1. Ch 12 Heart and Circulatory System
The Body’s Transport System

2. 4 Chambered Heart – size of clenched fist
2 Atria
2 Ventricles
Arteries (efferent vessels)
Veins (afferent vessels)
Layers of the Heart
Epicardium – outmost layer; covers surface of heart
Myocardium – muscle layer; contains cardiac muscle, blood vessels and nerves
Endocardium – lines heart’s chambers and valves; composed of simple squamous tissue

3. Two Circuits for Blood Pulmonary Circuit:
right side of heart; receives blood and transports de-oxygenated blood to lungs.
Systemic Circuit:
left side of heart; supplies body with oxygenated blood.

4. Pericardium is the shiny covering around the heart.
Function:
To reduce friction between surrounding surfaces as heart beats
Protect the heart
Anchor the surrounding structures

5. Characteristics of Heart Muscle. Intercalated discs. Involuntary
Characteristics of Heart Muscle Intercalated discs Involuntary Striated One nuclei per cell
Intercalated disks - allows heart to beat as one unit

6. Location of Heart

7. Structure of the Heart

8. Main Veins into heart Main Arteries Coronary Sinus Superior Vena Cava
Inferior Vena Cava
Pulmonary Vein
Main Arteries
Coronary Artery
Pulmonary Artery
Aorta 5 1 2 6

9. Blood flow through the Heart
De-oxygenated blood from the body enters the R atrium and is pumped to the R ventricle. From the R ventricle deO2 blood is sent to the lungs where gas exchange occurs.
Oxygenated blood enters the L atria and is sent to the L ventricle where it is sent to the body via the aorta.

10. Flow of blood through heartC
Superior Vena Cava
Inferior Vena Cava
R. atrium
R. ventricle
Pulmonary trunk (artery)
Pulmonary vein
L. atrium
L. ventricle
Aorta
A. Brachiocephalic
B. L. Common Carotid
C. L. Subclavian A 9 1 6 5 7 3 8 4 2

11. Coronary Arteries

12. Vein

13. Difference in myocardium thickness between R. ventricle and L
Difference in myocardium thickness between R. ventricle and L. ventricle.
Why?

14. Valves of the Heart Atrioventricular Valves
- one way valves; prevent back flow of blood
-chordae tendineae
- papillary muscles
Tricuspid – 3 flaps
Found between R atrium and R. ventricle
Bicuspid (mitral) – 2 flaps
Found between L atrium and L. ventricle

15. Anatomy of AV valves One-way valves
Atrioventricular valves
Chordae tendineae
Papillary muscles

16. Semilunar Valves Located in Pulmonary Artery and Aortic Artery 3 flaps
Prevents blood from flowing back into ventricles
Posterior
Anterior

17. Valve position when ventricles relaxed

18. Valve position when ventricles contract

19. Heart Sounds
Two sounds (lubb-dupp) associated with closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole
Second sound occurs when SL valves close at the beginning of ventricular diastole
Heart murmurs: abnormal heart sounds most often indicative of valve problems

20. Aortic valve sounds heard in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
Figure 18.19

22. Blood Flow and Valve Function

23. Cardiac Muscle Contraction
Rapid Depolarization: Threshold is reached along the membrane.
Causes Na+ channels in the sarcolemma to open
Na+ enters cell reversing membrane potential from –90 mV to +30 mV (Na+ gates close)
Plateau: Calcium channels open and Ca+2 enters sarcoplasm
Ca+2 also is released from SR
Ca+2 surge prolongs the depolarization phase and delays repolarization (excess + ions in cell)
Repolarization: Ca+2 begin to close; K+ channels open and K+ leaves the cell.

24. In Cardiac muscle, depolarization lasts longer
In Cardiac muscle, depolarization lasts longer. Thus cardiac muscle can’t increase tension with another impulse; tetanus doesn’t occur.
Why is this important?

25. Heart Physiology: Electrical Events
Intrinsic cardiac conduction system
A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart
Nodes – cells that are responsible for starting the impulse
Conducting cells – distribute the impulse to the myocardium
1 % of the heart’s cardiac cells have this capability

26. Internal Conduction System 1. Sinoatrial node 2. AV node
3. AV bundle or Bundle of HIS
4. R and L bundle branches
5. Purkinge fibers
Nodes – cluster of nervous tissue that begins an impulse. 5

27. Sequence of Excitation
Sinoatrial (SA) node (pacemaker)
Generates impulses about times/minute (sinus rhythm)
Depolarizes faster than any other part of the myocardium

28. Sequence of Excitation
Atrioventricular (AV) node
Delays impulses approximately 0.1 second
Allows for Atria to contract
Depolarizes times per minute in absence of SA node input

29. Sequence of Excitation
Conducting Cells
Atrioventricular (AV) bundle (bundle of His)
Right and left bundle branches
Two pathways in the interventricular septum that carry the impulses toward the apex of the heart
Sequence of Excitation

30. Sequence of Excitation
Purkinje fibers
Complete the pathway into the apex and ventricular walls

31. (a) Anatomy of the intrinsic conduction system showing the
Superior vena cava
Right atrium
The sinoatrial (SA)
node (pacemaker)
generates impulses. 1
Internodal pathway
The impulses
pause (0.1 s) at the
atrioventricular
(AV) node. 2
Left atrium
The atrioventricular
(AV) bundle
connects the atria
to the ventricles. 3
Purkinje
fibers
The bundle branches
conduct the impulses
through the
interventricular septum. 4
Inter-
ventricular
septum
The Purkinje fibers
depolarize the contractile
cells of both ventricles. 5
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
Figure 18.14a

32. Electrocardiography
Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time.
Three waves
P wave: depolarization of SA node
QRS complex: ventricular depolarization (AV node)
T wave: ventricular repolarization

33. Normal EKG has 3 distinct waves.
1st wave (P) - SA node fires
- Natural Pacemaker
- fires around times/minute
The atria depolarize Impulse is being generated across R and L atria via diffusion.
.1s after P wave, atria contract.

34. AV Node fires; depolarization of ventricles.
AV node – back up pacemaker
- Beats times/minute
- Impulse is delayed at bundle of HIS until Atria contract.
2nd wave (QRS)
AV Node fires; depolarization of ventricles.
Q-R interval represents beginning of atrial repolarization and AV node firing; ventricles depolarize
R-S interval represents beginning of ventricle contractions
S-T End of Ventricular depolarization

35. 3rd Wave (T)
T wave repolarization of ventricles
Ventricles return to normal relaxed state.
In a healthy heart, size, duration and timing of waves is consistent. Changes reveal a damage or diseased heart.

36. QRS complex Ventricular depolarization Ventricular Atrial
Sinoatrial
node
Ventricular
depolarization
Ventricular
repolarization
Atrial
depolarization
Atrioventricular
node
S-T
Segment
P-Q
Interval
Q-T
Interval
Figure 18.16

37. Atrial depolarization, initiated by the SA node, causes the P wave.
Repolarization P T Q S
Atrial depolarization, initiated by the SA node, causes the P wave. 1
Figure 18.17, step 1

38. Atrial depolarization, initiated by the SA node, causes the P wave.
Repolarization P T Q S
Atrial depolarization, initiated by the SA node, causes the P wave. 1 R
AV node P T Q S 2
With atrial depolarization complete, the impulse is delayed at the AV node.
Figure 18.17, step 2

39. Atrial depolarization, initiated by the SA node, causes the P wave.
Repolarization P T Q S
Atrial depolarization, initiated by the SA node, causes the P wave. 1 R
AV node P T Q S 2
With atrial depolarization complete, the impulse is delayed at the AV node. R P T Q S 3
AV node depolarizes; Ventricular
depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs.
Figure 18.17, step 3

40. Ventricular depolarization is complete.
Repolarization P T Q S
Ventricular depolarization is complete. 4
Figure 18.17, step 4

41. Ventricular depolarization is complete.
Repolarization P T Q S 4
Ventricular depolarization is complete. R P T Q S
Ventricular repolarization begins at apex, causing the T wave. 5
Figure 18.17, step 5

42. Ventricular depolarization is complete.
Repolarization P T Q S
Ventricular depolarization is complete. 4 R P T Q S
Ventricular repolarization begins at apex, causing the T wave. 5 R P T Q S
Ventricular repolarization is complete. 6
Figure 18.17, step 6

43. Atrial depolarization, initiated by the SA node, causes the P wave. Q
Repolarization R R P T Q P T S 1
Atrial depolarization, initiated by the SA node, causes the P wave. Q S
Ventricular depolarization is complete. 4
AV node R R P T P T Q S
With atrial depolarization complete, the impulse is delayed at the AV node. 2 Q S
Ventricular repolarization begins at apex, causing the T wave. 5 R R P T P T Q S Q 3 S
Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. 6
Ventricular repolarization is complete.
Figure 18.17

45. Homeostatic Imbalances
Defects in the intrinsic conduction system
may result in:
Arrhythmias: irregular heart rhythms
Uncoordinated atrial and ventricular contractions
Fibrillation: rapid, irregular contractions; useless for pumping blood

46. Problems with Sinus Rhythms
Tachycardia: Heart rate in excess of 100 bpm when at rest
If persistent, may lead to fibrillation
Bradycardia: Heart rate less than 60 bpm when at rest
May result in grossly inadequate blood circulation
May be desirable result of endurance training

47. Homeostatic Imbalances
Defective SA node may result
Ectopic focus: abnormal pacemaker takes over
No P waves; If AV node takes over, there will be a slower rhythm (40–60 bpm)
Defective AV node may result in
Partial or total heart block
Longer delay at AV node than normal
No all impulses from SA node reach the ventricles
Ventricular fibrillation:
cardiac muscle cells are overly sensitive to stimulation; no normal rhythm is established

48. Problems with Sinus Rhythms
2nd degree heart block; Missed QRS complex
SA node is sending impulses, but the AV node is not sending the impulses along the bundle branches
1st degree is represented by a longer delay between P & QRS

49. (a) Normal sinus rhythm. (b) Junctional rhythm. The SA
node is nonfunctional, P waves
are absent, and heart is paced by
the AV node at beats/min.
(c) Second-degree heart block.
Some P waves are not conducted
through the AV node; hence more
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
(d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
deflections are seen in acute
heart attack and electrical shock.
Figure 18.18

50. 1. 2.
Normal Rhythm
Bradycardia
tachycardia 3.

51. 4. 5.
Delayed AV Node (1st degree heart block) and missed QRS (2nd degree heart block)
Atrial fibulation
No P wave; Sa node not firing 6.

52. Pacemaker Used to correct nodes that are no longer are in rhythm.
Becomes the new heart’s pacemaker.

53. Myocardial Infarction
A Heart Attack is caused by oxygen not getting to the heart muscle usually by blockages in the coronary arteries
site of blockage

54. Stopping a Heart Attack
Breaking apart the blockage is done with:
Medication
Angioplasty
Stents
Coronary bypass surgery (CABG)
stent placement

55. Normal and Restricted Blood Circulation

56. Congestive Heart Failure (CHF)
Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs
Caused by
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts

57. Mechanical Events: The Cardiac Cycle
Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat
Systole—contraction
Diastole—relaxation

58. Phases of the Cardiac Cycle
Ventricular filling—takes place in mid-to-late diastole
AV valves are open
80% of blood passively flows into ventricles
Atrial systole occurs, delivering the remaining 20%
End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

59. Phases of the Cardiac Cycle
Ventricular systole
Atria relax and ventricles begin to contract
Rising ventricular pressure results in closing of AV valves
In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the Semilunar valves open
End systolic volume (ESV): volume of blood remaining in each ventricle

60. Phases of the Cardiac Cycle
Ventricles relax (diastole)
Decrease in pressure causes blood to flow backward
Backflow of blood in aorta and pulmonary trunk closes SL valves

61. Cardiac Cycle

62. EKG and One Cardiac Cycle

63. Cardiac Cycle & BP describes the contracting and relaxing stages of the heart.
Includes all events that occur in the heart during one complete heart beat.
Blood Pressure
Systolic pressure: (top number) measurement of the force on the arterial walls when the L ventricle contracts.
Diastolic pressure: (bottom number) measurement of the force on the arterial walls when the L ventricle is relaxed.
Normal BP = 120/80
Hypertension
Hypotension

64. Cardiac Output Volume of blood pumped by each ventricle in 1 minute.
CO = Heart rate (HR) x Stroke volume (SV)
Heart Rate (beats/minute)
Stroke Volume – volume of blood pumped out of the L. ventricle with each beat. Why Left ventricle?
SV = EDV(end diastolic volume) – ESV (end systolic volume)
Stroke volume can be determined by subtracting systolic BP volume from diastolic BP volume
Stroke volume/pulse pressure = SBP – DBP

65. Cardiac Output in a normal adult is 4.5 – 5 Liters of blood per minute
At rest: CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat) = 5.25 L/min
Varies with body’s demands
Change in HR or force of contraction
Cardiac Reserve – the heart’s ability to push cardiac output above normal limits
difference between resting and maximal CO
Healthier hearts can have a large increase in C.R.
Athlete 7X C.O. = 35L/minute
Nonathlete 4X C.O. = 20L/minute

66. Factors that Influence Heart Rate
Age
Gender
Exercise
Body temperature

67. Regulation of Stroke Volume
Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV
Factors which increase contractility
Increased Ca2+ influx due to sympathetic stimulation
Hormones (thyroxine and epinephrine)
Factors which decrease contractility
Increased extracellular K+
Calcium channel blockers

68. Factors that Control Cardiac Output
Blood volume reflexes
Autonomic Nervous System with assistance from neurotransmitters and hormones
Norepinephrine
Acethylcholine
Thyroxine
Ions
Temperature

69. Blood Volume Reflexes Frank Starling Law of the Heart
Stroke volume is controlled by Preload - the degree to which cardiac muscles are stretched just before they contract.
“More blood in = More blood out”
Increase in stretch is caused by an Increase in the venous return to the right atrium which causes the walls of the right atrium to stretch.
Increase in stretch causes SA node to depolarize faster; increasing HR
Increase in stretch also increases force of contraction; Stroke volume
At rest heart walls are not overstretched; ventricles don’t need forceful contractions

70. Autonomic Nervous System
Controlled by Medulla oblongata
Parasympathetic (Resting and Digesting)
Stimulates Vagus nerve (CN X) – decreases SV and HR; decreasing CO
Acetylcholine – decreases HR and SV; opposite action on cardiac muscle then on skeletal muscle (stimulates)
Sympathetic (Fight or Flight) – prepares the body for stress
Secretes Norephinephrine and epinephrine – increases HR and SV; increasing CO
Increasing HR causes overstretch (Frank S. law)
Beta blockers-

71. Dorsal motor nucleus of vagus The vagus nerve (parasympathetic)
decreases heart rate.
Cardioinhibitory center
Medulla oblongata
Cardio-
acceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15

72. Hypercalcemia
Excess Ca ions in muscle cell
Extended state of contraction; fatal
Hypocalcemia
Low Ca levels; results in no/weak contractions
Hyperkalemia
High levels of K
Interferes with depolarization of SA and AV nodes
Results in heart block
Increase in Na
Blocks Ca
No Ca; no T&T moving out of way
No/weak contractions

73. Temp > 98.6°F
Increases HR and SV
Increase CO
Temperature < 95° F
Slows depolarization
Slows contraction
Decrease CO

74. Exercise (by skeletal muscle and respiratory pumps; see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Exercise,
fright, anxiety
Venous
return
Sympathetic
activity
Parasympathetic
activity
Contractility
EDV
(preload)
ESV
Stroke
volume
Heart
rate
Cardiac
output
Initial stimulus
Physiological response
Result
Figure 18.22