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Differences from skeletal muscle
Cardiac muscles tissue has same arrangement of actin and myosin, zones, bands and Z lines as skeletal muscle. HOWEVER:
- Myofibrils of cardiac muscle cells vary in diameter
- Cardiac muscle contains less SR than skeletal muscle fibers
- Transverse tubules are larger
a. Have diameter 5x greater than T-tubules in skeletal muscle and volume 25x as great
b. Within cardiac T-tubules are mucopolysaccharides that attract Ca++ from extracellular fluid and allow for their storage. Extra Ca++ needed for contraction comes from T-tubules.
c. Quantity of Ca++ within T-tubules depends on extracellular fluid Ca++ ion concentration
- Heart has larger and more numerous mitochondria than skeletal muscle fiber
a. Cells rely almost exclusively on aerobic respiration to generate ATP
b. One-third of cell volume of cardiac contractile fibers is occupied by mitochondria
- Requires constant O2 supply
a. Cardiac muscle continuously contracts about 72 times/minute
b. Cardiac muscle extracts approx. 70-80% of O2 delivered to it by blood
Interruption of blood flow
Note: When coronary blood supply is interrupted and cells become oxygen starved, as with ischemia, oxidative ATP synthesis ceases. Glycolytic ATP production can only sustain the cell for seconds to minutes and cell becomes unable to remove Ca2+ from cytoplasm. Anaerobic glycolysis results in drop of pH as lactic acid builds up. The increase of Ca2+ and H+ acts to close gap junctions, electrically isolating the cells from the rest of the heart.
Length of action potentials
A key difference between skeletal muscle and cardiac muscle is length of action potentials.
- Longer cardiac action potentials allows for:
a. sustained force during ejection phase
b. prevention of tetanus: muscle relaxation and repolarization end almost at the same time due to long refractory period.
Conduction system: Autorhythmic cells
Do not contribute to contractile force of heart and are anatomically different from contractile cells. Smaller, do not contain organized sarcomeres. Characteristics:
1. Unstable resting membrane potential that drifts back toward threshold after repolarization
2. Fire spontaneous impulses (action potentials) that trigger contraction
3. Form conduction system that spreads impulses so heart contracts in coordinated manner. Responsible for inherent and rhythmic electrical activity of heart
4. Does not require extrinsic nerve stimulation. Nerve stimulation merely causes conducting fibers to increase or decrease rate of discharge
5. ANS and hormones do not establish fundamental rhythm; rather, modify the HR.
Physiology of autorhythmic cells
1. Resting membrane potential of -60mV and threshold of -40mV.
2. At -60mV ion (If) channels open allowing Na+ in and K+ out. Net Na+ influx inward is greater than net efflux of K+. Some slow Ca2+ channels open
3. Threshold is met
4. At -40 mV, fast Ca2+ gates open. This opens adjacent Ca2+ gates
5. Fast Ca2+ gates close at peak of AP and K+ channels open leading to repolarization
6. When repolarization hits -60mV, If channels open again
Serves as normal pacemaker of heart. Cardiac impulses originate in SA node and spread from R to L atrium via interatrial pathway (Bachmann's bundle). Impulse spreads from SA node to AV node.
Located at base of right atria near opening of coronary sinus. Cardiac impulse delayed for 0.08 to 0.12 seconds (ACh - rate of conduction through AV node. NE + rate of conduction). Spreads from AV node to Bundle of His. Divides into R and L bundle branches (descend on opposite sides of interventricular septum). Branch into Purkinje filaments (conduct impulse into mass of ventricular muscle tissue).
AP pathway through heart
SA node->atrial pathways->AV node->bundle of His->R&L bundle branches->Purkinje fibers
SA node: fastest intrinsic rate of impulse generation (60-100 bpm) SA node has most unstable RMP, reaching threshold before other cells and depolarizing them before they can generate their own AP (pacemaker)
Atrial foci: 60-80 bpm
AV node: 40-60 bpm
AV bundle: 25-45 bpm
Purkinje fibers: 20-40 bpm
Lower pacemakers serve critical function in prevention of cardiac asystole if SA node fails.
Myocardial contractile cells: Phase 4
RMP of -90 mV. Inward rectifier K+ channels open.
Myocardial contractile cells: Phase 0
1. Depolarization of autorhythmic cells spreads to gap junctions to depolarize contractile cells
2. As depolarizing currents move through gap junctions it opens Na+ gates in membrane
3. Na+ influx
4. Membrane potential hits +20mV
5. Na+ gates close
Myocardial contractile cells: Phase 1
Inward rectifier K+ gates remain open
Myocardial contractile cells: Phase 2
1. Slow Ca2+ gates open. Inward rectifier K+ channels close.
2. Delayed K+ channels open. Leads to plateau phase for 220 msec.
3. Ca2+ channels close.
Myocardial contractile cells: Phase 3
1. Delayed rectifier K+ channels close
2. Inward rectifier K+ channels begin to reopen
Phase 0: physiology
A: Autorhythmic cell depolarization and ion flow via gap junctions makes RMP of cardiac cell less negative.
1. m gates open->Na+ influx makes cell less negative->more m gates open
2. Accelerated Na+ influx->more m gates open->rapid and abrupt depolarization upstroke
B: Na+ entry progressively neutralizes negative membrane potential and thus electrostatic forces
1. Sodium influx continues b/c of concentration gradients
2. Note: Because only small amount of Na+ entry needed to alter membrane potential by more than 100mV AND significant ECF Na+ concentration, chemical forces remain constant and only electrostatic forces change
C: Na+ influx continues as chemical force exceeds outwardly directly chemical force; results in overshoot
1. At approx. +30mV the h, inactivation gates, are fully closed. Na+ channels inactivate.
Phase 1: physiology
1. h gates on Na+ channels completely closed
2. Slow closing of inward rectifier K+ channels combined with efflux of K+ results in short, rapid repolarization
3. Depolarization in phase 0 had set into motion 2 events:
a. closing of inward rectifier K+ channels (unusual b/c depolarization usually leads to K+ channels opening)
b. opening of voltage gated L-type Ca2+ channels
Phase 2: physiology
1. Opening of voltage regulated L-type Ca2+ channels allows Ca2+ to enter
2. Ca2+ influx is counter balanced by K+ efflux resulting in plateau. Also, Inward rectifier K+ channels close.
3. Ca2+ influx permits release of more Ca2+ from sarcoplasmic reticulum needed for myocardial contraction
4. Slow opening delayed rectifier K+ channels begin to open, gradually increasing efflux of K+. This occurs slowly over course of plateau phase.
Phase 3: physiology
1. Repolarization initiated as delayed rectifier K+ channels open fully and K+ efflux exceeds Ca2+ influx
2. Ca2+ channels close
3. Inward rectifier K+ begin to open again as Vm becomes more negative
4. Chemical forces beat electrostatic forces so K+ efflux exceeds K+ influx
Phase 4: physiology
1. RMP restored as Na+/K+ ATPase removes Na+ from cell and brings K+ back into cell
2. Ca2+ eliminated from interior cell. This happens when:
a. Na+/Ca2+ exchanges (3 Na+ in for 1 Ca2+ out. Na+/K+ ATPase then removes Na+ from cell).
b. Ca2+ ATPase pump (SERCA: sarcoplasmic endoplasmic reticulum Ca2+ ATPase)
3. At RMP chemical forces only slightly exceed electrostatic forces so K+ efflux barely exceeds K+ influx.
Role of Ca2+ in cardiac fiber contraction
EC Ca2+ enters cell and binds to ryanodine receptors in SR. Ryanodine receptor channels open, releasing additional Ca2+ from RyR2.
The greater the influx of Ca2+ from EC fluid, the greater the release of Ca2+ from SR and greater the force of contraction. Strength of contraction depends on EC Ca2+ ion concentration. Thus, if Ca2+ is removed from EC environment and cells depolarize, there will be no contraction.
Once released from SR, Ca2+ diffuses into sarcoplasm and results in sliding of actin and myosin filaments. Ca2+ binds troponin leading to contraction.
Epinephrine/Norepinephrine in cardiac fiber contraction
Epi and Norepi active Beta 1 receptors, opening more Ca2+ gates on cell membrane and increasing strength of contraction. They also activate phosopholamban, which enhances Ca2+-ATPase remove of Ca2+ from cytosol and thus shorting time Ca2+ is bound to troponin.
Measures electrical activity of heart by giving composite of AP produced by ALL the heart muscle fibers during each beat.
1st wave: Represents atrial depolarization.
Impulse moves from SA node throughout both atria. About 0.1 sec after P wave begins, atria contract.
Note: Unable to see atrial repolarization since it is osbscured by large QRS complex.
Represents length of time from start of atrial depolarization (P wave) to start of ventricular depolarization (QRS). This interval represents complete excitation of the autorhythmic pathway and contraction of atria (Initial SA impulse, atrial depolarization, AV node depolarization, His-Purkinje system depolarization)
Interval usually less than .2 sec (one large square on EKG). If interval is longer than .2, it indicates some type of AV block.
2nd wave: Represents onset of ventricular depolarization. This complex demonsrates the depolarization of the contractile myocytes as opposed to earlier depolarization of His-Purkinje system.
Represents time when ventricular contractile fibers are fully depolarized from end of R to start of T.
3rd wave: Represents ventricular repolarization.
Occurs just before ventricles start to relax. Smaller, more spread out than QRS wave b/c repolarization occurs more slowly than depolarization.
All events included in one complete heart beat
Repolarization of ventricular muscle fibers (T wave) initiates relaxation.
1. As ventricles relax, mmHg decreases and blood flows from pulmonary trunk and aorta back toward ventricles.
2. Semilunar valves close (DUBB)
Dicrotic wave: seen on aortic mmHg curve as blood rebounds off closed cusps
Isovolumetric relaxation: Ventricle pressure drops below aortic pressure but still exceeds atrial pressure.
When ventricular mmHg falls below atrial mmHg the AV valves open and ventricular filling begins
80% occurs between T and P wave. 20% occurs during atrial systole. SA node fires (P wave) leading to atrial contraction.
Note: Ventricular pressure does not significantly increase until ventricular volume exceeds 150 ml and then increases sharply as heart tissue and fibrous pericardium stretch to near max.
Contraction of ventricles (QRS complex).
Contraction of ventricles increase mmHg and pushes blood up into cusps of AV valves, closing them (LUBB) around 10 mmHg. Once mmHg surpasses aortic pressure at 80 mmHg and pulmonary pressure at 15-20 mmHg, semilunar valves open. Blood ejected from heart.
Isovolumetric contraction: Split-second period when AV valves closed but semilunar valves not yet open (R-S) as ventricles contract.
First sound: Lubb (created by blood turbulence associated with closure of AV valves @ beginning of ventricular systole)
Second sound: Dubb (created by closure of semilunar valves @ beginning of ventricular diastole)
Amount of blood pumped out of each ventricle in 1 minute. Determined by stroke volume and HR.
ex: CO=(average SV 70 ml/beat) x (average HR 75 beats/min)
CO=5250 ml/min or 5.25 liters/min
Total blood volume is 5-6 liters, thus heart pumps equivalent of total blood volume each minute under resting conditions.
Maximum percentage that the heart can increase the CO above an individual's normal CO.
Healthy adult typically able to raise CO 4-5 times normal.
If normal CO is 5.25 liters/min and CO during exercise is 21 liters/min, then cardiac reserve is about 400%.
Maximal cardiac output ranges
* 14-16 liters/min in untrained individuals
* 20-25 liters/min in trained individuals (CO=bpm x 130ml/min=20,800 ml/min=20.8l/m)
* Up to 40 liters/min in large highly conditioned endurance athletes
End diastolic volume (preload)
Volume of blood in ventricles at end of diastole just prior to contraction. Determined by length of ventricle diastole and venous mmHg
About 130 ml
End systolic volume (afterload)
Volume in blood in ventricles at end of systole and beginning of diastole. Determined by arterial BP. Increase in arterial BP increases ESV
About 60 ml
Amount of blood ejected by each ventricle per beat.
Heart pumps out 50-60% of blood that enters ventricles with each beat. 40-50% remains in ventricle.
Factors influencing stroke volume
2. Mean arterial pressure
EDV and stroke volume
Preload-about 130 ml. Major INTRINSIC factor influencing stroke volume.
The greater the preload stretch (EDV) the greater the force of contraction (Frank-Starlings law)
EDV determined by length of ventricular diastole and venous return (venous return influenced by: 1. skeletal pump 2. respiratory pump 3. increased sympathetic activity, which leads to constriction of veins which decreases volume in veins.
Frank-Starlings law and stroke volume
The more the heart is filled during diastole, the greater the force of contraction during systole. Thus, the greater preload stretch (EDV) the greater the force of contraction.
Thought to be due to optimizing the length tension relationship.
Evidence also suggests that stretching allows more Ca2+ to enter thus increasing strength of contraction.
Frank-Starlings explains why you can go from an unequal amount from R to L ventricle to an equal amount.
MAP (mean arterial pressure) and stroke volume
Represents an impedence to ejection of blood once contraction has begun. In other words, pressure that must be overcome before semilunar valves open. Thus MAP influences afterload (ESV).
If arterial BP increases, SV decreases and ESV increases. ESV represents afterload and is determined by arterial BP.
MAP=80 mmHg of pressure.
Contractibility and stroke volume
Strength of contraction at any given preload. An increase in SV independent of EDV. Major EXTRINSIC factor independent of preload stretch.
Positive inotropic sympathetic activation increases Ca2+ influx, which produces the more vigorous contraction at same EDV, and thus leads to an increase in blood ejection from the heart.
Generally an INTRINSIC function.
Without neural regulation, the heart will beat at rate set by SA node. Therefore, ANS innervation of SA node is major means by which cardiac rate is regulated.
Negative chronotropic effect
Parasympathetic NS has predominate inhibitory (negative chronotropic) effect on HR at rest via vagus nerve.
Parasympathetic NS releases Ach, which activates muscarinic receptors that:
1. influence increase in K+ ion permeability and hyperpolarize the cell
2. decrease permeability to Ca2+ which slows rate of depolarization
Both these influences hyperpolarizes the SA node and decreases rate of spontaneous firing.
Note: transecting vagus nerve would immediately increase HR approx. 30 bpm, up to inherent rate of SA node.
Positive chronotropic effect
Sympathetic NS has positive chronotropic effect.
Noepinephrine and epinephrine bind to Beta 1 receptors on autorhythmic cells. Activiates cAMP second messanger systems to increase ion flow through If channels and Ca2+ channels. Thus pacemaker fires action potentials at faster rate.
Note: Sympathetic has both positive chronotropic and positive inotropic effect on heart.
Inotropic vs. chronotropic
Inotropic-related to strength of muscular contractions of heart.
chronotropic-related to heart rate.
How EDV, MAP, contractility affect Stroke Volume
Increase in EDV: Increase in stroke volume
Decrease in EDV: Decrease in stroke volume
Increase in MAP: Decrease in stroke volume (ESV increase)
Decrease in MAP: Increase in stroke volume (ESV decrease)
Increase in contractility: Increase in stroke volume
Decrease in contractility: Decrease in stroke volume
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