1. Heart Topics Location of the Heart Chambers of the Heart Heart Valves
Coronary Circulation
Cardiac Muscle
Cardiac Conduction System
Cardiac Cycle
Cardiac Output

2. Cardiac Conduction System
Involuntary
Autorhythmic

3. Cardiac Conduction System

4. Assigned Reading
Review notes on diagram – go through this pathway several times.
Review your first term notes on:
Muscle contraction - Figures
Calcium extraction from bones
Types of action potentials

5. Action Potentials in Neurons
Depolarization
Plateau
Repolarization
Refractory Period

6. Action Potentials in SA Node
Depolarization
Plateau
Repolarization
Refractory Period

7. Action Potentials in Skeletal Cells
Depolarization
Plateau
Repolarization
Refractory Period

8. Action Potentials in Cardiac Cells
Rapid Depolarization
Plateau
Repolarization
Refractory Period

9. Cardiac ATP Production
High density of mitochondria in Cardiomyocytes = quick ATP production = resistance to fatigue.
Relies on aerobic cellular respiration (unlike skeletal muscle = anaerobic)
Fatty acid metabolism (60%)
Glucose metabolism (35%)
Creatine phosphate
Lactic acid metabolism - increases during exercise

10. Myocardial Infarction
Creatine kinase catalyzes the transfer of a phosphate group from creatine phosphate to ADP to make ATP.
Normally, CK and other enzymes are confined within cells.
Injured or dying cardiac or skeletal muscle fibers release CK into the blood.

11. The ECG Heart beat creates electrical currents on surface of body.
Recording of electrical changes of each cardiac cycle.
The initiation of each heartbeat and recording of the action of the entire heart.

12. The ECG
P Wave
QRS Complex
T Wave

13. ECG
Compare the electrical vs. mechanical activity on these diagrams as we can INFER the mechanical activity caused by the electrical activity.

14. ECG
AP in SA node propagates in atrial muscle  AV node  depolarizes atrial fibers = P wave
After start of P wave = atrial contraction (systole).
AP slows at AV node (anatomical diff) = atria time to contract = increases ventricular volume.

15. ECG
3. AP propagates fast again in bundle of HIS  bundle branches (septum = Q)  apex purkinje fibers  ventricles  QRS complex ms
Atrial repolarization hidden here

16. ECG 4. Shortly after QRS complex = ventricular fiber contraction
Continues during S-T segment
Contraction moves from apex to base
Blood squeezed towards semi-lunar valves

17. ECG
5. Repolarization of ventricular fibers starts at apex and spreads = T wave (0.4 sec after P wave)
6. Shortly after start of T wave = ventricular relaxation (diastole)
Once repolarization complete, fibers completely relax (by 0.6 sec)

18. Heart Topics Location of the Heart Chambers of the Heart Heart Valves
Coronary Circulation
Cardiac Muscle
Cardiac Conduction System
Cardiac Cycle
Cardiac Output

19. The Cardiac Cycle
Atrial Systole
Ventricular Systole
Relaxation Period

20. Atrial Systole ECG Connection: from P wave to Q wave AV valves: open
SL valves: closed

21. Atrial Systole Both atria contract Ventricles are relaxed
Atrial pressure increases
AV valves open
Blood flows into both ventricles
Ventricles are relaxed
Ventricular pressure too low to open SL valves
End-diastolic volume = EDV ~130 mL
Exercise increases EDV

22. Ventricular Systole Divided into two periods
Isovolumetric ventricular contraction
Ventricular ejection
Atria are relaxed and filling with blood .

23. Isovolumetric Ventricular Contraction
ECG Connection: begins with R wave
AV valves: closed
SL valves: closed

24. Isovolumetric Ventricular Contraction
Both ventricles begin contracting
Increases pressure
AV valves close
Ventricular pressure too low
SL valves remain closed
Isovolumetric

25. Ventricular Ejection ECG Connection: from S wave to T wave
AV valves: closed
SL valves: open

26. Ventricular Ejection Both ventricles continue contracting
Ventricular pressure continues to increase
AV valves remain closed
High ventricular pressure opens SL valves
Blood is ejected into pulmonary trunk and aorta
Max volume of blood ejected = ~70 mL / ventricle
60 mL remains = End-systolic volume (ESV)

27. Stroke Volume
The volume of blood ejected from each ventricle during systole.
SV= EDV-ESV
SV =130 ml – 60 ml
SV = 70 ml

28. Relaxation Period Divided into two periods:
Isovolumetric ventricular relaxation
Passive ventricular filling
Both atria and ventricles are relaxed and filling with blood

29. Isovolumetric Ventricular Relaxation
ECG Connection: begins at end of T wave
AV valves: closed
SL valves: closed

30. Isovolumetric Ventricular Relaxation
Both ventricles begin to relax
Ventricular pressure begins to decrease
Low ventricular pressure closes SL valves
Ventricular pressure too high to open AV valves

31. Passive Ventricular Filling
ECG Connection: after T wave to next P wave
AV valves: open
SL valves: closed

32. Passive Ventricular Filling
Both ventricles continue to relax
Ventricular pressure continues to decrease
SL valves remain closed
Atrial pressure exceeds ventricular pressure
AV valves open
Blood fills the ventricles

33. Cardiac Cycle and Heart Rate
Metabolic increase = HR increase
Durations of atrial and ventricular systole are relatively constant
Increased heart rate  decreased relaxation period

34. The Cardiac Cycle Pressure Heart sounds Ventricular volume
Left side vs. right

35. Types of questions asked
This diagram wouldn’t be on a test but all the content is!!
What electrical event initiates an action?
What is the pressure relationship on either side of a valve?
When are valves open or closed?
Where / when is blood moving?

36. Heart Topics Location of the Heart Chambers of the Heart Heart Valves
Coronary Circulation
Cardiac Muscle
Cardiac Conduction System
Cardiac Cycle
Cardiac Output

37. Cardiac Output
The heart’s ability to discharge oxygen rich blood needs to be variable to meet the work requirements of your cells.
CO = A measure of ejected blood from the ventricles every minute.

38. Cardiac Output Cardiac Output (CO) = SV X HR At rest CO = 70 X 75
At rest CO = 5.25 L/minute
CO adjusted by changing SV or HR
Cardiac Reserve = 5 X CO

39. Regulation of Stroke Volume
Preload
Contractility
Afterload

40. Preload Increased stretch  increased force of contraction
Increased filling during diastole  increased force of contraction during systole

42. Preload
Determined by:
Duration of ventricular diastole
Venous return

43. Why Preload?
The relationship between ventricular filling (EDV) and preload equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both systemic and pulmonary circulations.

44. Afterload
Afterload – the pressure that the ventricles must overcome to open the SL valves.
Increased afterload  decreased SV  increases ESV

45. Afterload
Hypertension

46. Contractility Positive inotropics increase contraction
Norepinephrine and epinephrine
Negative inotropics decrease contraction
Acetylcholine

47. Regulation of Heart Rate
Regulating HR is the body’s principal mechanism of short-term control of CO
Three main mechanisms:
ANS
Endocrine system
Other factors

48. Regulation of Heart Rate - ANS

49. Regulation of Heart Rate – Endocrine
Epinephrine and Norepinephrine
Increase HR and contractility
Thyroid hormone
Increases HR and contractility

50. Regulation of Heart Rate – other factors
Cations also affect heart rate:
Na+ and K+ decrease HR and contractility
Ca2+ increases HR and contractility

51. Exercise and the Heart