Chapters 26 & 27 (NO shock) Flashcards
(181 cards)
1
Q
the large
A
aorta
2
Q
medium
A
coronary
3
Q
small
A
ulcers
4
Q
pathology occurs by
A
impairment of blood flow
5
Q
ischemia
A
reduction in flow insufficient to meet oxygen demands of tissues
6
Q
injury
A
reversible
7
Q
infarction
A
irreversible with necrosis
8
Q
what has an active role in controlling vascular function
A
endothelium
9
Q
dysfunctional cells produce
A
inflammatory cytokines
10
Q
endothelial dysfunction
A
endothelial dysfunction describes potentially reversible changes in endothelial function that occur in response to environmental stimuli
11
Q
endothelial dysfunction: products that cause inflammation
A
cytokines, bacteria, viruses, hemodynamic stresses, lipid products, hypoxia
12
Q
dyslipidemia is a major cause of
A
atherosclerosis
13
Q
dyslipidemia is a imblance of
A
lipid components (triglycerides, phospholipids and cholesterol)
14
Q
5 types of lipoproteins but we only will be focusing on 2, what are they
A
LDL and HDL
15
Q
where is the synthesis of lipoproteins
A
small intestine and liver
16
Q
primary dyslipidemia
A
may have genetic basis, defective synthesis of apoproteins may occur, defective or lack of lipid receptors
17
Q
familial hypercholesterolemia is what kind of dyslipidemia
A
primary
18
Q
familial hypercholesterolemia ___ receptor is deficient of defective, autosomal _________ disorder. cholesterol levels can be as high as 1000
A
LDL, dominant
19
Q
secondary dyslipidemia
A
dietary, obesity, metabolic changes associated with DMT2
20
Q
hypercholesterolemia
A
increase in serum cholesterol levels
21
Q
screening for hypercholesterolemia is appropriate for children as young as two who have
A
a family history of heart disease or high cholesterol
22
Q
LDL is good or bad
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bad, LOSER CHOLESTEROL
23
Q
LDL is the main carrier for
A
cholesterol
24
Q
LDL receptors predominantly located in
A
hepatocytes
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_______ plays critical role in metabolism of LDL
liver
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LDL removal by scavenger cells such as
monocytes and macrophages
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uptake of LDL by macrophages in the arterial wall can result in accumulation of
insoluble cholesterol esters, foam cells, and atherosclerosis
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HDL
good, HAPPY CHOLESTEROL
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inverse relation between HDL and development of
atherosclerosis
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HDL facilitates in the clearance of cholesterol from atheromatous plaques and transports it back to the
liver
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HDL is responsible for
reverse cholesterol transport (returns excess cholesterol from tissues to liver)
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HDL inhibits uptake of _____ into arterial wall
LDL
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what increases HDL
regular exercise and moderate alcohol consumption
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what are associated with decreased levels of HDL
smoking and diabetes
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major risk factor for atherosclerosis is
hypercholesterolemia and elevations of LDL
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non modifiable risk factors for atherosclerosis is
age, gender, genetic history, family of premature CAD in a first degree relative
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nontraditional risk for atherosclerosis is
elevated serum C reactive protein
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inflammation marked by
elevated C reactive protein
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C reactive protein is
non specific
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nontraditional risk factors for coronary artery disease
c reactive protein, microbiome, medications, infection, airpolution
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modifiable risk factors for coronary artery disease
dislipidemia, hypertension, cigarette smoking, diabetes, obesity
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one pack of cigarette smoking a day _____ endothelial damage
doubles
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DM+hypertension+dyslipidemia= increases risk
20 times
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mechanisms for development of coronary artery disease
endothelial injury, fatty streak present in first year of life, fibrous atheromatous plaque, complicated lesion
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endothelial injury causes a migration of inflammatory cells which leads to ______ accumulation and smooth muscle ________ and ______ development
lipid, proliferation, plaque
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fatty streak
macrophages and smooth muscle cells distended with lipid to form foam cells
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fibrous atheromatous plaque
basic lesion accumulation of lipids, proliferation, scar tissue and calcification
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complicated lesion
hemorrhage, ulceration and scar tissue deposits with thrombosis
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vaculitides is a group of vascular disorders that cause ___________ injury and ________ of the blood vessel wall
inflammatory, necrossi
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vasculitides when in the large vessel is called
giant cell (temporal) arteritis
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giant cell (temporal) arteritis (AKA vasculitides) mainly affects arteries of the ______, this is a disease of the _______, symptoms may include:
inflammation of ophthalmic artery involvement can cause ______
head, elderly, stiffness of shoulder and headache and tenderness of temporal artery, blindness
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peripheral arterial disease is systemic atherosclerosis distal to the
arch of the aorta
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peripheral arterial strongest risk factors
smoking and DM
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peripheral arterial when you finally get symptoms you are already at __% narrowing
50
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peripheral arterial symptom will include
intermitten claduication or pain with walking in the calf
atrophic changes and thinning of the skin and sub q
ischemic pain at rest
ulceration and gangrene will develop
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why will you get pain in calf with peripheral arterial
because the gastrocnemius has the highest oxygen consumption of any muscle group in leg during walking
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it is important in peripheral arterial to look at what body part
feet
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acute arterial thrombus formation
activation of the coagulation cascade, intimal irritation and roughening, inflammation, trauma, infection, low BP, obstructions
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the 7 P's of acute arterial embolism
pistol shot (acute onset)
pallor
polar
pulselessness
pain
paresthesia
paralysis
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arterial disease of extremities peripheral vascular disorders
thromobangitis obliterans (Buerger's Disease), Raynaud's disease
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Buerger's Disease is ______ of medium arteries, usually affects ____, this is very ________
vaculitis, men, inflammed
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Raynaud's disease is caused by intense _______ of arteries and arterioles in ______, this is seen in _______, appear pale looking
vasospasm, fingers, women
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aneurysm is a localized _______ of blood vessle
dilatation
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aneurysm tension wall diameter increases with increasing size and may lead to
rupture
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aortic aneurysm is more frequent in men who are __________, most are _______
hypertensive, asymptomatic
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aortic dissection is acute and
life threatening
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aortic dissection is the hemorrhage into the vessel wall with
longitudinal tearing or separation of the vessel wall to form a blood filled channel
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aortic dissection is common with
Marfans syndrome
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BP is calculated how
cardiac output X peripheral vascular resistance
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pulse pressure
difference between systolic and diastolic
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systolic is normally the smaller or larger number
larger
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diastolic is normally the smaller or larger number
smaller
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mean arterial pressure
average blood pressure in systemic circulation
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how to calculate mean arterial pressure
1/3PP+DP
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mean arterial pressure is a good indicator of
tissue perfusion
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cardiovascular center is located in ____ and _______ where intergration with ANS occurs
pons, medulla
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pressure sensitive _________ are located in the blood vessels and heart
baroreceptors
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baroreceptors induces
heart rate increase and vasconstriction
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arterial chemoreceptors are located in _____ and _______ and respond to changes in oxygen, CO2 and H+, these control _________ and induce widespread ___________
carotids, aorta, ventilation, vasoconstriction
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Humoral BP regulation is regulated by
RAA, Vasopressin (ADH)
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RAA system steps
renin secreted by kidney in response to low BP, ECF volume/EC sodium,
renin converts to angiotensin to angiotensin 1
angiotensin 1 is converted to angiotensin II by enzyme in endothelial in lung
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Angiotensin 2 does what
its a strong vasoconstrictor and stimulates aldosterone
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aldosterone
secreted from adrenal glands which contributes to long term regulation by increasing salt and water retention by kidney
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undercuffing BP cuff
overestimates BP
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overcuffing BP cuff
underestimates BP
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primary/essential hypertension
no evidence of other disease, caused by consittutional or lifestyle,
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primary hypertension risk factors are things that cannot be changed like
genes, race, DM, age, gender
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primary hypertension lifestyle contributes
High NA intake, excessive calorie intake, obesity, inactivity, alcohol
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secondary hypertension may be
corrected or cured
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secondary hypertension causes
renal hypertension, pheochromocytoma, oral contraceptives, cocaine, amphetamines
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renal hypertension
largest single cause is renal disease, excess production of aldosterone and excess levels of glucocorotcoid
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pheochromocytoma
tumor of chromatin tissue which contains sympathetic nerve cells most often in adrenal medulla
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target organs of hypertension
heart, brain, kidney
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ACE inhibitors
inhibit conversion of angiotensin I to II reducing effect on vasoconstriction and aldosterone
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unique hypertensive situations include
pregnancy, elderly, children, orthostatic
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orthostatic
abnormal drop in standing position
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orthostatic is a sustained reduction in systolic pressure of at least __mmHg
20`
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causative factors of orthostatic hypotension
fluid deficit, medications, aging, defective function of ANS, effects of immobility
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disorders of venous circulation (one we need to know)
venous thrombosis
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venous thrombosis can be caused by
venous stasis
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venous stasis causes
bed rest, immobility, spinal cord injury. acute MI, congestive heart failure, shock, venous obstruction
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virchows triad associated with venous thrombosis
statuses of blood, increased blood coagulability, vessel wall injury
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hyperrreactivty genetic disease name
leiden 5 diease
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disorders of the cardiac pericardium
pericardial effusion, cardiac tamponade
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cardiac tamponade starts off as
pericardial effusion
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cardiac tamponade is an increase in
intrapericardial pressure
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cardiac tamponade is caused by
accumulation of fluid or blood in the pericardiac sac, trauma, cardiac surgery, cancer, uremia, cardiac rupture
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symptoms of cardiac tamponade depends on
how rapidly the fluid accumulates
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pulsus paradoxus
when you inspire your SBP drops a small amount
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in cardiac tamponade you have an exaggerated
pulsus paradoxus
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consequences of pericardial effusion
restricts heart expansion which causes the left ventricle to not accept enough blood which leads to decreased cardiac output and decreased BP and shock. This also causes the right ventricle to not accept enough blood which causes increased venous pressure; jugular distension
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right coronary artery supplies the ________ wall of the ventricle
inferior
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RCA supplies what else besides the inferior wall
SA and AV node
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left coronary artery has __ main branches
2
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what artery is known as your widowmaker
left coronary
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coronary heart disease is impaired coronary blood flow that may cause
angina, MI, cardiac arrhythmias, conduction defects, heart failure and sudden death
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coronary heart disease can be caused by
atherosclerotic plaques
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atherosclerotic plaques are made up of
soft lipid rich core with fibrous cap
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coronary heart disease plaque can occur with and without
thrombus
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_______ play a major role in linking plaque disruption to acute coronary syndrome
platelets
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in coronary heart diease with disruption platelets aggregate and release substances that
further propagate aggregation, vasoconstriction, and thrombus formation
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plaque disruption may occur
spontaneously
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plaque disruption could be triggered by
hemodynamic factors
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Diurnal variation
first hour after arising may favor platelet aggregation and fibrinolytic activity
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unstable plaque with ulceration or rupture and thrombosis could lead to
acute coronary syndromes
126
you need 3 things to diagnosis a MI
patient history, ECG changes, serum cardiac markers (troponin)
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STEMI has what elevation
ST elevation
128
NSTEMI has no ___ _________
ST elevation
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angina could be 2 types
stable and unstable
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stable angina
pain when hearts oxygen demand increases
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unstable angina
the pain has a more persistent and severe course and is characterized by at least one of three features
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unstable angina characterized by 1 of 3 factors
occurs at rest, lasting more than 20 mins
severe and described as pain and of new onset
occurs with a pattern that is more severe, prolonged, or frequent than previously experienced
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unstable angina causes
NSTEMI
134
unstable angina NSTEMI occurs at rest with minimal exertion usually lasting more than
20 mins
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NSTEMI reflects
ischemia server enough to cause myocardial damage which releases serum cardiac markers
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STEMI is a
MI
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STEMI is not treated by
nitroglycerin
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be careful with what 2 groups when they have a STEMI because they presentation is not conventional
women an diabetics
139
STEMI diabetic may
not experience pain
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STEMI women may
present with fatigue or shortness of breath
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referred pain
pain not related to origin
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if you have a 12 lead EKG change, markers and a clinical presentation you have
STEMI
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what part of the EKG will be changed when you have a STEMI
ST wave elevation
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cardiomyopathies
heterogenous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually exhibit inappropriate ventricular hypertrophy or dilatation and that are due to a variety of causes that frequently are genetic
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a example of a primary genetic cardiomyopathy is
hypertrophic
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an example of secondary cardiomyopathy found in women who just gave birth are
peripartum
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hypertrophic cardiomyopathy
unexplained ventricular hypertrophy with disproportionate thickening of the septum, abnormal diastolic filling and cardiac arrhythmias
148
what is the most common cause of death in young athletes
hypertrophic cardiomyopathy
149
syncope
fainting
150
hypertrophic cardiomyopathy is the enlargement of
myocardium
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mitral valve prolapse
floppy valve
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mitral valve prolapse is symptomatic or asymptomatic
asymptomatic
153
mitral valve is most commonly found in
females
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stenosis
narrowing of the valve opening, so it does not open properly
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if a valve is stenotic you will hear
murmur of blood shooting through the narrow opening when the valve is open
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incompetent or regurgitant valve
permits backward flow to occur when the valve should be closed
157
if a valve is regurgitant you will hear
murmur of blood leaking back through when the valve should be closed
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decrease in cardiac output with a consequent decrease in blood flow to
kidneys and other organs and tissues
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inotropic influence
is one that increases the ability of contractile elements of the heart muscle to interact and shorten against a load
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positive inotropic influence is caused by
sympathetic
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negative inotropic influences is caused by
acidosis
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SNS and RAA increase
heart rate
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what is preload
volume you have
164
what is the resistance heart has to pump against
afterload
165
how does tachycardia impact cardiac output and coronary artery filling
decreases time for coronary filling and ventricular filling leading to decreased cardiac output
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myocardial hypertrophy and remodeling is part of
RAA
167
angiotensin II causes
vasoconstriction (which leads to increased AL) and myocardium remodeling
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deleterious effects of norepinephrine and SNS
increased LV volumes and pressures, LV hypertrophy< arrhythmias, apoptosis
169
left sided vs right sided heart failure: left
decreased cardiac output and pulmonary congestion which leads to impaired gas exchange (leads to cyanosis and hypoxia) and pulmonary edema (leads to cough with frothy sputum, orthopena, paroxysmal nocturnal dyspnea)
170
left sided vs right sided heart failure: right
congestion of peripheral tissues which leads to dependent edema and ascites, GI tract congestion (anorexia, GI distress and weight loss) and liver congestion
171
symptoms of heart failure
orthopena, paroxysmal nocturnal dyspnea, fatigue, RUQ fullness and pain, anorexia, nausea and vomitting
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signs of heart failure
jugular venous distension, pulmonary crackles, cheyne stokes, S3 gallop, narrow pulse pressure, pale cool skin, decreased urine output
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cheyne stokes
gasping breathing
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pulmonary edema happens in
extreme heart failure
175
pulmonary edema happens when capillary fluid moves into
alveoli
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in pulmonary edema the hemoglobin is not completely
oxygenated
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as you get older in reaction to you cardiac function
increased vascular stiffness, left ventricular hypertrophy, heart compliance, reduced response to beta adrenergic
178
atrial fibrillation the blood is stagnant
in the atrias
179
atrial fibrillation is
irregularly irregular
180
when in atrial fibrillation you at risk for ______ ____, assess anticoagulant status
mural thrombi
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a person with a MI is releasing angiotensin II. how should the clinician interpret this findinf
counter productive, it causes the heart to work harder
