Studied by 3 peoplecardiac cycle
one complete contraction and relaxation of all four chambers of the heart
systole
contraction
diastole
Relaxation
atrial contraction
as the atria contracts, the blood atria fills
Blood is moving from the atria to the ventricles (ventricular filling)
AV valves are open and semilunar valves are closed
Atrial pressure exceeds ventricular pressure
isovolumetric contraction
when the ventricles begin to contract so there pressure, not enough pressure to open SL, but enough pressure to open the AV
Blood is not moving at the point, all 4 valves are temporarily close
As the ventricles begin to contact, the AV valves will close
No movement
Ventricular pressure is higher than atrial pressure and lower than the vessel pressure
ventricular ejection
when the ventricles are fully contracted and blood is ejected
Pressure in ventricle exceeds pressure in atria and vessels
Semilunars are open and AV valves are closed
isovolumetric relaxation
blood is not moving, all 4 valves are closed because the ventricles have started to relax
Enough pressure to keep AV closed, but not enough to keep SL open
atrial relaxation and ventricular filling
passive filling occurs
Blood is coming into the atria from the great veins
AV valves are open and semilunar valves are closed
Passive→ most of the EDV is from the passive filling
stroke volume
the amount of blood ejected from the ventricles in one beat
auscultation
Listening to sounds made by body
lub
Occurs with the closing of the AV valves
first heart sound
longer and louder
dub
Second heart sound
Softer and sharper
Occurs with the closure of semilunar valves
third heart sound
caused by a sudden deceleration of blood flow into the left ventricle from the left atrium
ventricular balance
equal amounts of blood are pumped by left and right sides of the heart
congestive heart failure
results from the failure of either ventricle to eject blood effectively
cardiac output
the amount of blood ejected by each ventricle in 1 minute
heart rate X stroke volume = amount of blood in one beat
cardiac reserve
Capacity to increase cardiac output above rest level
exercise output - cardiac output = level of exercise an individual can pursue
chronotropic agents
affect time or rate; change heart rate
Influence SA node to change its firing rate
Influence AV node to alter amount of delay
work via ANS or hormones
AV delay
AV node to AV bundle (P-R segment)
positive chronotropic agents
increase heart rate
ex.) electrolytes, hypercapnia, thyroid hormone, caffeine, nicotine, and cocaine
negative chronotropic agents
decrease heart rate
ex.) parasympathetic activity, beta-blocker drugs
bainbridge reflex
The reflex that involves baroreceptors found in the aortic arch and carotid sinus
venous return
volume of blood returned to the heart
determines end diastolic volume
preload
how much blood is loading into the heart
inotropic agents
external agents that alter contractility
Generally due to changes in calcium available in sarcoplasm
More calcium available → more crossbridges formed → greater contraction
afterload
the pressure in the aorta or the pulmonary trunk to open the semilunar valves
resistance in arteries
Pressure that must be exceeded before blood ejected
end diastolic volume
the amount of blood in each ventricle following ventricular filling
end systolic volume
the amount of blood remaining in the ventricle after ejection/after stroke volume
hypovolemia
low blood volume
starling law of the heart
Venous return increases during exercise and with a slower heart rate (e.g. in high-caliber athletes with strong hearts)
Increase EDV stretches the heart volume to contract with greater force
postive inotropic agents
increase available calcium
Epinephrine and norepinephrine increase calcium
Thyroid hormone increases number of receptors for epinephrine and norepinephrine
negative inotropic agents
decrease available Ca2+
Electrolyte imbalances such as increased K+ or H+
Certain drugs, e.g., Ca2+ channel-blocking blood
Note
Flashcard