1. The Heart
Chapter 18 – Day 4
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2. Wrap up Physiology Muscle contraction in cardiac tissue
Pacemaker cells (aka cells of the SA node)
Rhythmic depolarization and repolarization
Triggers depolarization through internodal cells (aka – start of action potential)
Cardiac tissue
Ca2+ enters muscle cells via “slow calcium channels”
This results in plateau (Fig )
Arrival of extracellular Ca2+ triggers the release of additional Ca2+ from reserves in SR
Sarcomeres shorten = muscle contraction
Period of active muscle contraction continues until the plateau ends
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3. Heart – Anatomy: Cardiac muscle
Fig. 18.5
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4. Order of Rhythm in Heart
Fig
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5. Fig
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6. Journal of Action Potential in Heart
Fig
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7. Wrap up Physiology Stimulates intercalated discs
Moves action potential nearly instantaneously cell-to-cell
Action potential simultaneously affects all tissue in the area
All muscle cells in ATRIA contract together
Action potential is transferred to AV node (100msec delay from SA node = Ventricles contract after atria)
All muscle cells in VENTRICLES contract together
We’ve covered EKG/ECG, make sure you are comfortable with it for lecture AND lab exam
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8. Heart
Fig
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9. Fig
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10. Cardiac Cycle Cardiac cycle = 1 heart beat Figure 18-16
2 important events
Systole = contraction
Diastole = relaxation
Each chamber has it’s own systole and diastole
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11. Cardiac Cycle ATRIAL SYSTOLE Ventricles build up pressure
Pushes blood into relaxed ventricles
Ventricles build up pressure
VENTRICULAR SYSTOLE
Early – there is enough pressure to close AV valves, but not enough to exceed pressure in blood vessels
Pressure exceeds that in blood vessels = 2nd phase of v. systole…
Ejects blood out of heart into circulation
Meanwhile….ATRIAL DIASTOLE is in progress
At the beginning of VENTRICULAR DIASTOLE
Atria fill up with blood (returning = venous return)
In late ventricular diastole all chambers are relaxed
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12. Fig
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13. Fig
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14. Fig
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15. Heart Health Resting heart rate is efficient
Cardiac cycle can give information about heart efficiency
As the heart rate increases, less time is spent in each phase, thus…
…blood is ejected at a different volume
Heart efficiency can be measured as CARDIAC OUTPUT
Heart sounds (p522)
4 distinct heart sounds (S1-S4)
Lubb (S1) = start of ventricular contraction when AV valves close
Dupp (S2) = beginning of ventricular filling when semilunar valves close
rushing/, gurgling sound = HEART MURMUR (regurgitation of blood through valves during diastole)
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16. Cardiac Output = volume of blood ejected every minute
P. 523 and on board
Example
Cardiac Output = a major factor in determining blood pressure
How hard does the heart have to work for proper circulation
Cardiac output (CO) = Stroke volume (SV) mL (VOLUME EJECTED AT EACH HEART BEAT – SYSTOLE) X heart rate (bpm)
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17. Cardiac Output Depends on Figure 18-23
Venous return
Stretching of heart muscles
Heart rate
End diastolic volume (EDV)
Volume remaining in ventricle after contraction b/c not all blood is ejected out
Figure 18-23
Amount of muscle stretching affects the force of contractions (e.g. pulling a rubber band)
Starlings Law of the Heart
“Stretch” builds up resistance against the blood
More blood is pushed out
Why is C.O. important?
Maintains proper BP levels to provide efficient blood supply
Starlings law of the heart:
general rule of “more in = more out”
Based on principle that ventricular expansion is limited by myocardial connective tissues, the fibrous skeleton and the pericardial sac
The relationship between the amt of vent. Stretching and the contractile force means that, within normal physiological limits, increasing the EDV results in a corresponding increase in the stroke volume.
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18. Factors Affecting Stroke Volume
Fig
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19. Cardiac Output Blood Pressure Pressure of blood within blood vessels
Pressure exerted on ARTERY walls
How would C.O. relate??
Higher cardiac output
More blood = ↑ BP
Less blood = ↓ BP
Resistance of blood vessel walls
Small diameter = ↑ BP
Blood flow is proportional to the radius of the “pipe”
Polycythemia (↑ in RBCs)
Thicker blood viscocity = ↑ BP (↑ RBCs or loss of water)
Length of blood vessel – longer length = ↑ BP
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20. Cardiac Output Cardiac output can be influenced by many factors
One of these is HEART RATE
Heart conduction system
Autonomic nervous system
Exercise can increase C.O.
Heart muscles are working out
Skeletal muscle cells need a fast blood supply
The heart has to meet that demand – when exercising, it meets increased demands
The force of contraction increases
Blood moves faster, so venous return is faster
More blood volume is pushed out
Does not increase indefinitely, the Heart Rate can out-compete C.O.
What is cardiac reserve and where does it fit here??
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21. Factors Affecting Heart Rate
Hormones, ions, nervous system…
ANS
Fibers connect to the SA node and the AV node
Sympathetic Control
Medulla – remember the cardiovascular center
Norepinephrine, epinephrine
Affects the SA node, AV node & myocardium
Cardiac Nerve
Dilates coronary vessels
Parasympathetic control
Medulla – cardio-inhibitory center
Vagus Nerve (at S.A. node & A.V. node)
Secretes ACh
ACh changes ion distribution = decrease in heart rate
Cardiovascular center of the medulla…
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22. Factors Affecting Heart Rate
Ions affect heart rate
Ca2+ , Na+ - needed for depolarization
K+ - needed for repolarization
Ion concentration in blood affects the action potential in the heart
Increase K+ outside
Less K+ will leave the cell
Partial repolarization – slower action potential  HR
Increase Ca2+ outside cell
 force of contraction – can lead to spasms
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23. Factors Affecting Cardiac Output
Fig
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24. Heart Problems
The normal rhythm of the heart can be disrupted in many ways – be ready to discuss on Friday those in book & those in handouts – you’ll also form your groups for the case study…
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