Exam 2: Ch 19 CHD, Fetal & Congenital Disorders Flashcards
__% of deaths in high income countries from heart disease
1 killer in USA
40%
the left and right coronary arteries begin just ____ to the ______ valve
distal, aortic
left main coronary artery gives rise to the ___ & ______
LAD, circumflex
left anterior descending supplies
septum and anterior wall of the LV
circumflex supplies
lateral (free) wall of LV
right coronary artery supplies
RV and gives rise to posterior descending artery
posterior descending artery supplies
posterior wall
gradual occlusion of CA does not produce symptoms until…
late because collaterals form
which artery BP reflects aortic pressure?
CA
CA flow is controlled by…
aortic BP: particularly DBP (intra myocardial vessels compressed during systole)
auto-regulation: CA flow increases to meet metabolic needs (O2 extraction high)
inadequate DBP leads to
ischemia
dilators include
NO and metabolites
CHD is divided into….
chronic ischemia heart disease
acute coronary syndromes
ischemia
any time cardiac oxygen demands are greater than supply
CHD caused by plaque categories
stable plaque
unstable plaque
fixed stable plaque
leads to stableangina
unstable plaques
rupture and form clots
lead to unstable angina and MI (ACS)
plaque rupture
can be spontaneous but often 2ndary SNS activity
vulnerable to rupture when they have a lipid core, inflammation, low SMC
plaque rupture occurs most often …
in the morning
during or after exercise
plaque rupture mechanisms
rupture exposes lipid core, causing platelets to adhere and release ADP and prostaglandins
more platelets leads to a thrombus
___ blocks prostaglandin synthesis
ASA – aspirin
_____ blocks ADP receptors on platelets
Plavix
3 types of acute coronary syndrome (ACS)
Q-wave MI (ST elevation)
non Q-wave MI (non ST elevation)
unstable angina
Q-wave MI generally occurs from a, and others from…
Q-wave: complete coronary artery occlusion
non Q-wave, unstable angina: incomplete or intermittent occlusion
T wave inversion
ischemia
ST changes in general
damage
ST depression
subendocardial injury
ST elecation
transmural injury
Q wave
old MI
serum markers
necrotic cells release contents into blood
myoglobin increased at 1hr, peaks in 4-8 hrs
not cardiac specific
will a Q-wave MI and non Q-wave MI show increased serum markers?
yes, then classified as MI
how is the area of infarct determined in Q-wave MI
which CA is blocked
cause and symptoms of non Q-wave MI and unstable angina
from: plaque disruption with clot and/or arterial spasm
pain occurs at rest and is severe, persistent (>20 min), not relieved by NTG
called MI if serum markers are elevated
symptoms of MI
acute pain, not relieved by rest or NTG
female more likely to have “discomfort”
elderly likely to have SOB (shortness of breath)
GI symptoms
30-50% die from VF (ventricular fibriliation) in 1st few hours
extent of pathologic changes in ACS determined by
which vessel is occluded
time of occlusion
metabolic needs of tissue
extent of collaterals
pathologic changes in ACS
immediate loss of contractility
irreversible damage and necrosis in 20-40min
reperfusion can reestablish blood flow, but “stuns” tissue
stunned tissue non functional
goal of managing ACS
prevent extent of injury/necrosis
prevent sudden cardiac death
cells may not die if reperfusion achieved in 20-40min
what happens in ER for ACS
evaluate for reperfusion w/ 12 lead ECG
watch for ST/T wave changes and PVCs (premature ventricular contractions)
O2 optimizes hemoglobin saturation
drugs given in ER for ACS
analgesia with MS (IV) relieves pain, decrease anxiety
beta blockers decrease myocardial O2 needs
aspirin inhibits prostaglandin syn. by platelets
Plavix blocks ADP receptor on platelets
NTG decreases preload/afterload
MS for pain and anxiety
management of ACS: fibrinolytic therapy
dissolves clots
limits infarct size
reduces mortality
best if begun within 90min of 1st symptoms
PCI - percutaneous coronary intervention
balloon tip catheter introduced to femoral or brachial artery
catheter advanced to blockage under fluoro
expand balloon to dilate stenosis
statins prevent vessel collapse when catheter withdrawn
acute and long term complications of PCI
acute: thrombosis, vessel dissection
long-term: restenosis (recurrence of stenosis)
CABG
done on or off the pump
graft from aorta to CA distal to blockage
venous or arterial graft
mammary artery used, saphenous vein
recovery from ACS
at 4-7 days the infarct is soft and can rupture
~7 weeks necrotic tissue replaced with granulation tissue (fibrous scar)
recovery complications of ACS
HF and cardiogenic shock from decreased contractility
Dressler’s syndrome
LV aneurysm and rupture from weakened wall
ventricular septal rupture
papillary muscle (mitral valve) rupture
Dressler’s syndrome
pericarditis – hypersensitivity to tissue necrosis
3 subtypes of chronic ischemia heart disease
stable angina
silent MI
vasospastic angina
stable angina
caused by fixed obstruction of CA, plaque > 75%
precipitated by increased O2 demands from exercise or emotional stress
generally relieved within 10 min of rest + NTG
silent MI
MI without angina
lack of pain may indicate high pain threshold or DM
vasospastic angina
spasm of CAs –> angina
occurs at rest
associated with life-threatening arrythmias
angina classification (4)
class 1: pain with prolonged exercise
class 2: slight limitation of normal activity
class 3: marked limitation of ordinary activity
class 4: pain at rest/any physical activity
diagnosis of chronic ischemic heart disease
rule out (R/O) non-cardiac pain – reflux, muscular
exercise stress test produces ST changes
holter monitor for vasospastic angina
treatment goal for chronic ischemic heart disease
reduce symptoms and prevent MI
treatment for chronic ischemic heart disease
angioplasty (PTCA) or CABG
therapeutic lifestyle changes (TLC)
anti-platelet drugs
beta blocks to decrease cardiac work
calcium channel blockers dilate arteries
NTG decreases preload/afterload
