The Heart - Collin College
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Transcript The Heart - Collin College
The Heart
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
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
Heart Wall
Epicardium – visceral layer of the serous
pericardium
Myocardium – cardiac muscle layer forming
the bulk of the heart
Fibrous skeleton of the heart – crisscrossing,
interlacing layer of connective tissue
Endocardium – endothelial layer of the inner
myocardial surface
Cardiac Muscle Bundles
External Heart: Major Vessels of
the Heart (Anterior View)
Vessels returning blood to the heart include:
Superior and inferior vena cava
Right and left pulmonary veins
Vessels conveying blood away from the heart:
Pulmonary trunk, which splits into right and
left pulmonary arteries
Ascending aorta (three branches) –
brachiocephalic, left common carotid, and
subclavian arteries
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)
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
External Heart: Arteries that Supply
the Heart
Coronary circulation is the functional blood
supply to the heart muscle itself
Collateral routes ensure blood delivery to heart
even if major vessels are occluded
External Heart: Arteries that Supply the
Heart
Right coronary artery (in atrioventricular groove)
Supplies
Right atrium
Portions of both ventricles
SA and AV nodes
Branches
Marginal artery
Posterior interventricular artery
External Heart: Arteries that Supply
the Heart
Left coronary artery
Supply
Left atrium
Portions of both ventricles
Branches
Circumflex
Anterior interventricular
Arterial Coronary Circulation
External Heart: Veins that Drain the
Heart
Veins that empty in the coronary sinus
Great cardiac vein
Posterior cardiac vein
Middle cardiac vein
Small cardiac vein
Vein that empty into the right atrium
Anterior cardiac vein
Venous Coronary Circulation
External Heart: Major Vessels of
the Heart (Posterior View)
Vessels returning blood to the heart include:
Right and left pulmonary veins
Superior and inferior vena cava
Vessels conveying blood away from the heart
include:
Aorta
Right and left pulmonary arteries
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
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)
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
Atria of the Heart
Atria are the receiving chambers of the heart
Each atrium has a protruding auricle
Pectinate muscles mark atrial walls
In the left atrium only in the wall of the
auricle
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
Papillary muscles and trabeculae carneae
muscles mark ventricular walls
Right ventricle pumps blood into the pulmonary
trunk
Left ventricle pumps blood into the aorta
Right and Left Ventricles
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
Heart Valves
Heart valves ensure unidirectional blood flow
through the heart
Atrioventricular (AV) valves lie between the
atria and the ventricles
AV valves prevent backflow into the atria when
ventricles contract
Chordae tendineae anchor AV valves to
papillary muscles
Heart Valves
Aortic semilunar valve lies between the left
ventricle and the aorta
Pulmonary semilunar valve lies between the
right ventricle and pulmonary trunk
Semilunar valves prevent backflow of blood
into the ventricles
Heart Valves
Heart Valves
Atrioventricular Valve Function
Semilunar Valve Function
Microscopic Anatomy of Heart
Muscle
Cardiac muscle is striated, short, fat, branched,
and interconnected
The connective tissue endomysium acts as
both tendon and insertion
Intercalated discs anchor cardiac cells together
and allow free passage of ions
Heart muscle behaves as a functional
syncytium
Microscopic Anatomy of Heart
Muscle
Heart is resistant to fatigue
Many mitochondria
Z discs, I band, A band,
Fewer and wider T tubules
Simpler sarcoplasmic reticulum
No triads
Microscopic Anatomy of Cardiac
Muscle
Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and is self-excitable
(automaticity)
Contracts as a unit or does not contract at all
Has a long absolute refractory period that
prevents tetany
Cardiac muscle contraction is similar to
skeletal muscle contraction
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
The intrinsic conducting system
Hyperpolarization leads to:
Loss of K
Opening of Na channels
Membrane becomes less and less negative
Threshold is reached
Ca channels opens
Influx of Ca causes the rising phase of the
action potential
Pacemaker and Action Potentials
Mechanisms of contraction
1) Rapid depolarization
Threshold
Opening of the voltage-regulated Na channels
Fast channels
Massive influx of Na
Mechanisms of contraction
2) Plateau
Transmembrane potential approaches +30mV
Na channels close and remain inactivated
Na is actively pumped out of the cell
Voltage-regulated Ca channels opens (slow
channels)
Ca enters the cytoplasma
It stimulates more Ca release from the SR
Mechanisms of contraction
This influx of Ca balances out the efflux of Na
Transmembrane potential is kept near 0mV
plateau
Mechanisms of contraction
3) Repolarization
Slow Ca channels start to close
Ca is reabsorbed by the SR or pumped out of
the cell
Slow K channels begin to open
Efflux of K causes the repolarization
Mechanisms of contraction
Heart Physiology: Sequence of
Excitation
Sinoatrial (SA) node generates impulses about
75 times/minute
Atrioventricular (AV) node delays the impulse
It generates impulses about 40-60 times/min
Smaller diameter of the fibers
Fewer gap junctions
Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)
Bundle of His is the only electrical
connection between atria and ventricle
Heart Physiology: Sequence of
Excitation
AV bundle splits into two pathways in the
interventricular septum (bundle branches)
Bundle branches carry the impulse toward
the apex of the heart
Purkinje fibers carry the impulse to the heart
apex and ventricular walls
Depolarize spontaneously at the rate of
20-40 beats/min
They supply the papillary muscles
Contract before the rest of the
ventricles
Cardiac Intrinsic Conduction
Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Impulse delayed
at AV node
AV node
Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Ventricular excitation
complete
Purkinje
fibers
Extrinsic Innervation of the Heart
Heart is stimulated
by the sympathetic
cardioacceleratory
center
Heart is inhibited by
the parasympathetic
cardioinhibitory
center
Electrocardiography
Electrical activity is recorded by
electrocardiogram (ECG)
P wave corresponds to depolarization of SA
node
QRS complex corresponds to ventricular
depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the
larger QRS complex
Electrocardiography
Electrocardiography
PR interval
Atrial depolarization and contraction
QT interval
Ventricular depolarization, contraction and
repolarization
PR segment
Atrial contraction
ST segment
Ventricular contraction
ECG Tracings
Heart
Sounds
Heart Sounds
Heart sounds (lub-dup) are associated with
closing of heart valves
First sound (S1)occurs as AV valves close
and signifies beginning of systole
Second sound (S2) occurs as SL valves
close at the beginning of ventricular diastole
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, then atrial systole
occurs
Phases of the Cardiac Cycle
Ventricular systole
Atria relax
Rising ventricular pressure results in closing
of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar
valves
Phases of the Cardiac Cycle
Isovolumetric relaxation – early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary
trunk closes semilunar valves
Dicrotic notch – brief rise in aortic pressure
caused by backflow of blood. This backflow
causes the valve to close and creates a slight
pressure rebound
Phases of the Cardiac Cycle
Cardiodynamics
End-diastolic volume (EDV)
Maximum amount of blood held in the
ventricles during diastole
End-systolic volume (ESV)
Amount of blood that remains in the
ventricles after the contraction and closing of
the semilunar valves
59
Cardiodynamics
Venous return- amount of blood returning to
the heart or blood flow during filling time
Heart rate – number of heart beats in a minute
Filling time- duration of ventricular diastole
Stroke volume (SV) – amount of blood
ejected from the ventricles with each beat
SV = EDV – ESV
60
Cardiodynamics
Cardiac output (CO) – the amount of blood
pumped by each ventricle in one minute
CO
Cardiac output
(ml/min)
=
HR
Heart rate
(beats/min)
X
SV
Stroke
volume
(ml/beat)
Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)
CO = 5250 ml/min (5.25 L/min)
Cardiac reserve is the difference between
resting and maximal CO
62
Factors Affecting stroke volume
(EDV-ESV)
EDV (end diastolic volume) is affected by:
Venous return
High venous return= high EDV
Exercise → ↑Venous return → ↑EDV→ ↑SV
↓Blood volume →↓Venous return→↓EDV→↓SV
63
Factors Affecting stroke volume
(EDV-ESV)
Filling
time
Depends on the heart rate
↑ HR → ↓Filling time→ ↓EDV→ ↓SV
64
Factors Affecting stroke volume
(EDV-ESV)
Preload
Stretchiness
of the ventricles during diastole
Directly proportional to the EDV
Frank-Starling principle (“more in = more out”)
or increased EDV=increased SV
65
Factors Affecting stroke volume
(EDV-ESV)
ESV (end systolic volume) is affected by:
Contractility
Force produced during a contraction
Positive inotropic (increases contractility)
Increased sympathetic stimuli
Certain hormones, some drugs
↑Contractility → ↓ESV→ ↑SV
66
Factors Affecting stroke volume
(EDV-ESV)
Negative
inotropic (decreases contractility)
Increased extracellular K+
Calcium channel blockers
↓Contractility → ↑ESV→ ↓SV
67
Heart Contractility
and Norepinephrine
Sympathetic
stimulation releases
norepinephrine and
initiates a cyclic
AMP secondmessenger system
Extracellular fluid
Norepinephrine
b 1-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
Sarcoplasmic
reticulum (SR)
Factors Affecting stroke volume
(EDV-ESV)
Afterload
The
pressure that must be overcome for the
ventricles to eject blood (back pressure exerted
by blood in the large arteries leaving the heart)
Increased by factors that restricts arterial blood
flow
↑Afterload→↑ESV →↓SV
69
Preload and Afterload
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
Atrial (Bainbridge) Reflex
Atrial reflex (Bainbridge Reflex) – a
sympathetic reflex initiated by increased blood
in the atria
↑Venous return→ Stimulates baroreceptors
in the atria→ ↑Sympathetic stimulation→
↑Stimulation of SA node→ ↑HR
72
Chemical Regulation of Heart Rate
The hormones epinephrine and thyroxine
increase heart rate
Intra- and extracellular ion concentrations must
be maintained for normal heart function
Hypocalcemia depresses the heart and
hypercalcemia stimulates the heart
Hyperkalemia causes heart block and
hypokalemia causes weak and irregular
contractions
Other factors influencing heart rate
Age
Exercise
Body temperature
Tachycardia
Bradycardia
Figure 20-23 Factors Affecting Stroke Volume
Factors Affecting Stroke Volume (SV)
Venous return (VR)
VR =
VR =
EDV
EDV
Filling time (FT)
FT = EDV
FT = EDV
Increased by
sympathetic
stimulation
Decreased by
parasympathetic
stimulation
Increased by E, NE,
glucagon,
thyroid hormones
Contractility (Cont)
of muscle cells
Cont =
Cont =
Preload
End-diastolic
volume (EDV)
ESV
ESV
End-systolic
volume (ESV)
STROKE VOLUME (SV)
EDV =
EDV =
SV
SV
ESV =
ESV =
SV
SV
Increased by
vasoconstriction
Decreased by
vasodilation
Afterload (AL)
AL = ESV
AL = ESV
Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)
Developmental Aspects of the
Heart
Developmental Aspects of the
Heart
Fetal heart structures that bypass pulmonary
circulation
Foramen ovale connects the two atria
Ductus arteriosus connects pulmonary trunk
and the aorta
Examples of Congenital Heart
Defects
Age-Related Changes Affecting the
Heart
Sclerosis and thickening of valve flaps
Decline in cardiac reserve
Fibrosis of cardiac muscle
Atherosclerosis