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HEART Part 2 Instructor Terry Wiseth A&P. 2 HEART CONDUCTION Throughout the heart are clumps of specialized cardiac muscle tissue whose fibers contain.

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Presentation on theme: "HEART Part 2 Instructor Terry Wiseth A&P. 2 HEART CONDUCTION Throughout the heart are clumps of specialized cardiac muscle tissue whose fibers contain."— Presentation transcript:

1 HEART Part 2 Instructor Terry Wiseth A&P

2 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 3 HEART CONDUCTION intrinsic ability to generate and conduct nerve impulses conducts impulse for proper contraction sequence of heart

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

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

6 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 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 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 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 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 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 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 15 ATRIOVENTRICULAR NODE damaged AV node  ventricles contract intrinsically slower  may require an artificial pacemaker

16 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 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 18 PURKINJE FIBERS conduction system fibers which form a rapid conduction network within the myocardium located at the ends of the bundle branches

19 19 PURKINJE FIBERS responsible for propagating the depolarization wave to all cardiac muscle cells QRS Complex 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 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 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 26 CARDIAC RHYTHM normal resting  beats/min Systole  Contraction Diastole  Expansion

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

28 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 29 VENTRICULAR SYSTOLE semilunar valves forced open

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

31 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 32 HEART SOUNDS closing of valves causes vibrations in heart wall “lubb-dupp” sound of heartbeat  “lubb” S 1  lower, louder  closing of AV valves  start of ventricular systole  “dupp” S 2  softer, sharper  closing of semilunar valves  end of ventricular systole

33 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

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

37 37 QRS COMPLEX Firing of SA node ventricular systole

38 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 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 41 READING EKG Important to note the size of the deflection waves at certain time intervals

42 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 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 44 ENLARGED Q-WAVES AND R-WAVES Enlarged R wave generally indicates enlarged ventricles Enlarged Q-wave may indicate a myocardial infarction

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

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

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

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

49 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 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 S 1 phase is indicated by the QRS complex

51 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 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 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 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 S 2

55 CARDIAC CYCLE

56 56 VOLUME CHANGES Ventricles pump as much blood as they receive both ventricles eject the same volume of blood  ESV (leftover) 60 ml  atrial diastole +30 ml  atrial systole +40 ml  total EDV 130 ml  stroke volume -70 ml  ESV 60 ml

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

58 58 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 VOLUME CHANGES

59 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 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 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 62 CARDIAC OUTPUT volume pumped by each ventricle per minute 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 63 CARDIAC OUTPUT Cardiac output and peripheral resistance determine blood pressure  Healthy young adult  120 mm Hg/ 80 mm Hg

64 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 65 STROKE VOLUME Governed by three factors  1) pre-load  2) contractility  3) after-load

66 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 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 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 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 71 MYOCARDIAL INFARCTION

72 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 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 74 MYOCARDIAL INFARCTION Myocardial infarction necrotic tissue

75 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 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 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 78 CARDIAC ARREST A cessation of cardiac output ventricles may be motionless or in fibrillation

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

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

81 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 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 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

87 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 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

91 91 BACTERIAL INFECTION Endocarditis 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 92 BACTERIAL INFECTION patient with infective endocarditis and blood culture positive for Staphylococcus aureus small linear subungual splinter hemorrhage

93 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 FEET HEAD RED BLOOD TO BODY BLUE BLOOD TO PUMP

98 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 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

100 100 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

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

103 103 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

106 106 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

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

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

109 109 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

111 111 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

113 113 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


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