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
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