Chapter 19: Heart Lecture Outline PDF

Chapter 19: Heart Lecture Outline ================================= - Describe the general structure and function of the cardiac muscle including how its energy needs are met. - Describe in detail the components and the processes associated with the heart's conduction system, including...

Chapter 19: Heart Lecture Outline ================================= - Describe the general structure and function of the cardiac muscle including how its energy needs are met. - Describe in detail the components and the processes associated with the heart's conduction system, including autonomic control. - Explain the events of cardiac muscle contraction, including refractory period and significance of the plateau phase. - Describe and identify the components of the ECG reading and discuss the clinical significance. - Explain in detail the cardiac cycle, its stages, and factors that influence the cycle. [19.4a Microscopic Structure of Cardiac Muscle ] - Myocardium is composed of cardiac muscle tissue - Cardiac muscle cells are short, branched - House one or two central nuclei - Supported by areolar connective tissue, called endomysium - Sarcolemma (plasma membrane) - Invaginates to form T-tubules extending into sarcoplasmic reticulum - Sarcoplasmic reticulum - Surrounds bundles of myofilaments - Myofilaments arranged in sarcomeres - Organization gives rise to striated appearance under microscope - Optimal length (maximum overlap of filaments) is seen when heart is stretched by blood filling the chamber - Allows filaments to contract with greater force with more blood - **Intercellular structures** - Sarcolemma is folded at connections between cells - Increases structural stability of myocardium - Facilitates communication between cells - Cells are connected with **intercalated discs** - **Desmosomes** mechanically join cells with protein filaments - **Gap junctions** electrically join cells (allow ion flow) to make each heart chamber a functional unit (**functional syncytium**) - **Cross Section of Cardiac Muscle Cells (Figure 19.12a,b)** - **Longitudinal View of Cardiac Muscle Cell (Figure 19.12c,d)** - Metabolism of cardiac muscle - High demand for energy - Extensive blood supply - Numerous mitochondria - **Myoglobin** and **creatine kinase** - Able to use different types of fuel molecules - Fatty acids, glucose, lactic acid, amino acids, and ketone bodies - Relies mostly on aerobic metabolism - Makes it susceptible to failure when **ischemic** (oxygen is low) - Interference with blood flow to heart muscle can cause cell death [19.5a The Heart's Conduction System ] - **Conduction system:** initiates and conducts electrical events to ensure proper timing of contractions - Specialized cardiac muscle cells that have action potentials but do not contract - Its activity is influenced by autonomic nervous system - **Sinoatrial (SA) node** initiates heartbeat (*pacemaker*) - Located high in posterior wall of right atrium - **Atrioventricular (AV) node** - Located in floor of right atrium (near right AV valve) - **Atrioventricular (AV) bundle** (*bundle of His*) - Extends from AV node though interventricular septum - Divides into **left** and **right bundles** - **Purkinje fibers** - Extend from left and right bundles at heart's apex - Couse through walls of ventricles - **Conduction System (Figure 19.13a)** [19.5b Innervation of the Heart] - **Cardiac center** of medulla oblongata - Contains cardioacceleratory and cardioinhibitory centers - Receives signals from baroreceptors and chemoreceptors in cardiovascular system - Sends signals via sympathetic and parasympathetic pathways - Modifies (does not initiate) cardiac activity - Influences rate and force of heart's contractions - **Parasympathetic innervation** decreases heart rate - Starts at medulla's **cardioinhibitory** **center** - Relayed via vagus nerves (CN X) - Right vagus innervates SA node - Left vagus innervates AV node - **Sympathetic innervation** increases heart rate and force of contraction - Starts at medulla's **cardioacceleratory** **center** - Relayed via neurons from T1--T5 segments of spinal cord - Extend to SA node, AV node, myocardium, and coronary arteries - Increases coronary vessel dilation - **Innervation of the Heartv (Figure 19.13b)** [19.6 Stimulation of the Heart] - Heart contraction involves two events - The **conduction system** initiates and propagates an action potential - **Cardiac muscle cells** initiate action potentials and contract - This process happens first in the atria and then the ventricles - **Physiologic Processes Associated with Heart Contraction: Conduction System (Fig19.14a)** - **Physiologic Processes Associated with Heart Contraction: Cardiac Muscle Cells (Fig19.14b)** [19.6a SA Nodal Cells at Rest] - **SA nodal cells** initiate heartbeat - Spontaneously depolarize and generate action potential - **Resting membrane potential (RMP)** is about -60mV - But these cells do not have a stable RMP - **Pacemaker potential** -- ability to reach threshold without stimulation - Have many common membrane proteins - Na^+^/K^+^ pumps, Ca^2+^ pumps, leak channels - Also have specific voltage-gated channels - Slow voltage-gated Na^+^ channels, fast voltage-gated Ca^2+^ channels, voltage-gated K^+^ channels - **SA Nodal Cells at Rest (Figure 19.15)** [19.6b Electrical Events at the SA Node: Initiation of the Action Potential ] - SA node cells exhibit **autorhythmicity** (spontaneous firing) 1. **Reaching threshold** - Slow voltage-gated Na^+^ channels open and Na^+^ flows in - Membrane potential changes from −60 mV to −40 mV (**threshold** value) 2. **Depolarization** - Fast voltage-gated Ca^2+^ channels open and Ca^2+^ flows in - Membrane potential changes from −40 mV to just above 0 mV 3. **Repolarization** - Calcium channels close and voltage-gated K^+^ channels open so K^+^ flows out - Membrane potential goes back to rest value (RMP = −60 mV) - Voltage-gated Na^+^ channels open at −60 mV and process begins again - At rest, one SA node action potential starts about 0.8 sec after the last - This translates to 75 heart beats per minute - Inherently, SA node would fire faster at 100 per minute - This is seen in heart tissue culture - In the body, **vagal tone** (parasympathetic activity relayed by the vagus nerve) keeps resting heart rate slower - **SA Node Cellular Activity (Figure 19.16)** [19.6c Conduction System of the Heart: Spread of the Action Potential ] - After starting at SA node the action potential spreads 1. Action potential is distributed through atria, reaches AV node - Excitation travels via gap junctions and the two atria contract together 2. Action potential is delayed at the AV node - AV nodal cells are slow because of small diameter and few gap junctions - Insulation of fibrous skeleton means AV node is bottleneck (only path) - Delay allows ventricles to fill before they contract 3. Action potential travels through AV bundle to Purkinje fibers - AV node → AV bundle → Bundle branches → Purkinje fibers 4. Action potential spreads through ventricles - Gap junctions allow impulse to spread through cardiac muscle fibers - Cells of the two ventricles contract nearly simultaneously - **Initiation and Spread of an Action Potential Through the Cardiac Conduction System (Figure 19.17 (steps 1-2))** - **Initiation and Spread of an Action Potential Through the Cardiac Conduction System (Figure 19.17 (steps 3-4))** - Specialized features associated with ventricles - Purkinje fibers larger in diameter than other cardiac fibers - Action potential extremely rapid - Ensures ventricles contract at same time - Papillary muscles stimulated to contract immediately - Muscles anchor chordae tendinae of AV cusps - Start to pull on cusps just prior to increase in pressure in ventricles - Stimulation begins at heart apex - Ensures blood efficiently ejected toward arterial trunks *[Clinical View: Ectopic Pacemaker]* - **Ectopic pacemaker**: Pacemaker other than SA node - Conduction system cells other than SA node - Also have ability to spontaneously depolarize - Depolarize at slower rates than SA node - AV node the default pacemaker if SA node impaired - AV node with inherent rhythm of 40 to 50 beats/min - Fast enough to sustain life - Cardiac muscle with rate of 20 to 40 beats/min - Usually too slow to sustain life [19.7a Cardiac Muscle Cells at Rest] - Cardiac muscle cells - Contain Na^+^/ K^+^ pumps, Ca^2+^ pumps, leakage channels for Na^+^ and K^+^ - Have a resting membrane potential of -90 mV - Contain specific voltage-gated channels: - Fast voltage-gated Na^+^ channels - Slow voltage-gated Ca^2+^ channels - Voltage-gated K^+^ channels - Voltage channels are closed when cell is at rest - **Cardiac Muscle Cell at Rest (Figure 19.18)** [19.7b Electrical and Mechanical Events of Cardiac Muscle Cells ] - Electrical events of cardiac muscle action potential 1. **Depolarization** - Impulse from conduction system (or gap junctions) opens fast voltage-gated Na^+^ channels - Na^+^ enters cell changing membrane potential from −90 mV to +30 mV - Voltage-gated Na^+^ channels start to inactivate 2. **Plateau** - Depolarization opens voltage-gated K^+^ and slow voltage-gated Ca^2+^ channels - K^+^ leaves cardiac muscle cell as Ca^2+^ enters - Stimulates sarcoplasmic reticulum to release more Ca^2+^ - Membrane remains depolarized 3. **Repolarization** - Voltage-gated Ca^2+^ channels close while K^+^ channels remain open - Membrane potential goes back to −90 mV - **Electrical Events at the Sarcolemma of a Cardiac Muscle Cell (Figure 19.19)** - Mechanical events (crossbridge cycling) - Ca^2+^ enters sarcoplasm from interstitial fluid and SR leading to contraction - As in skeletal muscle, it binds to troponin and initiates crossbridge cycling - Crossbridge formation, power stroke, release of myosin head, reset of myosin head - Ca^2+^ levels decrease leading to relaxation - Channels close and pumps move it into SR and out of cell [19.7c Repolarization and the Refractory Period] - Cardiac muscle *cannot* exhibit tetany - Unlike skeletal muscle, cardiac cells have a long **refractory period** - Cell cannot fire a new impulse during refractory period - Cardiac muscle cell's plateau phase leads to refractory period of about 250 ms - The heart cell contracts and relaxes before it can be stimulated again - Makes sustained (tetanic) contraction impossible - **Electrical and Mechanical Events in Skeletal Muscle Cells (Figure 19.20a,b)** - **Electrical and Mechanical Events in Cardiac Muscle Cells (Figure 19.20c,d)** [19.7d Electrocardiogram (ECG) ] - **Electrocardiogram (ECG/EKG)** - Skin electrodes detect electrical signals of cardiac muscle cells - Common diagnostic tool - Waves - **P wave** - Reflects electrical changes of **atrial depolarization** originating in SA node - **QRS complex** - Electrical changes associated with **ventricular depolarization** - Atria also simultaneously repolarizing - **T wave** - Electrical change associated with **ventricular repolarization** - Segments - Two segments between waves correspond to plateau phases of cardiac action potentials (no electrical change) - **P-Q segment** - Associated with atrial cells' plateau (atria are contracting) - **S-T segment** - Associated with ventricular plateau (ventricles are contracting) - **The Electrocardiogram (Figure 19.21a)** - **The Electrocardiogram 2 (Figure 19.21b)** - Electrical events of the heart and an ECG - Atria - **Atrial depolarization:** recorded as the P wave, muscle cells of atria stimulated to contract - **Atrial plaeau:** recorded as PQ segment, muscle cells of atria contract and relax - **Atrial repolarization:** not visible on ECG - Ventricles - **Ventricular depolarization:** recorded as the QRS wave, muscle cells of ventricles stimulated to contract - **Ventricular plateau**: recorded as ST segment, muscle cells of ventricles contract and relax - **Ventricular repolarization**: recorded as T wave - **Electrical Events of the Heart and an ECG (Figure 19.22)** - Intervals - **P-R interval** - Time from beginning of P wave to beginning of QRS deflection - From atrial depolarization to beginning of ventricular depolarization - Time to transmit action potential through entire conduction system - **Q-T interval** - Time from beginning of QRS to the end of T wave - Reflects the time of ventricular action potentials - Length depends upon heart rate - Changes may result in **tachyarrhythmia** (rapid, irregular heart rate) *[Clinical View: Cardiac Arrhythmia ]* - Any abnormality in heart's electrical activity - **Heart blocks:** impaired conduction - May result in light-headedness, fainting, irregular heartbeat, chest palpitations - **First-degree AV block:** *PR prolongation* - Slow conduction between atria and ventricles - **Second-degree AV block** - Failure of some atrial action potentials to reach ventricles - **Third-degree AV block:** complete - Failure of all action potentials to reach ventricles - **Premature ventricular contractions** - Result from stress, stimulants, or sleep deprivation - Abnormal action potential within AV node or ventricles - Not detrimental unless they occur in large numbers - **Atrial fibrillation:** chaotic timing of atrial action potentials - **Ventricular fibrillation:** chaotic electrical activity in ventricles - Uncoordinated contraction and pump failure - Leads to death of heart cells - Treated with paddle electrode defibrillator or **automated external defibrillator (AED)** [19.8a Overview of the Cardiac Cycle ] - **Cardiac cycle:** all events in heart from the start of one heart beat to start of the next - Includes both **systole** (contraction) and **diastole** (relaxation) - Contraction increases pressure; relaxation decreases it - Blood moves down its pressure gradient (high to low) - Valves ensure that flow is forward (closure prevents backflow) - Ventricular activity is most important driving force - **Ventricular contraction** raises ventricular pressure - AV valves pushed closed - Semilunar valves pushed open and blood ejected to artery - **Ventricular relaxation** lowers ventricular pressure - Semilunar valves close - No pressure from below keeping them open - AV valves open - No pressure pushing them closed [19.8b Events of the Cardiac Cycle ] - **See Figure 19.23a-c and Figure 19.23d-f: Phases of the Cardiac Cycle** - As the cardiac cycle begins - Four chambers at rest - Blood returning to both atria - Passive filling of ventricles - AV valves open - Atrial pressure \> ventricular pressure - Semilunar valves closed - Pressure in ventricles \< arterial trunk pressure - **Atrial contraction and ventricular filling** - SA node starts atrial excitation - Atria contract pushing remaining blood into ventricles - Ventricles filled to **end-diastolic volume (EDV)** - Atria relax for remainder of cardiac cycle - **Isovolumic contraction** - Purkinje fibers initiate ventricular excitation - Ventricles contract, pressure rises, and AV valves are pushed closed - Ventricular pressure is still less than arterial trunk pressure, so semilunar valves still closed - **Ventricular ejection** - Ventricles continue to contract so that ventricular pressure rises above arterial pressure - Semilunar valves forced open as blood moves from ventricles to arterial trunks - **Stroke volume (SV)** is amount of blood ejected by ventricle - **End systolic volume (ESV)** is amount of blood remaining in ventricle after contraction finishes - ESV = EDV − SV - For example, 60 mL = 130 mL − 70 mL - **Isovolumic relaxation** - Ventricles relax and start to expand, lowering pressure - Arterial pressure greater than ventricular pressure - By sliding back toward ventricles, blood closes semilunar valves - AV valves remain closed - When all valves are closed, blood neither enters nor leaves and the time is called "isovolumic" - **Atrial relaxation and ventricular filling** - All heart chambers are relaxed - Atrial blood pressure forces AV valves open and blood flows into ventricles - Semilunar valves remain closed since arterial pressure is greater than ventricular pressure - **Ventricular balance** - Equal amounts of blood are pumped by left and right sides of the heart - Left heart pumps blood farther and so must be stronger (thicker) - But ejected blood volumes must be the same or **edema** (swelling) can occur [19.9a Introduction to Cardiac Output ] - **Cardiac output (CO)** - Amount of blood pumped by a *single* ventricle in one minute - Measured in liters per minute - Measure of effectiveness of cardiovascular system - Increases in healthy individuals during exercise - Determined by **heart rate** (beats per minute) and **stroke volume** (amount of blood ejected per beat) - HR × SV = CO - For example, 75 beats/min × 70 ml/beat = 5.25 L/min - Maintaining resting cardiac output - CO must meet tissue needs - Individuals with smaller hearts have smaller stroke volume and so must have faster heart rate - For example, women and children - Individuals with stronger hearts have larger stroke volume and slower heart rate - For example, Endurance athletes have thicker heart walls and stronger hearts - **Cardiac reserve** - Capacity to increase cardiac output above rest level - Subtract cardiac output at rest from output with exercise - HR accelerates and stroke volume increases during exercise - Gives measure of level of exercise an individual can pursue - For example, CO can increase four-fold in healthy, nonathlete and up to seven-fold in athlete [19.9b Variables That Influence Heart Rate ] - **Chronotropic agents** change heart rate - Alter the activity of nodal cells (SA and/or AV node) - Often work via autonomic nervous system or hormones - **Positive chronotropic agents** increase heart rate - Sympathetic nerve stimulation - Causes norepinephrine (NE) release on heart - Causes adrenal to release epinephrine (EPI) and NE - NE and EPI bind to nodal cells and increase their firing rate - Receptors are beta-one adrenergic receptors - G-protein, adenylate cyclase, cAMP, protein kinase cascade - Phosphorylated Ca^2+^ channels enhance Ca^2+^ influx so cell fires sooner - Sympathetic Innervation of SA Nodal Cells (Figure 19.25) - Thyroid hormone - Increases number of β~1~-adrenergic receptors on nodal cells - Caffeine - Inhibits breakdown of cAMP - Nicotine - Increases release of norepinephrine - Cocaine - Inhibits reuptake of norepinephrine (more remains in cleft longer) - **Negative chronotropic agents** decrease heart rate - Parasympathetic activity - Parasympathetic axons release acetylcholine (ACh) onto nodal cells - ACh binds muscarinic receptors which are K^+^ channels - Channels open, K^+^ exits cell making it more negative - Longer time for nodal cell to reach threshold, so heart rate slower - Beta-blocker drugs - Interfere with EPI and NE binding to beta receptors - Used to treat high blood pressure - **Autonomic reflexes** - Baroreceptors and chemoreceptors send signals to cardiac center - Cardiac center influences sympathetic and parasympathetic systems to alter cardiac output as needed - **Atrial reflex** (*Bainbridge reflex*) - Protects heart from overfilling - Baroreceptors in atrial walls stimulated by increased venous return - Increased nerve signals to cardioacceleratory center - Increased excitation of sympathetic axons to heart - Heart rate increase to move blood through quickly (less atrial stretch) [19.9c Variables That Influence Stroke Volume ] - Stroke volume is amount of blood ejected in one beat - Stroke volume (SV) is influenced by: venous return, inotropic agents, and afterload - **Venous return:** volume of blood returned to the heart - Directly related to stroke volume - Determines amount of ventricular blood prior to contraction - That is, end-diastolic volume (EDV) - Volume determines **preload** - Pressure stretching heart wall before shortening - **Frank-Starling law** - As EDV increases, the greater stretch of heart wall results in more optimal overlap of thick and thin filaments - Heart contracts more forcefully when filled with more blood so SV increases - The Frank-Starling Law (Figure 19.27) - Venous return may be increased by increased venous pressure or increased time to fill - Venous pressure increases during exercise as muscles squeeze veins - Time to fill increases with slower heart rate (for example in high-caliber athletes with strong hearts) - Decreases with low blood volume (for example, with hemorrhage) or high heart rate - Results in smaller end diastolic volume, preload - Results in smaller stroke volume - Balanced ventricular output due largely to Frank-Starling law - As one side receives increased blood volume it contracts more forcefully - Leads to greater fill (and more forceful contraction) on the other side - Variables That Influence Stroke Volume: Venous Return (Figure 19.28a) - **Inotropic agents** change stroke volume - Alter **contractility** (force of contraction) - Generally due to a changes in Ca^2+^ available in sarcoplasm - Ca^2+^ levels directly relate to number of cross bridges formed - **Positive inotropic agents** increase available Ca^2+^ - EPI and NE work via β~1~-adrenergic receptors to increase Ca^2+^ - Thyroid hormone increases number of β~1~ receptors - Certain drugs, for example, digitalis, boost cardiac output by increasing contractility - **Negative inotropic agents** decrease available Ca^2+^ and thus lower contractility - Electrolyte imbalances such as increased K^+^ or H^+^ - Certain drugs, for example, Ca^2+^ channel-blocking blood pressure drugs - **Variables That Influence Stroke Volume: Inotropic Agents (Figure 19.28b)** - **Afterload** - Resistance in arteries to ejection of blood by ventricles - Pressure that must be exceeded before blood ejected - Atherosclerosis (plaque in vessel linings) increases afterload - Seen with aging - Smaller arterial lumen exerts greater resistance to movement of blood - Results in decreased stroke volume [19.9d Variables That Influence Cardiac Output] - Cardiac output varies directly with heart rate and stroke volume - **Heart rate** depends on chronotropic agents - Influence SA node to change its firing rate - Influence AV node to alter amount of delay - **Stroke volume** - Generally depends on state of myocardium - Venous return alters stretch of heart - Inotropic agents influence crossbridge formation - Increased afterload (arteries) decreases stroke volume - Relevant in elderly individuals - **Factors Affecting Cardiac Output (Figure 19.29)**