Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BSNC 3000 > Perfusion & MI > Flashcards

Perfusion & MI Flashcards

1
Q

Where are coronary arteries located

A

extend from aorta
located in epicardium
extend inwards via intramyocardial arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Coronary arteries

A

right coronary artery –> posterior descending

left coronary artery –> circumflex & anterior descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What region does the posterior descending artery supply?

A

posterior interventricular septum

posterior of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What region does the left circumflex artery supply?

A

left lateral side –> left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What region does the left anterior descending artery supply?

A

anterior interventricular septum

left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Factors affecting myocardial perfusion

A

central perfusion (coronary arteries orig in aorta)
coronary artery patency & diameter
heart relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When does the myocardium receive blood

A

during diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Types of angina

A

Stable
Unstable
Vasospastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Angina pain characteristics

A 
substernal or precordial chest pain
radiate --> up jaw, down arm 
tingling in arms
crushing, suffocating, strangulation
unstable --> doom, not relieved by rest/nitrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Duration of stable angina pain

A

2-5 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Duration of unstable angina

A

<20 min

relieved when fibrinolytic system kicks in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute MI duration

A

> 20 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Typical mechanism of AMI

A

unstable atherosclerotic plaque rupture –> thrombus formation that fully occludes the artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Angina pectoris

A

chest pain d/t insufficient oxygen supply (hypoxic injury) to myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Determinants of O2 supply

A

O2 content of blood (anemia, hypoxemia)

coronary blood flow (occlusion, hardening)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Determinants of O2 demand

A

metabolic demands of cardiac muscle

HR, BP (SVR = afterload), contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Atherosclerosis

A

build up of fatty plaques in arteries –> narrows lumen and causes arterial stiffening

stiffening = coronary arteries are unable to dilate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Types of autoregulation

A

mechanical –> high BP causes vasoconstriction

metabolic –> metabolic waste causes vasodilation (coronary arteries vasodilate in response to metabolic need)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Myocardium O2 extraction of arterial blood

A

60-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Factors impairing central perfusion

A 
hypovolemia
hypotension
aortic stenosis 
impaired contractility
impaired diastolic filling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factors impairing coronary patency

A

CAD
coronary vasospasm
coronary embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Factors impairing heart relaxation

A

tachyarrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Factors increasing O2 demand

A 
PSR
exercise 
ventricular hypertrophy (s/t HTN, stenosis, congenital defects)
large PE
sustained tachyarrhythmia 
hyperthermia/fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Factors decreasing arterial O2

A

anemia
hypoxemia d/t respiratory disease
hypovolemia
smoking –> carbon monoxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Unstable atherosclerotic plaque

A

thin fibrous cap
large lipid core
high risk for rupture –> platelet aggregation & thrombosis
implicated in unstable angina & MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Stable atherosclerotic plaque

A

thick fibrous cap
small fatty core
partially obstruct blood flow –> do not form thrombi
stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Stable angina triggers

A

exertion
emotional stress
predictable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Unstable angina triggers

A

unpredictable
at rest
*often precedes an MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Vasospastic angina triggers

A

nocturnal
at rest
smoking
lasts 5-15 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

RESP causes of chest pain

A

pleuritis, PE, pneumothorax, pneumonia, cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

GI causes of chest pain

A

GERD, swallowing disorders, cholecystitis, peptic ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CARDIAC causes of chest pain

A

angina, MI, pericarditis, aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MSK causes of chest pain

A

rib fracture
muscle strain
chrodroitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Angina pharmocotherapy

A

nitroglycerin
beta blockers
calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Collateral circulation

A

if atherosclerosis develops slowly –> coronary vessels can develop anastomoses to compensate for obstructed blood blow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

End arteries

A

arteries that are the only source of O2 blood to a tissue area
do not form anastomoses w/ other vascular beds
no collateral circulation
coronary arteries are end arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Nitroglycerin MOA

A

metabolized –> nitric oxide –> vasodilation
venous dilation > arterial dilation
reduces preload, contractility, afterload (arterial dilation)
coronary vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Acute myocardial infarction

A

tissue death that occurs d/t prolonged ischemia >20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Common causes of AMI

A

ruptured atherosclerotic plaque –> thrombus occlusion
coronary vasospasm (cocaine)
coronary embolism
CAD + O2 supply/demand imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Factors affecting severity of AMI

A

site of occlusion (proximal worse than distal)
which artery is occluded
degree of obstruction –> partial vs. complete
duration of ischemia –> before reperfusion occurs
extent of collateral circulation (takes time to develop)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

STEMI

A

elevated ST wave
transmural –> full thickness (occurs in 3-6 hrs)
assoc with fully obstructed arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

NSTEMI

A

depressed ST wave
subendocardial damage
assoc with partially occluded arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

NSTEMI

A

depressed ST wave
subendocardial damage (inner 1/3 to 1/2)
assoc with partially occluded arteries –> SOME blood flow still remains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where does necrosis initially begin?

A

in the subendocardium

furthest from the arterial blood supply, so will be the first to die from impaired blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which region of the heart most commonly affected by MI

A

left ventricle

supplied by all the coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Widow maker

A

an MI that occurs in the left main artery (short artery before branching into LAC & LCX)
high mortality rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Fx of ischemic on myocardium

A

anaerobic metabolism –> lactic acid
ATP depletion –> cellular swelling & increase in intracellular calcium
irreversible cell injury (>20-40 min)
cell lysis –> rls of proteins & potassium
necrotic tissue –> non functional, inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How long does post-MI inflammation last?

A

1-3 days
important for healing
physical rest during this stage to prevent rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Post-MI rupture

A

heart wall rupture –> cardiac tamponade –> bleed into pericardial cavity –> death
interventricular septum –> shunting of blood
papillary muscle –> mitral valve regurgitation

50
Q

Mechanisms of post-op MI

A

CAD rupture –> thrombus formation

CAD + O2 supply/demand imbalance

51
Q

PSR & hypercoagulability

A

increased platelet reactivity
increased clotting factors
decreased anticoagulant factors
*cortisol stimulates clotting factor/platelet synthesis

52
Q

Surgery & hypercoagulability

A

surgery –> trauma –> inflammation
inflammation = increase in clotting factors
injury = hemostasis

53
Q

PSR & O2 demand

A

increased HR
contractility
increased BP

54
Q

PSR & O2 supply

A

blood loss –> hypovolemia, anemia

55
Q

What type of MI is common post-op

A

NSTEMI

56
Q

When is risk of post-op MI highest

A

POD0-3

57
Q

S/S of MI

A 
chest pain --> radiating
diaphoresis
dyspnea
weakness
fatigue
dizziness, syncope
nausea/vomiting 
heartburn/indigestion
tachycardia, tachypnea, decreased SpO2
SOB, cough, crackles (pulmonary edema)
fever
58
Q

Silent MI

A

no symptoms reported by pt

59
Q

Unrecognized MI

A

symptoms are present but misidentified

delays treatment

60
Q

Diagnostic tests

A 
troponin T/I
creatinine kinase-MB
12 lead ECG 
CBC 
electrolytes
glucose
coagulation tests
BUN, Cr
61
Q

When is Troponin T or I detectable in blood?

A

3-4 hrs

remains in system for a few days

62
Q

Other conditions causing increased troponin

A 
myocarditis, pericarditis
heart failure
tachycardia, A. fib
cardiac contusion, trauma, CR, defibrillation 
extreme exertion
cardiotoxic medication
PE
63
Q

Other conditions causing increased troponin

A 
myocarditis, pericarditis
heart failure
tachycardia, A. fib
cardiac contusion, trauma, CR, defibrillation 
extreme exertion
cardiotoxic medication
PE
64
Q

AMI Pharmacotherapy

A 
nitrogclyerin
B-blockers
ACE-i
antiplatelet
anticoagulants
65
Q

1st generation B-blocker

A

propranolol

non-selective –> affects B1/B2

66
Q

2nd generation B-blocker

A

bisoprolol, metabolic

B1 selective

67
Q

3rd generation B blocker

A

carvedilol

non-selective –> B1/A1

68
Q

B2 receptors

A

B2 = VASODILATION
located in airways & livers
cause bronchodilation
induce glycogenolysis in liver

69
Q

Initial AMI treatment

A 
sit pt down --> encourage rest 
relieve pain/anxiety (morphine IV)
administer O2 PRn 
anti-platelet meds --> decrease thrombus formation 
B-blocker --> reduce work of heart 
ACE-i --> prevent remodeling
70
Q

Reperfusion therapy

A

percutaneous coronary intervention (PCI) –> balloon & stent
fibrinolysis –> thrombolytics
CABG –> coronary artery bypass graft (anastomoses made w/ aorta & distal region of artery w/ graft from saphenous vein)

71
Q

Therapeutic window for thromboltisc

A

within 12 hrs of symptom onset
want to initiate <30 min
followed by coronary angiography

72
Q

Post-MI treatment

A

antiplatelets –> prevent recurrent thrombosis
anticoagulants –> prevent L. ventricular thrombosis, thrombosis d/t A. fib, embolization
statin therapy –> decrease blood cholesterol
B-blocker –> reduce workload of heart
ACE-i –> prevent remodeling. manage workload of heart

73
Q

Immediate Post-MI complications (0-24 hrs)

A

dysrhythmias**

cardiogenic shock

74
Q

Short-term Post-MI complications (1-14 days)

A

pericarditis
mural thrombosis
myocardial rupture (during healing)

75
Q

Long-term MI complications (>2 weeks)

A

ventricular aneurysm

heart failure

76
Q

Sudden death s/t MI

A

death that occurs within 1 hr of an MI

usually caused by a fatal arrhythmia –> ventricular fibrillation

77
Q

Factors causing dysrhythmia

A

ischemia/injury to electrical conduction system

altered myocardial sensitivity to nerve impulses (electrolyte imbalances, SNS activation)

78
Q

What region does the right coronary artery supply?

A

right atrium/ventricle
SA node
AV node

79
Q

Common dysrhythmias post MI

A

sinus dysrhythmia –> tachycardia or bradycardia
atrial/ventricular fibrillation
AV bundle/branch blocks –> heart block
premature ventricular contractions

80
Q

When does cardiogenic shock occur

A

when >40% of left ventricular mass is damaged

–> acute LVHF –> cardiogenic shock

81
Q

S/S of cardiogenic shock

A

persistent hypotension SBP <90 mmHG
S/S of tissue hypoxia & congestion –> cool extremities, pallor, cyanosis, dizziness, oliguria, dyspnea, crackles
high perfusion organ damage

82
Q

When does pericarditis occur

A

2-3 days post infarction

inflammation of the pericardium (serous membrane)

83
Q

S/S of pericarditis

A 
pericardial friction rub on auscultation 
chest pain (sharp/stabbing) worse with deep inhalation
84
Q

How long does it take for heart to heal post-MI

A

necrotic tissue has to be replaced with scar tissue

~6 weeks

85
Q

When do mural thrombi develop

A

first 2 weeks post MI

86
Q

Mural Thrombosis patho

A

inflammation, blood stasis, hypercoagulability –> mural thrombi
can break off and cause an embolus

87
Q

Ventricular aneurysm patho

A

scar tissue over time becomes dilated & thin

rarely ruptures but contributes to blood stasis –> thrombosis

88
Q

Coronary artery disease

A

aka ischemic heart disease

atherosclerotic plaques accumulate in arteries –> myocardial ischemia

89
Q

Most common cause of acute MI death

A

acute death = w/i 1 hr of MI onset

usually d/t ventricular fibrillation

90
Q

Venticular fibrillation

A

uncoordinated ventricular contractions
ventricles quiver instead of contract = decreased cardiac output
**highest risk w/i first hour

91
Q

Dysrhythmia patho

A

physical injury to conduction system (ischemia, scarring)

conditions that alter myocardial sensitivity (electrolyte imbalances, SNS sensitivity)

92
Q

Common dysrhythmias

A 
sinus tachycardia
sinus bradycardia
atrial/ventricular fibrillation
AV (heart) block
premature ventricular contractions
93
Q

When does cardiogenic shock occur

A

when >40% of left ventricular mass affected (usually d/t new MI + existing scar tissue)
acute heart failure

94
Q

S/S of cardiogenic shock

A 
SBP <90 mm Hg
cool extremities 
pallor
weak pulses
dizziness
oliguria
cyanosis
dyspnea/crackles (pulmonary congestion)
multi-organ failure --> fatal
95
Q

Pericarditis

A

inflammation of pericardium (fibrous outer covering of heart)
extends to epicardial surface

96
Q

S/S pericarditis

A

chest pain –> worse w/ deep inhalation

pericardial friction rub (auscultation)

97
Q

Cardiac tamponade

A

restrictive heart condition

caused by excessive fluid in the pericardial cavity –> puts pressure on the heart preventing it from pumping properly

98
Q

Myocardial rupture

A

papillary muscle rupture –> valvular regurgitation

interventricular rupture –> shunting of blood

99
Q

Mural thrombosis patho

A

form in the heart over site of injury

d/t inflammation, blood pooling, hypercoagulability

100
Q

Ventricular aneurysm

A

caused by heart wall weakening –> begins to dilate & thin out
wall bulges outwards

101
Q

Systolic dysfunction

A

caused by scar tissue = reduced contractility = less pumping power

102
Q

Diastolic function

A

scar tissue = inelastic = decreased diastolic filling (preload)

103
Q

RF for atherosclerosis

A 
endothelial injury (smoking, hypertension)
lipid accumulation (LDL cholesterol, low HDL)
104
Q

How does atherosclerosis affect perfusion

A

plaques –> narrow artery lumen
thrombus can form on atheroma –> partial or full occlusion
thromboembolus –> blocks a distal artery
artery wall weakening –> aneurysm

105
Q

Where do atherosclerotic aneurysms typically form

A

the aorta

b/w renal or iliac arteries

106
Q

Hypoxia

A

insuff O2 to peripheral tissue

107
Q

Ischemia

A

cell injury caused by decreased blood flow

108
Q

Infarction

A

cell death caused by prolonged ischemia

109
Q

Why does ischemic injury occur faster than hypoxic injury?

A

ischemia = impaired delivery of nutrients, oxygen & removal of metabolic waste, CO2

110
Q

Ischemia & metabolism

A

ischemia causes cells to switch to anaerobic metabolism –> increased production of lactate

111
Q

Limits of anaerobic metabolism

A

glycolysis –> only uses glucose

pyruvic acid –> lactic acid = acidosis (decreases pH)

112
Q

ATP & Sodium

A

ATP required for the Na+/K+ pump

low ATP results in electrolyte imbalances –> cellular swelling

113
Q

Na+/Ca++ exchanger

A

antiporter
works to keep intracellular Ca++ levels low
requires ATP
exchanges Ca++ for Na++

114
Q

Cellular active transport pumps

A

Na+/K+ pump
Na+/Ca++ pump –> keep intracellular calcium low
Ca++ pump

115
Q

Sodium & Calcium

A

increased intracellular sodium –> ruins the concentration gradient needed for the na/ca antiporter
increased intracellular calcium = release of damaging enzymes

116
Q

Consequences of cell injury

A

ATP synthesis decreases
cells swell
protein synthesis decreases

117
Q

Consequences of cell death

A

no ATP synthesis
Ca++ accumulates
cell membranes rupture –> release of intracellular contents (K+, H+)

118
Q

Initial mgmt of ACS “MOAN”

A

Morphine
Oxygen
Aspirin/clopidogrel
Nitrates

119
Q

Post-MI Pharmacological mgmt “ABAS”

A

Ace-i/ARB
Beta blocker
Aspirin/clopidogrel
Statins

120
Q

Acute MI assessment

A

LOTTAARP –> hx of chest pain, assoc S/S

vital signs –> BP, HR (apical), SpO2

BSNC 3000 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions