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Heart Anatomy
Approximately the size of your fist
Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the sternum
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Heart Anatomy
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 18.1
Coverings of the Heart: Anatomy
Pericardium – a double-walled sac around the heart composed of:
The visceral layer or epicardium lines the surface of the heart
A superficial fibrous pericardium
A deep two-layer serous pericardium
The parietal layer lines the internal surface of the fibrous pericardium
They are separated by the fluid-filled pericardial cavity
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Coverings of the Heart: Physiology
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively frictionfree environment
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Pericardial Layers of the Heart
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Figure 18.2
Heart Wall
Epicardium – visceral layer of the serous pericardium
Myocardium – composed of aerobic muscle (contractile layer)
Composed of cardiac muscle bundles
Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue
Endocardium – endothelial layer of the inner myocardial surface
Lines the heart chamber and is continuous with the endothelial linings of the blood vessels
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Brachiocephalic trunk Superior vena cava
Left common carotid artery Left subclavian artery Aortic arch
Right pulmonary artery
Ligamentum arteriosum Left pulmonary artery
Ascending aorta Pulmonary trunk Right pulmonary veins Right atrium Right coronary artery (in coronary sulcus) Anterior cardiac vein Right ventricle Marginal artery Small cardiac vein Inferior vena cava (b) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Left pulmonary veins Left atrium Auricle Circumflex artery Left coronary artery (in coronary sulcus) Left ventricle Great cardiac vein Anterior interventricular artery (in anterior interventricular sulcus) Apex Figure 18.4b
Aorta Left pulmonary artery Left pulmonary veins Auricle of left atrium Left atrium
Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium
Great cardiac vein
Inferior vena cava
Posterior vein of left ventricle
Right coronary artery (in coronary sulcus) Coronary sinus
Apex
Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein
(d)
Right ventricle
Left ventricle
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Figure 18.4d
Aorta Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Fossa ovalis Pectinate muscles Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava (e) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Left pulmonary artery Left atrium Left pulmonary veins Mitral (bicuspid) valve Aortic valve Pulmonary valve Left ventricle Papillary muscle Interventricular septum Myocardium Visceral pericardium Endocardium Figure 18.4e
Atria of the Heart
Atria are the receiving chambers of the heart
Each atrium has a protruding auricle
Atria are relatively small, thin walled chambers
Atria contribute little to the propulsive pumping of the heart
Blood enters right atria from superior and inferior venae cavae and coronary sinus
Blood enters left atria from pulmonary veins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Ventricles of the Heart
Ventricles are the discharging chambers of the heart
Make up most of the volume of the heart
Trabeculae carnae are irregular ridges of myocardium
Papillary muscles are involved with valve function
Right ventricle pumps blood into the pulmonary trunk
Left ventricle pumps blood into the aorta
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Pathway of Blood Through the Heart and Lungs
Right atrium tricuspid valve right ventricle
Right ventricle pulmonary semilunar valve pulmonary arteries lungs
Lungs pulmonary veins left atrium
Left atrium bicuspid valve left ventricle
Left ventricle aortic semilunar valve aorta
Aorta systemic circulation
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Pathway of Blood Through the Heart
Pulmonary circuit is involved with gas exchange
Systemic circuit pumps oxygenated blood to the body
The two ventricles have unequal work loads
Right ventricle: short, low-pressure circulation
Left ventricle: long, high-pressure circulation, 5x more resistance than r. ventricle
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Coronary Circulation
Blood in the heart provides little nourishment to the heart
Coronary circulation is the shortest circulation in the body
Provided by the r. & l. coronary arteries arising from the base of the aorta & encircling the heart in the coronary sulcus
These vessels lie in the epicardium and send branches inward towards the myocardium
Venous blood is collected by the coronary veins following the same path as the arteries leading to the coronary sinus and then the r. atrium
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Coronary Circulation: Arterial Supply
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Figure 18.7a
Heart Valves
Heart valves ensure unidirectional blood flow through the heart
Atrioventricular (AV) valves lie between the atria and the ventricles & prevent backflow into the atria when ventricles contract
R. AV: tricuspid valve (3 cusps)
L. AV: bicuspid valve (2 cusps aka mitral valve)
Chordae tendineae anchor AV valves (in the closed position) to papillary muscles
Papillary muscles contract just prior to ventricular contraction
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Heart Valves
Aortic & pulmonary semilunar (SL) valves prevent backflow into the associated ventricles
Made of 3 cusps
Ventricular contraction forces valves open
Backflow fills the cusps thus moving (and closing them) backward
Due to low back pressure, they are not reinforced with cordae tendinae
Atrial contraction “pinches” off venae cavae and the pulmonary veins preventing substantial backflow through them
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Heart Valves
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Figure 18.8a, b
Heart Valves
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Figure 18.8c, d
Atrioventricular Valve Function
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Figure 18.9
Semilunar Valve Function
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Figure 18.10
Microscopic Anatomy of Heart Muscle
Cardiac muscle is striated, short, fat, branched, and interconnected
Contracts via the sliding filament mechanism
Connective tissue is found in the intercellular space
The connective tissue endomysium is connected to the fibrous skeleton and acts as both tendon and insertion
The plasma membrane of adjacent muscle fibers interlock at intercalated discs
The discs contain anchoring desmosomes & gap junctions
Cardiac cells are electrically coupled through these gap junctions
30% of the cell volume is mitochondria
70% of the cell is myofibrils containing typical sarcomeres
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Microscopic Anatomy of Cardiac Muscle
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Figure 18.11
Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and is self-excitable (automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period (skeletal muscle = 1-2 ms)
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Cardiac Contraction
Cardiac muscle contraction is similar to skeletal muscle contraction:
Depolarization opens a few fast voltage-gated Na+ channels
Presence of T-tubules
Ca++, troponin binding, sliding myofilaments
Cardiac muscle contraction differs from skeletal muscle contraction by:
Sarcoplasmic reticulum Ca++ release:
20% Ca++ from extracellular space (slow Ca++ channels)
80% Ca++ from S.R.
K+ permeability decrease preventing rapid repolarization
As long as Ca++ is entering, contraction continues
After 200ms, Ca++ channels close and K+ channels open
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Heart Physiology: Intrinsic Conduction System
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker potentials
Use calcium influx (rather than sodium) for rising phase of the action potential
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Energy & Electrical Requirements
The heart relies exclusively on aerobic respiration
Will use glucose and fatty acids, whichever is available
The heart does not rely on the nervous system to contract
However, autonomic nerve fibers can alter the basic rhythem
Setting the basic rhythem: Intrinsic Conduction System:
Presence of gap junctions
“In house” conduction
Consists of non-contractile cardiac cells that initiate and distribute impulses throughout the heart
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Action potential Initiation by Autorhythmic Cells
Autorhythmic cells do not maintain a stable resting membrane potential
Rather, they continuously depolarize drifting towards threshold initiating the action potential
This is due to ion channels in the sarcolemma
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Action potential Initiation by Autorhythmic Cells
Hyperpolarization closes K+ channels and opens slow Na+ channels
At 40 mV, Ca++ channels open producing the rising phase of the action potential and reversal of the membrane potential
Repolarization, as in skeletal muscle, reflects an increase in K+ permeability and efflux from the cell
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Pacemaker and Action Potentials of the Heart
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Figure 18.13
Cardiac Membrane Potential
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Figure 18.12
Heart Physiology: Sequence of Excitation
1) Sinoatrial (SA) node (located in the r. atrium) generates impulses about 100 times/minute
Sets pace for the heart as a whole (pacemaker)
2) Atrioventricular (AV) node delays the impulse approximately 0.1 second
3) Impulse passes from atria to ventricles via the atrioventricular bundle
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Heart Physiology: Sequence of Excitation
4) AV bundle splits into two pathways in the interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex of the heart
5) Purkinje fibers carry the impulse to the heart apex, ventricular walls, and papillary muscles Ventriclular contraction begins at the apex and moves superiorly SA node: 100x/min (dominates) AV node: 50x/min AVbunde (Purkinje fibers): 30x/min Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Cardiac Intrinsic Conduction
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Figure 18.14a
Heart Excitation Related to ECG
SA node generates impulse; atrial excitation begins
SA node
Impulse delayed at AV node
AV node
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Impulse passes to heart apex; ventricular excitation begins
Bundle branches
Ventricular excitation complete
Purkinje fibers
Figure 18.17
Extrinsic Innervation of the Heart
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
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Figure 18.15
Extrinsic Innervation of the Heart
Cardiac centers are located in the medulla oblongata
Cardioacceleratory center projects to sympathetic neurons in the T1-T5 level of the spinal cord
Cardioinhibitory center sends impulses to the parasympathetic dorsal vagus nucleus in the medulla
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Electrocardiography
Electrical activity is recorded by electrocardiogram (ECG)
Electrical currents generated in the heart spread throughout the body
3 waves (deflections)
P wave corresponds to depolarization of SA node thru the atria.
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex
P-Q interval is the time from the beginning of atrial excitation to the beginning of ventricular excitation
S-T segment is the time when the ventricle is depolarized
Q-T interval is the beginning of ventricular depolarization thru ventricular repolarization
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Electrocardiography
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Figure 18.16
Cardiac Cycle
Cardiac cycle refers to all events associated with blood flow through the heart
Systole – contraction of heart muscle
Diastole – relaxation of heart muscle
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Heart Sounds
Two sounds can be distinguished when the thorax is ausculated (listened to) w/ stethescope
They are associated w/ the closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole
Second sound occurs when SL valves close at the beginning of ventricular diastole
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Heart Sounds
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Figure 18.19
Phases of the Cardiac Cycle
Ventricular filling – mid-to-late diastole
Heart blood pressure is low as blood enters atria and flows into ventricles
AV valves are open but drift to closed position as blood fills ventricle (80%)
Atrial systole fills remaining 20% of ventricle
Atrial systole: depolarization (Pwave)
Atria contract, rise in atrial pressure
Ventricle in final part of diastole phase
Atrial diastole
Ventricles depolarize (QRS complex)
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Phases of the Cardiac Cycle
Ventricular systole
Atria are in diastole
Ventricles begin contracting
Rising ventricular pressure results in closing of AV valves
Ventricular ejection phase opens semilunar valves
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Phases of the Cardiac Cycle
Early diastole (following T wave)
Ventricles relax
SL valves close w/ backflow from aorta and pulmonary arteries
When blood pressure on the atrial side excedes that in the ventricles, the AV valves open and ventricular filling begins again
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Phases of the Cardiac Cycle
Notes:
Blood flow thru the heart is controlled totally by pressure changes
Blood flows down pressure gradients toward the lower pressure
Right side is low pressure
Left side is high pressure
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each ventricle in one minute
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a ventricle with each beat
Cardiac reserve is the difference between resting and maximal CO
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Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke Volume
SV = end diastolic volume (EDV; fill) minus end systolic volume (ESV; contraction)
EDV = End Diastolic Volume. Amount of blood collected in a ventricle during diastole
ESV = End Systolic Volume. Amount of blood remaining in a ventricle after contraction
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Factors Affecting Stroke Volume
Most important factors are:
Preload – amount ventricles are stretched by contained blood (affects EDV)
Contractility – cardiac cell contractile force due to factors other than EDV (affects ESV)
Afterload – back pressure exerted by blood in the large arteries leaving the heart (affects ESV)
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Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Slow heartbeat and exercise increase venous return to the heart, increasing SV by allowing more time to fill
Blood loss and extremely rapid heartbeat decrease SV
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Preload and Afterload
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Figure 18.21
Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength, independent of stretch and EDV
Enhanced contractility results in increased ejection from the heart (SV)
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Extrinsic Factors Influencing Stroke Volume
Afterload: back pressure exerted by arterial blood
The pressure that must be overcome for ventricles to eject blood
Hypertension (high blood pressure) reduces the ability of ventricles to eject blood
More blood remains in the heart after systole which increases ESV and decreases SV
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Regulation of Heart Rate
Autonomic Nervous System is the most important controller
NE binds to B-adrenergic receptors (GPCRs) in the heart causing threshold to be reached more quickly accelerating relaxation phase
Pacemaker fires more rapidly, heart rate increases
Also enhances Ca++ entry into contractile cells
ESV & EDV fall (less time to fill)
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Heart Contractility and Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Extracellular fluid Norepinephrine β1-Adrenergic receptor
Adenylate cyclase Ca2+ Ca2+ channel
Cytoplasm
GTP
GTP
1
GDP ATP
cAMP Active protein kinase A Ca2+
Inactive protein kinase A 3 Ca2+ 2
Enhanced actin-myosin interaction
Troponin
uptake pump
binds to Ca2+
SR Ca2+ channel Cardiac muscle force and velocity
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Sarcoplasmic reticulum (SR)
Figure 18.22
Regulation of Heart Rate: Autonomic Nervous System
Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
E.g. cutting the vagus nerve results in increased heart rate equal to that of the pacemaker (100 beats/min)
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Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex
Increased atrial filling leads to increased heart rate by stimulating both the SA node and atrial stretch receptors
This leads to reflex adjustments causing increased stimulation of the heart
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Chemical Regulation of the Heart
The hormones epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations must be maintained for normal heart function
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Here endth the lesson
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