Quiz 1 Flashcards
1
Q
what are the ischemic heart diseases?
A
atherosclerosis, coronary artery disease (CAD), acute MI, hypertension (HTN), cerebral vascular disease (CVD), peripheral artery disease (PAD), renal artery disease, and aneurysms
2
Q
who is at the greatest risk for CV disease?
A
minority groups
3
Q
t/f: COVID leads to an increased risk for CV disease
A
true :(
4
Q
what is the PT’s role in treatment of CV disease?
A
educate pts on risk factor modification
manage cardiometabolic diseases and risk factors
fitness and exercise programs
vitals on EVERY pt
SHOULD be part of preventative medicine programs
5
Q
what are some modifiable risk factors for CV disease?
A
smoking
body weight
physical activity
diet
BP
cholesterol
stress
blood glucose
6
Q
what are non-modifiable risks for CV disease?
A
heredity
male sex
increased age
7
Q
how does cigarette smoking contribute to the development of CVD?
A
leukocytosis (increased WBCs) leads to the development of ATHEROSCLEROSIS, PLAQUES, and lowered HDL
increased fibrinogen, BP, and inflammation
constriction of the arteries increases the pressure in the arteries leading to high BP
8
Q
smoking ____ times a day leads to an increased risk of CVD above a non-smoker
A
4
9
Q
what percentage of adults don’t engage in the minimum amount of physical activity?
A
60%
10
Q
sedentary lifestyle is increased in _____ and _____
A
women, diabetics
11
Q
physical activity has a beneficial effect on…
A
lipid profile
BP
insulin sensitivity
12
Q
what are the long term benefits of physical activity?
A
increased fibrinolysis and RBC deformability
decreased platelet aggregability
13
Q
exercise can be ____, _____, or both
A
resistive, aerobic
14
Q
what is the goal for exercise?
A
150 minutes per week of moderate intensity OR 75 minutes per week of vigorous intensity
15
Q
what is considered the MAIN risk for CVD?
A
body weight
16
Q
what percentage of the population is obese/overweight?
A
68%
17
Q
what BMI is associated with increased risk for CVD?
A
greater than or equal to 30 kg/m^2
18
Q
adipose tissue where in the body is especially associated with increased significance of CVD risk?
A
abdomen
19
Q
adequate nutrition can decrease the risk of what?
A
HTN
hyperlipidemia
obesity
glucose levels
20
Q
what are the nutritional goals to decrease CVD risk?
A
4 1/2 cups fruits and veg
2 servings fish/week
3 servings whole grains daily
limit sugary drinks to 36 oz/week or less
limits sodium intake to less than 150 mg/day
21
Q
t/f: BP is considered an independent risk factor for the development of CVD
A
true!
22
Q
t/f: decreased BP lowers the risk of stroke more than MI
A
true
23
Q
increase BP can cause…
A
increased pressure on arteries, injuring the vascular endothelium
increased permeability of vessel wall to LDL
increased foam cell and smooth muscle production leads to increased LDL in the intima layer causing plaques to form
increased systemic inflammation stimulates oxidative stress and cytokine production
24
Q
t/f: there is a direct link b/w increased cholesterol and the development of CAD
A
true!
25
how does high cholesterol contribute to development of atherosclerosis?
high cholesterol leads to abnormal circulating lipid levels, especially LDL
26
can increased saturated fat in the diet contribute to increased cholesterol levels?
yes
27
how does increased HDL levels protect against development of atherosclerosis?
it transports cholesterol away from peripheral tissues
28
poorly controlled diabetes can ____ HDL levels
lower
29
what is HDL?
carries good cholesterol in blood to the liver where it is broken down and removed from your body
30
what is LDL?
carries cholesterol to your cells and arteries causing buildup
hardens and narrows vessels so less blood can flow through
31
what makes up total cholesterol?
HDL, LDL, and triglycerides
32
what is the best predictor for the development of CVD?
cholesterol levels
33
what ratio of total cholesterol to HDL leads increased risk of atherosclerosis?
greater than 4.5
34
triglyceride level of ____ can contribute to atherosclerosis
greater than 150 mg/dL
35
HDL level of ____ can contribute to atherosclerosis
less than 35 mg/dL
36
_____ _____ influences development of atherosclerosis 20x more than cholesterol content of food
saturated fat
37
what are ideal LDL levels?
less than 70 mg/dL
38
what is the suggested blood glucose levels to reduce risk of diabetics getting CAD?
less then 100 mg/dL
39
why does blood glucose levels increase risk for CAD?
the binding of glucose to proteins or fibrinogen w/o enzymes leads to increased risk for thrombus formation
diabetes can cause impaired endothelial function which allows for accumulation of cholesterol in arterial walls
40
t/f: family history is considered a major risk for CAD
false, it's a "minor" risk bc there's not much good evidence yet
41
is there a genetic link established for CAD?
no
42
what doubles risk for CAD?
premature/early CAD in your family
43
what is recommended in pt's with a strong family history of CAD?
aspirin use
44
what is the average age of MI in men?
64.7 y/o
45
what is the average age of MI in women?
72.2 y/o
46
who is at a larger risk for acute MI before 55 y/o, men or women?
men
47
what is the leading cause of death in both men and women?
CAD
48
who has a higher mortality rate after a 1st MI, men or women?
women
49
what women are at an increased risk for CAD?
post-menopausal and diabetic women (estrogen may play protective role)
women who had pre-eclampsia w/pregnancy
50
t/f: increased hostility/anger leads to increased risk for CVD?
true
51
what are other factors that affect CVD?
homocysteine
lipoprotein
c-reactive protein
52
homocysteine
may contribute to oxidative stress, vascular inflammation, and platelet adhesiveness
53
lipoprotein
a varient of LDL that encourages inflammation and thrombosis
can't be effected by diet and exercise
54
what has the greatest effect against lipoprotein
niacin
55
c-reactive protein
marker of systemic inflammation
56
t/f: c-reactive protein can be an independent predictor of MI, stroke, PAD, and sudden cardiac death
true
57
what is arterial pressure regulated by?
baroreceptor reflex
58
where are the baroreceptor reflex receptors?
the aortic arch and carotid sinuses
59
what do baroreceptors monitor?
stretch and deformation of arteries
60
can the baroreceptor response regulate BP long term?
no
61
how does the baroreceptor response work?
the baroreceptors are stimulated by increased arterial pressure and signal the CNS to send negative feedback to circulation via the ANS to bring the BP back to baseline
62
how does the ANS lower BP?
by lowering peripheral vascular resistance and cardiac output due to vasodilation, and decreased HR and contractility
63
what is HTN?
diastolic BP over 90 mmHg OR systolic BP consisttently over 140 mmHg
64
when does the heart relax?
during diastole
65
what is the role of diastole?
allows blood to fill coronary arteries to supply the heart w/blood supply
66
why is high DBP bad?
is leads bad blood supply to heart tissues
67
what is SBP?
the heart contracting to supply the body with blood or blood to the lungs
68
what are the types of HTN?
labile, primary/essential, secondary, and malignant
69
what is labile HTN?
BP that fluctuates b/w normal and hypertensive values
70
what type of HTN is the most common?
labile HTN
71
labile HTN is most common in what group?
advanced age groups
72
labile HTN is most likely due to...
multiple defects in BP regulation along with environmental stressors, possible insulin resistance, obesity, and diabetes
73
what is primary/essential HTN?
HTN with no discernable cause
74
what are some suspected causes of primary/essential HTN?
genetics, environment, high sodium intake, stress, obesity, alcohol, or smoking
75
what is secondary HTN?
there is an identifiable medical condition/cause of the HTN
76
what a percentage of HTN cases are secondary HTN?
5-10%
77
what is secondary HTN associated with?
renovascular health conditions and endocrine disorders
78
what is malignant HTN?
a hypertensive crisis where there is marked elevated BP w/target organ damage
79
what are some effects of malignant HTN?
retinal hemorrhages, heart failure, encephalopathy, renal insufficiency, stroke
80
in malignant HTN, DBP is...
over 125 mmHg
81
what is normal BP?
SBP: <120
and
DBP: <80
82
what is high-normal, elevated, pre-hypertensive BP?
SBP: 120-129
and
DBP: <80
83
what is stage 1 HTN?
SBP: 130-139
or
DBP: 80-89
84
what is stage 2 HTN?
SBP: >140
or
DBP: >90
85
what is hypertensive crisis?
SBP: >180
and/or
DBP: >120
86
what are symptoms?
what the patient tells us
87
what are signs?
changes in body structure and function
88
what are the symptoms of HTN?
headache
spontaneous epitaxis (bloody nose)
dizziness
flushing
sweating
blurred vision
nocturnal urinary frequency
89
what are the signs of HTN?
L ventricular hypertrophy (thickened myocardium)
retinopathy (vision changes)
arterial bruits in carotid and femoral arteries
90
why does a thickened myocardium affect BP?
the tissue becomes stiff and can't pump properly
91
what are bruits?
swooshing artery sounds
turbulence due to atherosclerosis
S2 heart sounds due to L atrium contractions in a stiff LV
92
what happens as BP continues to increase?
1. destruction of arterial bed and narrowing of arterioles
2. elasticity of arteries decreases (can't return to og shape)
3. viscocity of blood increases (doesn't move through as well)
4. decrease in tissue perfusion (target organs-heart, kidneys, brain)
5. increase in wall tension of LV
6. acceleration of atherosclerosis
93
with HTN, there is a _____ in TPR and _____ in CO (cardiac output)
increase, decrease
94
what happens to the renal system with increased BP?
activation of the renin-angiotensin system
95
what is the renin-angiotensin system?
a decrease in blood flow to kidneys causes the secretion of renin and formation of angiotensin which causes the secretion of aldosterone, promoting sodium and water retention by the kidneys
the retention causes increased intravascular volume and continues the cycle that increases BP
96
what would continued abnormal BP cause?
abnormal calcium metabolism leading to loss of calcium
97
when is there secondary activation of the parathyroid gland?
when there is a loss of blood calcium
98
what does the parathyroid do to raise blood calcium levels?
increases movement of calcium from the bone
99
what is the downside of parathyroid increasing calcium from the bone to the blood?
risk for urinary tract stones and osteoporosis
100
t/f: pts with mild-moderate HTN are usually asymptomatic
true
101
why should we ALWAYS take BP?
mild to moderate HTN is usually asymptomatic
102
what is hypertensive heart disease?
changes in body structure and function related to the heart as a result of persistently elevated BP
103
what happens to the LV in hypertensive heart disease?
it hypertrophies (stiffens) so it can't relax and fill as well
LV filling pressures increase
104
what other structure is enlarged due to LV hypertrophy?
the L atrium
105
what are the effects of LV hypertrophy in hypertensive heart disease?
decreased ability to fill and perfuse the coronaries
LA enlargement
myocardium ischemia or necrosis
106
what are the changes in structure and function of the LV with HTN?
increased pressure causes the muscles to hypertrophy
hypertrophy impairs filling ability
decreased compliance of the LV also impairs its filling ability
decreased filling decreases coronary perfusion
107
HTN leads to ____ O2 demand and ____ blood supply
increased, decreased
108
what does persistent HTN lead to?
decreased coronary perfusion
cardiac arrythmias
decreased compliance
decreased blood volume in the LV
stroke
end result is that HTN causes LV failure if left untreated
usually ends in CHF
109
what does decreased coronary perfusion lead to?
myocardial injury, ischemia, death
110
HTN is a major contributor to the development of ____ and ____
MI and CAD
111
what causes cardiac arrythmias?
electrolyte imbalance
112
what does decreased compliance lead to?
decreased blood filling the LV
113
what does decreased blood volume lead to?
decreased CO and SV
114
what does persistent HTN usually end up as?
CHF (congestive heart failure)
115
if HTN leads to to heart failure and decreased CO, what CV s/s would you expect to see?
fatigue, angina, edema in LE, pulmonary edema, SOB, dizziness, or palpitations
116
what is the most common way to manage HTN?
pharmacological methods
117
other than meds what lifestyle modifications can be done to manage HTN?
decrease weight
decrease sodium
decrease alcohol consumption
smoking cessation
regular aerobic exercise
118
what are common meds used to manage HTN?
diuretics
beta-blockers
alpha adrenergic blockers
vasodilators
centrally acting adrenergic antagonists
calcium channel blockers
angiotensin 2 receptor blockers
ACE inhibitors
119
how do diuretics work to manage HTN?
they increase fluid output to lower BP and stop pulmonary and LE edema
120
how do beta-blockers work to manage HTN?
they keep the HR down
121
are HTN meds more effective at rest or with exercise?
at rest
122
what happens to BP measurements in pts on anti-hypertensive meds?
they are exaggerated with exercise
123
what are the benefits of exercise for pts with HTN?
exercise controls BP better w/o or w/less meds
help the pt from going into hypertensive crisis
124
medical clearance is necessary and on prescribed meds if the SBP is _____ and DBP is ____
greater or equal to 180 mmHg, greater or equal to 110 mmHg
125
if retinopathy, renal disease, or LVH (LV hypertrophy) are present...
BP MUST be controlled at rest and w/activity b4 PT
126
exercise should be terminated if BP increases above SBP of _____ or DBP of ____
greater than 250 mmHg , greater than 115 mmHg
127
patients with HTN have an increased risk of what?
myocardial ischemia
128
what are the 3 ischemic heart diseases?
1. atherosclerosis
2. coronary artery disease (CAD)
3. acute myocardial infarction (MI)
129
myocardial ischemia results from atherosclerosis which causes what 3 things?
1. endothelial cells dysfunction
2. arterial vessel narrowing
3. abnormal vascular tone
130
when does the myocardium receive blood supply?
during diastole (relaxation)
131
the myocardium receives its own blood supply via...
coronary arteries
132
when are the coronary arteries perfused?
during diastole
133
what artery is extremely important in supplying the LV?
left anterior descending artery
134
what arteries are often diseased in CAD?
left main
left anterior descending
left circumflex
obtuse marginal
right coronary artery
posterior descending artery
135
what 4 things determine myocardial blood flow?
1. DBP
2. vasomotor tone
3. resistance to flow
4. left ventricular end diastolic pressure (LVEDP)
136
what is diastolic blood pressure (DBP)?
the force that drives blood into the myocardium during diastole
137
what is vasomotor tone?
force that regulates the caliber of artery and volume of blood delivered to the tissue
138
does vasomotor tone differ throughout the coronary tree?
no, it is uniform throughout the coronary tree
139
what maintains optimal resting level of contraction of smooth muscle fibers?
the vasomotor tone
140
does atherosclerosis increase or decrease resistance to flow?
increase
141
do collaterals increase or decrease resistance to flow?
decrease
142
how do collaterals decrease resistance to flow?
they provide a route for blood to flow around obstructions
143
what are collateral arteries?
small arteries that develop over time if there is a blockage in myocardial blood flow to try and provide a different route around the obstruction
144
what is left ventricular end diastolic pressure?
pressure in the LV at the end of diastole
145
what is the normal LVEDP?
3-5 mmHg
146
when LVEDP is elevated, it leads to _____ blood flow and ______ myocardial oxygen demand.
decreased, increased
147
if LVEDP remains elevated, what can it lead to?
MI bc the myocardium will become ischemic and maybe even necrotic
148
what is the difference b/w coronary and peripheral vasculature?
coronary arteries have anastomotic connections that lack capillary beds called collateral vessels
149
do collaterals vessels have a role under normal circumstances?
no, they are only present with issues
150
what is a possible downside of collateral vasculature in coronaries?
they can prolong the onset of symptoms related to coronary atherosclerosis and ischemia so the patient won't know they have an obstruction
151
what are the 3 determinants for myocardial oxygen demand?
1. ventricular wall stress
2. heart rate
3. contractility
152
what is ventricular wall stress?
measure of the force acting on the myocardial fibers that pulls them apart
153
when ventricular wall stress increases, does myocardial oxygen demand increase or decrease?
increase
154
what changes in heart structure and function would causes increased ventricular wall stress?
HTN, valve stenosis, valve regurgitation, and atherosclerosis
155
when HR increases, does the myocardial oxygen demand increase or decrease?
increase
156
why does myocardial oxygen demand increase when HR increases?
bc there is an increased ATP consumption that demands more blood flow from the coronary arteries
157
what is considered the most important factor in determining myocardial oxygen demand?
HR
158
what is contractility?
a measure of the force of contraction
159
contractility increases with the use of what?
catecholamines or meds that increase oxygen consumption
160
contractility decreases with what?
meds that decrease oxygen consumption
161
t/f: a small amount of oxygen is consumed for cardiac basal metabolism and electrical depolarization
true
162
decreased coronary blood flow caused by ______ leads to decreased blood flow to the myocardium
atherosclerosis
163
when oxygen demand increases but coronary blood flow is inadequate, oxygen ______ exceeds oxygen _____
demand, supply
164
myocardial ischemia occurs at what percentage occlusion of the artery?
70%
165
at what percent occlusion of the artery lumen are basal oxygen requirements not met and ischemia can develop AT REST?
90%
166
when will ischemia occur at rest?
when the basal oxygen requirements are not met
90% occlusion of the artery
167
t/f: decreased oxygen to tissues is accompanied by electrolyte disturbances
true
168
with myocardial ischemia, there is cellular loss of what 3 minerals?
1. potassium
2. calcium
3. magnesium
169
cellular loss of potassium, calcium, and magnesium can lead to what?
further loss of cardiac contractility and pumping ability
170
with myocardial ischemia, what is released that can cause serious imbalance in sympathetic and parasympathetic function, arrhythmias, and heart failure
catecholamines (E and NE)
171
can ischemia be reversed?
yes! as long as it is reversed b4 tissue death starts to occur
172
what is atherosclerosis?
pathologic process that causes progressive buildup of plaque and hardening and narrowing of systemic arteries
173
what vessels can be affected by atherosclerosis?
any blood vessels
174
t/f: ischemia can cause stroke
true
175
atherosclerosis results in dysfunction of what cells?
endothelial
176
what can cause the dysfunction of endothelial cells that's seen in atherosclerosis?
toxic substances, abnormal circulating lipid levels, diabetes, and increased pressure from HTN
177
damage to endothelial cells can lead to increase in what 2 things?
1. inflammation and release of cytokines
2. permeability to LDL
178
LDL accumulates in what layer?
intima layer
179
what are plaques composed of?
lipids (cholesterol) and thrombus (platelets)
180
plaques develop in what layers?
endothelium and intima layers
181
what is the first visible sign of endothelial damage?
fatty streak
182
what does the fatty streak consist of?
lipid laden macrophages and smooth muscle cells
183
where does the fatty streak build up?
in the endothelial and intima layers
184
the fatty streak causes the endothelium to stretch and separate, which exposes ____ and _____ to circulation
intima, CT
185
how does a rupture in the tan fibrous cap cause a thrombus to form?
when it ruptures, plaque content is released into the blood stream which stimulates a response to injury cascade and platelet activation and aggregation
186
what is the difference b/w an obstruction and a rupture?
an obstruction is when plaque completely blocks the artery
a rupture is when the plaque causes a blood clot to form and block the artery or the clot becomes an embolus and travels to occlude a vessel
187
what is the presentation of coronary artery disease?
sudden cardiac death
chronic unstable angina
acute coronary syndrome (ACS)/myocardial ischemia
cardiac muscle dysfunction
188
what is sudden cardiac death?
occurs w/in an hour of the onset of symptoms and v fib leads to no cardiac output and death
189
does sudden cardiac death have any symptoms?
it may or may not
190
what is coronary muscle dysfunction?
heart failure
191
what is angina?
substernal pressure
192
where can angina be located?
from the epigastric region to the jaw
193
what are some common symptoms of angina?
squeezing, tightness, crushing, feeling like an elephant/rock on the chest
194
what is angina a result of?
temporary lack of blood flow to the myocardium due to an imbalance in supply and demand of blood
195
what causes symptoms in angina?
ischemia of the myocardium
196
what are typical male symptoms of angina?
central crushing chest pain, left arm pain, sweating
197
what are typical female symptoms of angina?
jaw pain, shoulder blade pain, right arm pain sometimes, nausea, indigestion-like symptoms, SOB, fatigue
198
what is usually the #1 symptom of angina in people with diabetes?
SOB
199
what is chronic stable angina?
angina with a predictable onset of symptoms that develop w/exertion and diminish w/rest
associated with a set level of myocardial oxygen demand
200
how is chronic stable angina controlled?
decreased intensity of activity or use of sublingual nitroglycerine
201
what is unstable angina?
angina where the symptoms get worse in frequency or severity and may even occur AT REST
symptoms occur w/o and increased in myocardial O2 demand
202
which type of angina has increased mortality and morbidity rates
unstable angina
203
what is acute coronary syndrome?
MI
defined as unstable angina that lasts>20 minutes
204
what 3 things cause an acute MI?
1. lack of blood flow
2. myocardial ischemia
3. myocardial necrosis
205
what 3 things define an acute MI? (VERY IMPORTANT)
1. increased troponin I blood serum levels
2. ECG changes
3. echocardiogram imaging abnormalities
206
what are ECG changes seen with acute MI?
pathologic Q wave
ST segment changes (elevated/depressed)
new left bundle branch block (LBBB) which supplies the LV
207
what are echocardiogram imaging abnormalities seen with acute MI?
cardiac muscle damage
ventricular wall motion abnormalities
208
what are the 3 ways to diagnose an acute MI?
1. specific blood serum enzyme levels
2. troponin I
3. CPK-MB isoenzymes
209
what are specific blood serum enzyme levels?
cardiac enzymes released into circulation when myocardial damage occurs
released at variable rates
210
t/f: absence of specific blood serum enzymes means there was no injury
false, the absence of enzymes doesn't mean no injury!!!
211
what is the gold stand for diagnosing an acute MI
troponin I
212
what is normal troponin I levels?
<0.1 ug/mL
213
why is troponin I the gold standard?
bc it occurs earlier and lasts longer in the blood (up to 10 days post-MI)
214
t/f: troponin I had a high sensitivity and specificity
true
215
troponin I can also be elevated in what 2 conditions?
CHF and acute pulmonary embolism
216
what is CPK-MB isoenzyme?
creatine phosphate myocardial band
217
why is CPK-MB not always the best diagnostic test?
it rises quickly, but also disappears quickly
218
when else can CPK-MB levels be elevated?
post bypass surgery, sepsis, or renal failure
219
if a patient is still symptomatic, should you continue with PT?
NO! don't continue with PT until the patient is medically stable
220
what determines if a patient is medically stable for PT following an acute MI?
decreasing trend in serial troponin I levels
221
what is a STEMI?
ST elevation MI
transmural infarct (full thickness or near full thickness)
abnormal Q wave with 24-48 hours
ST segment elevation
injury distal to TOTALLY occluded coronary
due to thrombus and plaque OR ruptured plaque
extent of injury determined by collateral blood flow and vasospasm
more significant
increased short-term mortality
222
what is a NSTEMI?
non-ST elevation MI
subendocardial infarct (circumferential)
no Q wave abnormality
increased troponin I levels
ST segment DEPRESSION or inverted t-wave
due to INCOMPLETE occlusion
risk for death and another heart attack is higher when troponin I is higher
223
is a STEMI or NSTEMI transmural?
STEMI
224
is a STEMI or NSTEMI due to INCOMPLETE occlusion?
NSTEMI
225
does a STEMI or NSTEMI have greater risk for death and another heart attack?
NSTEMI
226
does a STEMI or NSTEMI have an abnormal Q wave?
STEMI
227
does a STEMI or NSTEMI had an inverted T-wave?
NSTEMI
228
does a STEMI or NSTEMI have ST segment elevation?
STEMI
229
is a STEMI or NSTEMI due to thrombus and plaque or ruptured plaque?
STEMI
230
is a STEMI or NSTEMI more significant?
STEMI
231
does a STEMI or NSTEMI have increase troponin I levels?
NSTEMI
232
is a STEMI or NSTEMI due to COMPLETE occlusion?
STEMI
233
t/f: a STEMI has increased short term mortality?
true
234
is a STEMI or NSTEMI subendocardial?
NSTEMI
235
what is embolization?
rare
emboli in the LA from a clot in the LV from aneurysms/failure, prosthetic heart valve, infected heart valve
236
what is arteritis-?
inflammation of the arteries that can affect the coronaries
237
what is amyloidosis?
a metabolic disease that causes thickened arteries
238
what is coronary artery vasospasm?
Prinzmetal angina
chest pain from a coronary artery vasospasm where the heart thinks it's not getting enough blood
239
what are medical/surgical management methods for acute coronary syndrome?
early reperfusion through thrombolytic agents, coronary angioplasty or CABG
meds
supplemental oxygen
angioplasty/stenting
treatment of arrythmias
treatment of complications
240
what are common meds used to manage acute coronary syndrome?
aspirin, plavix, brilinta, anti-coagulants, nitrates (for chest pain), and beta blockers
241
what are some complications of acute MI?
ventricular wall motion abnormalities (abnormal contraction patterns)
damage to myocardium of LV
persistent arrythmias post STEMI
pulmonary, endocrine, circulation, and renal problems
RAS system activation
242
what are some ventricular wall motion abnormalities?
dyssynchrony
hypokinesis
akinesis
dyskinesis
243
what is dyssynchrony?
uncoordinated contraction
244
what is hypokinesis?
reduced strength of contraction
245
what is akinesis?
no contraction
246
what is dyskinesis?
abnormal movement during contraction
247
15% damage to the myocardium of the LV leads to what?
decreased SV and coronary perfusion
increased EDP
248
25% damage of the LV leads to what?
s/s of CHF and poor long term prognosis
249
40% damage of the LV leads to what?
can lead to patient death
250
a left infarct results in...
LBBB
251
a right infarct results in...
SA node dysfunction or atrial arrythmias
252
what are pulmonary problems that result from acute MI?
problems with gas exchange
pulmonary edema from CHF
253
what are endocrine problems that result from acute MI?
impaired glucose tolerance
hyperglycermial insulin resistance
increased secretion of catecholamines
254
what are circulation problems that result from acute MI?
increased platelet aggregation
decreased affinity of Hgb for O2
255
what are renal problems that result from acute MI?
acute renal failure due to decreased CO (cardiac output)
256
what does increased RAS system activation result in?
vasocontriction
sodium retention
257
what does the prognosis of acute MI depend on?
complications
infarct size
presence of disease on other coronary arteries
improvements in ventricular function
