Anatomy & Physiology Chapter 17 Heart PDF

Anatomy & Physiology Seventh Edition Chapter 17 Part B The Cardiovascular System: The Heart PowerPoint® Lectures Slides...

Anatomy & Physiology Seventh Edition Chapter 17 Part B The Cardiovascular System: The Heart PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Community College Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.5 Electrical Events of the Heart Heart depolarizes and contracts without nervous system stimulation, although rhythm can be altered by autonomic nervous system Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (1 of 8) Coordinated heartbeat is a function of: – Presence of gap junctions – Intrinsic cardiac conduction system ▪ Network of noncontractile (autorhythmic) cells ▪ Initiate and distribute impulses to coordinate depolarization and contraction of heart Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (2 of 8) Action potential initiation by pacemaker cells – Cardiac pacemaker cells have unstable resting membrane potentials called pacemaker potentials or prepotentials – Three parts of action potential 1. Pacemaker potential: K+ channels are closed, but slow Na+ channels are open, causing interior to become more positive Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (3 of 8) Action potential initiation by pacemaker cells 2. Depolarization: Ca2+ channels open (around 40 m V), illi allowing huge influx of Ca2+, leading to rising phase of action potential 3. Repolarization: K+ channels open, allowing efflux of K+, and cell becomes more negative Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.12 Pacemaker and Action Potentials of Typical Cardiac Pacemaker Cells (3 of 3) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (4 of 8) Sequence of excitation – Cardiac pacemaker cells pass impulses, in following order, across heart in ~0.22 seconds 1. Sinoatrial node → 2. Atrioventricular node → 3. Atrioventricular bundle → 4. Right and left bundle branches → 5. Subendocardial conducting network (Purkinje fibers) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (5 of 8) Sinoatrial (SA) node – Pacemaker of heart in right atrial wall ▪ Depolarizes faster than rest of myocardium – Generates impulses about 75×/minute (sinus rhythm) ▪ Inherent rate of 100×/minute tempered by extrinsic factors – Impulse spreads across atria and to AV node Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (6 of 8) Atrioventricular (AV) node – In inferior interatrial septum – Delays impulses approximately 0.1 second ▪ Because fibers are smaller in diameter, have fewer gap junctions ▪ Allows atrial contraction prior to ventricular contraction – Inherent rate of 50×/minute in the absence of SA node input Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (7 of 8) Atrioventricular (AV) bundle (bundle of His) – In superior interventricular septum – Only electrical connection between atria and ventricles ▪ Atria and ventricles not connected via gap junctions Right and left bundle branches – Two pathways in interventricular septum – Carry impulses toward apex of heart Copyright © 2020 Pearson Education, Inc. All Rights Reserved Setting the Basic Rhythm: The Intrinsic Conduction System (8 of 8) Subendocardial conducting network ▪ Also referred to as Purkinje fibers – Complete pathway through interventricular septum into apex and ventricular walls – More elaborate on the left side of the heart – AV bundle and subendocardial conducting network depolarize 30×/minute in the absence of AV node input – Ventricular contraction immediately follows from apex toward atria – Process from initiation at SA node to complete contraction takes ~0.22 seconds Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.13 Intrinsic Cardiac Conduction System and Action Potential Succession During One Heartbeat (4 of 4) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.4 (1 of 3) Defects in intrinsic conduction system may cause: – Arrhythmias: irregular heart rhythms – Uncoordinated atrial and ventricular contractions – Fibrillation: rapid, irregular contractions ▪ Heart becomes useless for pumping blood, causing circulation to cease; may result in brain death ▪ Treatment: defibrillation interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.4 (2 of 3) Defective SA node may cause ectopic focus, an abnormal pacemaker that takes over pacing – If AV node takes over, it sets junctional rhythm at 40–60 beats/min ute – Extrasystole (premature contraction): ectopic focus of small region of heart that triggers impulse before SA node can, causing delay in next impulse ▪ Heart has longer time to fill, so next contraction is felt as thud as larger volume of blood is being pushed out ▪ Can be from excessive caffeine or nicotine Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.4 (3 of 3) To reach ventricles, impulse must pass through AV node If AV node is defective, may cause a heart block – Few impulses (partial block) or no impulses (total block) reach ventricles – Ventricles beat at their own intrinsic rate ▪ Too slow to maintain adequate circulation – Treatment: artificial pacemaker, which recouples atria and ventricles Copyright © 2020 Pearson Education, Inc. All Rights Reserved Modifying the Basic Rhythm: Extrinsic Innervation of the Heart Heartbeat modified by ANS via cardiac centers in medulla oblongata – Cardioacceleratory center: sends signals through sympathetic trunk to increase both rate and force ▪ Stimulates SA and AV nodes, heart muscle, and coronary arteries – Cardioinhibitory center: parasympathetic signals via vagus nerve to decrease rate ▪ Inhibits SA and AV nodes via vagus nerves Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.14 Autonomic Innervation of the Heart Copyright © 2020 Pearson Education, Inc. All Rights Reserved Action Potentials of Contractile Cardiac Muscle Cells (1 of 3) Contractile muscle fibers make up bulk of heart muscle and are responsible for pumping action – Different from skeletal muscle contraction; cardiac muscle action potentials have plateau Steps involved in AP: – Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell ▪ Positive feedback influx of Na+ causes rising phase of AP (from 90 m V to +30 mV) illi Copyright © 2020 Pearson Education, Inc. All Rights Reserved Action Potentials of Contractile Cardiac Muscle Cells (2 of 3) – Depolarization by Na+ also opens slow Ca2+ channels ▪ At +30 m V, Na+ channels close, but slow Ca2+ illi channels remain open, prolonging depolarization – Seen as a plateau – After about 200 ms, slow Ca2+ channels are closed, and voltage-gated K+ channels are open ▪ Rapid efflux of K+ repolarizes cell to RMP ▪ Ca2+ is pumped both back into SR and out of cell into extracellular space Copyright © 2020 Pearson Education, Inc. All Rights Reserved Action Potentials of Contractile Cardiac Muscle Cells (3 of 3) Difference between contractile muscle fiber and skeletal muscle fiber contractions – AP in skeletal muscle lasts 1–2 m s; in cardiac muscle, illi it lasts 200 m s illi econd – Contraction in skeletal muscle lasts 15–100 m s ; in illi econd cardiac contraction, it lasts over 200 ms econd Benefit of longer AP and contraction: – Sustained contraction ensures efficient ejection of blood – Longer refractory period prevents tetanic contractions Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.15 The Action Potential of Contractile Cardiac Muscle Cells (3 of 3) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Electrocardiography (1 of 2) Electrocardiograph can detect electrical currents generated by heart Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity – Composite of all action potentials at given time; not a tracing of a single AP – Electrodes are placed at various points on body to measure voltage differences ▪ 12 lead ECG is most typical Copyright © 2020 Pearson Education, Inc. All Rights Reserved Electrocardiography (2 of 2) Main features: – P wave: depolarization of SA node and atria – QRS complex: ventricular depolarization and atrial repolarization – T wave: ventricular repolarization – P-R interval: beginning of atrial excitation to beginning of ventricular excitation – S-T segment: entire ventricular myocardium depolarized – Q-T interval: beginning of ventricular depolarization through ventricular repolarization Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.16a The Electrocardiogram (ECG) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.16b The Electrocardiogram (ECG) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.17 The Sequence of Depolarization and Repolarization of the Heart Related to the E CG Waves (6 of 6) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.5 (1 of 2) Changes in patterns or timing of ECG may reveal diseased or damaged heart, or problems with heart’s conduction system Problems that can be detected: – Enlarged R waves may indicate enlarged ventricles – Elevated or depressed S-T segment indicates cardiac ischemia Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.5 (2 of 2) Problems that can be detected: – Prolonged Q-T interval reveals a repolarization abnormality that increases risk of ventricular arrhythmias Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.18a Normal and Abnormal ECG Tracings Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.18b Normal and Abnormal ECG Tracings Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.18c Normal and Abnormal ECG Tracings Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.18d Normal and Abnormal ECG Tracings Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.6 Mechanical Events of Heart (1 of 5) Systole: period of heart contraction Diastole: period of heart relaxation Cardiac cycle: blood flow through heart during one complete heartbeat – Atrial systole and diastole are followed by ventricular systole and diastole – Cycle represents series of pressure and blood volume changes – Mechanical events follow electrical events seen on E CG Three phases of the cardiac cycle (following left side, starting with total relaxation) Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.6 Mechanical Events of Heart (2 of 5) – Ventricular filling: mid-to-late diastole ▪ Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SL valves closed) ▪ Atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle – End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole ▪ Depolarization spreads to ventricles (QRS wave) ▪ Atria finish contracting and return to diastole, while ventricles begin systole Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.6 Mechanical Events of Heart (3 of 5) – Isovolumetric contraction ▪ Atria relax; ventricles begin to contract ▪ Rising ventricular pressure causes closing of AV valves ▪ Isovolumetric contraction phase is split-second period when ventricles are completely closed (all valves closed), volume remains constant, ventricles continue to contract ▪ When ventricular pressure exceeds pressure in large arteries, SL valves are forced open – Pressure in aorta reaches about 120 mm Hg Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.6 Mechanical Events of Heart (4 of 5) – Isovolumetric relaxation: early diastole ▪ Following ventricular repolarization (T wave), ventricles relax ▪ End systolic volume (ESV): volume of blood remaining in each ventricle after systole ▪ Ventricular pressure drops causing backflow of blood from aorta and pulmonary trunk that triggers closing of SL valves ▪ Ventricles are completely closed chambers momentarily – Referred to as isovolumetric relaxation phase Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.6 Mechanical Events of Heart (5 of 5) ▪ Closure of aortic valve raises aortic pressure as backflow rebounds off closed valve cusps – Referred to as dicrotic notch ▪ Atria continue to fill during ventricular systole and when atrial pressure exceeds ventricular pressure, A V valves open; cycle begins again ▪ Heart beats around 75 times per minute ▪ Cardiac cycle lasts about 0.8 seconds – Atrial systole lasts about 0.1 seconds – Ventricular systole lasts about 0.3 seconds – Quiescent period is total heart relaxation that lasts about 0.4 seconds Copyright © 2020 Pearson Education, Inc. All Rights Reserved Focus Figure 17.2 The Cardiac Cycle (1 of 2) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Focus Figure 17.2 The Cardiac Cycle (2 of 2) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Heart Sounds (1 of 2) Two sounds (lub-dup) associated with closing of heart valves – First sound is closing of AV valves at the beginning of ventricular systole – Second sound is closing of SL valves at the beginning of ventricular diastole – Pause between lub-dups indicates heart relaxation Copyright © 2020 Pearson Education, Inc. All Rights Reserved Heart Sounds (2 of 2) Mitral valve closes slightly before tricuspid, and aortic closes slightly before pulmonary valve – Differences allow auscultation of each valve when stethoscope is placed in four different regions Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.19 Areas of the Thoracic Surface Where the Sounds of Individual Valves Are Heard Most Clearly Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.6 Heart murmurs: abnormal heart sounds heard when blood hits obstructions Usually indicate valve problems – Incompetent (or insufficient) valve: fails to close completely, allowing backflow of blood ▪ Causes swishing sound as blood regurgitates backward from ventricle into atria – Stenotic valve: fails to open completely, restricting blood flow through valve ▪ Causes high-pitched sound or clicking as blood is forced through narrow valve Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.7 Regulation of Pumping (1 of 2) Cardiac output: amount of blood pumped out by each ventricle in 1 minute – Equals heart rate (HR) times stroke volume (SV) ▪ Stroke volume: volume of blood pumped out by one ventricle with each beat – Correlates with force of contraction At rest: CO ml / min  HR 75 beats / min  SV 70 ml / beat   5.25 L / min Copyright © 2020 Pearson Education, Inc. All Rights Reserved 17.7 Regulation of Pumping (2 of 2) Maximal CO is 4–5 times resting CO in nonathletic people (20–25 L/min) Maximal CO may reach 35 L/min in trained athletes Cardiac reserve: difference between resting and maximal CO CO changes (increases/decreases) if either or both S V or HR is changed CO is affected by factors leading to: – Regulation of stroke volume – Regulation of heart rates Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.20 Factors Involved in Determining Cardiac Output (1 of 2) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Stroke Volume (1 of 5) Mathematically: SV = EDV − ESV – EDV is affected by length of ventricular diastole and venous pressure (~120 ml/beat) – ESV is affected by arterial BP and force of ventricular contraction (~50 m l /beat) illi iter – Normal SV = 120 m l − 50 m l = 70 ml /beat illi iter illi iter iter Three main factors that affect SV: – Preload – Contractility – Afterload Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Stroke Volume (2 of 5) Preload: degree of stretch of heart muscle – Preload: degree to which cardiac muscle cells are stretched just before they contract ▪ Changes in preload cause changes in SV – Affects EDV – Relationship between preload and SV called Frank-Starling law of the heart – Cardiac muscle exhibits a length-tension relationship ▪ At rest, cardiac muscle cells are shorter than optimal length; leads to dramatic increase in contractile force Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Stroke Volume (3 of 5) Preload – Most important factor in preload stretching of cardiac muscle is venous return—amount of blood returning to heart ▪ Slow heartbeat and exercise increase venous return ▪ Increased venous return distends (stretches) ventricles and increases contraction force  Venous Return   EDV     SV   CO Frank-Starling Law Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Stroke Volume (4 of 5) Contractility – Contractile strength at given muscle length ▪ Independent of muscle stretch and EDV – Increased contractility lowers ESV; caused by: ▪ Sympathetic epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations ▪ Positive inotropic agents increase contractility – Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+ – Decreased by negative inotropic agents ▪ Acidosis (excess H+), increased extracellular K+, calcium channel blockers Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.21 Norepinephrine Increases Heart Contractility Via a Cyclic AMP Second-Messenger System Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Stroke Volume (5 of 5) Afterload: back pressure exerted by arterial blood – Afterload is pressure that ventricles must overcome to eject blood ▪ Back pressure from arterial blood pushing on SL valves is major pressure – Aortic pressure is around 80 mmHg – Pulmonary trunk pressure is around 10 mm Hg – Hypertension increases afterload, resulting in increased ESV and reduced SV Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (1 of 7) If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR and contractility – Positive chronotropic factors increase heart rate – Negative chronotropic factors decrease heart rate Heart rate can be regulated by: – Autonomic nervous system – Chemicals – Other factors Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (2 of 7) Autonomic nervous system regulation of heart rate – Sympathetic nervous system can be activated by emotional or physical stressors – Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing: ▪ Pacemaker to fire more rapidly, increasing HR – EDV decreased because of decreased fill time ▪ Increased contractility – ESV decreased because of increased volume of ejected blood Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (3 of 7) Autonomic nervous system regulation of heart rate – Because both EDV and ESV decrease, SV can remain unchanged – Parasympathetic nervous system opposes sympathetic effects ▪ Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels, which slows HR ▪ Has little to no effect on contractility Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (4 of 7) Autonomic nervous system regulation of heart rate – Heart at rest exhibits vagal tone ▪ Parasympathetic is dominant influence on heart rate ▪ Decreases rate about 25 beats/min ute ▪ Cutting vagal nerve leads to HR of ~100 Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (5 of 7) Autonomic nervous system regulation of heart rate – When sympathetic is activated, parasympathetic is inhibited, and vice-versa – Atrial (Bainbridge) reflex: sympathetic reflex initiated by increased venous return, hence increased atrial filling ▪ Atrial walls are stretched with increased volume ▪ Stimulates SA node, which increases HR ▪ Also stimulates atrial stretch receptors that activate sympathetic reflexes Copyright © 2020 Pearson Education, Inc. All Rights Reserved Figure 17.20 Factors Involved in Determining Cardiac Output (2 of 2) Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (6 of 7) Chemical regulation of heart rate – Hormones ▪ Epinephrine from adrenal medulla increases heart rate and contractility ▪ Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine – Ions ▪ Intracellular and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function – Imbalances are very dangerous to heart Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.7 Hypocalcemia: depresses heart Hypercalcemia: increases HR and contractility Hyperkalemia: alters electrical activity, which can lead to heart block and cardiac arrest Hypokalemia: results in feeble heartbeat; arrhythmias Copyright © 2020 Pearson Education, Inc. All Rights Reserved Regulation of Heart Rate (7 of 7) Other factors that influence heart rate – Age ▪ Fetus has fastest HR; declines with age – Gender ▪ Females have faster HR than males – Exercise ▪ Increases HR ▪ Trained athletes can have slow HR – Body temperature ▪ HR increases with increased body temperature Copyright © 2020 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 17.8 Tachycardia: abnormally fast heart rate (>100 beats/min ) ute – If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 beats/min ute – May result in grossly inadequate blood circulation in nonathletes – May be desirable result of endurance training Copyright © 2020 Pearson Education, Inc. All Rights Reserved Homeostatic Imbalance of Cardiac Output (1 of 3) Congestive heart failure (CHF) – Progressive condition; CO is so low that blood circulation is inadequate to meet tissue needs – Reflects weakened myocardium caused by: ▪ Coronary atherosclerosis: clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells – Heart becomes hypoxic, contracts inefficiently Copyright © 2020 Pearson Education, Inc. All Rights Reserved Homeostatic Imbalance of Cardiac Output (2 of 3) Congestive heart failure (CHF) ▪ Persistent high blood pressure: aortic pressure 90 mm Hg causes myocardium to exert more force – Chronic increased ESV causes myocardium hypertrophy and weakness ▪ Multiple myocardial infarcts: heart becomes weak as contractile cells are replaced with scar tissue ▪ Dilated cardiomyopathy (DCM): ventricles stretch and become flabby, and myocardium deteriorates – Drug toxicity or chronic inflammation may play a role Copyright © 2020 Pearson Education, Inc. All Rights Reserved Homeostatic Imbalance of Cardiac Output (3 of 3) Congestive heart failure (CHF) – Either side of heart can be affected: ▪ Left-sided failure results in pulmonary congestion – Blood backs up in lungs ▪ Right-sided failure results in peripheral congestion – Blood pools in body organs, causing edema – Failure of either side ultimately weakens other side ▪ Leads to decompensated, seriously weakened heart ▪ Treatment: removal of fluid, drugs to reduce afterload and increase contractility Copyright © 2020 Pearson Education, Inc. All Rights Reserved