What kind of anticoag med is given in unstable angina?

A
  • Enoxaparin (Lovenox): LMWH
    1 mg/kg subq
  • essence trial: decreased rate of death, MI, recurrent angina or revascularization procedure at 30 days and 1 year compared to Heparin (UFH)
  • no diff in bleeding complications
58
Q

Anticoag for NSTEMI?

A
  • synergy trial: higher incidence of bleeding with enoxaparin compared to UFH and no difference in death or nonfatal MI in 2 groups
  • NSTEMI pts receiveing P2Y12 inhibitor along with aspirin (irreversible - account for bleeding) so use heparin to decrease bleeding
  • if pt not receiving P2Y12 inhibitor than cardiologist may want to give IV or SQ enoxaparin (CHECK with cardiologist first!!)
59
Q

If an early invasive approach is selected (High risk NSTEMI pt) then what may you want to add on to UFH?

A
  • a GP IIb/IIIa inhibitor:
    abciximab (Reo Pro)
    eptifibatide (integrilin)
    tirofiban (aggrastat)
60
Q

Tx for USA?

A
  • aspirin + lovenox
61
Q

Tx for NSTEMI?

A
  • aspirin + plavix+ heparin

- if early invasive approach - GP II/IIIa inhibitor also

62
Q

What should pts be d/c on after NSTEMI/USA?

A
  • statin therapy
  • trials suggest high dose therapy
  • atorvastatin (Lipitor) 80 mg daily
  • switch pts who are on alt statins if no CIs
63
Q

What can you use to determine management strategy?

A
  • can be determined after risk stratification
  • helps to ID pts at highest risk for further cardiac events who may benefit from an aggressive approach
  • TIMI score for risk stratification: % of risk at 14 days of all cause mortalitiy, new or recurrent MI or severe recurrent ischemia requiring urgent revasc.
    4 pts - 20%
64
Q

Choice of early cardiac cath is determined by what?

A
  • extent of EKG and cardiac biomarker abnormalities
  • evidence of hemodynamic instability
  • persistent chest pain despite approp medical therapy
  • severe LV dysfxn or HF
  • ventricular arrhythmias
  • new or worsening mitral regurg or new VSD
65
Q

Person with NSTEMI tx options?

A
  • admit pt to hospital and determine course of action
  • early invasive approach (cath and potential reverse)
  • or medical therapy only
  • or invasive approach just not urgent (within the next day)
  • if unstable angina continue checking cardiac biomarkers at least 3 more times and esc therapy if they become positive
66
Q

How do you manage cocaine assoc MI?

A
  • similar to other ACS pts except:
    give benzodiazepines early
  • don’t use BB due to possibility of inducing further coronary vasospasm
67
Q

What is a STEMI?

A
  • MI due to complete obstruction of coronary artery

- myocardium is at risk

68
Q

First step in tx a STEMI?

A
  • recognizing the problem
  • high index of suscpicion
  • remember elderly, women and diabetics may present with atypical sxs
  • EKG: ST elevation
69
Q

Goals of STEMI therapy?

A
  • relief of ischemic pain
  • assessment of hemodynamic state and reversal of abnormalities
  • reperfusion therapy with PCI or fibrinolysis
  • antithrombotic therapy to prevent rethrombosis
  • BB therapy to prevent recurrent ischemia and ventricular arrhythmias
70
Q

Medical therapy for STEMI?

A
  • O2
  • nitro
  • morphine
  • BBs
  • all 4 relieve ischemic pain and decrease myocardial O2 consumption
  • antiplatelet therapy
  • anticoag
    • fibrinolytic therapy or PCI!!!
71
Q

First line therapy for reperfusion in STEMI?

A
  • PCI unless not available within 90-120 minutes
  • second line:
    fibrinolytics if PCI not available within 90-120 min, sxs less than 12 hrs and no CIs
72
Q

Antiplatelet forSTEMI pt having fibrinolytic?

A
  • clopidogrel (plavix) 300 mg but if 75 or older - 75 mg
73
Q

Antiplatelet for STEMI pt with no reperfusion?

A
  • Ticagrelor (brilinta) 180 mg
74
Q

Antiplatelet therapy for STEMI pt receiving PCI?

A
  • Ticagrelor (Brilinta) 180 mg or

PRasugrel (Effient) 60 mg

75
Q

antiplatelet tx for STEMI pt with high risk of bleeding

A
  • clopidogrel (plavix) 300-600 mg

* * always consult with cardiologist when admin P2Y12 inhibitors in STEMI pts

76
Q

Anticoag therapy options for STEMI pts?

A
  • UFH: undergoing PCI and who received fibrinolyis
  • Bivalrudin (angiomax) PLUS GP IIb/IIIa inhibitor
  • LMWH (enoxaparin/lovenox): small loading dose IV followed by SQ admin - can’t reverse lovenox effects, cant do PCI
77
Q

Most common fibrinolytic used?

A
  • Alteplase: tPA
78
Q

MOA of fibrinolytics?

A
  • initiation of local fibrinolysis by binding to fibrin in the thrombus and converts entrapped plasminogen to plasmin
79
Q

Absolute CIs to fibrinolytics?

A
  • Hx of intracranial hemorrhage
  • ischemic stroke within last 3 months
  • cerebral vascular malformation
  • primary metastatic intracranial malignancy
  • suspicion for aortic dissection
  • bleeding disorder or active bleeding
  • sig closed head injury or facial trauma in the last 3 months
80
Q

Relative CIs to fibrinolytics?

A
  • severe uncontrolled HTN: SBP greater than 180 and or DBP greater than 110
  • ischemic stroke more than 3 months ago
  • dementia
  • any known intracranial disease
  • traumatic or prolonged (greater than 10 min) CPR
  • major surgery within last 3 weeks
  • pregnancy
  • noncompressable vascular punctures
  • internal bleeding within the last 2-4 weeks or active peptic ulcer
  • for streptokinase or anistreplase - prior exposure or allergic rxn to these drugs
81
Q

Complications of an AMI?

A
  • pump failure: lead to CHF, pulm edema, cardiogenic shock
  • mechanical: LV free wall rupture, VSD, pap muscle dysfxn (acute MR)
  • pericarditis: can be early or late
  • ventricular aneurysm: CHF, ventricular arrhythmia, thromboemboli
  • electrical: arrhythmias, conduction disturbances, sudden cardiac death
  • arterial and venous thrombosis and embolism: LV mural thrombus, venous thrombus resulting in PE
82
Q

MI mortality of STEMI and NSTEMI?

A
  • 30 days:
    STEMI: 6.1%
    NSTEMI: 3.8%

1 year:
STEMI: 9.6%
NSTEMI: 8.8%

2 years:
STEMI: 11%
NSTEMI: 20% - may be due to the fact that pver half of pts with NSTEMI have multivessel disease and greater likelihood of residual ischemia

Cardiology (20 decks)

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