Quiz 1 Flashcards
what are the ischemic heart diseases?
atherosclerosis, coronary artery disease (CAD), acute MI, hypertension (HTN), cerebral vascular disease (CVD), peripheral artery disease (PAD), renal artery disease, and aneurysms
who is at the greatest risk for CV disease?
minority groups
t/f: COVID leads to an increased risk for CV disease
true :(
what is the PT’s role in treatment of CV disease?
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
what are some modifiable risk factors for CV disease?
smoking
body weight
physical activity
diet
BP
cholesterol
stress
blood glucose
what are non-modifiable risks for CV disease?
heredity
male sex
increased age
how does cigarette smoking contribute to the development of CVD?
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
smoking ____ times a day leads to an increased risk of CVD above a non-smoker
4
what percentage of adults don’t engage in the minimum amount of physical activity?
60%
sedentary lifestyle is increased in _____ and _____
women, diabetics
physical activity has a beneficial effect on…
lipid profile
BP
insulin sensitivity
what are the long term benefits of physical activity?
increased fibrinolysis and RBC deformability
decreased platelet aggregability
exercise can be ____, _____, or both
resistive, aerobic
what is the goal for exercise?
150 minutes per week of moderate intensity OR 75 minutes per week of vigorous intensity
what is considered the MAIN risk for CVD?
body weight
what percentage of the population is obese/overweight?
68%
what BMI is associated with increased risk for CVD?
greater than or equal to 30 kg/m^2
adipose tissue where in the body is especially associated with increased significance of CVD risk?
abdomen
adequate nutrition can decrease the risk of what?
HTN
hyperlipidemia
obesity
glucose levels
what are the nutritional goals to decrease CVD risk?
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
t/f: BP is considered an independent risk factor for the development of CVD
true!
t/f: decreased BP lowers the risk of stroke more than MI
true
increase BP can cause…
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
t/f: there is a direct link b/w increased cholesterol and the development of CAD
true!
how does high cholesterol contribute to development of atherosclerosis?
high cholesterol leads to abnormal circulating lipid levels, especially LDL
can increased saturated fat in the diet contribute to increased cholesterol levels?
yes
how does increased HDL levels protect against development of atherosclerosis?
it transports cholesterol away from peripheral tissues
poorly controlled diabetes can ____ HDL levels
lower
what is HDL?
carries good cholesterol in blood to the liver where it is broken down and removed from your body
what is LDL?
carries cholesterol to your cells and arteries causing buildup
hardens and narrows vessels so less blood can flow through
what makes up total cholesterol?
HDL, LDL, and triglycerides
what is the best predictor for the development of CVD?
cholesterol levels
what ratio of total cholesterol to HDL leads increased risk of atherosclerosis?
greater than 4.5
triglyceride level of ____ can contribute to atherosclerosis
greater than 150 mg/dL
HDL level of ____ can contribute to atherosclerosis
less than 35 mg/dL
_____ _____ influences development of atherosclerosis 20x more than cholesterol content of food
saturated fat
what are ideal LDL levels?
less than 70 mg/dL
what is the suggested blood glucose levels to reduce risk of diabetics getting CAD?
less then 100 mg/dL
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
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
is there a genetic link established for CAD?
no
what doubles risk for CAD?
premature/early CAD in your family
what is recommended in pt’s with a strong family history of CAD?
aspirin use
what is the average age of MI in men?
64.7 y/o
what is the average age of MI in women?
72.2 y/o
who is at a larger risk for acute MI before 55 y/o, men or women?
men
what is the leading cause of death in both men and women?
CAD
who has a higher mortality rate after a 1st MI, men or women?
women
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
t/f: increased hostility/anger leads to increased risk for CVD?
true
what are other factors that affect CVD?
homocysteine
lipoprotein
c-reactive protein
homocysteine
may contribute to oxidative stress, vascular inflammation, and platelet adhesiveness
lipoprotein
a varient of LDL that encourages inflammation and thrombosis
can’t be effected by diet and exercise
what has the greatest effect against lipoprotein
niacin
c-reactive protein
marker of systemic inflammation
t/f: c-reactive protein can be an independent predictor of MI, stroke, PAD, and sudden cardiac death
true
what is arterial pressure regulated by?
baroreceptor reflex
where are the baroreceptor reflex receptors?
the aortic arch and carotid sinuses
what do baroreceptors monitor?
stretch and deformation of arteries
can the baroreceptor response regulate BP long term?
no
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
how does the ANS lower BP?
by lowering peripheral vascular resistance and cardiac output due to vasodilation, and decreased HR and contractility
what is HTN?
diastolic BP over 90 mmHg OR systolic BP consisttently over 140 mmHg
when does the heart relax?
during diastole
what is the role of diastole?
allows blood to fill coronary arteries to supply the heart w/blood supply
why is high DBP bad?
is leads bad blood supply to heart tissues
what is SBP?
the heart contracting to supply the body with blood or blood to the lungs
what are the types of HTN?
labile, primary/essential, secondary, and malignant
what is labile HTN?
BP that fluctuates b/w normal and hypertensive values
what type of HTN is the most common?
labile HTN
labile HTN is most common in what group?
advanced age groups
labile HTN is most likely due to…
multiple defects in BP regulation along with environmental stressors, possible insulin resistance, obesity, and diabetes
what is primary/essential HTN?
HTN with no discernable cause
what are some suspected causes of primary/essential HTN?
genetics, environment, high sodium intake, stress, obesity, alcohol, or smoking
what is secondary HTN?
there is an identifiable medical condition/cause of the HTN
what a percentage of HTN cases are secondary HTN?
5-10%
what is secondary HTN associated with?
renovascular health conditions and endocrine disorders
what is malignant HTN?
a hypertensive crisis where there is marked elevated BP w/target organ damage
what are some effects of malignant HTN?
retinal hemorrhages, heart failure, encephalopathy, renal insufficiency, stroke
in malignant HTN, DBP is…
over 125 mmHg
what is normal BP?
SBP: <120
and
DBP: <80
what is high-normal, elevated, pre-hypertensive BP?
SBP: 120-129
and
DBP: <80
what is stage 1 HTN?
SBP: 130-139
or
DBP: 80-89
what is stage 2 HTN?
SBP: >140
or
DBP: >90
what is hypertensive crisis?
SBP: >180
and/or
DBP: >120
what are symptoms?
what the patient tells us
what are signs?
changes in body structure and function
what are the symptoms of HTN?
headache
spontaneous epitaxis (bloody nose)
dizziness
flushing
sweating
blurred vision
nocturnal urinary frequency
what are the signs of HTN?
L ventricular hypertrophy (thickened myocardium)
retinopathy (vision changes)
arterial bruits in carotid and femoral arteries
why does a thickened myocardium affect BP?
the tissue becomes stiff and can’t pump properly
what are bruits?
swooshing artery sounds
turbulence due to atherosclerosis
S2 heart sounds due to L atrium contractions in a stiff LV
what happens as BP continues to increase?
- destruction of arterial bed and narrowing of arterioles
- elasticity of arteries decreases (can’t return to og shape)
- viscocity of blood increases (doesn’t move through as well)
- decrease in tissue perfusion (target organs-heart, kidneys, brain)
- increase in wall tension of LV
- acceleration of atherosclerosis
with HTN, there is a _____ in TPR and _____ in CO (cardiac output)
increase, decrease
what happens to the renal system with increased BP?
activation of the renin-angiotensin system
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
what would continued abnormal BP cause?
abnormal calcium metabolism leading to loss of calcium
when is there secondary activation of the parathyroid gland?
when there is a loss of blood calcium
what does the parathyroid do to raise blood calcium levels?
increases movement of calcium from the bone
what is the downside of parathyroid increasing calcium from the bone to the blood?
risk for urinary tract stones and osteoporosis
t/f: pts with mild-moderate HTN are usually asymptomatic
true
why should we ALWAYS take BP?
mild to moderate HTN is usually asymptomatic
what is hypertensive heart disease?
changes in body structure and function related to the heart as a result of persistently elevated BP
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
what other structure is enlarged due to LV hypertrophy?
the L atrium
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
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
HTN leads to ____ O2 demand and ____ blood supply
increased, decreased
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
what does decreased coronary perfusion lead to?
myocardial injury, ischemia, death
HTN is a major contributor to the development of ____ and ____
MI and CAD
what causes cardiac arrythmias?
electrolyte imbalance
what does decreased compliance lead to?
decreased blood filling the LV
what does decreased blood volume lead to?
decreased CO and SV
what does persistent HTN usually end up as?
CHF (congestive heart failure)
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
what is the most common way to manage HTN?
pharmacological methods
other than meds what lifestyle modifications can be done to manage HTN?
decrease weight
decrease sodium
decrease alcohol consumption
smoking cessation
regular aerobic exercise
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
how do diuretics work to manage HTN?
they increase fluid output to lower BP and stop pulmonary and LE edema
how do beta-blockers work to manage HTN?
they keep the HR down
are HTN meds more effective at rest or with exercise?
at rest
what happens to BP measurements in pts on anti-hypertensive meds?
they are exaggerated with exercise
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
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
if retinopathy, renal disease, or LVH (LV hypertrophy) are present…
BP MUST be controlled at rest and w/activity b4 PT
exercise should be terminated if BP increases above SBP of _____ or DBP of ____
greater than 250 mmHg , greater than 115 mmHg
patients with HTN have an increased risk of what?
myocardial ischemia
what are the 3 ischemic heart diseases?
- atherosclerosis
- coronary artery disease (CAD)
- acute myocardial infarction (MI)
myocardial ischemia results from atherosclerosis which causes what 3 things?
- endothelial cells dysfunction
- arterial vessel narrowing
- abnormal vascular tone
when does the myocardium receive blood supply?
during diastole (relaxation)
the myocardium receives its own blood supply via…
coronary arteries
when are the coronary arteries perfused?
during diastole
what artery is extremely important in supplying the LV?
left anterior descending artery
what arteries are often diseased in CAD?
left main
left anterior descending
left circumflex
obtuse marginal
right coronary artery
posterior descending artery
what 4 things determine myocardial blood flow?
- DBP
- vasomotor tone
- resistance to flow
- left ventricular end diastolic pressure (LVEDP)
what is diastolic blood pressure (DBP)?
the force that drives blood into the myocardium during diastole
what is vasomotor tone?
force that regulates the caliber of artery and volume of blood delivered to the tissue
does vasomotor tone differ throughout the coronary tree?
no, it is uniform throughout the coronary tree
what maintains optimal resting level of contraction of smooth muscle fibers?
the vasomotor tone
does atherosclerosis increase or decrease resistance to flow?
increase
do collaterals increase or decrease resistance to flow?
decrease
how do collaterals decrease resistance to flow?
they provide a route for blood to flow around obstructions
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
what is left ventricular end diastolic pressure?
pressure in the LV at the end of diastole
what is the normal LVEDP?
3-5 mmHg
when LVEDP is elevated, it leads to _____ blood flow and ______ myocardial oxygen demand.
decreased, increased
if LVEDP remains elevated, what can it lead to?
MI bc the myocardium will become ischemic and maybe even necrotic
what is the difference b/w coronary and peripheral vasculature?
coronary arteries have anastomotic connections that lack capillary beds called collateral vessels
do collaterals vessels have a role under normal circumstances?
no, they are only present with issues
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
what are the 3 determinants for myocardial oxygen demand?
- ventricular wall stress
- heart rate
- contractility
what is ventricular wall stress?
measure of the force acting on the myocardial fibers that pulls them apart
when ventricular wall stress increases, does myocardial oxygen demand increase or decrease?
increase
what changes in heart structure and function would causes increased ventricular wall stress?
HTN, valve stenosis, valve regurgitation, and atherosclerosis
when HR increases, does the myocardial oxygen demand increase or decrease?
increase
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
what is considered the most important factor in determining myocardial oxygen demand?
HR
what is contractility?
a measure of the force of contraction
contractility increases with the use of what?
catecholamines or meds that increase oxygen consumption
contractility decreases with what?
meds that decrease oxygen consumption
t/f: a small amount of oxygen is consumed for cardiac basal metabolism and electrical depolarization
true
decreased coronary blood flow caused by ______ leads to decreased blood flow to the myocardium
atherosclerosis
when oxygen demand increases but coronary blood flow is inadequate, oxygen ______ exceeds oxygen _____
demand, supply
myocardial ischemia occurs at what percentage occlusion of the artery?
70%
at what percent occlusion of the artery lumen are basal oxygen requirements not met and ischemia can develop AT REST?
90%
when will ischemia occur at rest?
when the basal oxygen requirements are not met
90% occlusion of the artery
t/f: decreased oxygen to tissues is accompanied by electrolyte disturbances
true
with myocardial ischemia, there is cellular loss of what 3 minerals?
- potassium
- calcium
- magnesium
cellular loss of potassium, calcium, and magnesium can lead to what?
further loss of cardiac contractility and pumping ability
with myocardial ischemia, what is released that can cause serious imbalance in sympathetic and parasympathetic function, arrhythmias, and heart failure
catecholamines (E and NE)
can ischemia be reversed?
yes! as long as it is reversed b4 tissue death starts to occur
what is atherosclerosis?
pathologic process that causes progressive buildup of plaque and hardening and narrowing of systemic arteries
what vessels can be affected by atherosclerosis?
any blood vessels
t/f: ischemia can cause stroke
true
atherosclerosis results in dysfunction of what cells?
endothelial
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
damage to endothelial cells can lead to increase in what 2 things?
- inflammation and release of cytokines
- permeability to LDL
LDL accumulates in what layer?
intima layer
what are plaques composed of?
lipids (cholesterol) and thrombus (platelets)
plaques develop in what layers?
endothelium and intima layers
what is the first visible sign of endothelial damage?
fatty streak
what does the fatty streak consist of?
lipid laden macrophages and smooth muscle cells
where does the fatty streak build up?
in the endothelial and intima layers
the fatty streak causes the endothelium to stretch and separate, which exposes ____ and _____ to circulation
intima, CT
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
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
what is the presentation of coronary artery disease?
sudden cardiac death
chronic unstable angina
acute coronary syndrome (ACS)/myocardial ischemia
cardiac muscle dysfunction
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
does sudden cardiac death have any symptoms?
it may or may not
what is coronary muscle dysfunction?
heart failure
what is angina?
substernal pressure
where can angina be located?
from the epigastric region to the jaw
what are some common symptoms of angina?
squeezing, tightness, crushing, feeling like an elephant/rock on the chest
what is angina a result of?
temporary lack of blood flow to the myocardium due to an imbalance in supply and demand of blood
what causes symptoms in angina?
ischemia of the myocardium
what are typical male symptoms of angina?
central crushing chest pain, left arm pain, sweating
what are typical female symptoms of angina?
jaw pain, shoulder blade pain, right arm pain sometimes, nausea, indigestion-like symptoms, SOB, fatigue
what is usually the #1 symptom of angina in people with diabetes?
SOB
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
how is chronic stable angina controlled?
decreased intensity of activity or use of sublingual nitroglycerine
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
which type of angina has increased mortality and morbidity rates
unstable angina
what is acute coronary syndrome?
MI
defined as unstable angina that lasts>20 minutes
what 3 things cause an acute MI?
- lack of blood flow
- myocardial ischemia
- myocardial necrosis
what 3 things define an acute MI? (VERY IMPORTANT)
- increased troponin I blood serum levels
- ECG changes
- echocardiogram imaging abnormalities
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
what are echocardiogram imaging abnormalities seen with acute MI?
cardiac muscle damage
ventricular wall motion abnormalities
what are the 3 ways to diagnose an acute MI?
- specific blood serum enzyme levels
- troponin I
- CPK-MB isoenzymes
what are specific blood serum enzyme levels?
cardiac enzymes released into circulation when myocardial damage occurs
released at variable rates
t/f: absence of specific blood serum enzymes means there was no injury
false, the absence of enzymes doesn’t mean no injury!!!
what is the gold stand for diagnosing an acute MI
troponin I
what is normal troponin I levels?
<0.1 ug/mL
why is troponin I the gold standard?
bc it occurs earlier and lasts longer in the blood (up to 10 days post-MI)
t/f: troponin I had a high sensitivity and specificity
true
troponin I can also be elevated in what 2 conditions?
CHF and acute pulmonary embolism
what is CPK-MB isoenzyme?
creatine phosphate myocardial band
why is CPK-MB not always the best diagnostic test?
it rises quickly, but also disappears quickly
when else can CPK-MB levels be elevated?
post bypass surgery, sepsis, or renal failure
if a patient is still symptomatic, should you continue with PT?
NO! don’t continue with PT until the patient is medically stable
what determines if a patient is medically stable for PT following an acute MI?
decreasing trend in serial troponin I levels
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
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
is a STEMI or NSTEMI transmural?
STEMI
is a STEMI or NSTEMI due to INCOMPLETE occlusion?
NSTEMI
does a STEMI or NSTEMI have greater risk for death and another heart attack?
NSTEMI
does a STEMI or NSTEMI have an abnormal Q wave?
STEMI
does a STEMI or NSTEMI had an inverted T-wave?
NSTEMI
does a STEMI or NSTEMI have ST segment elevation?
STEMI
is a STEMI or NSTEMI due to thrombus and plaque or ruptured plaque?
STEMI
is a STEMI or NSTEMI more significant?
STEMI
does a STEMI or NSTEMI have increase troponin I levels?
NSTEMI
is a STEMI or NSTEMI due to COMPLETE occlusion?
STEMI
t/f: a STEMI has increased short term mortality?
true
is a STEMI or NSTEMI subendocardial?
NSTEMI
what is embolization?
rare
emboli in the LA from a clot in the LV from aneurysms/failure, prosthetic heart valve, infected heart valve
what is arteritis-?
inflammation of the arteries that can affect the coronaries
what is amyloidosis?
a metabolic disease that causes thickened arteries
what is coronary artery vasospasm?
Prinzmetal angina
chest pain from a coronary artery vasospasm where the heart thinks it’s not getting enough blood
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
what are common meds used to manage acute coronary syndrome?
aspirin, plavix, brilinta, anti-coagulants, nitrates (for chest pain), and beta blockers
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
what are some ventricular wall motion abnormalities?
dyssynchrony
hypokinesis
akinesis
dyskinesis
what is dyssynchrony?
uncoordinated contraction
what is hypokinesis?
reduced strength of contraction
what is akinesis?
no contraction
what is dyskinesis?
abnormal movement during contraction
15% damage to the myocardium of the LV leads to what?
decreased SV and coronary perfusion
increased EDP
25% damage of the LV leads to what?
s/s of CHF and poor long term prognosis
40% damage of the LV leads to what?
can lead to patient death
a left infarct results in…
LBBB
a right infarct results in…
SA node dysfunction or atrial arrythmias
what are pulmonary problems that result from acute MI?
problems with gas exchange
pulmonary edema from CHF
what are endocrine problems that result from acute MI?
impaired glucose tolerance
hyperglycermial insulin resistance
increased secretion of catecholamines
what are circulation problems that result from acute MI?
increased platelet aggregation
decreased affinity of Hgb for O2
what are renal problems that result from acute MI?
acute renal failure due to decreased CO (cardiac output)
what does increased RAS system activation result in?
vasocontriction
sodium retention
what does the prognosis of acute MI depend on?
complications
infarct size
presence of disease on other coronary arteries
improvements in ventricular function
