1. Ellen Rasche Darcy Holzum Ariel Dunteman
Cardiac Cycle
Ellen Rasche
Darcy Holzum
Ariel Dunteman

2. Diastole and Systole Diastole- Relaxation of the heart
Systole- Contraction of the heart

4. Heart Sounds Action of the heart valves “lubb” “dubb”
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

5. 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

6. 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

7. 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

8. Calculate Your Cardiac Output
Cardiac output = stroke volume x Heart Rate
(mL/min) (mL/beat) (beats/min)

9. 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

10. 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
Occurs in right atrium and affects heart rate
Ventricular reflex than affects stroke volume

11. 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

12. 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

13. 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

14. 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

15. 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

16. 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

17. 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