Norton - IHD Flashcards Preview

T&D III exam 1 > Norton - IHD > Flashcards

Flashcards in Norton - IHD Deck (54):
1

IHD - general

imbalance - supply and demand for oxygenated blood for the heart

reduced nutrients, waste removal

2

IHD is also called

CAD, coronary heart disease

3

>90% of IHD is caused by

reduced coronary blood flow due to atherosclerotic coronary arterial obstruction

4

Clinical manifestation - IHD

angina pectoris
MI
Chronic IHD w/ HF
Sudden cardiac death

5

#1 cause of death of both men and women in US

IHD

6

Pathogenesis IHD

demand > coronary perfusion

7

What can increase the demand while perfusion is low

Fixed obstruction
acute plaque change

coronary thrombus
vasospasm

8

obstruction needed to cause symptomatic ischemia with:

exercise

at rest

> 70% w/ exercise
> 90% at rest

9

what can protect distal myocardium from ischemia

collateral

10

triggering factors for acute plaque change

- adrenergic stimulation
- dynamic changes of the structure and composition of plaque
- moderately stenotic are most dangerous

11

most dangerous trigger factor for acute plaque change

moderately stenotic

12

Coronary thrombus can

- partial occlusion -- eventually lead to total occlusion
- emolize
- activate SM growth-related signals

13

Vasoconstriction is stimulated by

adrenergic agonist

platelet contents

14

How does angina pectoris present?

Paroxysmal
Recurrent
Substernal/precordial chest discomfort - constricting, squeezing, choking, knifelike

lasts at most 15 min - no infarction

15

what is angina pectoris due to

myocardial ischemia

16

Stable angina - decreased coronary perfusion due to

fixed obstruction

17

Unstable angina is due to

disruption of atherosclerotic plaque with superimposed partially occluding thrombus

18

#1 of the acute coronary syndromes

unstable angina

19

Prinzmetal angina is not related to

physical activity
HR
BP

20

#2 of the acute coronary syndromes

MI

21

Acute plaque disruption

- hemorrhage
- erosion/ulceration
- rupture or fissuring

22

90% of transmural infarcts

acute plaque disruption -- platelets adhere to exposed subendothelial collagen/necrotic plaque contents, release aggregators -- vasospasms -- other extrinsic coag pathway also gets activated -- Thrombus quickly occludes lumen

23

myocardial response to ischemia at ~ 1 sec

cessation of aerobic glycolysis

decreased creatine phosphate, ATP

Accumulate lactic acid

24

when does loss of contractility occur

after 2 min

25

when does injury to myocyte become irreversible?

20-40min

26

microvascular injury occurs

after 1 hr

27

_____ may occur even due to ischemia

arrhythmias

28

Subendocardial infarct is NOT due to

plaque disruption
superimposed thrombus

29

Subendocardial infarct is majorly due to

diffuse stenosing coronary atherosclerosis with reduction of blood flow

30

Morphology of MI depends on

- Location, severity and rate of dev of coronary obstruction
- size of area perfused by obstructed vessel
- duration of occlusion
- metabolic/oxygen demand
- extent of collateral
- coronary vasospasm
- BP, HR, rhythm
- Necrosis (complete in 6 hrs)

31

Infarct modification by reperfusion

Thrombolysis
Angioplasty w/ stent placement
CABG

32

Grafting of

RCA
LAD

RCA - saphenous vein
LAD - internal mammary artery

33

Factors associated with poor prognosis (MI)

Advanced age
female gender
DM
previous MI

34

Consequence and complications of MI

Contractile dysfunction (htn, pulmonary vascular congestion, cardiogenic shock if severe)

Arrhythmias

Myocardial rupture

Pericarditis

right ventricular infarct

Mural thrombus

Ventricular aneurysm

Papillary m. dysfunction

Progressive late heart failure

35

Most common to least common myocardial rupture

Ventricular free wall -- cardiac tamponade
Intraventrucular septum -- L-R shunting
Papillary m. -- severe mitral regurgitation

36

What is a later complication of MI

ventricular aneurysm

37

is rupture common with ventricular aneurysm?

no - scar tissue is strong

38

Complications of MI depend on

infarct size, site, transmural extent

39

Large transmural infarct

Cardiogenic shock
Arrhythmias
late CHF

40

Anterior transmural infarct

Free-wall rupture
expansion
Mural thrombi
aneurysm
worse clinical course

41

Inferior transmural infarct

conduction blocks
RV involvement

42

Most important factors affecting prognosis after an MI

- quality of LV function
- extent of vascular obstruction perfusing viable myocardium

43

Often elderly, ptns develop ________ due to ischemic myocardial damage

progressive HF

44

Chronic ischemic heart dz

hypertrophy, dilation, stenosis of coronary, healed previous infarcts

45

is prior sx or history necessary to present with CHF?

no

46

Sudden Cardiac death

Unexpected death from cardiac causes - no symptomatic heart dz or early after the onset of sx (less than 1 hr)

47

Sudden cardiac death is usually due to

IHD

48

Other causes of Sudden cardiac death

- congenital
- valvular issues (aortic)
- myocarditis
- cardiomyopathy

49

Ultimate mechanism of Sudden cardiac death

lethal ARRHYTHMIA

50

#3 of the acute coronary syndromes

Sudden cardiac death

51

Morphology of sudden cardiac death

- coronary artery occlusion 75% in one or more of the three major vessels
High grade stenosis

52

Prognosis in survivors of sudden cardiac death is improved by

implanting automatic cardioverter-defibrillator

53

The acute coronary syndromes:

unstable angina
acute MI
sudden cardiac death

54

What do acute coronary syndromes share?

- common pathophys -
coronary atherosclerotic plaque disruption and assoc. intraluminal platelet-fibrin thrombus formation