1. Figure 22.6

2. joined by intercalated discs
CARDIAC MUSCLE CELLS
Branched
joined by intercalated discs
desmosomes: tightly bind cells & transfer of tension
gap junction: electrical synapses that directly transfer electrical activity/AP from one cell to the next
Contractile/myocardial Cells => contract and conduct AP’s
Conductile/autorhythmic cells => produce and conduct action potentials

4. AP in SA conductile/nodal/autorhythmic cells
VG Na+ channels
HCN channels: VG ion channels, open due to hyperpolarization,
allow Na+ in
VG Ca channels cause depolarization of AP
VG K channels cause repolarization

5. Fig
Conduction System

6. AP/Stimulus begins in SA node
Transmitted through conduction system and from cell to cell via gap junctions
Both Atria contract, then both ventricles contract

7. AP in Contractile/Myocardial Cells
Plateau cause by slow VG Ca+ channels & Ca+ inflow
this prolonged state of depolarization results in long period of refractory.
Long refractory prevents heart from entering tetanus (which is a good thing as heart needs to relax to fill)

8. AP and Excitation-Contraction Coupling in Myocardial cells (contractile cells)
AP formation and propagation as in axons and skeletal muscle
opening of VG Ca+  Ca+ flows in
Ca+ entering cytoplasm causes Ca release channels to open
massive Ca release from SR
“calcium induced calcium release”
actin and mysin interact as in skeletal muscle
Extracellular calcium plays bigger role in myocardial contraction than in skeletal muscle fiber contraction
Fig 8

9. Fig

10. Table 13.6

11. Fig

12. the repeating sequence of contraction and relaxation of the heart.
Fig
Cardiac Cycle:
the repeating sequence of contraction and relaxation of the heart.
Diastole = relaxation
filling
Systole = contraction
ejection of blood

13. Fig

14. Isovolumetric contraction Ejection Isovolumetric relaxation
Fig
Isovolumetric contraction
Ejection
Isovolumetric relaxation
Rapid refilling
Atrial contraction

16. ECG: measures overall electrical activity of the whole heart
PR interval:
time it takes for depolarization that begins in SA to spread to ventricles
Long PR represent damage to atria conductive system or AV note
QT interval:
time of ventricles to depolairze and repolarize.
Can Ax electrolytes imbalance, tissue damage, ischemia

18. Fig

19. Maintenance of proper blood pressure (BP) is critical for proper CVS function
BP is influenced by:
cardiac output (CO)
heart function
peripheral resistance
vessel activity and blood characteristics
Cardiac Output = Heart Rate (HR) x stroke volume (SV)

20. Page 470

21. Relationship among factors that determine cardiac output

22. Heart activity is regulated by
Autonomic Nervous System (ANS)
Sympathetic Nerves
Parasympathetic nerves—vagus nerve
Hormones
Intrinsic Regulation

23. Cardiac Control Centers is in medulla
Fig
Cardiac Control Centers is in medulla
influenced by higher brain centers
Cardiac centers recieve sensory input from
vagus nerve
hypoglossal nerve
barroreceptors—pressure
chemoreceptors—blood chemistry
Medulla Signals heart via
vagus nerve-parasympathetic
sympathetic cardiac nerves

24. Fig

26. Regulation of Heart Rate
Nervous system
SD and PD inneration of SA node
Endocrine System
hormone affects on SA node
Intrinsic (autoregulation)
stretch of nodal cells directly increases rate of depolarization

27. Vagus Nerve (parasympathetic)
Ach—muscarinic receptors (g-proteins—ion channels)
innervates atria/SA node & AV node
Sympathetic Nerves (sympathetic)
Norepinephrine (NE)—Beta 1 (β1) receptors
innervates ventricles
sympathetic nervous system also signals the heart via the endocrine system/epinephrine

28. Autonomic Innervation
Parasymphathetic division slows heart rate
slows rate of SA node depolarization
Sympathetic division increases heart rate
speeds up rate of SA node depolarization
Heart receives constant input from BOTH systems
balance of SD and PD determines if HR goes up or down
At rest Parasympathetic signals predominate and this depresses the heart rate below the SA nodes intrinsic rate of ~100 bpm

29. Nervous Regulation of HR
Parasympathic:
Ach-muscarinic receptors
opens K+ gates
slows pacemaker potential
decreases HR
Sympathetic:
NE-- β1 opens Na-Ca+ channels
speeds up pacemaker potential
increases HR
/ Natural rate

32. Interplay between PD and SD activity
Increasing PD—slows heart
decreasing PD—speeds heart
increasing SD—speeds heart
decreasing SD—slows heart

33. Hormones and HR
N.E., Epinephrine (E), and Thyroid Hormones delivered through blood can also increase HR
increasing levels increase HR
decreasing levels decrease HR
mechanism similar to nervous system mechanisms (alters rate of pacemaker potential)

34. Atrial Reflex (SD regulation of heart)
Atrial Reflex (Bainbridge reflex)
Increased filling of atria (i.e., increased venous return or increased blood volume) stretches atrial wall
sensory neurons relay stretch to medulla
medulla increase rate of SD signaling of heart (or decreasin PD, literature is unclear)
HR increases (in either case).

35. Intrinsic Regulation (autoregulation) of the Heart Rate
Increased filling of atria (i.e., increased venous return or increased blood volume) stretches nodal cells of atrial wall
stretching of the cells directly causes their rate of depolarization to increase

36. Regulation of Stroke Volume
Stroke Volume influenced by:
ESV
EDV SV
Preload (directly related to EDV)
Afterload (equivalent to peripheral resistance/arterial blood pressure)

37. EDV: the amount of blood in each ventricle at the end of diastole (i.e., how much blood fills ventricles)
ESV: amount of blood in each ventricle at end of systole (how much blood is left after ejection/contraction
SV: how much blood is ejected from each ventricle during systole
EDV-ESV=SV

38. Interactions between EDV, Preload, SV and CO
Preload: amount of stretching of ventricular wall
Caused by filling of ventricle and directly related to EDV
↑ EDV  ↑ Preload
↓ EDV  ↓ Preload
EDV is influenced by venous return (rate of blood return to heart through veins)
↑ venous return  ↑ EDV/ Preload
↓ venous return  ↓ EDV/Preload

39. Interactions between EDV, Preload, SV and CO: Frank-Starling
↑ venous return  ↑ EDV/ Preload  increased ventricular stretching  ↑ ventricular contraction strength  ↑ SV  ↑ CO
“more in, more out”
intrinsic regulation that makes output match return (also keeps two circuits in synch by making sure amount through systemic circuit keeps pace with amount through pulmonary
Increased contraction strength due to lengthening of sarcomeres to a more optimum overlap length  stronger contraction

40. Fig. 14.3

41. Contractility: ↑ contractility--↑ SV, ↓ contractility-- ↓ SV
Contractility=Increase in contraction strength due to ionotropic effects (i.e., for reasons other than fiber length/overlap)
due to Ca+ availability in cytoplasm
Causes of Increased Contractility
SD fibers to ventricles—NE– Beta 1-- ↑ contractility-- ↑ SV
Adrenal medulla—E-- Beta 1(in venricles)-- ↑ contractility-- ↑ SV
Although PD technically innervates ventricles their role is negligable
Hormones (other than E)
Thyroid hormone and glucagon also increase contractility

42. Topics Related to contractility
Beta 1 stimulators or drugs that increase intracellular calcium (like digitalis) increase contractility/CO
Beta blockers drugs decrease Ca+, decrease contractility, decrease CO
used to treat hypertension
Ca+ channels blockers (nifedipine): Ca+, decrease contractility, decrease CO

43. Afterload and CO
Afterload: amount of pressure ventricles need to produce/overcome to eject blood
directly related to arterial blood pressure (i.e., peripheral resistance)
↑ afterload  ↓ ejection  ↓ SV  ↓ CO
chronic high blood pressure = chronic high afterload causing heart to work excessively hard/stress to maintain CO
weakened or diseased heart may be unable to overcome relatively small increases in afterload causing significant problems in maintain CO/BP

44. ~TPR

47. Table 14.1

48. Fig. 14.2

49. Table 14.3

50. Fig. 14.7

51. Fig. 14.5
P.R.