Post on 08-Jan-2018
description
Outline
• Comparison of types of muscle tissue • Circulatory system overview• Anatomy• Electrical activity• Mechanical events• Cardiac output• Coronary circulation
Comparison of Role of Calcium In Bringing About Contraction in Smooth, Skeletal, and Cardiac Muscle
Cardiac muscle
Cardiac Muscle Fibers• Interconnected by intercalated discs and form functional syncytia• Within intercalated discs – two kinds of membrane junctions
– Desmosomes– Gap junctions
• Ap’s
fig 16-8b, pg 487
Myofibril
Opening of Transversetubule
Intercalateddisc
Transversetubule
Longitudinalsystem
SacrolemmaBasal laminaMyofibrils
Mitochondria
Nucleus
Skeletal Muscle Fiber
fig 16-9a, pg 479
Nucleus
RoughEndoplasmicreticulum
Glycogengranules
Mitochondria
Thin filament
Thick filament
Densebodies
Plasmamembrane
Smooth Muscle Fiber
Outline
• Comparison of types of muscle tissue • Circulatory system overview• Anatomy• Electrical activity• Mechanical events• Cardiac output• Coronary circulation
Human heart.
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AnatomyHeartHollow, muscular organ about the size of a clenched fistPositioned between two bony structures – sternum and vertebrate
Circulatory System• Three basic components
– Heart• Serves as pump that establishes
the pressure gradient needed for blood to flow to tissues
– Blood vessels• Passageways through which
blood is distributed from heart to all parts of body and back to heart
– Blood • Transport medium within which
materials being transported are dissolved or suspended
• Pulmonary circulation– Closed loop of vessels carrying
blood between heart and lungs• Systemic circulation
– Circuit of vessels carrying blood between heart and other body systems
Circulatory System• Heart• Arteries
• Carry blood away from ventricles to tissues• Veins
• Vessels that return blood from tissues to the atria• Septum
– Continuous muscular partition that prevents mixture of blood from the two sides of heart
• Dual pump– Right and left sides of heart function as two separate pumps– Divided into right and left halves and has four chambers
• Atria– Upper chambers– Receive blood returning to heart and transfer it to lower chamber
• Ventricles – Lower chambers which pump blood from heart
Outline
• Internal Anatomy– Thoracic cavity, base, apex– AV and semilunar valves– endothelium, myocardium, epicardium– cardiac cells, intercalated disks– Comparison of cardiac cells to skeletal and
smooth muscle cells– pericardium
Blood Flow Through and Pump Action of the Heart
What are the parts and what do they do?Know the flow of blood in order.
Heart Valves• Atrioventricular (AV) valves
– Name = position– Prevent backflow of blood from ventricles into atria during ventricular emptying– Right AV valve = tricuspid valve– Left AV valve = bicuspid valve or mitral valve– Chordae tendinae
• Fibrous cords which prevent valves from being everted• Papillary muscles
• Semilunar valves– Aortic and pulmonary valves– Lie at juncture where major arteries leave ventricles– Prevented from everting by anatomic structure and positioning of cusps
• No valves between atria and veins– Reasons
• Atrial pressures usually are not much higher than venous pressures• Sites where venae cavae enter atria are partially compressed during atrial contraction
Endocardium
MyocardiumEpicardium
• 3 layers• Consists of three distinct layers
– Endothelium• Thin inner tissue• Epithelial tissue which lines entire
circulatory system– Myocardium
• Middle layer• Composed of cardiac muscle• Constitutes bulk of heart wall
– Epicardium • Thin external layer which covers the heart
• Pericardium– the fluid filled sac that surrounds the heart
Outline
• Electrical activity of the heart– Autorhymicity– Pacemaker (function, ions)– Conductive system (SA, AV, bundle of His,
Purkinje fibers)– Abnormal rhythms– Spread of cardiac excitation– Cardiac cell action potentials
• Characteristics vary by location
Electrical Activity of Heart• Heart beats rhythmically as result of action potentials it generates by
itself (autorhythmicity)• Two specialized types of cardiac muscle cells
– Contractile cells• 99% of cardiac muscle cells, do mechanical work of
pumping,normally do not initiate own action potentials– Autorhythmic cells
• Do not contract but send electrical signals to the contractile cells, specialized for initiating and conducting action potentials responsible for contraction of working cells
Electrical Activity of Heart• Locations of noncontractile cells capable of autorhymicity
– Sinoatrial node (SA node)• Specialized region in right atrial wall near opening of superior
vena cava• Pacemaker of the heart
– Atrioventricular node (AV node)• Small bundle of specialized cardiac cells located at base of
right atrium near septum– Bundle of His (atrioventricular bundle)
• Cells originate at AV node and enters interventricular septum• Divides to form right and left bundle branches which travel
down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls
– Purkinje fibers• Small, terminal fibers that extend from bundle of His and
spread throughout ventricular myocardium
Electrical Activity of Heart • Cardiac impulse originates at SA node• Action potential spreads throughout right and left atria• Impulse passes from atria into ventricles through AV node
(only point of electrical contact between chambers)• Action potential briefly delayed at AV node (ensures atrial
contraction precedes ventricular contraction to allow complete ventricular filling)
• Impulse travels rapidly down interventricular septum by means of bundle of His
• Impulse rapidly disperses throughout myocardium by means of Purkinje fibers
• Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions
Electrical Activity of Heart
• Atria contract as single unit followed after brief delay by a synchronized ventricular contraction
• Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction– Ensures adequate ejection time– Plateau primarily due to activation of slow L-type
Ca2+ channels
Electrical Activity of Heart
• Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum– Ca2+ induced Ca2+ release leads to cross-bridge
cycling and contraction• Because long refractory period occurs in conjunction
with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible– Ensures alternate periods of contraction and
relaxation which are essential for pumping blood– Refractory= unresponsive to stimulus
Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle
Physiology of contractile cell
fig. 18-13; pg: 568
Milliseconds
SA nodepacemaker
Atrial muscle
Atrioventricular
Bundle branch
Purkinje fibers
Ventricularmuscle
Coordination of noncontractile and contractile cells
Electrocardiogram (ECG)• Record of overall spread of electrical activity through heart• Represents
– Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body surface
• Not direct recording of actual electrical activity of heart– Recording of overall spread of activity throughout heart
during depolarization and repolarization• Not a recording of a single action potential in a single cell at
a single point in time– Comparisons in voltage detected by electrodes at two
different points on body surface, not the actual potential• Does not record potential at all when ventricular muscle is
either completely depolarized or completely repolarized
ST segment =Time during whichventricles are contractingand emptying
T wave =Ventricularrepolarization
TP interval =Time during whichventricles arerelaxing and filling
Rec
orde
d po
tent
ial
P
PR segment =AV nodal delay
QRS complex =Ventricular depolarizationatria repolarizingsimultaneously)
P wave =Atrial depolarization
SA nodefires
TPinterval
STsegment
PRsegment
Q
P
S
200 msecR
T
Fig. 9-14, p. 320
Abnormalities in Rhythm and rate• Rhythm
– Regularity or spacing of ECG waves• Arrhythmia
– Variation from normal rhythm and sequence of excitation of the heart
• Atrial flutter (200-300 BPM)• Atrial fibrillation• Ventricular fibrillation• Heart block
• Tachycardia >100 beats per minute• Bradycardia < 60 beats per minute
• Damage of the heart muscle– Myocardial ischemia
• Inadequate delivery of oxygenated blood to heart tissue– Necrosis
• Death of heart muscle cells– Acute myocardial infarction (heart attack)
• Occurs when blood vessel supplying area of heart becomes blocked or ruptured
Fig. 9-17, p. 316
•http://library.med.utah.edu/kw/pharm/hyper_heart1.html
Cardiac Output
• Volume of blood ejected by each ventricle each minute
• Determined by heart rate times stroke volume
Thresholdpotential
Thresholdpotential
= Inherent SA node pacemaker activity= SA node pacemaker activity on parasympathetic stimulation= SA node pacemaker activity on sympathetic stimulation Fig. 9-20, p. 322
• Heart rate is varied by altering balance of parasympathetic and sympathetic influence on SA node:
– Parasympathetic stimulation slows heart rate
– Sympathetic stimulation speeds it up
Cardiac Output
• Stroke volume– Determined by extent of venous return and by
sympathetic activity– Influenced by two types of controls
• Intrinsic control• Extrinsic control
– Both factors increase stroke volume by increasing strength of heart contraction
Frank-Starling Law of the Heart
• States that heart normally pumps out during systole the volume of blood returned to it during diastole
Coronary circulationNourishing the Heart Muscle
• Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers
• Heart receives most of its own blood supply that occurs during diastole– During systole, coronary vessels are compressed
by contracting heart muscle• Coronary blood flow normally varies to keep pace
with cardiac oxygen needs
Coronary Artery Disease (CAD)
• Pathological changes within coronary artery walls that diminish blood flow through the vessels
• Leading cause of death in United States• Can cause myocardial ischemia and possibly lead to
acute myocardial infarction– Three mechanisms
• Profound vascular spasm of coronary arteries• Formation of atherosclerotic plaques• Thromboembolism
Collagen-richsmooth musclecap of plaque
Normal bloodvessel wall
Lipid-rich coreof plaque
Endothelium
Plaque
Fig. 9-29, p. 328
Rightcoronaryartery
Leftcoronaryartery
Rightventricle
Leftventricle
Area of cardiacmuscle deprivedof blood supplyif coronary vesselis blocked at point
Area of cardiacmuscle deprivedof blood supplyif coronary vesselis blocked at point
Fig. 9-31, p. 331