Ischemic Heart Disease Flashcards
what is Ischemic Heart Disease?
inadequate supplu of blood and oxygen to a portion of the myocardium
when does atherosclerosis begin
childhood
Where is nitric oxide produced
endothelial cells
what does nitric oxide do
inhibits plaque formation
anti-inflammatory properties
what causes endothelial dysfunction
LDL and oxidized LDL
Women that present without chest pain with Ischemic heart disease have a greater likelihood of being induced by what
rest, sleep and mental stress rather than activity
characteristics of stable angina (angina pectoris)
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
presentation of stable angina
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
presentation of atypical stable angina
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
Diagnostics for angina
-EKG
may have ST depression
-chest radiograph
-cardiac biomarkers- cardiac enzymes
troponin
CK
Diagnosis
cardiac stress testing
coronary angiography
what is Bruce Protocol for exercise stress test
speed and incline are increased every 3 minutes until pt heart rate is at 85% of maximum HR
what is the gold standard for diagnosing CAD
coronary angiography aka cardiac catheterization
meds that DECREASE oxygen demand
-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
meds that INCREASE oxygen supply
- nitrates - dilate coronary arteries
0. 3-0.6 mg sublingually every 5 min up to 3 doses
-calcium channel blockers: act as coronary vasodilators
3 antiplatelet meds
aspirin 75-325 mg daily
clopidogrel (plavix)
combo of ASA and clopidogrel
what do statins do
STABILIZE PLAQUES
reduce clinical events
slow progression of coronary atherosclerosis
induce regression of coronary atherosclerosis
two types of revascularization
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
characteristics of acute coronary syndrome (ACS)
unstable angina
MI
non-st elevation MI (NSTEMI)
ST elevation MI
4 pathophysiological processes
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
presentation of prinzmetal’s angina
-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
presentation of ACS
ischemic pain SOB weakness nausea anxiety sense of doom atypical presentation in women, diabetics and elderly pts
Presentation of unstable angina (UA)/NSTEMI
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
clinical features of Unstable angina UA
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
management of UA/NSTEMI
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
ST-elevation MI (STEMI) identifiable precipitating factors
vigorous exercise
extreme emotional stress
medical or surgical illness
common within a few hours of awakening in the a.m.
STEMI causes
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
management of STEMI
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
absolute contras to thrombolytic (fibrinolytic) therapy
hx of intracranial hemorrhage hx of stroke past year poorly controlled HTN systolic >180 and/or >110 suspected aortic dissection active internal bleeding
