NURS1004 Week 10 Lecture the Heart Part II Prepared by Didy Button.
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1 NURS1004 Week 10 Lecture the Heart Part II Prepared by Didy Button.
2 20-2 The Conducting System Heartbeat A single contraction of the heart The entire heart contracts in series First the atria Then the ventricles
3 20-2 The Conducting System Cardiac Physiology Two Types of Cardiac Muscle Cells 1. Conducting system Controls and coordinates heartbeat 2. Contractile cells Produce contractions that propel blood
4 20-2 The Conducting System The Cardiac Cycle Begins with action potential at SA node Transmitted through conducting system Produces action potentials in cardiac muscle cells (contractile cells) Electrocardiogram (ECG or EKG) Electrical events in the cardiac cycle can be recorded on an electrocardiogram
5 20-2 The Conducting System The Conducting System A system of specialized cardiac muscle cells Initiates and distributes electrical impulses that stimulate contraction Automaticity Cardiac muscle tissue contracts automatically
6 20-2 The Conducting System Structures of the Conducting System Sinoatrial (SA) node - wall of right atrium Atrioventricular (AV) node - junction between atria and ventricles Conducting cells - throughout myocardium
7 20-2 The Conducting System Conducting Cells Interconnect SA and AV nodes Distribute stimulus through myocardium In the atrium Internodal pathways In the ventricles AV bundle and the bundle branches
8 20-2 The Conducting System Prepotential Also called pacemaker potential Resting potential of conducting cells Gradually depolarizes toward threshold SA node depolarizes first, establishing heart rate ANIMATION The Heart: Conduction System
9 Figure 20-11a The Conducting System of the Heart Sinoatrial (SA) node Internodal pathways Atrioventricular (AV) node AV bundle Purkinje fibers Components of the conducting system Bundle branches
10 Figure 20-11b The Conducting System of the Heart Threshold Prepotential (spontaneous depolarization) Time (sec) Changes in the membrane potential of a pacemaker cell in the SA node that is establishing a heart rate of 72 beats per minute. Note the presence of a prepotential, a gradual spontaneous depolarization.
11 20-2 The Conducting System Heart Rate SA node generates action potentials per minute Parasympathetic stimulation slows heart rate AV node generates action potentials per minute
12 20-2 The Conducting System The Sinoatrial (SA) Node In posterior wall of right atrium Contains pacemaker cells Connected to AV node by internodal pathways Begins atrial activation (Step 1)
13 Figure Impulse Conduction through the Heart (Step 1) SA node activity and atrial activation begin. SA node Time = 0
14 20-2 The Conducting System The Atrioventricular (AV) Node In floor of right atrium Receives impulse from SA node (Step 2) Delays impulse (Step 3) Atrial contraction begins
15 Figure Impulse Conduction through the Heart (Step 2) Stimulus spreads across the atrial surfaces and reaches the AV node. AV node Elapsed time = 50 msec
16 Figure Impulse Conduction through the Heart (Step 3) There is a 100-msec delay at the AV node. Atrial contraction begins. AV bundle Elapsed time = 150 msec Bundle branches
17 20-2 The Conducting System The AV Bundle In the septum Carries impulse to left and right bundle branches Which conduct to Purkinje fibers (Step 4) And to the moderator band Which conducts to papillary muscles
18 Figure Impulse Conduction through the Heart (Step 4) The impulse travels along the interventricular septum within the AV bundle and the bundle branches to the Purkinje fibers and, via the moderator band, to the papillary muscles of the right ventricle. Moderator Elapsed time = 175 msec band
19 20-2 The Conducting System Purkinje Fibers Distribute impulse through ventricles (Step 5) Atrial contraction is completed Ventricular contraction begins
20 Figure Impulse Conduction through the Heart (Step 5) The impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium. Atrial contraction is completed, and ventricular contraction begins. Elapsed time = 225 msec Purkinje fibers
21 20-2 The Conducting System Abnormal Pacemaker Function Bradycardia - abnormally slow heart rate Tachycardia - abnormally fast heart rate Ectopic pacemaker Abnormal cells Generate high rate of action potentials Bypass conducting system Disrupt ventricular contractions
22 20-2 The Conducting System The Electrocardiogram (ECG or EKG) A recording of electrical events in the heart Obtained by electrodes at specific body locations Abnormal patterns diagnose damage
23 Figure 20-13a An Electrocardiogram Electrode placement for recording a standard ECG.
24 20-2 The Conducting System Features of an ECG P wave Atria depolarize QRS complex Ventricles depolarize T wave Ventricles repolarize
25 20-2 The Conducting System Time Intervals between ECG Waves P R interval From start of atrial depolarization To start of QRS complex Q T interval From ventricular depolarization To ventricular repolarization
26 Figure 20-13a An Electrocardiogram Electrode placement for recording a standard ECG.
27 Figure 20-13b An Electrocardiogram 800 msec R R P wave (atria depolarize) T wave (ventricles repolarize) P R segment S T segment Millivolts P R interval Q S S T interval Q T interval QRS interval (ventricles depolarize)
28 Figure Cardiac Arrhythmias Premature Atrial Contractions (PACs) P P P Paroxysmal Atrial Tachycardia (PAT) P P P P P P Atrial Fibrillation (AF)
29 Figure Cardiac Arrhythmias Premature Ventricular Contractions (PVCs) P T P T P T Ventricular Tachycardia (VT) P Ventricular Fibrillation (VF)
30 20-2 The Conducting System Refractory Period Absolute refractory period Long Cardiac muscle cells cannot respond Relative refractory period Short Response depends on degree of stimulus
31 20-2 The Conducting System The Role of Calcium Ions in Cardiac Contractions Contraction of a cardiac muscle cell Is produced by an increase in calcium ion concentration around myofibrils
32 20-2 The Conducting System The Energy for Cardiac Contractions Aerobic energy of heart From mitochondrial breakdown of fatty acids and glucose Oxygen from circulating hemoglobin Cardiac muscles store oxygen in myoglobin
33 20-3 The Cardiac Cycle The Cardiac Cycle Is the period between the start of one heartbeat and the beginning of the next Includes both contraction and relaxation
34 20-3 The Cardiac Cycle Two Phases of the Cardiac Cycle Within any one chamber 1. Systole (contraction) 2. Diastole (relaxation)
35 Figure Phases of the Cardiac Cycle Start msec msec 100 msec Cardiac cycle 370 msec
36 Start Figure 20-16a Phases of the Cardiac Cycle Atrial systole begins: Atrial contraction forces a small amount of additional blood into relaxed ventricles. 800 msec 0 msec 100 msec Cardiac cycle
37 Figure 20-16b Phases of the Cardiac Cycle Atrial systole ends, atrial diastole begins 100 msec Cardiac cycle
38 Figure 20-16c Phases of the Cardiac Cycle Cardiac cycle Ventricular systole first phase: Ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.
39 Figure 20-16d Phases of the Cardiac Cycle Cardiac cycle 370 msec Ventricular systole second phase: As ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected.
40 Figure 20-16e Phases of the Cardiac Cycle Cardiac cycle 370 msec Ventricular diastole early: As ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves and forces them closed. Blood flows into the relaxed atria.
41 Figure 20-16f Phases of the Cardiac Cycle 800 msec Ventricular diastole late: All chambers are relaxed. Ventricles fill passively. Cardiac cycle
42 Blood Pressure 20-3 The Cardiac Cycle In any chamber Rises during systole Falls during diastole Blood flows from high to low pressure Controlled by timing of contractions Directed by one-way valves
43 20-3 The Cardiac Cycle Cardiac Cycle and Heart Rate At 75 beats per minute (bpm) Cardiac cycle lasts about 800 msec When heart rate increases All phases of cardiac cycle shorten, particularly diastole
44 20-3 The Cardiac Cycle Phases of the Cardiac Cycle Atrial systole Atrial diastole Ventricular systole Ventricular diastole
45 Atrial Systole 20-3 The Cardiac Cycle 1. Atrial systole Atrial contraction begins Right and left AV valves are open 2. Atria eject blood into ventricles Filling ventricles 3. Atrial systole ends AV valves close Ventricles contain maximum blood volume Known as end-diastolic volume (EDV)
46 20-3 The Cardiac Cycle Ventricular Systole 4. Ventricles contract and build pressure AV valves close cause isovolumetric contraction 5. Ventricular ejection Ventricular pressure exceeds vessel pressure opening the semilunar valves and allowing blood to leave the ventricle Amount of blood ejected is called the stroke volume (SV)
47 20-3 The Cardiac Cycle Ventricular Systole 6. Ventricular pressure falls Semilunar valves close Ventricles contain end-systolic volume (ESV), about 40% of enddiastolic volume
48 Left ventricular volume (ml) Pressure (mm Hg) Figure Pressure and Volume Relationships in the Cardiac Cycle ATRIAL ATRIAL DIASTOLE SYSTOLE VENTRICULAR DIASTOLE VENTRICULAR SYSTOLE ATRIAL DIASTOLE Aortic valve opens Aorta Left ventricle Left atrium Left AV valve closes Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. End-diastolic volume Stroke volume Time (msec)
49 20-3 The Cardiac Cycle Ventricular Diastole 7. Ventricular diastole Ventricular pressure is higher than atrial pressure All heart valves are closed Ventricles relax (isovolumetric relaxation) 8. Atrial pressure is higher than ventricular pressure AV valves open Passive atrial filling Passive ventricular filling
50 Left ventricular volume (ml) Pressure (mm Hg) VENTRICULAR SYSTOLE Figure Pressure and Volume Relationships in the Cardiac Cycle ATRIAL DIASTOLE VENTRICULAR DIASTOLE ATRIAL SYSTOLE Aortic valve closes Dicrotic notch Left AV valve opens Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. End-systolic volume Time (msec)
51 Heart Sounds S 1 Loud sounds 20-3 The Cardiac Cycle Produced by AV valves S 2 Loud sounds Produced by semilunar valves ANIMATION The Heart: Cardiac Cycle
52 S 3, S 4 Soft sounds 20-3 The Cardiac Cycle Blood flow into ventricles and atrial contraction Heart Murmur Sounds produced by regurgitation through valves
53 Figure 20-18a Heart Sounds Sounds heard Valve location Aortic valve Valve location Sounds heard Pulmonary valve Sounds heard Valve location Left AV valve Valve location Sounds heard Right AV valve Placements of a stethoscope for listening to the different sounds produced by individual valves
54 Pressure (mm Hg) Figure 20-18b Heart Sounds Semilunar valves open Semilunar valves close Left ventricle Left atrium AV valves close AV valves open Heart sounds S 1 S 4 S 4 S 2 S 3 Lubb Dubb The relationship between heart sounds and key events in the cardiac cycle
55 Cardiodynamics 20-4 Cardiodynamics The movement and force generated by cardiac contractions End-diastolic volume (EDV) End-systolic volume (ESV) Stroke volume (SV) SV = EDV ESV Ejection fraction The percentage of EDV represented by SV
56 Figure A Simple Model of Stroke Volume Start Filling Ventricular diastole End-systolic volume (ESV) End-diastolic volume (EDV) Stroke volume Pumping Ventricular systole
57 Figure A Simple Model of Stroke Volume Start When the pump handle is raised, pressure within the cylinder decreases, and water enters through a one-way valve. This corresponds to passive filling during ventricular diastole. Filling Ventricular diastole
58 Figure A Simple Model of Stroke Volume At the start of the pumping cycle, the amount of water in the cylinder corresponds to the amount of blood in a ventricle at the end of ventricular diastole. This amount is known as the end-diastolic volume (EDV). End-diastolic volume (EDV)
59 Figure A Simple Model of Stroke Volume Pumping Ventricular systole As the pump handle is pushed down, water is forced out of the cylinder. This corresponds to the period of ventricular ejection.
60 Figure A Simple Model of Stroke Volume End-systolic volume (ESV) Stroke volume When the handle is depressed as far as it will go, some water will remain in the cylinder. That amount corresponds to the end-systolic volume (ESV) remaining in the ventricle at the end of ventricular systole. The amount of water pumped out corresponds to the stroke volume of the heart; the stroke volume is the difference between the EDV and the ESV.
61 20-4 Cardiodynamics Cardiac Output (CO) The volume pumped by left ventricle in 1 minute CO = HR SV CO = cardiac output (ml/min) HR = heart rate (beats/min) SV = stroke volume (ml/beat)
62 Figure Factors Affecting Cardiac Output Factors Affecting Heart Rate (HR) Factors Affecting Stroke Volume (SV) Autonomic innervation Hormones End-diastolic volume End-systolic volume HEART RATE (HR) STROKE VOLUME (SV) = EDV ESV CARDIAC OUTPUT (CO) = HR SV
63 20-4 Cardiodynamics Autonomic Innervation Cardiac plexuses innervate heart Vagus nerves (N X) carry parasympathetic preganglionic fibers to small ganglia in cardiac plexus Cardiac centers of medulla oblongata Cardioacceleratory center controls sympathetic neurons (increases heart rate) Cardioinhibitory center controls parasympathetic neurons (slows heart rate)
64 Autonomic Innervation 20-4 Cardiodynamics Cardiac reflexes Cardiac centers monitor: Blood pressure (baroreceptors) Arterial oxygen and carbon dioxide levels (chemoreceptors) Cardiac centers adjust cardiac activity Autonomic tone Dual innervation maintains resting tone by releasing ACh and NE Fine adjustments meet needs of other systems
65 Cardioinhibitory center Figure Autonomic Innervation of the Heart Vagal nucleus Cardioacceleratory center Medulla oblongata Vagus (N X) Spinal cord Sympathetic Sympathetic ganglia (cervical ganglia and superior thoracic ganglia [T 1 T 4 ]) Sympathetic preganglionic fiber Sympathetic postganglionic fiber Cardiac nerve Parasympathetic Parasympathetic preganglionic fiber Synapses in cardiac plexus Parasympathetic postganglionic fibers
66 20-4 Cardiodynamics Effects on the SA Node Membrane potential of pacemaker cells Lower than other cardiac cells Rate of spontaneous depolarization depends on: Resting membrane potential Rate of depolarization
67 Figure 20-22a Autonomic Regulation of Pacemaker Function Membrane potential (mv) Normal (resting) Prepotential (spontaneous depolarization) Threshold Heart rate: 75 bpm Pacemaker cells have membrane potentials closer to threshold than those of other cardiac muscle cells ( 60 mv versus 90 mv). Their plasma membranes undergo spontaneous depolarization to threshold, producing action potentials at a frequency determined by (1) the resting-membrane potential and (2) the rate of depolarization.
68 20-4 Cardiodynamics Effects on the SA Node Sympathetic and parasympathetic stimulation Greatest at SA node (heart rate) ACh (parasympathetic stimulation) Slows the heart NE (sympathetic stimulation) Speeds the heart
69 Figure 20-22b Autonomic Regulation of Pacemaker Function Parasympathetic stimulation Membrane potential (mv) Threshold Hyperpolarization Heart rate: 40 bpm Slower depolarization Parasympathetic stimulation releases ACh, which extends repolarization and decreases the rate of spontaneous depolarization. The heart rate slows.
70 Figure 20-22c Autonomic Regulation of Pacemaker Function Sympathetic stimulation Membrane potential (mv) Threshold Reduced repolarization Heart rate: 120 bpm More rapid depolarization Time (sec) Sympathetic stimulation releases NE, which shortens repolarization and accelerates the rate of spontaneous depolarization. As a result, the heart rate increases.
71 Atrial Reflex 20-4 Cardiodynamics Also called Bainbridge reflex Adjusts heart rate in response to venous return Stretch receptors in right atrium Trigger increase in heart rate Through increased sympathetic activity
72 20-4 Cardiodynamics Hormonal Effects on Heart Rate Increase heart rate (by sympathetic stimulation of SA node) Epinephrine (E) Norepinephrine (NE) Thyroid hormone
73 20-4 Cardiodynamics Factors Affecting the Stroke Volume The EDV amount of blood a ventricle contains at the end of diastole Filling time Duration of ventricular diastole Venous return Rate of blood flow during ventricular diastole
74 20-4 Cardiodynamics Preload The degree of ventricular stretching during ventricular diastole Directly proportional to EDV Affects ability of muscle cells to produce tension
75 20-4 Cardiodynamics The EDV and Stroke Volume At rest EDV is low Myocardium stretches less Stroke volume is low With exercise EDV increases Myocardium stretches more Stroke volume increases
76 20-4 Cardiodynamics The Frank Starling Principle As EDV increases, stroke volume increases Physical Limits Ventricular expansion is limited by: Myocardial connective tissue The cardiac (fibrous) skeleton The pericardial sac
77 20-4 Cardiodynamics End-Systolic Volume (ESV) Is the amount of blood that remains in the ventricle at the end of ventricular systole
78 20-4 Cardiodynamics Three Factors That Affect ESV 1. Preload Ventricular stretching during diastole 2. Contractility Force produced during contraction, at a given preload 3. Afterload Tension the ventricle produces to open the semilunar valve and eject blood
79 Contractility Is affected by: 20-4 Cardiodynamics Autonomic activity Hormones
80 20-4 Cardiodynamics Effects of Autonomic Activity on Contractility Sympathetic stimulation NE released by postganglionic fibers of cardiac nerves Epinephrine and NE released by adrenal medullae Causes ventricles to contract with more force Increases ejection fraction and decreases ESV
81 20-4 Cardiodynamics Effects of Autonomic Activity on Contractility Parasympathetic activity Acetylcholine released by vagus nerves Reduces force of cardiac contractions
82 Afterload 20-4 Cardiodynamics Is increased by any factor that restricts arterial blood flow As afterload increases, stroke volume decreases
83 Figure Factors Affecting Stroke Volume Factors Affecting Stroke Volume (SV) Venous return (VR) Filling time (FT) VR = EDV FT = EDV VR = EDV FT = EDV Increased by sympathetic stimulation Decreased by parasympathetic stimulation Increased by E, NE, glucagon, thyroid hormones Preload Contractility (Cont) of muscle cells Cont = ESV Increased by Cont = ESV vasoconstriction Decreased by vasodilation End-diastolic volume (EDV) End-systolic volume (ESV) Afterload (AL) AL = ESV AL = ESV EDV = EDV = SV SV STROKE VOLUME (SV) ESV = ESV = SV SV
84 20-4 Cardiodynamics Summary: The Control of Cardiac Output Heart Rate Control Factors Autonomic nervous system Sympathetic and parasympathetic Circulating hormones Venous return and stretch receptors
85 20-4 Cardiodynamics Summary: The Control of Cardiac Output Stroke Volume Control Factors EDV ESV Filling time, and rate of venous return Preload, contractility, afterload
86 Cardiac Reserve 20-4 Cardiodynamics The difference between resting and maximal cardiac output
87 20-4 Cardiodynamics The Heart and Cardiovascular System Cardiovascular regulation Ensures adequate circulation to body tissues Cardiovascular centers Control heart and peripheral blood vessels Cardiovascular system responds to: Changing activity patterns Circulatory emergencies
88 Figure A Summary of the Factors Affecting Cardiac Output Factors affecting heart fate (HR) Factors affecting stroke volume (SV) Skeletal muscle activity Blood volume Changes in peripheral circulation Atrial reflex Venous return Filling time Autonomic innervation Hormones Preload Contractility Vasodilation or vasoconstriction Autonomic innervation Hormones End-diastolic volume End-systolic volume Afterload HEART RATE (HR) STROKE VOLUME (SV) = EDV ESV CARDIAC OUTPUT (CO) = HR SV
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