1. Instructor Terry Wiseth
HEART Part 2
A&P
Instructor Terry Wiseth

2. HEART CONDUCTION
Throughout the heart are clumps of specialized cardiac muscle tissue whose fibers contain only a few myofibrils
Initiate and distribute cardiac impulses throughout the myocardium

3. HEART CONDUCTION
intrinsic ability to generate and conduct nerve impulses
conducts impulse for proper contraction sequence of heart

4. HEART CONDUCTION
intrinsic ability to generate and conduct nerve impulses
conducts impulse for proper contraction sequence of heart

5. HEART CONDUCTION
intrinsic ability to generate and conduct nerve impulses
conducts impulse for proper contraction sequence of heart

6. SINOATRIAL NODE
Cell area located on the posterior part of the right atrial wall, adjacent to the junction of the superior vena cava and the right atrium
“Pacemaker”
signals atria to contract

7. SINOATRIAL NODE
depolarization of the SA node is the first step of the cardiac cycle
does not produce enough energy to be recorded by the EEG
cells in the SA node transmit impulses six times faster than do ordinary cell-to-cell interconnections

8. SINOATRIAL NODE The SA node sets the heart rate at 95 beats per minute
60 beats per minute is intrinsic to the atria alone
beats per minute is intrinsic to the ventricles alone

9. HEART CONDUCTION

10. SINOATRIAL NODE
Acetycholine released by parasympathetic system of ANS slows SA node to 72 beats per minute
Other hormones affect heart rate by influencing SA node

11. ECTOPIC PACEMAKER
Site other than SA node develops an abnormal self-excitability
Produces extra beats
Irregularly pace the heart for short periods of time
Nicotine and caffeine can trigger these events

12. ATRIOVENTRICULAR NODE
made up of another cluster of specialized cardiac conduction system cells
forms a pathway for impulse conduction that bridges between the atria and ventricles
delays impulse for atria to finish contraction

13. HEART CONDUCTION

14. ATRIOVENTRICULAR NODE
Depolarization of the AV node is relatively slow due to the intrinsic characteristics of its cells
This causes a delay in the transmission of the depolarization wave to the ventricles
transmission of the wave through the AV node is relatively weak
considered silent on the electrocardiogram

15. ATRIOVENTRICULAR NODE
damaged AV node
ventricles contract intrinsically slower
may require an artificial pacemaker

16. BUNDLE OF HIS a compact tract of cardiac conduction system fibers
also called the AV bundle
route for signals to leave the AV node

17. BUNDLE OF HIS tract down the interventricular septum
The right and left branches spread the electrical impulse to the right and left ventricles

18. PURKINJE FIBERS
conduction system fibers which form a rapid conduction network within the myocardium
located at the ends of the bundle branches

19. PURKINJE FIBERS
responsible for propagating the depolarization wave to all cardiac muscle cells
The QRS Complex of the electrocardiogram represents the ventricular depolarization of contraction

20. HEART CONDUCTION

21. CONDUCTION
SA node
AV node
bundle of His
Purkinje fibers

22. CONDUCTION Contraction begins at the heart apex and progresses upwards
milking action of ventricular contraction and the spiral arrangement of the ventricular muscle fibers twist and wring out the blood

23. HEART CONDUCTION

24. CONTROL OF CONTRACTION
brain is able to affect heart rate via
1) parasympathetic nerve impulses
heart-slowing
2) sympathetic nerve impulses
increase heart rate

25. CONTROL OF CONTRACTION
Click to View Baroreceptor control of heart rate

26. CARDIAC RHYTHM Systole Diastole normal resting 70-80 beats/min
Contraction
Diastole
Expansion

27. VENTRICULAR DIASTOLE
during ventricular diastole cusps hang loosely into ventricular chamber

28. VENTRICULAR SYSTOLE
during (at start of ) ventricular systole the resulting increased blood pressure developing in the ventricle forces the flaps up together shutting the AV valves

29. VENTRICULAR SYSTOLE
semilunar valves forced open

30. VENTRICULAR DIASTOLE
semilunar valves closed from back flow pressure of aortic and pulmonary trunks

31. HEART SOUNDS
Lubb - dupp sounds are due to vibrations in the heart tissues
created as the blood flow is suddenly increased or slowed with the contraction and relaxation of the heart chambers
created with the opening and closing of the valves

32. HEART SOUNDS closing of valves causes vibrations in heart wall
“lubb-dupp” sound of heartbeat
“lubb” S1
lower, louder
closing of AV valves
start of ventricular systole
“dupp” S2
softer, sharper
closing of semilunar valves
end of ventricular systole

33. ELECTROCARDIGRAM Comprehensive image of the hearts electrical activity
supplies a composite recording of all action potentials produced by nodal and muscle cells
three principle deflections
P wave
QRS complex
T wave

34. EKG COMPONENTS

35. EKG COMPONENTS

36. P WAVE Signal from the SA node spreads through the atria
atrial systole

37. QRS COMPLEX
Firing of SA node
ventricular systole

38. S-T SEGMENT
Following ventricular contraction and the QRS complex is a brief period of low electrical activity
On the electrocardiogram this appears as the S-T segment

39. T WAVE
Ventricular repolarization is represented by the T-wave on the electrocardiogram
The T-wave deflection is also in the same direction of the largest deflection of the QRS complex

40. EKG SUMMARY
depolarization
repolarization

41. READING EKG
Important to note the size of the deflection waves at certain time intervals

42. ENLARGEMENT OF P-WAVE Indicates enlargement of the atria
atrial stenosis
mitral valve narrows
blood backs into the left atrium and there is an expansion of the atrial wall

43. LENGTHENED P-R INTERVAL
Occurs because the heart tissue, covered by the P-Q interval, namely the atria and A-V node is scarred or inflamed
Impulse, as a result, travels at a slower rate and the interval is lengthened
Atherosclerotic disease
Rheumatic fever

44. ENLARGED Q-WAVES AND R-WAVES
Enlarged R wave generally indicates enlarged ventricles
Enlarged Q-wave may indicate a myocardial infarction

45. S-T SEGMENT Elevated S-T segment acute myocardial infarction
Depressed S-T segment
heart muscle receives insufficient oxygen

46. T-WAVE Flat when the heart muscle is receiving insufficient oxygen
May be elevated during hyperkalemia
High levels of potassium in bloodstream

47. CARDIAC CYCLE 1) Ventricular filling 2) Atrial systole
3) Isovolumetric ventricular contraction
4) Rapid ventricular ejection
5) Isovolumetric ventricular relaxation

48. 1) VENTRICULAR FILLING AV valves open due to low ventricular pressure
blood passively enters the ventricles
P wave starts

49. 2) ATRIAL SYSTOLE SA node fires
contraction of the atrium stops the pulmonary venous and systemic inflow
atrial contraction completes the filling of the ventricles
pressure in the ventricles increases closing the AV valves
phase is indicated by the P wave

50. 3) ISOVOLUMETRIC CONTRACTION
ventricular contraction causes the pressure to rise in the ventricles
AV valves close
blood is not ejected from the ventricles
atria relax
heart sound S1
phase is indicated by the QRS complex

51. 4) VENTRICULAR EJECTION
the pressure in the ventricles exceed the pulmonary and systemic pressures causing the semilunar valves to open
ventricle continues to contract rapidly ejecting blood to the aorta and pulmonary trunk

52. 4) VENTRICULAR EJECTION
Ventricle contains 130 ml blood
EDV (End Diastolic Volume)
ventricles eject 54% (ejection fraction) of the EDV during contraction
blood remaining behind is called ESV (End Systolic Volume)
during rigorous exercise 90% may be ejected
ejection fraction is an important measure of cardiac health

53. 5) ISOVOLUMETRIC RELAXATION
Ventricles expand causing pressure to drop
semilunar valves close as the ventricular pressure falls below the systemic and pulmonary diastolic level

54. 5) ISOVOLUMETRIC RELAXATION
ventricular pressures continue to fall until it is slightly below atrial pressure
AV valves open
blood begins to fill the ventricles
phase is indicated by the T wave
heart sound S2

55. CARDIAC CYCLE

56. VOLUME CHANGES Ventricles pump as much blood as they receive
both ventricles eject the same volume of blood
ESV (leftover) ml
atrial diastole ml
atrial systole ml
total EDV ml
stroke volume ml
ESV ml

57. VOLUME CHANGES If RV pumped more than LV could handle on return
causes hypertension and edema in the lungs
fluid swells the lungs impairing gas exchange

58. VOLUME CHANGES If LV pumped more blood than RV can handle on return
results in hypertension and edema in the body
can lead to aneurysms, stroke, kidney failure, heart failure

59. CONGESTIVE HEART FAILURE
Failure of either ventricle to eject blood effectively
can be caused by:
1) myocardial infarcted weakened heart muscle
2) chronic hypertension
3) valvular insufficiency
4) congenital defects

60. CONGESTIVE HEART FAILURE
Left ventricle failure
pulmonary edema
shortness of breath
sense of suffocation
Right ventricle failure
systemic edema
enlargement of liver
swelling of fingers, ankles, feet

61. CONGESTIVE HEART FAILURE
Left ventricle failure
pulmonary edema
shortness of breath
sense of suffocation
Right ventricle failure
systemic edema
enlargement of liver
swelling of fingers, ankles, feet

62. CARDIAC OUTPUT volume pumped by each ventricle per minute HR = 75 bpm
CO = Heart Rate (HR) X Stroke Volume (SV)
HR = 75 bpm
SV = 70 ml/beat
CO = 75 X 70 = 5,250 ml/min = 5.25 L/min
total volume of blood is 4-6 L
thus entire volume of body’s blood is pumped through each minute
vigorous exercise increases CO up to 21 L/min

63. CARDIAC OUTPUT
Cardiac output and peripheral resistance determine blood pressure
Healthy young adult
120 mm Hg/ 80 mm Hg

64. HEART RATE Normal 72 bpm Tachycardia rate above 100 bpm
stress, anxiety, drugs, disease, elevated body temperature
Bradycardia
HR below 60 bpm
sleep, well trained athlete, low body temperature

65. STROKE VOLUME Governed by three factors 1) pre-load 2) contractility
3) after-load

66. PRE-LOAD Determined by volume of blood in ventricles
stretched myocardial muscle is able to contract more forcefully
thus expel more blood and increasing CO

67. CONTRACTILITY
Refers to the strength of contraction for a given pre-load
measures myocyte receptivity to stimulation
solutions of glucagon and calcium chloride are standard emergency treatment for heart attacks
digitalis acts as a cardiac stimulant to treat congestive heart failure
barbiturates are negative agents which reduce myocyte response to stimulation

68. AFTER-LOAD Blood pressure in arteries outside the semilunar valve
opposes the opening of semilunar valves
increased after-load reduces the stroke volume

69. AFTER-LOAD
arterial circulation impediments increase after-load
scar tissue (lung diseases)
emphysema, chronic bronchitis
cor pulmonale
RV failure due to obstructed pulmonary circulation
Emphysema

70. HEART ABORMALITIES Cardiomyopathy
The myocardium functions poorly and the heart is large and dilated

71. MYOCARDIAL INFARCTION

72. MYOCARDIAL INFARCTION
MI ,“heart attack”
Within the lumen of the coronary can be seen a dark red recent coronary thrombosis
The dull red color to the myocardium to the lower right of the thrombus is consistent with underlying myocardial infarction

73. MYOCARDIAL INFARCTION
left ventricular wall sectioned lengthwise to reveal a recent myocardial infarction
The center of the infarct contains necrotic muscle that appears yellow-tan
Remaining viable myocardium is reddish- brown

74. MYOCARDIAL INFARCTION
Myocardial infarction necrotic tissue

75. MYOCARDIAL INFARCTION
histological acute myocardial infarction
contraction band necrosis
myocardial fibers are beginning to lose cross striations
nuclei are not clearly visible
many irregular darker pink wavy contraction bands extending across the fibers

76. ATRIAL FLUTTER Cells in the atria set off extra contractions
the atria beats beats per minute
early firing can cause premature ventricular contractions (PVCs)
often due to irritation of the heart by stimulants, emotional stress, or lack of sleep
can lead to ventricular fibrillation

77. VENTRICULAR FIBRILLATION
An arrhythmia caused by electrical signals arriving at different regions of the myocardium at widely different times
squirming, uncoordinated contractions “bag of worms”
no pumping of blood
ischemia rapidly follows

78. CARDIAC ARREST A cessation of cardiac output
ventricles may be motionless or in fibrillation

79. DEFIBRILLATION
Heart is given a strong electric shock with a pair of electrodes

80. Defibrillation shocks
Depolarizes the entire myocardium and stops the fibrillation
hope that the SA node will resume in sinus rhythm
Atrial fibrillation
Normal sinus rhythm
Defibrillation shocks

81. PACEMAKER
A pacing system stimulates the heart muscle with precisely timed discharges of electricity
cause the heart to beat in a manner very similar to a naturally occurring heart rhythm

82. PACEMAKER
The pacemaker sends tiny electrical impulses to start a heartbeat
The electrode is designed to relay information (sense) about your heart's own electrical activity to the pacemaker and to deliver electrical impulses (paces) only when the heart needs them

83. PACEMAKER

84. DYNAMIC CARDIOMYOPLASTY
involves harvesting the the Latissimus Dorsi
the muscle is wrapped around the surface of the heart
the nerve to the muscle is stimulated (with a specialized pacemaker device) allowing the muscle to contract
improves the ejection of blood from the heart
lessens the symptoms of heart failure

85. DYNAMIC CARDIOMYOPLASTY

86. DYNAMIC CARDIOMYOPLASTY

87. HYPERTENSION
The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years
hypertension creates a greater pressure load on the heart to induce the hypertrophy

88. AORTIC TEAR
a sudden deceleration injury in a vehicular accident can produce a tear in the aorta
tear is just distal to the great vessels
the tear leads to sudden loss of blood and shock
It is widely believed that Princess Diana died from an aortic tear brought on by a sudden deceleration

89. AORTIC TEAR

90. AORTIC TEAR

91. BACTERIAL INFECTION Endocarditis
blue bacterial colonies on the lower left
extending into the pink connective tissue of the valve
valves are relatively avascular
high dose antibiotic therapy is needed to eradicate the infection

92. BACTERIAL INFECTION
patient with infective endocarditis and blood culture positive for Staphylococcus aureus
small linear subungual splinter hemorrhage

93. HEART TUMOR heart of a two year old child who died suddenly
at autopsy, a large firm, white tumor mass was found filling much of the left ventricle
tumors of the heart are rare

94. HEART TUMOR

95. PULMONARY THROMBOEMBOLUS
Blood clots formed elsewhere in the body can dislodge and move through the larger blood vessels and heart and become lodged in the smaller pulmonary circuit blood vessels causing a blockage or bursting of the blood vessel

96. HEART LUNG MACHINE

97. HEART LUNG MACHINE
FEET
BLUE BLOOD TO PUMP
RED BLOOD TO BODY
HEAD

98. ATRIAL SEPTAL DEFECT
A defect involving both the atrial and the ventricular septums allows blood to pass freely between the two ventricles and the atriums

99. ATRIAL SEPTAL DEFECT
The valve apparatus at the junction between atriums and ventricles is "shared"
effectively only one valve instead of the normal two
Blood flow and pressure in the lung circulation is substantially increased

100. ATRIAL SEPTAL DEFECT often results in early onset of symptoms with:
breathlessness
poor feeding
slow weight gain
defect is very common in babies with Down syndrome

101. VENTRICULAR SEPTAL DEFECT

102. FOSSA OVALIS depression in interatrial septum
opening which exists in fetal heart
foramen ovale
RA RV

103. HEART CHANGES AT BIRTH At birth, the first breath inflates the lungs
lowers the resistance to blood flow
thus increases the volume of blood flowing through them
thereby increasing the amount of blood returning from the pulmonary trunk to the heart
all of which results in increased pressure in the left atrium

104. FETAL CIRCULATION

105. FETAL CIRCULATION

106. HEART CHANGES AT BIRTH increased pressure in the left atrium
forces the flap covering the foramen ovale against the interatrial septum
blocking off communication between the right and left atrium

107. HEART CHANGES AT BIRTH closure of the ductus arteriosus
takes place almost immediately after birth
due to muscular contraction
mediated by, bradykinin
released from the lungs after the newborn's first breath

108. HEART CHANGES AT BIRTH
In some instances, the ductus arteriosus does not obliterate within the first few days leaving a left to right shunt

109. HEART CHANGES AT BIRTH
There are two shortcuts; normally, both of them close up at birth or shortly thereafter
ductus arteriosus
a small blood vessel connecting the pulmonary artery and aorta
foramen ovale
a small hole between the left and right atria

110. DUCTUS ARTERIOSUS BEFORE AND AFTER

111. HEART CHANGES AT BIRTH
Openings and blood vessels close at birth and if they do not two conditions may result:
Patent Ductus Arteriosus (PDA)
Patent Foramen Ovale (PFO)

112. PATENT DUCTUS ARTERIOSUS

113. HEART CHANGES AT BIRTH Either of these conditions can cause fatigue
difficult or rapid breathing
failure to grow normally
chronic respiratory infections
Large openings can lead to heart failure and death

114. DUCTUS ARTERIOSUS REPAIR

115. END HEART Part 2