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

Norton - IHD Flashcards

1
Q

IHD - general

A

imbalance - supply and demand for oxygenated blood for the heart

reduced nutrients, waste removal

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2
Q

IHD is also called

A

CAD, coronary heart disease

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3
Q

> 90% of IHD is caused by

A

reduced coronary blood flow due to atherosclerotic coronary arterial obstruction

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4
Q

Clinical manifestation - IHD

A

angina pectoris
MI
Chronic IHD w/ HF
Sudden cardiac death

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5
Q

1 cause of death of both men and women in US

A

IHD

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6
Q

Pathogenesis IHD

A

demand > coronary perfusion

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7
Q

What can increase the demand while perfusion is low

A

Fixed obstruction
acute plaque change

coronary thrombus
vasospasm

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8
Q

obstruction needed to cause symptomatic ischemia with:

exercise

at rest

A

> 70% w/ exercise

> 90% at rest

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9
Q

what can protect distal myocardium from ischemia

A

collateral

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10
Q

triggering factors for acute plaque change

A
  • adrenergic stimulation
  • dynamic changes of the structure and composition of plaque
  • moderately stenotic are most dangerous
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11
Q

most dangerous trigger factor for acute plaque change

A

moderately stenotic

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12
Q

Coronary thrombus can

A
  • partial occlusion – eventually lead to total occlusion
  • emolize
  • activate SM growth-related signals
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13
Q

Vasoconstriction is stimulated by

A

adrenergic agonist

platelet contents

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14
Q

How does angina pectoris present?

A

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

lasts at most 15 min - no infarction

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15
Q

what is angina pectoris due to

A

myocardial ischemia

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16
Q

Stable angina - decreased coronary perfusion due to

A

fixed obstruction

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17
Q

Unstable angina is due to

A

disruption of atherosclerotic plaque with superimposed partially occluding thrombus

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18
Q

1 of the acute coronary syndromes

A

unstable angina

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19
Q

Prinzmetal angina is not related to

A

physical activity
HR
BP

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20
Q

2 of the acute coronary syndromes

A

MI

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21
Q

Acute plaque disruption

A
  • hemorrhage
  • erosion/ulceration
  • rupture or fissuring
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22
Q

90% of transmural infarcts

A

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
Q

myocardial response to ischemia at ~ 1 sec

A

cessation of aerobic glycolysis

decreased creatine phosphate, ATP

Accumulate lactic acid

24
Q

when does loss of contractility occur

A

after 2 min

25
Q

when does injury to myocyte become irreversible?

A

20-40min

26
Q

microvascular injury occurs

A

after 1 hr

27
Q

_____ may occur even due to ischemia

A

arrhythmias

28
Q

Subendocardial infarct is NOT due to

A

plaque disruption

superimposed thrombus

29
Q

Subendocardial infarct is majorly due to

A

diffuse stenosing coronary atherosclerosis with reduction of blood flow

30
Q

Morphology of MI depends on

A
  • 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
Q

Infarct modification by reperfusion

A

Thrombolysis
Angioplasty w/ stent placement
CABG

32
Q

Grafting of

RCA
LAD

A

RCA - saphenous vein

LAD - internal mammary artery

33
Q

Factors associated with poor prognosis (MI)

A

Advanced age
female gender
DM
previous MI

34
Q

Consequence and complications of MI

A

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
Q

Most common to least common myocardial rupture

A

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

36
Q

What is a later complication of MI

A

ventricular aneurysm

37
Q

is rupture common with ventricular aneurysm?

A

no - scar tissue is strong

38
Q

Complications of MI depend on

A

infarct size, site, transmural extent

39
Q

Large transmural infarct

A

Cardiogenic shock
Arrhythmias
late CHF

40
Q

Anterior transmural infarct

A 
Free-wall rupture
expansion
Mural thrombi
aneurysm
worse clinical course
41
Q

Inferior transmural infarct

A

conduction blocks

RV involvement

42
Q

Most important factors affecting prognosis after an MI

A
  • quality of LV function

- extent of vascular obstruction perfusing viable myocardium

43
Q

Often elderly, ptns develop ________ due to ischemic myocardial damage

A

progressive HF

44
Q

Chronic ischemic heart dz

A

hypertrophy, dilation, stenosis of coronary, healed previous infarcts

45
Q

is prior sx or history necessary to present with CHF?

A

no

46
Q

Sudden Cardiac death

A

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

47
Q

Sudden cardiac death is usually due to

A

IHD

48
Q

Other causes of Sudden cardiac death

A
  • congenital
  • valvular issues (aortic)
  • myocarditis
  • cardiomyopathy
49
Q

Ultimate mechanism of Sudden cardiac death

A

lethal ARRHYTHMIA

50
Q

3 of the acute coronary syndromes

A

Sudden cardiac death

51
Q

Morphology of sudden cardiac death

A
  • coronary artery occlusion 75% in one or more of the three major vessels
    High grade stenosis
52
Q

Prognosis in survivors of sudden cardiac death is improved by

A

implanting automatic cardioverter-defibrillator

53
Q

The acute coronary syndromes:

A

unstable angina
acute MI
sudden cardiac death

54
Q

What do acute coronary syndromes share?

A
  • common pathophys -

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

T&D III exam 1 (11 decks)

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