Perfusion & MI Flashcards
1
Q
Where are coronary arteries located
A
extend from aorta
located in epicardium
extend inwards via intramyocardial arteries
2
Q
Coronary arteries
A
right coronary artery –> posterior descending
left coronary artery –> circumflex & anterior descending
3
Q
What region does the posterior descending artery supply?
A
posterior interventricular septum
posterior of the heart
4
Q
What region does the left circumflex artery supply?
A
left lateral side –> left ventricle
5
Q
What region does the left anterior descending artery supply?
A
anterior interventricular septum
left ventricle
6
Q
Factors affecting myocardial perfusion
A
central perfusion (coronary arteries orig in aorta)
coronary artery patency & diameter
heart relaxation
7
Q
When does the myocardium receive blood
A
during diastole
8
Q
Types of angina
A
Stable
Unstable
Vasospastic
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
10
Q
Duration of stable angina pain
A
2-5 minutes
11
Q
Duration of unstable angina
A
<20 min
relieved when fibrinolytic system kicks in
12
Q
Acute MI duration
A
> 20 min
13
Q
Typical mechanism of AMI
A
unstable atherosclerotic plaque rupture –> thrombus formation that fully occludes the artery
14
Q
Angina pectoris
A
chest pain d/t insufficient oxygen supply (hypoxic injury) to myocardium
15
Q
Determinants of O2 supply
A
O2 content of blood (anemia, hypoxemia)
coronary blood flow (occlusion, hardening)
16
Q
Determinants of O2 demand
A
metabolic demands of cardiac muscle
HR, BP (SVR = afterload), contractility
17
Q
Atherosclerosis
A
build up of fatty plaques in arteries –> narrows lumen and causes arterial stiffening
stiffening = coronary arteries are unable to dilate
18
Q
Types of autoregulation
A
mechanical –> high BP causes vasoconstriction
metabolic –> metabolic waste causes vasodilation (coronary arteries vasodilate in response to metabolic need)
19
Q
Myocardium O2 extraction of arterial blood
A
60-80%
20
Q
Factors impairing central perfusion
A
hypovolemia hypotension aortic stenosis impaired contractility impaired diastolic filling
21
Q
Factors impairing coronary patency
A
CAD
coronary vasospasm
coronary embolism
22
Q
Factors impairing heart relaxation
A
tachyarrhythmia
23
Q
Factors increasing O2 demand
A
PSR exercise ventricular hypertrophy (s/t HTN, stenosis, congenital defects) large PE sustained tachyarrhythmia hyperthermia/fever
24
Q
Factors decreasing arterial O2
A
anemia
hypoxemia d/t respiratory disease
hypovolemia
smoking –> carbon monoxide
25
Unstable atherosclerotic plaque
thin fibrous cap
large lipid core
high risk for rupture --> platelet aggregation & thrombosis
implicated in unstable angina & MI
26
Stable atherosclerotic plaque
thick fibrous cap
small fatty core
partially obstruct blood flow --> do not form thrombi
stable angina
27
Stable angina triggers
exertion
emotional stress
predictable
28
Unstable angina triggers
unpredictable
at rest
*often precedes an MI
29
Vasospastic angina triggers
nocturnal
at rest
smoking
lasts 5-15 minutes
30
RESP causes of chest pain
pleuritis, PE, pneumothorax, pneumonia, cancer
31
GI causes of chest pain
GERD, swallowing disorders, cholecystitis, peptic ulcer
32
CARDIAC causes of chest pain
angina, MI, pericarditis, aortic dissection
33
MSK causes of chest pain
rib fracture
muscle strain
chrodroitis
34
Angina pharmocotherapy
nitroglycerin
beta blockers
calcium channel blockers
35
Collateral circulation
if atherosclerosis develops slowly --> coronary vessels can develop anastomoses to compensate for obstructed blood blow
36
End arteries
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
37
Nitroglycerin MOA
metabolized --> nitric oxide --> vasodilation
venous dilation > arterial dilation
reduces preload, contractility, afterload (arterial dilation)
**coronary vasodilation**
38
Acute myocardial infarction
tissue death that occurs d/t prolonged ischemia >20 minutes
39
Common causes of AMI
ruptured atherosclerotic plaque --> thrombus occlusion
coronary vasospasm (cocaine)
coronary embolism
CAD + O2 supply/demand imbalance
40
Factors affecting severity of AMI
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)
41
STEMI
elevated ST wave
transmural --> full thickness (occurs in 3-6 hrs)
assoc with fully obstructed arteries
42
NSTEMI
depressed ST wave
subendocardial damage
assoc with partially occluded arteries
43
NSTEMI
depressed ST wave
subendocardial damage (inner 1/3 to 1/2)
assoc with partially occluded arteries --> SOME blood flow still remains
44
Where does necrosis initially begin?
in the subendocardium
| furthest from the arterial blood supply, so will be the first to die from impaired blood flow
45
Which region of the heart most commonly affected by MI
left ventricle
| supplied by all the coronary arteries
46
Widow maker
an MI that occurs in the left main artery (short artery before branching into LAC & LCX)
high mortality rate
47
Fx of ischemic on myocardium
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
48
How long does post-MI inflammation last?
1-3 days
important for healing
physical rest during this stage to prevent rupture
49
Post-MI rupture
heart wall rupture --> cardiac tamponade --> bleed into pericardial cavity --> death
interventricular septum --> shunting of blood
papillary muscle --> mitral valve regurgitation
50
Mechanisms of post-op MI
CAD rupture --> thrombus formation
| CAD + O2 supply/demand imbalance
51
PSR & hypercoagulability
increased platelet reactivity
increased clotting factors
decreased anticoagulant factors
*cortisol stimulates clotting factor/platelet synthesis
52
Surgery & hypercoagulability
surgery --> trauma --> inflammation
inflammation = increase in clotting factors
injury = hemostasis
53
PSR & O2 demand
increased HR
contractility
increased BP
54
PSR & O2 supply
blood loss --> hypovolemia, anemia
55
What type of MI is common post-op
NSTEMI
56
When is risk of post-op MI highest
POD0-3
57
S/S of MI
```
chest pain --> radiating
diaphoresis
dyspnea
weakness
fatigue
dizziness, syncope
nausea/vomiting
heartburn/indigestion
tachycardia, tachypnea, decreased SpO2
SOB, cough, crackles (pulmonary edema)
fever
```
58
Silent MI
no symptoms reported by pt
59
Unrecognized MI
symptoms are present but misidentified
| delays treatment
60
Diagnostic tests
```
troponin T/I
creatinine kinase-MB
12 lead ECG
CBC
electrolytes
glucose
coagulation tests
BUN, Cr
```
61
When is Troponin T or I detectable in blood?
3-4 hrs
| remains in system for a few days
62
Other conditions causing increased troponin
```
myocarditis, pericarditis
heart failure
tachycardia, A. fib
cardiac contusion, trauma, CR, defibrillation
extreme exertion
cardiotoxic medication
PE
```
63
Other conditions causing increased troponin
```
myocarditis, pericarditis
heart failure
tachycardia, A. fib
cardiac contusion, trauma, CR, defibrillation
extreme exertion
cardiotoxic medication
PE
```
64
AMI Pharmacotherapy
```
nitrogclyerin
B-blockers
ACE-i
antiplatelet
anticoagulants
```
65
1st generation B-blocker
propranolol
| non-selective --> affects B1/B2
66
2nd generation B-blocker
bisoprolol, metabolic
| B1 selective
67
3rd generation B blocker
carvedilol
| non-selective --> B1/A1
68
B2 receptors
B2 = VASODILATION
located in airways & livers
cause bronchodilation
induce glycogenolysis in liver
69
Initial AMI treatment
```
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
Reperfusion therapy
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
Therapeutic window for thromboltisc
within 12 hrs of symptom onset
want to initiate <30 min
followed by coronary angiography
72
Post-MI treatment
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
Immediate Post-MI complications (0-24 hrs)
dysrhythmias**
| cardiogenic shock
74
Short-term Post-MI complications (1-14 days)
pericarditis
mural thrombosis
myocardial rupture (during healing)
75
Long-term MI complications (>2 weeks)
ventricular aneurysm
| heart failure
76
Sudden death s/t MI
death that occurs within 1 hr of an MI
| usually caused by a fatal arrhythmia --> ventricular fibrillation
77
Factors causing dysrhythmia
ischemia/injury to electrical conduction system
| altered myocardial sensitivity to nerve impulses (electrolyte imbalances, SNS activation)
78
What region does the right coronary artery supply?
right atrium/ventricle
SA node
AV node
79
Common dysrhythmias post MI
sinus dysrhythmia --> tachycardia or bradycardia
atrial/ventricular fibrillation
AV bundle/branch blocks --> heart block
premature ventricular contractions
80
When does cardiogenic shock occur
when >40% of left ventricular mass is damaged
| --> acute LVHF --> cardiogenic shock
81
S/S of cardiogenic shock
persistent hypotension SBP <90 mmHG
S/S of tissue hypoxia & congestion --> cool extremities, pallor, cyanosis, dizziness, oliguria, dyspnea, crackles
high perfusion organ damage
82
When does pericarditis occur
2-3 days post infarction
| inflammation of the pericardium (serous membrane)
83
S/S of pericarditis
```
pericardial friction rub on auscultation
chest pain (sharp/stabbing) worse with deep inhalation
```
84
How long does it take for heart to heal post-MI
necrotic tissue has to be replaced with scar tissue
| ~6 weeks
85
When do mural thrombi develop
first 2 weeks post MI
86
Mural Thrombosis patho
inflammation, blood stasis, hypercoagulability --> mural thrombi
can break off and cause an embolus
87
Ventricular aneurysm patho
scar tissue over time becomes dilated & thin
| rarely ruptures but contributes to blood stasis --> thrombosis
88
Coronary artery disease
aka ischemic heart disease
| atherosclerotic plaques accumulate in arteries --> myocardial ischemia
89
Most common cause of acute MI death
acute death = w/i 1 hr of MI onset
| usually d/t ventricular fibrillation
90
Venticular fibrillation
uncoordinated ventricular contractions
ventricles quiver instead of contract = decreased cardiac output
**highest risk w/i first hour
91
Dysrhythmia patho
physical injury to conduction system (ischemia, scarring)
| conditions that alter myocardial sensitivity (electrolyte imbalances, SNS sensitivity)
92
Common dysrhythmias
```
sinus tachycardia
sinus bradycardia
atrial/ventricular fibrillation
AV (heart) block
premature ventricular contractions
```
93
When does cardiogenic shock occur
when >40% of left ventricular mass affected (usually d/t new MI + existing scar tissue)
acute heart failure
94
S/S of cardiogenic shock
```
SBP <90 mm Hg
cool extremities
pallor
weak pulses
dizziness
oliguria
cyanosis
dyspnea/crackles (pulmonary congestion)
multi-organ failure --> fatal
```
95
Pericarditis
inflammation of pericardium (fibrous outer covering of heart)
extends to epicardial surface
96
S/S pericarditis
chest pain --> worse w/ deep inhalation
| pericardial friction rub (auscultation)
97
Cardiac tamponade
restrictive heart condition
| caused by excessive fluid in the pericardial cavity --> puts pressure on the heart preventing it from pumping properly
98
Myocardial rupture
papillary muscle rupture --> valvular regurgitation
| interventricular rupture --> shunting of blood
99
Mural thrombosis patho
form in the heart over site of injury
| d/t inflammation, blood pooling, hypercoagulability
100
Ventricular aneurysm
caused by heart wall weakening --> begins to dilate & thin out
wall bulges outwards
101
Systolic dysfunction
caused by scar tissue = reduced contractility = less pumping power
102
Diastolic function
scar tissue = inelastic = decreased diastolic filling (preload)
103
RF for atherosclerosis
```
endothelial injury (smoking, hypertension)
lipid accumulation (LDL cholesterol, low HDL)
```
104
How does atherosclerosis affect perfusion
plaques --> narrow artery lumen
thrombus can form on atheroma --> partial or full occlusion
thromboembolus --> blocks a distal artery
artery wall weakening --> aneurysm
105
Where do atherosclerotic aneurysms typically form
the aorta
| b/w renal or iliac arteries
106
Hypoxia
insuff O2 to peripheral tissue
107
Ischemia
cell injury caused by decreased blood flow
108
Infarction
cell death caused by prolonged ischemia
109
Why does ischemic injury occur faster than hypoxic injury?
ischemia = impaired delivery of nutrients, oxygen & removal of metabolic waste, CO2
110
Ischemia & metabolism
ischemia causes cells to switch to anaerobic metabolism --> increased production of lactate
111
Limits of anaerobic metabolism
glycolysis --> only uses glucose
| pyruvic acid --> lactic acid = acidosis (decreases pH)
112
ATP & Sodium
ATP required for the Na+/K+ pump
| low ATP results in electrolyte imbalances --> cellular swelling
113
Na+/Ca++ exchanger
antiporter
works to keep intracellular Ca++ levels low
requires ATP
exchanges Ca++ for Na++
114
Cellular active transport pumps
Na+/K+ pump
Na+/Ca++ pump --> keep intracellular calcium low
Ca++ pump
115
Sodium & Calcium
increased intracellular sodium --> ruins the concentration gradient needed for the na/ca antiporter
increased intracellular calcium = release of damaging enzymes
116
Consequences of cell injury
ATP synthesis decreases
cells swell
protein synthesis decreases
117
Consequences of cell death
no ATP synthesis
Ca++ accumulates
cell membranes rupture --> release of intracellular contents (K+, H+)
118
Initial mgmt of ACS "MOAN"
Morphine
Oxygen
Aspirin/clopidogrel
Nitrates
119
Post-MI Pharmacological mgmt "ABAS"
Ace-i/ARB
Beta blocker
Aspirin/clopidogrel
Statins
120
Acute MI assessment
LOTTAARP --> hx of chest pain, assoc S/S
| vital signs --> BP, HR (apical), SpO2
