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Function of the heart Chapter 17 1. Cardiac Cycle Sequence of events that occurs during one heartbeat Coordinated contraction and relaxation of the chambers.

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Presentation on theme: "Function of the heart Chapter 17 1. Cardiac Cycle Sequence of events that occurs during one heartbeat Coordinated contraction and relaxation of the chambers."— Presentation transcript:

1 Function of the heart Chapter 17 1

2 Cardiac Cycle Sequence of events that occurs during one heartbeat Coordinated contraction and relaxation of the chambers of the heart Systole- contraction of myocardium Diastole- relaxation of myocardium 2

3 Systole & Diastole Systole –Contraction of heart muscle forces blood out of the chamber Diastole –Relaxation of heart muscle allows the chamber to fill with blood Atrial and ventricular activity are closely coordinated: atrial systole = ventricular diastole 3

4 Three Stages of Cardiac Cycle Atrial Systole –Atria contract; pump blood into ventricles –AV valves open, ventricles relaxed Ventricular Systole Ventricles contract; pushes AV valves closed; pushes semilunar valves open Blood pumped to pulmonary artery & aorta 4

5 Three Stages of Cardiac Cycle Diastole –Brief time when both atria and ventricles are relaxed –Blood flows into atria; some blood flows passively into ventricles –Diastole is a “filling” period Cycle repeats itself starting with atrial contraction again 5

6 6

7 Position of valves during systole & diastole 7

8 Which of the following occurs during ventricular diastole? 1.The ventricles fill with blood. 2.The atrioventricular valves close. 3.The ventricles pump blood into the great vessels. 4.The semilunar valves open. 8

9 Cardiac Cycle Cardiac cycle is repeated with every heartbeat; if heart rate is 70 bpm, then cardiac cycle lasts approx. 0.8 sec; diastole lasts approx. 0.4 sec If heart rate increases, diastole shortens- can impact cardiac function. How? Decreased filling time reduces the amount of blood that enters the ventricles; and coronary blood flow occurs during diastole 9

10 Autonomic Control of the Heart If cardiac cells can initiate cardiac impulses, why are autonomic nerves needed? Affect the rate at which cardiac impulses are fired Affects how fast the impulses travel through the heart Affects how forcefully the heart contracts 10

11 ANS The autonomic nervous system allows the heart to respond to increased oxygen demand by increasing the rate and force of cardiac contraction. 11

12 Autonomic Wiring Sympathetic –Supply the SA node, AV node and ventricular myocardium Parasympathetic –Vagus nerve –SA node and AV node (does not innervate the ventricles) 12

13 Autonomic Firing Sympathetic stimulation –Increases SA node activity ( HR) –Increases speed of impulse (from SA node to His-Purkinje) –Increases strength of contraction 13

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15 Important points to remember Excessive sympathetic activity leads to “fight or flight” response (panic causes racing and pounding heart) May be involved in certain illnesses- shock, heart failure (need to treat with drugs that reduce excessive sympathetic firing) 15

16 Important points to remember Causes tachydysrhythmias Nurses often give drugs that mimic or block sympathetic activity –Drugs that mimic sympathetic activity increase HR and force of contraction (epinepherine & dopamine); called sympathomimetic drugs –Drugs that inhibit SNS effects are called sympatholytic drugs (clonidine) 16

17 Autonomic Firing Paraympathetic stimulation –Decreases SA node activity ( HR) –Decreases the speed of cardiac impulses from SA to AV node –Does not affect strength of myocardial contraction (no innervation of ventricles) 17

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19 Important points to remember Parasympathetic effects are exerted by the vagus nerve In the resting heart, the vagus nerves slows the firing of the SA node (SA node wants to fire at 90 bpm, vagus nerve keeps it around 70) Excessive vagal discharge can be caused by different things, including certain drugs(digoxin) and conditions (MI) 19

20 Important points to remember Excessive vagal discharge causes bradycardia (<60 bpm); it also increases the likelyhood of lethal dysrhythmias Vagal stimulation can also slow conduction through the heart, leading to potentially lethal heart blocks 20

21 Important points to remember Drugs that mimic the effects of vagal activity (slow HR or conduction) are called vagomimetic (or, parasympathomimetic) drugs (digoxin) Drugs that inhibit vagal discharge (like atropine) are called vagolytic (or, parasympatholytic) drugs 21

22 Cardiac Output Cardiac output is the amount of blood pumped by each ventricle each minute Normal cardiac output is 5 liters per minute (an average adults entire blood volume) Cardiac output is determined by heart rate and stroke volume CO = HR x SV 22

23 Heart Rate The number of times the heart beats in one minute (avg 72 bpm for adult) Resting HRs differ because of size, age and gender –Larger size- slower HR –Women tend to have faster HR than men –Age- generally, younger hearts beat faster (fetal HR avgerages 140’s) 23

24 Heart Rate Other factors that affect HR –Exercise- increases HR (response to increased oxygen demand) –Stimulation of ANS (sympathetic stim causes increased HR, parasympathetic (vagus) stim causes decreased HR –Hormone secretion- epi, norepi and thyroid hormones increase HR 24

25 Heart Rate Pathology- certain diseases or conditions can affect HR (sick sinus syndrome, MI, fever) Medications- many drugs can affect the heart rate (digoxin, epi/ norepi, caffeine); important to know effects of drugs and the patients HR before giving them 25

26 Stroke Volume The amount of blood pumped by the ventricles per beat Average is ml per beat Normally, ventricles pump out about 65% of the blood they contain; if force of contraction is increased, more blood will be forced out 26

27 Changing Stroke Volume Stroke volume can be changed though Starling’s Law or through an inotropic effect (strength of contraction) 27

28 Starling’s Law Depends on the degree of stretch of the myocardial fibers Greater the stretch, greater the force of contraction If more blood enters the ventricle, the fibers are stretched more, the ventricle contracts more forcefully (conversely, less blood = less stretch, decreased force of contraction) So, stroke volume can be increased by increasing venous return to the heart 28

29 Starling’s Law 29

30 An increase in end diastolic volume 1.elicits Starling’s law of the heart. 2.decreases stroke volume. 3.decreases cardiac output. 4.All of the above 30

31 Inotropic Effect Increasing the force of myocardial contraction without stretching the myocardial fibers; called (+) inotropic effect Stimulation of the heart by sympathetic nerves causes +inotropic effect; epi and digoxin are +inotropes (-)Inotropic effects decrease the force of contraction (excessive depression can lead to heart failure) 31

32 Cardiac Output Since cardiac output is determined by heart rate and stroke volume, changing one or both can affect output Cardiac reserve refers to the capacity to increase cardiac output above normal resting state Diseased hearts often have little reserve, so the person may become easily tired with minimal exertion 32

33 Clinical Terminology Special vocabulary related to the heart 33

34 End Diastolic Volume The amount of blood in the ventricle at the end of diastole (resting phase) Determines the amount of stretch in the muscle fibers; basis for Starling’s Law 34

35 Preload Same as EDV; amount of blood in the ventricles after diastole; increased preload stretches the ventricles, causing stronger force of contraction (which increases stroke volume, and therefore cardiac output) Drugs can affect preload- dilate veins to decrease preload, constrict veins to increase preload 35

36 Ejection Fraction Remember ventricles pump about 65-67% of their volume; this is referred to as the ejection fraction Indicated cardiac health- a healthy heart can increase EF to 90% with exercise; diseased or weakened heart are much lower, may be less than 30% 36

37 Afterload Refers to resistance against blood as it is pumped out of the heart From the LV, blood must push against blood already in the aorta; increased resistance (stenosis, high pressure) causes the heart to work harder Continued increased resistance (hypertension, especially) can cause LV hypertrophy 37

38 Afterload Afterload in the right ventricle is determined by the pulmonary artery; high pressure can be caused by chronic lung diseases (asthma, emphysema) RV hypertrophy and increased pulmonary artery pressure is referred to as cor pulmonale (often causes RV failure) 38

39 Afterload Drugs can alter afterload by relaxing or dilating blood vessels in the periphery; decreases workload of the heart Drugs that constrict blood vessels will increase afterload and increase the workload of the heart 39

40 40

41 Which of the following is most related to preload? 1.Blood pH 2.End-diastolic volume 3.Cyanosis 4.Coronary blood flow 41

42 Inotropic Effect Refers to change in myocardial contraction not due to stretching of fibers + inotrope increases contractile force - inotrope decreases contractile force Sympathetic nerve stimulation causes a positive inotropic effect 42

43 Chronotropic Effect Refers to a change in heart rate + chronotropic effect increases HR - chronotropic effect decreases HR Sympathetic nerve stimulation causes a + chronotropic effect Parasympathetic (vagal) stimulation causes a – chronotropic effect 43

44 Dromotropic Effect Refers to a change in the speed at which the cardiac impulse travels through the conduction system + dromotropic effect increases speed of conduction - dromotropic effect decreases speed of conduction Pronounced (-) dromotropic effects may lead to heart block 44

45 A (+) inotropic effect increases cardiac output because it 1.decreases afterload. 2.increases stroke volume. 3.intensifies vagal discharge. 4.expands blood volume. 45

46 Autonomic Receptors 46

47 Beta 1 adrenergic receptors The adrenergic neurotransmitter is norepinepherine (NE) The cardiac receptors for NE are beta 1 - adrenergic receptors Activation of beta 1 receptors cause –+chronotropic effects –+dromotropic effects –+inotropic effects 47

48 Beta 1 adrenergic receptors Drugs that activate beta 1 -adrenergic receptors increase HR, stroke volume and overall cardiac output These drugs are called beta 1 -adrenergic agonists (or simply “beta agonists”) Include dopamine and epinephrine Note: beta 1 receptor activation is the same as a sympathomimetic effect 48

49 Beta 1 Receptor Blockade Blockade of the beta 1 -adrenergic receptors prevents receptor activation People taking beta 1 -adrenergic blockers (or, “beta blockers”) will not increase their heart rate when sympathetic nerves fire (stress or exercise) 49

50 Beta 1 Receptor Blockade May be administered to tachycardic patients or patients having an MI; reduces HR and force of contraction… reduces workload of heart and therefore oxygen demand of the heart Beta 1 -adrenergic blockade is the same as a sympatholytic effect 50

51 Cholinergic (muscarinic) Receptors The cholinergic neurotransmitter is acetylcholine (ACh) (vagus nerve) The cardiac cholinergic receptors are called muscarinic receptors Activation of muscarinic receptors causes –(-)chronotropic effect –(-) dromotropic effect –No inotropic effect (vagus does not innervate ventricles) –Same as parasympathomimetic effect 51

52 Cholinergic (muscarinic) Blockade Muscarinic/ cholinergic blockers act by blocking the effects of ACh at the muscarinic receptors Therefore, HR and speed of conduction is increased (atropine) Muscarinic (cholinergic)-receptor blockade is the same as parasympatholytic effect 52

53 Tricky terminology… Muscarinic agonist = cholinergic agonist Muscarinic blocker = antimuscarinic agent = cholinergic blocker = anticholinergic agent Beta 1 receptor activation = sympathomimetic effect Beta 1 -adrenergic blockade = sympatholytic effect 53

54 Tricky terminology… Muscarinic (cholinergic) receptor activation = parasympathomimetic effect Muscarinic (cholinergic) receptor blockade = parasympatholytic effect 54

55 Which of the following is least apt to slow heart rate? 1.Activation of the muscarinic receptors 2.Firing of the vagus nerve 3.A sympathomimetic effect 4.Binding of ACh to its receptor on the SA node 55

56 The Failing Heart When the heart can’t pump 56

57 The heart as a double pump… Remember the heart functions as two pumps The right side of the heart pumps blood to the lungs for oxygenation The left side of the heart pumps blood to the aorta and to the systemic circulation 57

58 Left-Heart Failure Two main components –Blood backs up in the lungs –Insufficient amount of blood is pumped out to the systemic circulation Can be described in terms of forward failure of backward failure 58

59 Backward Failure Blood backs up in structures behind the left ventricle- left atrium, pulmonary veins and pulmonary capillaries Increased pressure in the pulmonary capillaries forces fluid into the lungs Called pulmonary edema Fluid in the lungs impairs the lungs’ ability to oxygenate blood 59

60 Backward Failure Pulmonary Edema –Signs & symptoms (S&S) include: exertional dyspnea (-pnea means breathing) –Cyanosis –Blood tinged sputum and cough –Orthopnea (pillows?) –Tachycardia and restlessness 60

61 Backward Failure Most symptoms are respiratory Treatment includes: –+inotropic agent (increase force of myocardial contraction to push excess blood out) –Nitroglycerine (NTG) (decreases preload) –Oxygen (increase oxygenation) –Morphine (decrease workload, anxiety) –Upright position (ease work of breathing) –Diuretic (relieve edema) 61

62 62

63 Left-sided heart failure 63

64 Forward Failure The damaged ventricle cannot pump adequate blood to the systemic circulation S&S include: –kidneys filter less water and reabsorb excess salt and water, increases blood volume and edema –Decreased cardiac output stimulates sympathetic activity- temporarily improves C.O. but eventually the heart wears out 64

65 Left-Heart Failure Commonly caused by myocardial infarction and chronic, uncontrolled hypertension (HTN) In MI, if the damaged tissue is in the left ventricle, the heart may fail as a pump (LAD- the “widow maker”) In HTN, the LV has to continuously pump against resistance- LV hypertrophies and eventually fails 65

66 Right-Heart Failure Blood backs up in the veins that return blood to the heart Superior vena cava receives blood from the jugular veins; congestion in the jugular veins is known as jugular vein distention (JVD) Blood also backs up into major viscera, causing enlargement- hepatomegaly and splenomegaly (-megaly means enlargement) 66

67 Right-Heart Failure Edema also found in the feet and ankles- pedal edema; pitting edema is severe edema that will indent when pressed Right-heart failure is usually a result of left heart failure; can also be caused by chronic lung disease (emphysema) 67

68 Marked pitting edema of leg (arrow) as a result of chronic heart failure. 68

69 69

70 Right-sided heart failure 70

71 Treatment of Heart Failure Goals of treatment –Strengthen myocardial contraction –Remove excess edema –Decrease workload of heart –Protect the heart from excess sympathetic activity 71

72 NCLEX Question After an anterior wall myocardial infarction (MI), which problem is indicated by auscultation of crackles in the lungs? 1.left sided heart failure 2.right sided heart failure 3.pulmonic valve dysfunction 4.tricuspid valve malformation 72

73 Rationale 1. Anterior wall MIs usually cause extensive damage to the left ventricle, resulting in left sided heart failure. The symptoms of left sided failure are predominantly pulmonary in nature- usually resulting in pulmonary edema 73

74 NCLEX Question Which drug class protects the ischemic myocardium by decreasing catecholamines and sympathetic nerve stimulation? 1.opiods 2.beta-adrenergic blockers 3.nitrates 4.calcium channel blockers 74

75 Rationale 2. Beta-adrenergic blockers work by blocking receptors activated by norepinepherine, thereby decreasing the sympathetic stimulation to the heart 75

76 NCLEX Question With which disorder is jugular vein distention (JVD) most prominent? 1.abdominal aortic aneurysm 2.anterior wall myocardial infarction 3.right sided heart failure 4.pneumothorax 76

77 Rationale 3. Right sided heart failure results in congestion of the superior vena cava, which drains the jugular veins 77

78 NCLEX Question Stool softeners would be given to a client after a myocardial infarction for which reason? 1.to stimulate the bowel because of loss of nerve innervation 2.to prevent the Valsalva maneuver, which may lead to bradycardia 3.to prevent straining, which increases intracranial pressure (ICP) 4.to prevent constipation when osmotic diuretics are used 78

79 Rationale 2. Straining to have a bowel movement may stimulate the vagus nerve, resulting in bradycardia. This can be potentially life- threatening in a patient with damage to the myocardium 79

80 NCLEX Question A nurse is collecting data from a client with left-sided heart failure. The client states that it is necessary to use three pillows under the head and chest at night to be able to breathe comfortably while sleeping. The nurse documents that the patient is experiencing: 1.orthopnea 2.dyspnea on exertion 3.dyspnea at rest 4.paroxysmal nocturnal dyspnea 80

81 Rationale 1. Left sided heart failure results in pulmonary edema. This is exacerbated by lying flat. The patient will find it easier to breath while sitting up, called orthopnea 81

82 NCLEX Question A nurse is performing a cardiovascular assessment on a client. Which of the following items should the nurse check to obtain the best information about the client’s left-sided heart function. 1.status of breath sounds 2.presence of hepatojugular reflex 3.presence of peripheral edema 4.presence of jugular vein distention 82

83 Rationale Left sided heart failure will result in pulmonary edema, so a client’s lung sounds need to be assessed frequently 83

84 THE END 84


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