damage to the semilunar valve on the R side of the heart would affect blood flow to which vessel?
would affect blood flow to the pulmonary artery
what prevents the AV valves from swinging into the atria?
contraction of the papillary muscles (just before the rest of the ventricular myocardium contracts) pulls on the chordae tendineae, which prevent the AV valves from opening back into the atria
why is the L ventricle more muscular than the R ventricle?
because the L ventricle must generate enough force to propel blood throughout the body, except the alveoli of the lungs; whereas the R ventricle must generate only enough force to propel blood a few centimeters to the lungs
or autorhythmicity, is the ability of cardiac muscle tissue to contract without neural or hormonal stimulation
which structure of the heart is known as the cardiac pacemaker or the natural pacemaker?
sinoatrial node (SA node)
if the cells of the SA node failed to function, how would the heart rate be affected?
the heart would still continue to beat, but at a slower rate; the AV node would act as the pacemaker
why is it important for impulses from the atria to be delayed at the av node before they pass into the ventricles?
if impulses weren't delayed, they would be conducted through the ventricles so quickly by the bundle brances and purkinje cells that the ventricles would begin contracting immediately, before the atria had finished their contraction
- as a result, the ventricles wouldnt be as full of blod as they could be, and the pumping of the heart would not be efficient, esp. during activity
provide the alternate terms for heart contraction and heart relaxation
alternate term for contraction= systole
for relaxation= diastole
list the phases of the cardiac cycle
is the heart always pumping blood when pressure in the L ventricle is rising? Explain
-when pressure in the L ventricle 1st rises, the heart is contracting BUT no blood is leaving the heart
- during the initial phase of contraction, BOTH the AV valves and semilunar valves are CLOSED
-the increase in pressure is the result of increased tension as the cardiac muscle contracts
-when the pressure in the ventricle EXCEEDS the pressure in the aorta, the aortic semilunar valves are FORCED OPEN, and blood is rapidly EJECTED from the ventricle
what factor or factors could cause an increase in the size of the QRS complex in an electrocardiogram?
(which is indicated by a larger than normal amt of electrical activity during ventricular depolarization)
-one possible cause is AN ENLARGED HEART.
- because more cardiac muscle is depolarizing, the magnitude of the electrical event would be greater
caffeine has effects on conducting cells and contractile cells that are similar to those of NE. what effect would drinking large amounts of caffeinated drinks have on the heart?
-caffeine acts directly on the conducting system and contractile cells of the heart.
- it increases the rate at which they depolarize
-drinking large amts of caffeinated drinks would increase the HR
if the cardioinhibitory center of the medulla oblongata were damaged , which part of the autonomic nervous system would affected, and how would the heart be influenced?
-part of the parasympathetic division.
-would reduce parasympathetic action potentials to the heart
-the resulting sympathetic dominance would increase the HR
how does a drug that increases the length of time required for the repolarization of pacemaker cells affect the heart rate?
would decrease the heart rate, because the pacemaker cells would generate fewer action potentials per minute
why is it a potential prob if the heart beats too rapidly?
- the heart pumps in proportion to the amt of blood that enters.
- a heart that beats too fast doesnt have sufficient time to fill completely btw beats
- this, when the heart beats too fasts, very little blood leaves the ventricles and enters the circulation,
- so tissues suffer damage from inadequate blood supply
what effects would stimulating the Ach receptors of the heart have on cardiac output?
-it would slow the heart
- since cardiac output is the product of stroke volume and HR, a reduction in HR will lower the cardiac output (assuming that the stroke volume doesn't change)
what effect would an increased in venous return have on the stroke volume?
- the venous return fills the heart with blood, stretching the heart muscle.
- according tot he frank-starling principle, the more the heart muscle is stretched, the more forcefully it will contract (to a point)
- the more forceful the contraction, the more blood the heart will eject with each beat (stroke volume)
-therefore, increased venous return would increase the stroke volume (if all the other factors are constant)
how would an increase in sympathetic stimulation of the heart affect the end-systolic volume?
- increased sympathetic stim. would increase HR and force of contraction
- the end-systolic volume (ESV) is the amt of blood that remains in a ventricle after a contraction (systole)
-the more forcefully the heart contracts, the more blood it ejects and the lower the ESV is.
-therefore increases sympathetic stim. should result in a lower ESV