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Clin Med - Cardio II > CAD > Flashcards

CAD Flashcards

1
Q

definition of CAD

A

coronary artery dz - narrowing or blockage of arteries and vessels that provide oxygen and nutrients to the heart

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2
Q

definition of CVD

A

cardiovascular dz - broader category which includes CAD, arrhythmias, stroke (CVA) and heart valve disorders

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3
Q

definitions of atherosclerosis

A

buildup of plaque (choesterold, fat, calcium) withing blood vessles

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4
Q

definition of angina pectoris

A

dz marked by brief paroxysmal attacks of chest pain precipitated by deficient oygenation of the heart muscles
myocardial O2 demand exceeds supply which is reveresed by decreasing demand

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5
Q

definition of MI

A

myocardial infarction
heart attack further differentiated into
STEMI (ST segment elevation MI)
or NSTEMI (non ST segment MI)

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6
Q

etiology of CAD

A

significances of age, sex, incr BP, cholesterol, and obesity in predicting future CHD

Framingham Coronary Heart Dz risk score

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7
Q

risk factors for males

A 
total cholesterol
HTN
smoking
low HDL
diabetes
age
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8
Q

risk factors for females

A 
low HDL
diabetes 
total cholesterol
HTN
age
smoking
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9
Q

CAD factors unique to women

A
  1. smaller coronary arteries and less developed collateral cirucation = symptoms with less occlusion
  2. elevated inflammatory state with loss of estrogen - risk doubles 10 years over 55yo
  3. lower baseline HDL levels
  4. vague symptoms are the norm = 50% report no pain, OSB MC, other symptoms include: fatigue weakness, palpitations, midback pain
  5. less symptoms relief with treatments and poorer outcomes from CABG
  6. higher rates of post MI heart failure
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10
Q

cigarette smoking

A

1 preventable cause of death and illness in US including 2nd hand smoke

  1. risk of CAD decreases by 50 % after cessation x 1 year; 10-15 yr until same as nonsmoker
  2. CO high affinity to bind to hemoglobin: decr O2 binding capacity and release of O2 = incr RBC mass resulting in hypercoagulable state
  3. inhalation of CO reduces threshold for Vfib
  4. nicotine increases HR by avg 7 beats/minute
  5. oxidizing chemicals and metals cause inflammation, endothelia dysfunction, lipid abnormalities, and platelet activation
  6. end result = incr demand, decreases O2 to tissues, hypercoag state, damaged endothelium
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11
Q

CAD and lipids

A

LDL cholesterol: main component in atherosclerotic plaques
TGs: lipid made from converting foods high in carbs or fat; also component of plaques
HDL cholesterol: absorbs other cholesterol and carries it back to liver; can reduce risk of heart dz and stroke

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12
Q

CAD and diabetes

A
  1. diabetes tends to lower HDL and raise triglyceride and LDL
    contributes to hypercoagulable state: increased fibrinogen and plasminogen activator inhibitor -1 and various platelet abnormalities
    nephropathy leading to cardio-renal syndrome
    neuropathy allows multi vessel atherosclerosis to develop before ischemic symptoms occur resulting in cardiomyopathy
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13
Q

CAD and HTN

A

causes microscopic tears to artery walls allowing for accumulation of atherosclerosis
causes decreased elasticity of arteries resulting in increased afterload leading to more strain on the heart resulting in cardiomyopathy

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14
Q

CAD - sleep apnea

A
  • paused or shallow breathing while sleeping
  • obstructive most common vs central, generally associated with obesity
  • increased negative intrathoracic pressures increases after load resulting in increased demand in an already hypoxemic state
  • pro-inflammatory and oxidative state promoting atherosclerosis
  • increased platelet activity and reduced fibrinogen promoting thrombus
  • up to 40% of pts with CAD have sleep apnea, generally under considered when working up CAD = question partner about snoring or apneic events while sleeping
    rx: sleep study if suspected, CPAP
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15
Q

hx to determine stable vs unstable angina

A
  1. aggravating
  2. relieving - aggravating
  3. descriptors
  4. location/radiation
  5. frequency/duration
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16
Q

hx often determine angina

A
  • exertion (? less activity required)
  • supine (incr preload)
  • emotional stress
  • am symptoms (incr sympathetic NS tone and cortisol elevls during this time can lead to the rupture of cholesterol plaques in coronary arteris ultimately leading to a four fold higher risk of heart attack early in the morning)
  • post prandial or cold exposure (vasoconstriction)
  • intercourse
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17
Q

hx to determine angina vs unstable angina - relieving

A

how long after cessation of aggravating factor does pain - descriptors resolve? generally stops

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18
Q

hx to determine stable vs unstable angina

A

tightness, squeezing, burning, pressing, choking, aching, gas busting or tearing usually associated with thoacic aneurysm

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19
Q

hx to determine stable vs unstable angina - location/radiation

A

clenched fist over chest, substernal or left sided, loess frequently right sided, radiates to shoulder arm neck jaw back or abdomen

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20
Q

hx to determine stable vs unstable angina - frequency/duration

A

how often or number of incidence increasing, longer duration more likely unstable angina or MI

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21
Q

CAD epidemiology

A 
#1killer of US women, greater then all forms of cancer combined
usual onset M>45 F>55
CAD is leading global cause of death
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22
Q

exam to differentiate stable vs unstable angina

A
  1. cardiac murmurs: mitral prolapse, AS, AR
  2. diabetes: retinopathy, neuropathy
  3. hypercholesterolemia: xanthelasma
  4. hypothyroid: myxedema (cardiomegaly, fluid retention, bradycardia, lethargy)
  5. peripheral artery dz: claudication, diminished pulses, lower ext atrophy, extremity hair loss or thinning of skin, rub of feet w/ blanching on elevation
  6. active angina - hypertensive gallop rhythm, tachy-arrythmias, mitral regurg, diaphoretic, restless
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23
Q

w/u for CAD

A
  1. risk stratification: framingham, ascvd, QRISK, HEART, reynolds
  2. labs: CBC, chem7, lips, a1c, cardiac enzymes, crp,
  3. ekg: normla, LVH, ST elevations/depressions, t inversions during pain
    cxr: normal or cardiomegaly, assess for non cardiac etiology
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24
Q

CRP levels and CAD risk

A

3x increased risk o of heart dz with elevated levels

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25
Q

CAD and stress test

A
  1. exercise stress is most common,
    - utilizes bruce protocol which increases treadmill speed/elevation q3min while monitoring ekg for changes
  2. pharmacologic stress uses dobutamine or adenosine rather then exercise to elicit angina or ischemia
  3. stress echo - adds ultrasound to eval for wall motion abnormalities
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26
Q

indications for stress test

contraindications

A
  • confirm dx, determine severity and prognosis, eval response to tx
  • pain at rest or with minimal activity, AS
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27
Q

positive test in stress test for CAD

A

1mm horizontal or down sloping ST depression measured 80 msec past the j point

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28
Q

echo indication for CAD

A

clarification if underlying ekg changes, confirmation if possible false positive exercise, ischemia vs infarcted, tx response, monitor for dz progression

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29
Q

what is myocardial perfusion scintigraphy

A

radioactive tracer injected pre and post exercise or dobutamine, images taken to assess for changes. provides simultaneous assessment of myocardial perfusion and fucntion with only wone study. dipyridamole may be used as a vasodilatro to enchance study

30
Q

indications for myocardial perfusion scintigraphy

A
  1. resting ST segment depression
31
Q

what is radionuclide angiography (MUGA)

A

radioactive tracer eval of ventricle contractility and very accurate EF measurement

  • monitor cardiotoxic chemo drug effects during tx
  • indications: safe in renal pts, nucleotide excreted via liver to GI
  • contradiction: similar to exercise MD preference
  • limitations - can’t assess valves. artifacts (breasts, diaphragm) LBBB
32
Q

CT angiography

A

detects CA stenosis with high accuracy, can establish stent or bypass graft patency, can visualize cardiac and coronary venous anatomy, and can assess calcified and noncalcified plaque burden. coronary artery calcium score can be generated and used to calculate risk .

  • indications: low intermediate probabilities pt’s, quick r/o, inconclusive stress
  • limitations: moderate radiation exposure, contraindicated in renal failure hHR should be
33
Q

cardiac catherterization

A

catheter introduced via radial artery or femoral artery into aorta then into cardiac vessels. dye injected to assess for blockages. suction, angioplasty (balloon inflation) or stenting can then be performed

  • indications: unstable angina or angina refractory to medical therapy, further work-up after positive stress test, final r/o after other causes of pain excluded and stress negative, intervention of acute MI
  • contraindications: renal insufficiency, dye allergy, sepsis , coagulopathy
34
Q

medical management of CAD - general, plt, nitro

A
  1. general: BP control (JNC), DM control, lifestyle (smoking, diet, exercise)
  2. platelet inhibitions: ASA +/- plavix for ASA sensitive pt or acute coronary syndrome; no significant decrease in MI, CVA or death vs ASA when used daily; main side effect is increased bleeding
  3. nitro (NTG): sublingual, spray, paste or long acting tablet. sublingual r spray used prior to exertion or with angina event. long acting tabs and paste for prevention. main side effects are h/a, nausea, hypotension
35
Q

medical management of CAD - bb, ranolazine, statins

A
  1. beta blockers: HR and BP reduction - 1st line therapy in angina. main side effect is bradycardia, hypotension, fatigue, reactive airway exacerbation
  2. ranolazine: uncertain mechanism of action but no affect on HR or BP. 1st line therapy in chronic angina, main side effects are QT prolongation, dizziness
  3. statin reduction: follow guidelines updated regularly. multiple options, main side effect is myositis or rhabdo
36
Q

1st line for symptom relief in CAD

A

short acting nitrates + beta blockers or CCB

37
Q

2nd line for symptom relief in CAD

A 
ivabradine
long acting nitrates
nicorandil
ranolazine
trimetazidine
38
Q

CAD event prevention

A 
lifestyle management
control of risk factors
educate pt
aspirin
statins
ACE-I or ARBs
39
Q

what is an MI/ACS

A

myocardial infarction/acute coronary syndrome

-blockage of flow to one or more coronary arteries not relieveed by decreased demand
results in damage to myocardium

40
Q

what is STEMI

A

ST elevation MI

–acute occlusion of an atherosclerotic area resulting full thickness necrosis of myocardium

41
Q

etiology of STEMI

A

thrombus or plaque rupture most common, vasospasm, hypotension, coronary artery dissection, cocaine

42
Q

hx of STEMI

A

increased severity of angina symptoms if previously diagnosed

diaphoresis, nausea, dyspnea, arrhythmia, or suddendeath.
up to 1/3 may be painless or have vague symptoms (elderly, somen, DM)

43
Q

PE of STEMI

A

anxious, uncomfortable

  • bradycardia/tachycardia/arrhythmia possible
  • heart sounds usually WNL, gallops or mitral regurg (papillary muscle dysfunction possible)
  • JVD possible with large infarct
44
Q

labs for STEMI

A

CPK, CKMB, troponin (most specific)

-may be withing normal limits if pt presents early

45
Q

ekg findings with CAD

A
  1. ST segment elevation greater than 1mm in 2 or more contiguous precordial leads or 2 or more adjacent limb leads OR new or presumed new left bundle branch block
  2. pathologic Q waves - occurs in 50-70% of infarcts. may take hrs to days; >1mm wide OR >2mm deep OR >25% of depth of QRS complex
    - usually seen in leads V1-3
    - most never fully resolve
  3. hyperacute T waves may be present early
46
Q

tx of CAD STEMI

A
  1. emergent percutaneous coronary intervention = time is muscle
  2. oxygen
  3. asa 325mg chewed plus clopidogrel (plavix)
  4. NTG - sublingual up to 3 doses if not hypotensive
    5: morphine - IV prn for pain
  5. heparin - weigh based protocol with bolus
  6. beta blocker
    8: fibrinolytic: contraindicated: CVA
47
Q

what is NSTEMI

A

non ST elevation

48
Q

etiology of NSTEMI

A

same as stemi

49
Q

labs for NSTEMI

A

cardiac enzymes most reliable way to dx NSTEMI

50
Q

EKG for NSTEMI

A
  • may appear normal or subtle changes.
  • ST segment depression of 0.5mm or greater
  • OR dynamic T wave inversion with pain or discomfort/ transient ST elevation of 0.5mm or greater for less than 20 minutes
51
Q

tx of NSTEMI

A
  • oxygen
  • ASA 325 chewed plus plavix
  • NTG
  • morphine
  • additional antiplatelets
  • anticoagulants - heparin, lovenox, etc
  • cath lab if unable to get pain free - serial ekg’s
  • post event - initiate lifestyle modifications and meds
52
Q

what is prinzmetal angina

A

coronary artery spasm generally in the setting of clean coronary arteries

  • rare
  • more common in younger pt’s and women and geranally occurs in early AM
53
Q

etiology of prinzemtal angina

A

cold, stress, cocain, smoking, vasoconstriction meds (beta blockers, antihistmaines, decongestants, ADHD stimulants)

54
Q

EKG of prinzmetal angina

A

usually presents as STEMI

55
Q

w/u of prinzmetal angina

A

cardiac cath due to STEMI appearance

56
Q

tx of prinzmetal angina

A
  • generally responds well to NTG
  • long acting nitrates and or Ca+ channel blockers for prophylaxis
  • avoidance of precipitants is key
57
Q

MI complications

A
  1. cardiogenic shock
  2. heart failure
  3. dressler’s syndrome
  4. arrhythmias
58
Q

MI complications - cardiogenic shock

A

large L venntricle infarct leads to sig. decr. in contractility
-results in very low BP with an inadequate supply of O2 rich blood to the tissues of the body

59
Q

MI compliations - heart failure

A

acute (may lead to shock) or chronic (develop over time)

60
Q

MI complications - Dressler’s syndrome

A

fever, pleuritis, and pericarditis,

it is caused by an autoimmune rxn to damage heart muscle, can occur weeks or months after an MI

61
Q

MI complications - arrhythmias

A
  1. bradycardia - inferior infarcts or meds. atropine. pacing may be needed
  2. SVT - adrenergic stimulations vs hypovolumemia. check lytes. rate control ?cardiovert
  3. Vtach/fib - most common 1st few hours post MI. Lido/Amio/procainamide. shock Vfib
  4. AV block - 1st degree at the level of the AV node most common. atropine. pacing
62
Q

what factors are taken into account for the TMII RISK SCORE for UA/NSTEMI?

A
  1. age >65
  2. > 3 CAD risk factors
  3. known CAD (stenosis >50%)
  4. ASA use in past 7 days
  5. recent severe angina
  6. incr cardiac markers
  7. ST deviation >0.5mm
63
Q

what factors are taken into account for TIMI risk score for STEMI

A 
age >75 or 65-74
DM or HTN or angina
SBP 100bpm
Killip II-Iv
Weight 4hrs
64
Q

what is a CABG

A

coronary artery bypass graft
inidicated in pts with STEMI and coronary anatomy not amenable to PCI who have ongoing or recurrent ischemia, cardiogenic shock, severe HF, or other high risk features. saphenous vein or internal thoracic artery most common

65
Q

what is cardiac rehab

A

education, counseling and exervcise services to help heart pts increase physical fitness, reduce cardiac symptoms, imporve mental/physical health and reduce the risk of futrue heart problesms

66
Q

ACE/ARB use in CAD

A

have been shown to minimize LV dilations post MI resulting in lower rates of heart failure and improved survival

67
Q

what is therapeutic hypthermia

A

consider in post arrest pt’s

  • goal is to reduce anoxic/reperfusion brain injury and improve neurological morbidity and mortality
  • initiate as early as possible
68
Q

what is inclusion criteria for therapeutic hypothermia

A

code time

69
Q

what is exclusion criteria for therapeutic hypohermia

A

pregnancy, hemodynamic, instability, trauma, arrest, sepsis, significant bleeding

70
Q

what are complications of therapeutic hypothermia

A 
coagulopathy
dysrhythmias(bradycardia, blocks, afib/vfib)
hypotension
hyperglycemia
pancreatitis
electrolyte abnormalities (K, MG, PHos)

Clin Med - Cardio II (12 decks)

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