Heart Anatomy

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

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


Heart Anatomy

Figure 18.1


Coverings of the Heart: Anatomy

Pericardium – a double-walled sac around the heart composed of:

A superficial fibrous pericardium

A deep two-layer serous pericardium

The parietal layer lines the internal surface of the fibrous pericardium

The visceral layer or epicardium lines the surface of the heart

They are separated by the fluid-filled pericardial cavity


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 friction-free environment


Pericardial Layers of the Heart

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

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.4b

(b)

BrachiocephalictrunkSuperiorvena cava

Rightpulmonary artery

AscendingaortaPulmonary trunk

Rightpulmonary veinsRight atriumRight coronaryartery (in coronarysulcus)Anteriorcardiac veinRight ventricleMarginal arterySmall cardiac veinInferiorvena cava

Left commoncarotid arteryLeftsubclavian arteryAortic arch

Ligamentumarteriosum

Left pulmonary artery

Left atrium

Auricle

CircumflexarteryLeft coronaryartery (in coronarysulcus)

Anteriorinterventricular artery(in anteriorinterventricular sulcus)

Great cardiac vein

Apex

Left pulmonary veins

Left ventricle

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.4d

(d)

Superiorvena cavaRightpulmonary artery

Rightpulmonary veins

Right atrium

Right coronaryartery (in coronarysulcus)

Right ventricle

Coronary sinus

Middle cardiac vein

Left pulmonary artery

Left atrium

Auricleof left atrium

Left ventricle

Posterior veinof left ventricle

Posteriorinterventricular artery(in posteriorinterventricular sulcus)

Great cardiac vein

Apex

Leftpulmonary veins

Inferiorvena cava

Aorta

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.4e

(e)

Superior vena cava

Rightpulmonary arteryPulmonary trunk

Right atriumRightpulmonary veinsFossaovalisPectinatemuscles

TricuspidvalveRight ventricle

ChordaetendineaeTrabeculaecarneaeInferiorvena cava

Aorta

Leftpulmonary arteryLeft atriumLeftpulmonary veins

Pulmonaryvalve

Aorticvalve

Mitral (bicuspid) valve

Left ventricle

PapillarymuscleInterventricularseptumMyocardium

VisceralpericardiumEndocardium


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


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


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


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


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


Coronary Circulation: Arterial Supply

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


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


Heart Valves

Figure 18.8a, b


Heart Valves

Figure 18.8c, d


Atrioventricular Valve Function

Figure 18.9


Semilunar Valve Function

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


Microscopic Anatomy of Cardiac Muscle

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)


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


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


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


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


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


Pacemaker and Action Potentials of the Heart

Figure 18.13


Cardiac Membrane Potential

Figure 18.12


Heart Physiology: Sequence of Excitation

1) Sinoatrial (SA) node (located in the r. atrium) generates impulses about 75 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


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

Contraction begins at the apex and moves superiorly

SA node: 75x/min (dominates)

AV node: 50x/min

AVbunde (Purkinje fibers): 30x/min


Cardiac Intrinsic Conduction

Figure 18.14a


Cardiac Membrane Potential

Figure 18.12


SA node generates impulse;atrial excitation begins

Impulse delayedat AV node

Impulse passes toheart apex; ventricular

excitation begins

Ventricular excitationcomplete

SA node AV node Purkinjefibers

Bundlebranches

Figure 18.17

Heart Excitation Related to ECG


Extrinsic Innervation of the Heart

Heart is stimulated by the sympathetic cardioacceleratory center

Heart is inhibited by the parasympathetic cardioinhibitory center

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


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


Electrocardiography

Figure 18.16


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


Heart Sounds

Figure 18.19


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


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 (P-wave) Atria contract, rise in atrial

pressure Ventricle in final part of diastole

phase Atrial diastole Ventricles depolarize (QRS complex)


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



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



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


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


Cardiac Output: Example

CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)

CO = 5250 ml/min (5.25 L/min)


Regulation of Stroke Volume

SV = end diastolic volume (EDV; fill) minus end systolic volume (ESV; contraction)

EDV = amount of blood collected in a ventricle during diastole

ESV = amount of blood remaining in a ventricle after contraction


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)


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


Preload and Afterload

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


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


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

Pacemaker fires more rapidly, heart rate increases

Also enhances Ca++ entry into contractile cells

ESV falls but SV does not decline


GTP GDP

Inactive protein kinase A

Active protein kinase A

ATP cAMP

GTP

SR Ca2+

channel

Ca2+

Ca2+

bindsto

TroponinEnhancedactin-myosininteraction

Extracellular fluid

Cytoplasm

Adenylate cyclase

Ca2+

channel

Ca2+1-Adrenergicreceptor

Norepinephrine

Ca2+

uptakepump

Sarcoplasmicreticulum (SR)

Cardiac muscleforce and velocity

1

3

2

Heart Contractilityand Norepinephrine

Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system

Figure 18.22


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)

Regulation of Heart Rate: Autonomic Nervous System


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


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

Heart Anatomy

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