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Download NURS1004 Week 10 Lecture the Heart Part II Prepared by Didy
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NURS1004 Week 10 Lecture the Heart Part II Prepared by Didy Button. 20-2 The Conducting System • Heartbeat – A single contraction of the heart – The entire heart contracts in series • First the atria • Then the ventricles 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 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 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 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 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 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 Figure 20-11a The Conducting System of the Heart Sinoatrial (SA) node Internodal pathways Atrioventricular (AV) node AV bundle Bundle branches Purkinje fibers Components of the conducting system 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. 20-2 The Conducting System • Heart Rate – SA node generates 80–100 action potentials per minute – Parasympathetic stimulation slows heart rate – AV node generates 40–60 action potentials per minute 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) Figure 20-12 Impulse Conduction through the Heart (Step 1) SA node activity and atrial activation begin. Time = 0 SA node 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 Figure 20-12 Impulse Conduction through the Heart (Step 2) Stimulus spreads across the atrial surfaces and reaches the AV node. AV node Elapsed time = 50 msec Figure 20-12 Impulse Conduction through the Heart (Step 3) There is a 100-msec delay at the AV node. Atrial contraction begins. AV bundle Bundle branches Elapsed time = 150 msec 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 Figure 20-12 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 band Elapsed time = 175 msec 20-2 The Conducting System • Purkinje Fibers – Distribute impulse through ventricles (Step 5) – Atrial contraction is completed – Ventricular contraction begins Figure 20-12 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. Purkinje Elapsed time = 225 msec fibers 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 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 Figure 20-13a An Electrocardiogram Electrode placement for recording a standard ECG. 20-2 The Conducting System • Features of an ECG – P wave • Atria depolarize – QRS complex • Ventricles depolarize – T wave • Ventricles repolarize 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 Figure 20-13a An Electrocardiogram Electrode placement for recording a standard ECG. Figure 20-13b An Electrocardiogram 800 msec R P wave (atria depolarize) R T wave (ventricles repolarize) P–R segment S–T segment Millivolts Q S P–R interval S–T interval Q–T interval QRS interval (ventricles depolarize) Figure 20-14 Cardiac Arrhythmias Premature Atrial Contractions (PACs) P P P Paroxysmal Atrial Tachycardia (PAT) P P P Atrial Fibrillation (AF) P P P Figure 20-14 Cardiac Arrhythmias Premature Ventricular Contractions (PVCs) P T P T Ventricular Tachycardia (VT) P Ventricular Fibrillation (VF) P T 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 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 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 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 20-3 The Cardiac Cycle • Two Phases of the Cardiac Cycle – Within any one chamber 1. Systole (contraction) 2. Diastole (relaxation) Figure 20-16 Phases of the Cardiac Cycle Start 0 800 msec msec 100 msec Cardiac cycle 370 msec Figure 20-16a Phases of the Cardiac Cycle Start Atrial systole begins: Atrial contraction forces a small amount of additional blood into relaxed ventricles. 0 800 msec msec Cardiac cycle 100 msec Figure 20-16b Phases of the Cardiac Cycle Atrial systole ends, atrial diastole begins 100 msec Cardiac cycle 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. 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. 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. Figure 20-16f Phases of the Cardiac Cycle 800 msec Cardiac cycle Ventricular diastole—late: All chambers are relaxed. Ventricles fill passively. 20-3 The Cardiac Cycle • Blood Pressure – 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 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 20-3 The Cardiac Cycle • Phases of the Cardiac Cycle – Atrial systole – Atrial diastole – Ventricular systole – Ventricular diastole 20-3 The Cardiac Cycle • Atrial Systole 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) 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) 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 Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle ATRIAL ATRIAL DIASTOLE SYSTOLE VENTRICULAR DIASTOLE ATRIAL DIASTOLE VENTRICULAR SYSTOLE Aortic valve opens Aorta Pressure (mm Hg) Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Left ventricle Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. Left AV valve closes Left atrium AV valves open; passive ventricular filling occurs. Left ventricular volume (mL) End-diastolic volume Stroke volume Time (msec) 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 Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle ATRIAL SYSTOLE ATRIAL DIASTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE Aortic valve closes Dicrotic notch Atrial contraction begins. Pressure (mm Hg) Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Left ventricular volume (mL) Left AV valve opens End-systolic volume Time (msec) Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. 20-3 The Cardiac Cycle • Heart Sounds – S1 • Loud sounds • Produced by AV valves – S2 • Loud sounds • Produced by semilunar valves ANIMATION The Heart: Cardiac Cycle 20-3 The Cardiac Cycle • S3, S4 – Soft sounds – Blood flow into ventricles and atrial contraction • Heart Murmur – Sounds produced by regurgitation through valves 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 Figure 20-18b Heart Sounds Semilunar valves close Pressure (mm Hg) Semilunar valves open Left ventricle Left atrium AV valves open AV valves close S1 S4 S2 S3 Heart sounds “Lubb” “Dubb” The relationship between heart sounds and key events in the cardiac cycle S4 20-4 Cardiodynamics • 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 Figure 20-19 A Simple Model of Stroke Volume Start Filling Ventricular diastole End-systolic volume (ESV) End-diastolic volume (EDV) Stroke volume Pumping Ventricular systole Figure 20-19 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 Figure 20-19 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) Figure 20-19 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. Figure 20-19 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. 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) Figure 20-20 Factors Affecting Cardiac Output Factors Affecting Heart Rate (HR) Autonomic innervation Hormones HEART RATE (HR) Factors Affecting Stroke Volume (SV) End-diastolic volume End-systolic volume STROKE VOLUME (SV) = EDV – ESV CARDIAC OUTPUT (CO) = HR SV 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) 20-4 Cardiodynamics • Autonomic Innervation – 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 Figure 20-21 Autonomic Innervation of the Heart Vagal nucleus Cardioinhibitory center Cardioacceleratory center Medulla oblongata Vagus (N X) Spinal cord Sympathetic Sympathetic ganglia (cervical ganglia and superior thoracic ganglia [T1–T4]) Sympathetic preganglionic fiber Sympathetic postganglionic fiber Cardiac nerve Parasympathetic Parasympathetic preganglionic fiber Synapses in cardiac plexus Parasympathetic postganglionic fibers 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 Figure 20-22a Autonomic Regulation of Pacemaker Function Normal (resting) Prepotential (spontaneous depolarization) Membrane potential (mV) 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. 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 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. 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. 20-4 Cardiodynamics • Atrial Reflex – 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 20-4 Cardiodynamics • Hormonal Effects on Heart Rate – Increase heart rate (by sympathetic stimulation of SA node) • Epinephrine (E) • Norepinephrine (NE) • Thyroid hormone 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 20-4 Cardiodynamics • Preload – The degree of ventricular stretching during ventricular diastole – Directly proportional to EDV – Affects ability of muscle cells to produce tension 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 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 20-4 Cardiodynamics • End-Systolic Volume (ESV) – Is the amount of blood that remains in the ventricle at the end of ventricular systole 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 20-4 Cardiodynamics • Contractility – Is affected by: • Autonomic activity • Hormones 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 20-4 Cardiodynamics • Effects of Autonomic Activity on Contractility – Parasympathetic activity • Acetylcholine released by vagus nerves • Reduces force of cardiac contractions 20-4 Cardiodynamics • Afterload – Is increased by any factor that restricts arterial blood flow – As afterload increases, stroke volume decreases Figure 20-23 Factors Affecting Stroke Volume Factors Affecting Stroke Volume (SV) Venous return (VR) VR = VR = EDV EDV Filling time (FT) FT = EDV FT = EDV Increased by sympathetic stimulation Decreased by parasympathetic stimulation Increased by E, NE, glucagon, thyroid hormones Contractility (Cont) of muscle cells Cont = Cont = Preload End-diastolic volume (EDV) ESV ESV End-systolic volume (ESV) STROKE VOLUME (SV) EDV = EDV = SV SV ESV = ESV = SV SV Increased by vasoconstriction Decreased by vasodilation Afterload (AL) AL = ESV AL = ESV 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 20-4 Cardiodynamics • Summary: The Control of Cardiac Output – Stroke Volume Control Factors • EDV – Filling time, and rate of venous return • ESV – Preload, contractility, afterload 20-4 Cardiodynamics • Cardiac Reserve – The difference between resting and maximal cardiac output 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 Figure 20-24 A Summary of the Factors Affecting Cardiac Output Factors affecting heart fate (HR) Factors affecting stroke volume (SV) Skeletal Blood Changes in muscle volume peripheral activity circulation Venous return Atrial reflex Autonomic innervation Hormones HEART RATE (HR) Filling time Autonomic innervation Preload Contractility End-diastolic volume End-systolic volume Hormones STROKE VOLUME (SV) = EDV – ESV CARDIAC OUTPUT (CO) = HR SV Vasodilation or vasoconstriction Afterload