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Heart- Cardiac Cycle, Stroke Volume, Cardiac Output, and Heart Rate

Terms in this set (38)

What leads to mechanical activity in the heart?
electrical activity (depolarization and repolarization)
how does blood move?
pressure gradients; differences in pressure- blood will flow to where pressure is lower
Cardiac cycle main phases
- ventricular filling
- ventricular systole
- isovolumetric relaxation
ventricular filling
Phase of the cardiac cycle in which the ventricles expand, their pressure drops, and the AV valves open and blood flows into the ventricles; ~70% is passive filling and ~30% is active filling as a result of atrial systole
end diastolic volume (EDV)
volume of blood in each ventricle at end of ventricular diastole and end of ventricular filling
isovolumetric contraction
refers to the short period during ventricular systole when the ventricles are completely closed chambers
ventricular systole
contraction of ventricles; semilunar valves open and stroke volume is ejected; remaining blood is the end systolic volume
What causes the AV valves to close?
When ventricular pressure > atrial pressure
What causes the semilunar valves to open?
As ventricles contract and intraventricular pressure rises, blood is pushed up against the SL valves, forcing them to open; artey pressure < ventricular pressure
isovolumetric relaxation
period when all four valves are closed and ventricular blood volume does not change; comes directly after systole but before the ventricles are relaxed enough to reopen the AV valves
End Systolic Volume (ESV)
volume of blood remaining in each ventricle after systole
Wiggers Diagram
cardiac output
The volume of blood ejected from each ventricle per minute; SV x HR
Stroke Volume (SV)
The volume of blood pumped forward with each ventricular contraction. EDV-ESV
Factors impacting end diastolic volume
Filling time and venous return
filling time
determined by heart rate; slow heart rate = more time to fill, fast heart rate = less time to fill; fast heart rate can be balanced by increased contractility from epinephrine
venous return
The amount of blood returned to the heart by the veins
What impacts venous return?
venous pressure, venoconstriction, muscular pump, and inspiration all increase it; an increase in blood volume will increase venous return while a decrease in blood volume will decrease venous return
factors impacting end systolic volume (ESV)
related to ease of contraction from ventricles; affected by afterload and ventricular contractility
Afterload
The force or resistance against which the heart pumps. How much blood is left after the ventricle contracts
ventricular contractility
Capacity of heart ventricles to contract. Impacted by positive and negative inotropic agents
positive inotropic agents
increase contractility; make contraction stronger. ex.= epinephrine, norepinephrine, thyroxine, increased calcium, and digitalis
negative inotropic agents
decrease contractility, make contraction weaker. ex.= hyperkalemia, hypocalcemia, acidosis, and calcium channel blockers
Heart Rate (HR)
number of heart beats per minute
heart rate set by
SA node
What is intrinsic rate impacted by?
temperature, hormones, ion concentrations, and neurotransmitters
temperatures impact
temp impacts diffusion rates; increased temp= faster heart rate
hormonal impact
epinephrine, norepinephrine, and thyroxine all increase heart rate but also increase contractility
ionic conditions increasing heart rate
decreased Ca2+ (hypocalcemia)
ionic conditions decreasing heart rate
-increased Ca2+ (hypercalcemia)
-decreased K+ (hypokalemia)
-highly increased K+ (severe hyperkalemia)
Beta Blockers
beta-adrenergic receptor blockers block epinephrine from binding, slowing heart rate
Baroreceptors
detect changes in blood pressure; on atria and carotid arteries
neural response to increased blood pressure
1. more stim of baroreceptors
2. sensory neurons more stimulates
3. inhibit cardiac acceleratory center
4. less norepinephrine released
OR
1. more stim of baroreceptors
2. sensory neurons more stimulates
3. activates cardiac inhibitory center
4. APs sent back to heart
5. Acetylcholine released
6. Heart rate and BP slow
neural response to decreased blood pressure
1. decreased BP
2. less stim of baroreceptors
3. less afferent impulses to cardiac acceleratory center
4. activation of CAC leads to epinephrine release
5. increase of HR and BP
Bainbridge reflex
occurs when mechanoreceptors embedded within the right atrial myocardium respond to an increase in pressure and stretch (distention of the right atrium). stimulates the vasomotor centers of the medulla and results in increased sympathetic input and heart rate. reflex can also influence a decrease in heart rate when heart is beating too fast.
where are the cardiac acceleratory and inhibitory centers found?
interneuron integration center of the medulla oblongata
chemoreceptor reflexes
respond to changes in chemical composition, particularly pH and dissolved gases; decrease of O2 or pH lead to increased impulses at CAC which in turn increase sympathetic outlfow, HR, and BP
congestive heart failure
inability to balance stroke volume and venous return; caused by weakening of ventricle due to over stretching. heart can't efficiently eject blood to arteries
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