Exam 2: Ch 19 CHD, Fetal & Congenital Disorders Flashcards Preview

Pathophysiology > Exam 2: Ch 19 CHD, Fetal & Congenital Disorders > Flashcards

Flashcards in Exam 2: Ch 19 CHD, Fetal & Congenital Disorders Deck (54):
1

__% of deaths in high income countries from heart disease

40%

#1 killer in USA

2

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

distal, aortic

3

left main coronary artery gives rise to the ___ & ______

LAD, circumflex

4

left anterior descending supplies

septum and anterior wall of the LV

5

circumflex supplies

lateral (free) wall of LV

6

right coronary artery supplies

RV and gives rise to posterior descending artery

7

posterior descending artery supplies

posterior wall

8

gradual occlusion of CA does not produce symptoms until...

late because collaterals form

9

which artery BP reflects aortic pressure?

CA

10

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)

11

inadequate DBP leads to

ischemia

12

dilators include

NO and metabolites

13

CHD is divided into....

chronic ischemia heart disease

acute coronary syndromes

14

ischemia

any time cardiac oxygen demands are greater than supply

15

CHD caused by plaque categories

stable plaque

unstable plaque

16

fixed stable plaque

leads to stableangina

17

unstable plaques

rupture and form clots

lead to unstable angina and MI (ACS)

18

plaque rupture

can be spontaneous but often 2ndary SNS activity

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

19

plaque rupture occurs most often ...

in the morning

during or after exercise

20

plaque rupture mechanisms

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

more platelets leads to a thrombus

21

___ blocks prostaglandin synthesis

ASA -- aspirin

22

_____ blocks ADP receptors on platelets

Plavix

23

3 types of acute coronary syndrome (ACS)

Q-wave MI (ST elevation)

non Q-wave MI (non ST elevation)

unstable angina

24

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

25

T wave inversion

ischemia

26

ST changes in general

damage

27

ST depression

subendocardial injury

28

ST elecation

transmural injury

29

Q wave

old MI

30

serum markers

necrotic cells release contents into blood

myoglobin increased at 1hr, peaks in 4-8 hrs

not cardiac specific

31

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

yes, then classified as MI

32

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

which CA is blocked

33

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

34

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

35

extent of pathologic changes in ACS determined by

which vessel is occluded

time of occlusion

metabolic needs of tissue

extent of collaterals

36

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

37

goal of managing ACS

prevent extent of injury/necrosis

prevent sudden cardiac death

cells may not die if reperfusion achieved in 20-40min

38

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

39

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

40

management of ACS: fibrinolytic therapy

dissolves clots

limits infarct size

reduces mortality

best if begun within 90min of 1st symptoms

41

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

42

acute and long term complications of PCI

acute: thrombosis, vessel dissection

long-term: restenosis (recurrence of stenosis)

43

CABG

done on or off the pump

graft from aorta to CA distal to blockage

venous or arterial graft

mammary artery used, saphenous vein

44

recovery from ACS

at 4-7 days the infarct is soft and can rupture

~7 weeks necrotic tissue replaced with granulation tissue (fibrous scar)

45

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

46

Dressler's syndrome

pericarditis -- hypersensitivity to tissue necrosis

47

3 subtypes of chronic ischemia heart disease

stable angina

silent MI

vasospastic angina

48

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

49

silent MI

MI without angina

lack of pain may indicate high pain threshold or DM

50

vasospastic angina

spasm of CAs --> angina

occurs at rest

associated with life-threatening arrythmias

51

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

52

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

53

treatment goal for chronic ischemic heart disease

reduce symptoms and prevent MI

54

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