Exam 2 Study Guide Flashcards
anastomoses
collateral / alternative routes to prevent blockage of blood supply
bradycardia
persistent resting adult heart rate <60 BPM
tachycardia
persistent resting adult heart rate > 100 BPM; may lead to fibrillation
fibrillation
rapid, irregular contractions; useless for pumping blood ➡️ circulation ceases ➡️ brain death
ex) “looks like a bag of worms”
angina pectoris
imbalance associated with coronary circulation; temporary ischemia (blockage) of circulation; can be caused by spasms of coronary arteries or increased demand on the heart; cells are weakened
cardiac tamponade
too much fluid in pericardium ➡️ compresses heart ➡️ limits pumping ability
pericarditis
inflammation of pericardium; not enough serous fluid
ductus arteriosis
connects pulmonary trunk to aorta in baby
ligamentum arteriosum
connects pulmonary trunk to aorta in adults
auricles
found in atria; appendage that increases atrial volume
pectinate muscles
mark right atrial wall and auricles; resemble teeth of a comb
fossa ovalis
remnant of foramen ovale in adult; depression in right atrium @ level of interatrial septum
foramen ovale
opening that connects atria in baby
trabeculae carneae
rounded / irregular muscular columns which project from inner surface of right + left ventricle
valvular prolapse
“incompetent valve”; blood backflows so heart repumps same blood over and over; caused by improper closing of valves
myocardial infarction
heart attack; prolonged ischemia; fibrosis (no longer functional cells)
congestive heart failure (CHF)
progressive condition; due to weakened heart caused by
1) coronary atherosclerosis = plaque buildup
2) persistent high bp
3) multiple MIs
4) valvular insufficiency = leaky valves
5) dilated cardiomyopathy (DCM): ventricles stretch & become flabby; causes = unknown, alcohol
inotropic (pos. & neg.)
substances that control contractility
1) positive inotropic agents increase contractility: hypercalcemia; certain hormones (glucagon, thyroxine, epinephrine)
2) negative inotropic agents decrease contractility: acidosis created by hypercapnia (increase in CO2 & H+); hyperkalemia (too much K in blood); hypocalcemia (calcium channel blockers)
chronotropic (pos. & neg.)
- positive factors = ⬆️HR
- negative factors= ⬇️HR
- K+ has greatest chronotropic effect
cardiac reserve
difference between resting and maximal cardiac output (CO)
- greater w/ fitness
- less w/ disease
baroreceptors
stretch receptors; monitor changes in BP; causes increased ANS stimulation; pressure sensors in aortic arch, carotid sinuses & large arteries of neck & thorax
-⬇️BP = ⬆️HR
-⬆️BP= ⬇️HR
by cardiac center to match HR
chordae tendineae
anchor cusps of AV valves to papillary muscles
papillary muscles
muscles located in ventricles; attach to cusps of AV valves via chordae tendineae
coronary circulation
circulation to the heart itself
layers of heart wall / pericardium (from outer ➡️ inner)
epicardium ➡️ myocardium ➡️ endocardium
epicardium
visceral layer of serous pericardium; infiltrated w/ fat
myocardium
bundle of cardiac muscle cells forming bulk of fat
-contains fibrous cardiac skeleton of heart= crisscrossing layer of connective tissue; prevents electrical signal to move from contracted atria to relaxed ventricles or vice versa; nonconductor
endocardium
inner myocardial surface
- simple squamous epithelium (endothelium)
- inside lining of heart is continuous with inside lining of blood vessels which is continuous with lining of lymphoid tissues
importance of ventricle wall thickness
thickest in left ventricle so chamber can create enough pressure needed to pump blood into aorta and throughout systemic circulation
purpose of heart valves (why do they open & close?)
- ensure unidirectional blood flow through heart
- open & close in response to pressure changes
major types of valves (2)
1) atrioventricular valves between atria & ventricles
2) semilunar valves between ventricles & major arteries
what is the “lub-dup” sound associated with?
closing of the heart valves
first sound (S1)
occurs as AV valve closes & signifies beginning of ventricular systole (contraction)
- S1 is louder & longer
second sound (S2)
occurs when SL valves close at the beginning of ventricular diastole (relaxation)
-S2 is softer & shorter
systole
contraction of heart muscle
diastole
relaxation of heart muscle
trace path of blood through heart
right atrium ➡️ tricuspid valve ➡️ right ventricle ➡️ pulmonary semilunar valve ➡️ pulmonary trunk ➡️ pulmonary arteries ➡️ lungs ➡️ pulmonary veins ➡️ left atrium ➡️ bicuspid valve ➡️ left ventricle ➡️ aortic semilunar valve ➡️ aorta ➡️ body
right side of heart
{pulmonary vs systemic circuit}
pumps blood to lungs to get rid of CO2 & pick up O2 via pulmonary circuit
left side of heart
{pulmonary vs systemic circuit}
receives oxygenated blood from lungs; pumps blood to body tissues via systemic circuit
right atrium
{receiving chamber of heart}
receives blood returning from systemic circuit
left atrium
{receiving chamber of heart}
receives blood returning from pulmonary circuit