1. Cardiac Muscle Contraction
Heart (cardiac) muscle is stimulated by:
Self-excitation (automaticity:1% of cardiac cells)
Nerves (autonomic nervous system)
Contracts as a unit (presence of gap junctions & branching)
Has a long (250 ms) absolute refractory period (tetanic contraction prevention)
Remaining cardiac cells contracts similarly to skeletal muscle

2. Intrinsic Conduction System
Autorhythmic cells:
Specialized noncontractile cells
Initiate action potentials
Have unstable potential:
Continuously depolarize
Slowly drifting toward threshold)
Such potential is called pacemaker potentials
Initiate and spread action potential
Use calcium influx (rather than sodium) to produce the rising phase of the action potential

3. Sequence of Excitation
Sinoatrial (SA) node:
Located in right atrial wall (inferior to superior vena cava)
Generates impulses about 75 times/minute
Atrioventricular (AV) node:
Located in the inferior part of the interatrial septum (above tricuspid valve)
Delays the impulse approximately 0.1 second (why?)
Atrioventricular bundle (bundle of His):
Located in the superior part of interventricular septum
conveys impulses from atria to ventricles

4. Sequence of Excitation (cont’d)
AV bundle (bundle of His) splits into:
Two pathways (bundle branches) in the interventricular septum
Bundle branches:
Carry the impulse toward the apex of the heart
Purkinje fibers:
Carry the impulse to the heart apex and ventricular walls

5. Cardiac Intrinsic Conduction
Figure 18.14a

6. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Figure 18.17

7. Heart Excitation Related to ECG
Impulse delayed
at AV node
AV node
Figure 18.17

8. Heart Excitation Related to ECG
Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Figure 18.17

9. Heart Excitation Related to ECG
Ventricular excitation
complete
Purkinje
fibers
Figure 18.17

10. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
Impulse delayed
at AV node
Impulse passes to
heart apex; ventricular
excitation begins
Ventricular excitation
complete
SA node
AV node
Bundle
branches
Purkinje
fibers
Figure 18.17

11. Extrinsic Innervation of the Heart
Heart is stimulated by:
The sympathetic cardioacceleratory center
Located in the medulla oblongata
Heart is inhibited by:
The parasympathetic cardioinhibitory center
Figure 18.15

12. Electrical activity is recorded by electrocardiogram (ECG)
Electrocardiography
Electrical activity is recorded by electrocardiogram (ECG)
P wave corresponds to atrial depolarization
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex
PLAY
InterActive Physiology ®:
Intrinsic Conduction System, pages 3–6

13. ECG Tracings
Figure 18.18

14. Electrocardiography
Figure 18.16

15. Two distinguishable sounds with each heart beat
Heart Sounds
Two distinguishable sounds with each heart beat
Sounds (lub-dup pause lub-dup) are associated with closing of heart valves
First sound:
Occurs as AV valves close
Signifies the beginning of ventricular blood pressure rising above atrial pressure (beginning of ventricular systole)
Second sound:
Occurs when SL valves snap shut
At the beginning of ventricular diastole

16. Break Slide
June 15

17. Heart Sounds
Figure 18.19

18. Cardiac Cycle
Cardiac cycle refers to all events associated with blood flow through the heart
Systole:
Contraction of heart muscle
Diastole:
Relaxation of heart muscle

19. Phases of the Cardiac Cycle
Ventricular filling
Between mid-to-late diastole
Heart blood pressure is low
Blood enters atria and flows into ventricles
AV valves are open,
Then atrial systole occurs

20. Phases of the Cardiac Cycle
Ventricular systole
Atria relax
Ventricular pressure rises
AV valves close
Isovolumetric contraction phase (split-second when ventricles are completely closed & volume remain constant)
Ventricular ejection phase opens semilunar valves
During vent.ejection phase, the pressure in the aorta reaches 120 mmHg

21. Phases of the Cardiac Cycle
Isovolumetric relaxation
At early diastole (ventricles are completely closed)
Ventricles relax
Ventricular pressure drops
Blood in aorta and pulmonary trunk backflows
Backflowing blood closes semilunar valves (SL)
Dicrotic notch:
Brief rise in aortic pressure caused by:
Backflow of blood rebounding off SL valves
PLAY
InterActive Physiology ®: Cardiac Cycle, pages 3–18

22. Cardiac Output (CO) CO (cardiac output): HR (heart rate):
Is the amount of blood pumped by each ventricle in one minute
Is the product of heart rate (HR) and stroke volume (SV)
HR (heart rate):
Is the number of heart beats per minute
SV (stroke volume):
Is the amount of blood pumped out by one ventricle with each beat (correlates with the force of ventricular contraction)
It is equal to 70 ml/beat

23. Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min
= (5.25 L/min)

24. Regulation of Stroke Volume
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV :
Amount of blood collects in a ventricle during diastole
Normally about 120 ml
Determined by:
Duration of ventricular diastole
Venous pressure

25. Regulation of Stroke Volume
ESV = amount of blood remaining in a ventricle after contraction
Approximately 50 ml
Determined by:
Arterial blood pressure
Force of ventricular contraction
SV= EDV – ESV
= 120 ml/beat – 50 ml/beat
= 70 ml/beat

26. Factors Affecting Stroke Volume
Preload:
Degree of stretch of cardiac muscle cells before they contract
Contractility:
Contractile strength achieved at a given muscle length
Afterload:
Back pressure exerted by blood in the large arteries leaving the heart

27. Preload and Afterload
Figure 18.21

28. Extrinsic Factors Influencing Stroke Volume
Increased contractility comes from:
Increased sympathetic stimuli
Hormones: Glucagon,thyroxine, epinephrine
High levels of extracellular Ca2+
Some drugs e.g. digitalis
Impaired contractility comes from:
Acidosis (high H+)
High levels of extracellular K+
Drugs called calcium channels blockers

29. Regulation of Heart Rate: Autonomic N. S.
Sympathetic nervous system (SNS)
Its stimulation is activated by:
Stress
Anxiety
Excitement
Exercise

30. Regulation of Heart Rate: Autonomic N. S.
Parasympathetic nervous system (PNS) stimulation:
Mediated by acetylcholine & opposes the sympathetic nervous system (SNS)
Dominates the autonomic stimulation
Slows heart rate
Causes vagal tone (dominant inhibitory effect at rest )
What is the effect of cutting the vagal nerves to the heart?

31. Atrial (Bainbridge) Reflex
A sympathetic reflex
Initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates stretch receptors in the atria causing increased sympathetic nervous system (SNS) stimulation

32. Chemical Regulation of the Heart
Hormones:
Epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations:
Ion concentration must be maintained for normal heart function
Hypo & Hypercalcemia (low & high blood ca2+):
Depresses & stimulate the heart, respectively
Hypo & Hyperkalemia (low & high blood K+):
Causes heart block & arrhythmia, respectively
PLAY
InterActive Physiology ®: Cardiac Output, pages 3–9