Exam 2: Ch 19 CHD, Fetal & Congenital Disorders

Question 1

__% of deaths in high income countries from heart disease

Answer 1

1 killer in USA

40%

Question 2

the left and right coronary arteries begin just ____ to the ______ valve

Answer 2

distal, aortic

Question 3

left main coronary artery gives rise to the ___ & ______

Answer 3

LAD, circumflex

Question 4

left anterior descending supplies

Answer 4

septum and anterior wall of the LV

Question 5

circumflex supplies

Answer 5

lateral (free) wall of LV

Question 6

right coronary artery supplies

Answer 6

RV and gives rise to posterior descending artery

Question 7

posterior descending artery supplies

Answer 7

posterior wall

Question 8

gradual occlusion of CA does not produce symptoms until…

Answer 8

late because collaterals form

Question 9

which artery BP reflects aortic pressure?

Answer 9

CA

Question 10

CA flow is controlled by…

Answer 10

aortic BP: particularly DBP (intra myocardial vessels compressed during systole)

auto-regulation: CA flow increases to meet metabolic needs (O2 extraction high)

Question 11

inadequate DBP leads to

Answer 11

ischemia

Question 12

dilators include

Answer 12

NO and metabolites

Question 13

CHD is divided into….

Answer 13

chronic ischemia heart disease

acute coronary syndromes

Question 14

ischemia

Answer 14

any time cardiac oxygen demands are greater than supply

Question 15

CHD caused by plaque categories

Answer 15

stable plaque

unstable plaque

Question 16

fixed stable plaque

Answer 16

leads to stableangina

Question 17

unstable plaques

Answer 17

rupture and form clots

lead to unstable angina and MI (ACS)

Question 18

plaque rupture

Answer 18

can be spontaneous but often 2ndary SNS activity

vulnerable to rupture when they have a lipid core, inflammation, low SMC

Question 19

plaque rupture occurs most often …

Answer 19

in the morning

during or after exercise

Question 20

plaque rupture mechanisms

Answer 20

rupture exposes lipid core, causing platelets to adhere and release ADP and prostaglandins

more platelets leads to a thrombus

Question 21

___ blocks prostaglandin synthesis

Answer 21

ASA – aspirin

Question 22

_____ blocks ADP receptors on platelets

Answer 22

Plavix

Question 23

3 types of acute coronary syndrome (ACS)

Answer 23

Q-wave MI (ST elevation)

non Q-wave MI (non ST elevation)

unstable angina

Question 24

Q-wave MI generally occurs from a, and others from…

Answer 24

Q-wave: complete coronary artery occlusion

non Q-wave, unstable angina: incomplete or intermittent occlusion

Question 25

T wave inversion

Answer 25

ischemia

Question 26

ST changes in general

Answer 26

damage

Question 27

ST depression

Answer 27

subendocardial injury

Question 28

ST elecation

Answer 28

transmural injury

Question 29

Q wave

Answer 29

old MI

Question 30

serum markers

Answer 30

necrotic cells release contents into blood myoglobin increased at 1hr, peaks in 4-8 hrs not cardiac specific

Question 31

will a Q-wave MI and non Q-wave MI show increased serum markers?

Answer 31

yes, then classified as MI

Question 32

how is the area of infarct determined in Q-wave MI

Answer 32

which CA is blocked

Question 33

cause and symptoms of non Q-wave MI and unstable angina

Answer 33

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

Question 34

symptoms of MI

Answer 34

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

Question 35

extent of pathologic changes in ACS determined by

Answer 35

which vessel is occluded time of occlusion metabolic needs of tissue extent of collaterals

Question 36

pathologic changes in ACS

Answer 36

immediate loss of contractility irreversible damage and necrosis in 20-40min reperfusion can reestablish blood flow, but "stuns" tissue stunned tissue non functional

Question 37

goal of managing ACS

Answer 37

prevent extent of injury/necrosis prevent sudden cardiac death cells may not die if reperfusion achieved in 20-40min

Question 38

what happens in ER for ACS

Answer 38

evaluate for reperfusion w/ 12 lead ECG watch for ST/T wave changes and PVCs (premature ventricular contractions) O2 optimizes hemoglobin saturation

Question 39

drugs given in ER for ACS

Answer 39

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

Question 40

management of ACS: fibrinolytic therapy

Answer 40

dissolves clots limits infarct size reduces mortality best if begun within 90min of 1st symptoms

Question 41

PCI - percutaneous coronary intervention

Answer 41

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

Question 42

acute and long term complications of PCI

Answer 42

acute: thrombosis, vessel dissection long-term: restenosis (recurrence of stenosis)

Question 43

CABG

Answer 43

done on or off the pump graft from aorta to CA distal to blockage venous or arterial graft mammary artery used, saphenous vein

Question 44

recovery from ACS

Answer 44

at 4-7 days the infarct is soft and can rupture ~7 weeks necrotic tissue replaced with granulation tissue (fibrous scar)

Question 45

recovery complications of ACS

Answer 45

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

Question 46

Dressler's syndrome

Answer 46

pericarditis -- hypersensitivity to tissue necrosis

Question 47

3 subtypes of chronic ischemia heart disease

Answer 47

stable angina silent MI vasospastic angina

Question 48

stable angina

Answer 48

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

Question 49

silent MI

Answer 49

MI without angina lack of pain may indicate high pain threshold or DM

Question 50

vasospastic angina

Answer 50

spasm of CAs --> angina occurs at rest associated with life-threatening arrythmias

Question 51

angina classification (4)

Answer 51

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

Question 52

diagnosis of chronic ischemic heart disease

Answer 52

rule out (R/O) non-cardiac pain -- reflux, muscular exercise stress test produces ST changes holter monitor for vasospastic angina

Question 53

treatment goal for chronic ischemic heart disease

Answer 53

reduce symptoms and prevent MI

Question 54

treatment for chronic ischemic heart disease

Answer 54

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