Ischemic Heart Disease Flashcards

1
Q

what is Ischemic Heart Disease?

A

inadequate supplu of blood and oxygen to a portion of the myocardium

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2
Q

when does atherosclerosis begin

A

childhood

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3
Q

Where is nitric oxide produced

A

endothelial cells

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4
Q

what does nitric oxide do

A

inhibits plaque formation

anti-inflammatory properties

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5
Q

what causes endothelial dysfunction

A

LDL and oxidized LDL

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6
Q

Women that present without chest pain with Ischemic heart disease have a greater likelihood of being induced by what

A

rest, sleep and mental stress rather than activity

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7
Q

characteristics of stable angina (angina pectoris)

A

chest discomfort
exertional or stress-related chest or arm discomfort that resolves with rest and/or the use of sublingual nitro
usually not greater than 5-10 MINS

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8
Q

presentation of stable angina

A

heaviness or pressure
tightness squeezing, smothering, choking
“Levine’s sign” Fist over sternum
radiation: shoulders, arms, neck, jaw teeth, epigastrum, midback
duration 2-10 mins
crescendo-decrescendo
relief in <10 min with rest or taking sublingual nitro
PE: tachycardia, hypertension, abnormal heart sounds

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9
Q

presentation of atypical stable angina

A

DYSPNEA, NAUSEA, FATIGUE, FAINTNESS
more common in elderly and diabetic patients
dyspnea common in women

symptoms not likely to be ischemia or angina
sharp, fleeting stabs of chest pain
prolonged, dull ache in the left precordial area
any discomfort localized with one finger
pain lasting for seconds or constant pain lasting for days

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10
Q

Diagnostics for angina

A

-EKG
may have ST depression

-chest radiograph

-cardiac biomarkers- cardiac enzymes
troponin
CK

Diagnosis
cardiac stress testing
coronary angiography

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11
Q

what is Bruce Protocol for exercise stress test

A

speed and incline are increased every 3 minutes until pt heart rate is at 85% of maximum HR

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12
Q

what is the gold standard for diagnosing CAD

A

coronary angiography aka cardiac catheterization

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13
Q

meds that DECREASE oxygen demand

A

-nitrates- PRELOAD reduction
First line for acute angina

-Beta blockers decrease HR, BP, and contractility, AFTERLOAD reduction
first line for chronic angina

-calcium channel blockers decrease BP, and contractility, AFTERLOAD reduction
indicated for pts that do not respond to nitrates and beta blockers

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14
Q

meds that INCREASE oxygen supply

A
  • nitrates - dilate coronary arteries
    0. 3-0.6 mg sublingually every 5 min up to 3 doses

-calcium channel blockers: act as coronary vasodilators

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15
Q

3 antiplatelet meds

A

aspirin 75-325 mg daily
clopidogrel (plavix)
combo of ASA and clopidogrel

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16
Q

what do statins do

A

STABILIZE PLAQUES
reduce clinical events
slow progression of coronary atherosclerosis
induce regression of coronary atherosclerosis

17
Q

two types of revascularization

A

percutaneous coronary intervention PCI
(stent?)

Coronary artery bypass grafting (CABG)
left main coronary stenosis
triple vessel disease
typically use saphenous vein or internal mammary arteries

18
Q

characteristics of acute coronary syndrome (ACS)

A

unstable angina
MI
non-st elevation MI (NSTEMI)
ST elevation MI

19
Q

4 pathophysiological processes

A

plaque rupture or erosion with a superimposed OCCLUSINVE THROMBUS (most common)

dynamic obstruction
coronary artery spasm

progressive mechanical obstruction
progressive atherosclerosis or restenosis following percutaneous coronary intervention (PCI)

UA secondary to increased myocardial oxygen demand and/or decreased supply
tachycardia or anemia

20
Q

presentation of prinzmetal’s angina

A

-ischemic symptoms secondary to VASOSPASM
-chest pain occuring at rest with TRANSIENT ST-SEGMENT ELEVATION
-usually younger pts with fewer risk factors
-diagnostics
coronary angiography
-treatment:
NITRATES
CALCIUM CHANNEL BLOCKERS

21
Q

presentation of ACS

A
ischemic pain
SOB
weakness
nausea
anxiety
sense of doom
atypical presentation in women, diabetics and elderly pts
22
Q

Presentation of unstable angina (UA)/NSTEMI

A

UA:
ischemic discomfort and at least one of the following
occurs at REST
severe and of NEW ONSET
occurs with a CRESCENDO pattern
more severe, prolonged, frequent than previously

Non ST elevation MI (NSTEMI)
similar symptoms with continued worsening

23
Q

clinical features of Unstable angina UA

A

NO ELEVATION OF CK-MB OR TROPONIN (not actual cell death)
may have ST depression or T wave inversion on ECG’
rare transient ST elevation

Non-ST elevation MI (NSTEMI)
DEFINITE ELEVATION OF CK-MB AND/OR TROPONIN
typically no ST elevation
may have ST depression or T wave inversion

24
Q

management of UA/NSTEMI

A

bedrest, cardiac monitoring, IV access and labs
oxygen if <90%
sublingual NO x3 5 min intervals
morphone avoided unless pain unacceptable
beta blockers start within 24 hrs
high intensity statin therapy 80 mg
antiplatelet therapy in NSTEMI clopidogrel
anticoagulation (ASA, heparin)
risk stratification, angiography and revascularization with PCI and CABG

25
Q

ST-elevation MI (STEMI) identifiable precipitating factors

A

vigorous exercise
extreme emotional stress
medical or surgical illness

common within a few hours of awakening in the a.m.

26
Q

STEMI causes

A

RUPTURE OF A VULNERABLE PLAQUE (ASCAD)
results in a COMPLETE OCCLUSION of a coronary artery
(most common)

slowly developing stenosis of a coronary artery
collateral vessels usually develop as stenosis increases, providing blood flow to the affected areas

27
Q

management of STEMI

A

bed rest, cardiac monitoring, IV access and labs
ASA 325 chewed and swallowed
cardiac enzymes
sublingual nitro
beta blockers
high intensity statin
select reperfusion strategy
fibrinolysis if PCI not available within 120 min, symptoms less than 12 hrs
anticoagulant therapy, and antiiplatelet therapy

28
Q

absolute contras to thrombolytic (fibrinolytic) therapy

A
hx of intracranial hemorrhage
hx of stroke past year
poorly controlled HTN
systolic >180 and/or >110
suspected aortic dissection
active internal bleeding