Transcript Cardaic Cycle

Cardiac Cycle
Ellen Rasche
Darcy Holzum
Ariel Dunteman
Diastole and Systole
• Diastole- Relaxation of the heart
• Systole- Contraction of the heart
Heart Sounds
• Action of the heart valves
• “lubb”
– AV valves close and semilunars open
– Marks the start of the ventricular systole
– Longer than second sound
• “dubb”
– Beginning of ventricular diastole, when the
smilunanr valves close
Heart Sounds (cont.)
• Third and fourth sounds may be audible
– Usually faint and seldom detectable
– Are associated with atrial contraction and blood
flowing into the ventricles rather than with valve
action
Heart Dynamics
• Heart dynamics – refers to movements and
forces generated during cardiac contractions
• Each time t he heart beats, 2 ventricles eject
equal amounts of blood
• The stroke volume is the amount ejected by a
ventricle during a single beat
– Stroke volume varies beat to beat so physicians
are often more interested in cardiac output
Heart Dynamics
• Cardiac output is the amount of blood
pumped by each ventricle in 1 minute
– Provides indication of blood flow through
peripheral tissues; without adequate blood flow,
homeostasis cannot be maintained
Calculate Your Cardiac Output
Cardiac output = stroke volume x Heart Rate
(mL/min)
(mL/beat)
(beats/min)
Factors controlling Cardiac Output
• The major factors that regulate cardiac output
often affect both heart rate and stroke volume
• Primary factors include:
– Blood volume reflexes
– Autonomic innervation
– hormones
Blood Volume Reflexes
• There is a direct relation between the amount
of blood entering the heart and the amount of
blood ejected during the contraction
• 2 heart reflexes respond to changes in blood
volume
1. Occurs in right atrium and affects heart rate
2. Ventricular reflex than affects stroke volume
Blood Volume Reflexes con’t
• Ariel reflex produces adjustments in heart
rate in response to an increase in the venous
return
– Venous return: flow of venous blood to the heart
– The entry of blood stimulates stretch receptors on
the right atrial walls, triggering a reflexive increase
in heart rate through increased sympathetic
activity
Blood Volume Reflexes con’t
• The amount of blood pumped out of a
ventricle each heartbeat (stroke volume)
depends not only venous return but also on
the filling time - the duration of ventricular
diastole, when blood can flow into the
ventricles
• The filling time depends primarily on the heart
rate: the faster the heart rate, the shorter the
available filling time
Blood Volume Reflexes
• Over the range of normal activities, the greater
the volume of blood entering the ventricles, the
more powerful the contraction (and the more
pumping force is produced), and the greater the
stroke volume
• If more blood flows into the heart, the ventricles
produce greater force upon contraction
– “more in = more out”
– This is the Frank-Starling Principle
– Output of blood from both ventricles is balanced
under a variety of conditions
Factors Controlling Cardiac Output
• Autonomic Innervation
– The basic heart rate is established by pacemaker
cells of the SA node
• This rate can be modified by the autonomic nervous
system (ANS)
– Both they sympathetic and parasympathetic
divisions of the ANS innervate the heart
– Postganglionic sympathetic fibers extend from
neurons
• Located in the cervical and upper thoracic ganglia
Autonomic Innervation (cont.)
• The vagus nerve carries parasympathetic
preganglionic fibers to small ganglia near the
heart
• Both ANS divisions innervated the SA and AV
nodes
– Atrial and ventricular cardiac muscles cells
Autonomic Effects on Heart Rate
• Reflect the responses of the SA node to
acetylcholine (Ach) and to norepinephine (NE)
• ACh results in a lower heart rate
• Norepinephrine released by sympathetic
neurons increases the heart rate
• Release of epinephrine € and norepinephrine
by the adrenal medullae produces a more
sustained rise in heart rate
Autonomic Effect on Stroke Volume
• Release of Ne, E and Ach, the ANS affects
stroke volume by altering force of myocardial
contractions:
– Effects of Ne and E: increase the force and degree
of contraction, resulting in an increase of stroke
volume