Heart

Heart as a pump Two separate pumps Right heart Left heart Blood to respiratory system Left heart Blood to the peripheral organs

Chambers Muscle composition Atrium (Primer pump) Ventricle Atrial muscle Ventricular muscle Specialized muscles Excitatory Conductive

Atrial and ventricular muscles Similar to skeletal muscles Longer duration of contraction Excitatory and conductive fibers Few contractile fibrils Contract freely Automatic rhythmical electrical discharge Conduction of action potential

Cardiac muscle Striated Arranged in a latticework Division Recombination Spreading Myosin and actin filaments

Cardiac muscle Syncytium Muscle cells connected to each other via intercalated discs Gap junctions (free diffusion of ions) Action potential Many cells act as one large unit

Two different syncytium Atrial syncytium Ventricular syncytium Separation of atria from ventricle Fibrous tissue surrounding atrioventricular (A-V) valvular openings Prevents atrial action potential from traveling to ventricle Allows contraction of atria ahead of ventricles

Ventricular action potential 150 mV Plateau (15 times longer contraction)

Cause of plateau and longer action potential Fast Na channels Slow Ca channels (Na-Ca channels) Longer flow of Na and Ca ions (prolonged deolarization) Decreased K permeability after the onset of action potential Prevents flow of K out of the cells

Ventricular Muscle Action Potential Ca++ Channels Open More K+ Channels Open K+ Channels Open More Slow Ca++ Channels Open 1 2 3 4 phase +20 -20 Membrane Potential (mV) -40 -60 -80 Fast Na+ Channels Open -100 1 2 3 4 phase 0- Fast Na+ channels open then slow Ca++ channels phase 1- K+ channels open phase 2- Ca++ channels open more phase 3- K+ channels open more phase 4- Resting membrane potential Seconds Copyright © 2006 by Elsevier, Inc.

Velocity of signal conduction 0.3 to 0.5 mSec Purkinje fibers Refractory period Absolute refractory period 0.25 to 0.3 sec in ventricular muscle 0.15 sec in atrial muscle Relative refractory period 0.05 sec Cause premature contraction

Excitation-contraction coupling Specific mechanism Large influx of Ca from extracellular fluid via T-tubules (critical for generating stronger contraction) Poorly developed SR Larger T-tubules Mucopolysaccharides (negatively charged molecule) inside of the T-tubules Ca ion storage

Cardiac cycle Between the beginning of one heartbeat to the beginning of next heartbeat Initiated by spontaneous generation of action potential Sinus node Action potential to atrium Action potential to ventricles via A-V bundle Delayed by 0.1 sec

Diastole Systole period of relaxation Blood fills the heart Contraction

Cardiac Cycle (cont’d) Figure 9-5; Guyton & Hall

Electrocardiogram and cardiac cycle Five waves (P, Q, R, S, and T) Electrical voltages generated by the heart P-wave Spread of depolarization through atria (contraction of atria) Q, R, and S waves Depolarization of ventricle T wave Repolarization of ventricle

Pressure changes in atria Atria as primer pumps 80 % of blood flows directly through atria into the ventricle 20 % by contraction of atria Pressure changes in atria a-wave (contraction) c-wave (bulging of A-V valves due to ventricular contraction) v-wave (filling of atria while A-V valve is closed)

Ventricles as pump Systole Isovolumetric contraction Ejection Rapid rise in ventricular pressure A-V valve closure Contraction without emptying of ventricle Ejection Opening of semilunar valve (aortic and plumonary) Rapid (first 1/3, 70% emptying) Slow (last 2/3, 30 % emptying)

Cardiac Cycle (cont’d) Figure 9-5; Guyton & Hall

Diastole Dramatic fall of ventricular pressure after ejection Closure of semilunar valves Isovolumic relaxation Opening of A-V valves Rapid filling of ventricles (first 1/3 of diastole)

Cardiac Cycle (cont’d) Figure 9-5; Guyton & Hall

Stroke volume End-diastolic volume Stroke volume/ejection fraction 110-120 ml Stroke volume/ejection fraction 70 ml End-systolic volume 40 to 50 ml Increased end-diastolic volume and decreased end-systolic volume Greater stroke volume

Cardiac output Stroke volume X # heartbeat (per minute)

Function of valves Tricuspid and mitral valves Prevent backflow of blood from ventricle to atria Open and close passively Changes in pressure Chordae tendinea Connection between vanes of valve and papillary muscle Prevent valves from bulging too far during ventricular contraction

Aortic pressure curve Opening of aortic valves Ventricular pressure Stretching of aortic wall 120 mm Hg pressure Continuous blood flow Closure of aortic valves Decrease in aortic pressure 80 mm Hg pressure

Work output Two forms Volume-pressure work (external work, major proportion) Moving blood from low pressure (vein) to high pressure (artery) Kinetic energy of blood flow Acceleration of velocity to ejection speed through valves

Volume-pressure diagram Four stages associated with cardiac cycle Period of filling End-systolic to end-diastolic volume Isovolumetric contraction Valve closure Ejection Isovolumetric relaxation

Pre- and afterload Preload A Left Ventricular Volume Left Ventricular Pressure A 3 4 1 2 Increased preload Preload Degree of muscle tension when contraction beigns End-diastolic pressure Ventricle is filled Abnormal Alteration in pressure of ventricular filling

Afterload B Tension which the muscle exerts its contractile force Corresponds to systolic pressure Abnormal Arterial pressure (ventricle must contract against) Left Ventricular Volume Left Ventricular Pressure B Increased afterload 3 4 2 1

Regulation of heart pumping Intrinsic regulation Changes in volume of blood flowing to the heart Autonomic nervous system

Intrinsic regulation Frank-Starling mechanism Adaptation of the heart in response to increasing flow of blood from veins Venous return Greater the stretch of heart muscle during filling, greater the force of contraction Greater the volume of blood being pumped Stretching of right atrium

Ventricular function curves Stroke output curve Relationship between atrial pressure and ventricular output

Ventricular function curves Ventricular volume output curve Relationship between two ventricles Overall relationship Filling of ventricle by increased atrial pressure Increased ventricular volume and strength of pressure

Role of autonomic nervous system Sympathetic nerves Increases heart rate (70/min to 180-200/min) Increases contraction force Increases amount of blood being pumped out Increases ejection pressure Increase in maximum cardiac output by 2 to 3 X Addition to Frank-Starling mechanism Decreases heart rate (30 %) if inhibited Sympathetic stimulation causes pumping to be maintained at 30 % above the level without stimulation

Parasympathetic nerves (Vagus nerves) Innervates atrium Strong stimulation can stop heartbeat for a few seconds Heart “escapes” and beats 20-40/min as long as being stimulated Decreases the strength of heart muscle contraction (20-30 %) Decreases ventricular pumping by 50 % or more

Effects on cardiac function curve Right atrial pressure Controls cardiac output Sympathetic stimulation Increased cardiac output Parasympathetic stimulation Decreased cardiac output Caused by: Changes in heart rate Changes in contractile strength of heart muscle

Role of ions Excess potassium (2 to 3 x above normal) Calcium Dilation Flaccid heart (soft/flabby) Decreased heart rate Block conduction of cardiac impulses from atria to ventricle Decreased resting membrane potential Calcium Spastic contraction if excess Flaccid when deficient

Rhythmic excitation of heart Components Sinus node (sinoatrial/S-A) Internodal pathway Atrioventricular node (A-V node) A-V Bundle Bundle branches of Purkinje nerves

Rhythmic excitation of heart Special system Generation of rhythmical electrical impulses Sinus node Rapid conduction of impulses Internodal pathway A-V bundle Left and right bundle branches of Purkinje nerve Spread impulse throughout the ventricle Impulse delayed by A-V node

Sinus node Specialized cardiac muscle Absent of contractile muscle filament Smaller size (3 to 5 mm) compared to surrounding atrial muscle (10-15 mm) Capable of self-excitation Controls the rate of beat Entire heart Pacemaker Leaky membrane to Ca and Na ions Cause of self-excitation

Higher resting membrane potential (-55 to -60 mV) Higher Na ion concentrations Generation of action potential Slow Na channels Rapid opening and closing of Na-Ca channels Opening of K channel Hyperpolarization of membrane to bring membrane potential to -55 to -60 mV

Membrane Potential (mV) Rhythmical Discharge of Sinus Nodal Fiber Slow Ca++ Channels Open Sinus Nodal Fiber Ventricular Muscle fiber K+ Channels Open more +20 Threshold -20 -40 Membrane Potential (mV) } -60 “Resting Potential” -80 Na+ Leak -100 1 2 3 4 Seconds

Internodal pathways Action potential from S-A node Spread throughout atrium and reach A-V node Specialized fiber to increase speed of conduction (0.3 m/sec to 1 m/sec) Three pathway Anterior Middle Posterior Anterior interatrial band Transmit impulse from atria to the left atrium

A-V node Delayed conduction Caused by reduced number of gap junction Greater resistance to conduction of ions Emptying of atria before ventricular contraction

Internodal pathways Initial conduction delay from S-A node to internodal pathway (0.03 sec) About 0.1 sec (0.09 sec) delay from the time action potential arrives via internodal pathway Another 0.04 sec delay in the penetration portion of A-V bundle Total delay from S-A node to A-V bundle (0.16 sec)

Ventricular Purkinje system Purkinje fibers A-V node through A-V bundle into the ventricle Very large fiber Rapid conduction of action potential Instantaneous transmission of action potential throughout the ventricle High level of permeability by gap junction Very few myofibrils

Left and right branches Action potential One-way conduction Atria to ventricle Arrhythmia prevention Prevention of re-entry Fibrous barrier between atria and ventricle Insulator Left and right branches

Main Arrival Times S-A Node 0.00 sec A-V Node 0.03 sec A-V Bundle 0.12 sec Ventricular Septum 0.16 sec

Control of excitation Sinus node Faster discharge rate compared to A-V node or Purkinje fibers Pacemaker Ectopic pacemaker (other parts of heart) Shift from sinus node to A-V node or Purkinje fibers Excessive excitability Blockage of transmission Delayed initiation of impulse (Stoke-Adams syndrome)

Control of rhythmicity Parasympathetic nerves (Vagus) Release of acetylcholine when stimulated Increased permeability/leakage of K (hyperpolarization) Decreased resting potential to -65 to -70 mV Decrease rate of rhythm by S-A node Decrease excitability of A-V junctional fibers

Sympathetic stimulation Releases norepinephrine Increased Na and Ca permeability Increased resting membrane potential Acceleration of self-excitation Increased rate of sinus nodal discharge Increased rate of conduction and level of excitability Increased force of atrial and ventriclular contraction