Professional Documents
Culture Documents
prepared by
Barbara Heard,
Atlantic Cape Community
College
CHAPTER 18
The
Cardiovascular
System: The
Heart: Part A
Annie Leibovitz/Contact Press Images 2013 Pearson Education, Inc.
The Pulmonary and Systemic Circuits
Pulmonary Circuit
Pulmonary
arteries Pulmonary veins
Aorta and branches
Venae
cavae
Left
atrium
Left
Right ventricle
atrium Heart
Right
ventricle
Systemic Circuit
Midsternal line
2nd rib
Sternum
Diaphragm Location of
apical impulse
Superior Aorta
vena cava Parietal pleura
(cut)
Pulmonary Left lung
trunk
Pericardium (cut)
Apex of heart
Diaphragm
Double-walled sac
Superficial fibrous pericardium
Protects, anchors to surrounding structures,
and prevents overfilling
Pulmonary
trunk Fibrous pericardium
Parietal layer of serous
Pericardium pericardium
Myocardium Pericardial cavity
Epicardium (visceral
layer of serous
pericardium) Heart
Myocardium wall
Endocardium
Heart chamber
Pericarditis
Inflammation of pericardium
Roughens membrane surfaces pericardial
friction rub (creaking sound) heard with
stethoscope
Cardiac tamponade
Excess fluid sometimes compresses heart
limited pumping ability
Epicardium
Visceral layer of serous pericardium
Myocardium
Spiral bundles of contractile cardiac muscle
cells
Cardiac skeleton: crisscrossing, interlacing
layer of connective tissue
Anchors cardiac muscle fibers
Supports great vessels and valves
Limits spread of action potentials to specific paths
Pulmonary
trunk Fibrous pericardium
Parietal layer of serous
Pericardium pericardium
Myocardium Pericardial cavity
Epicardium (visceral
layer of serous
pericardium) Heart
Myocardium wall
Endocardium
Heart chamber
Cardiac
muscle
bundles
Four chambers:
Two superior atria
Two inferior ventricles
Interatrial septum separates atria
Fossa ovalis remnant of foramen ovale of
fetal heart
Interventricular septum separates
ventricles
Aorta
Left pulmonary artery
Superior vena cava
Left atrium
Right pulmonary artery
Left pulmonary veins
Pulmonary trunk
Right atrium
Mitral (bicuspid) valve
Right pulmonary veins
Frontal section
Small, thin-walled
Contribute little to propulsion of blood
Three veins empty into right atrium:
Superior vena cava, inferior vena cava,
coronary sinus
Four pulmonary veins empty into left
atrium
Pulmonary trunk
Auricle of right atrium
Anterior interventricular
artery
Right ventricle
Aortic valve
Right ventricle anterior
wall (retracted)
Pulmonary valve
Trabeculae carneae
Interventricular
septum (cut)
Opening to right
atrium Left ventricle
Right ventricle
Cusp of
2 As ventricles fill, AV valve flaps atrioventricular
hang limply into ventricles. valve (open)
Chordae
3 Atria contract, forcing additional tendineae
blood into ventricles. Papillary
Ventricle muscle
AV valves open; atrial pressure greater than ventricular pressure
Atrium
Cusps of
1 Ventricles contract, forcing atrioventricular
blood against AV valve cusps. valve (closed)
Aorta
Pulmonary
trunk
As ventricles contract
and intraventricular
pressure rises, blood
is pushed up against
semilunar valves,
forcing them open.
As ventricles relax
and intraventricular
pressure falls, blood
flows back from
arteries, filling the
cusps of semilunar
valves and forcing
them to close.
Myocardium
Mitral
(left atrioventricular)
valve
Tricuspid
(right atrioventricular)
valve
Aortic valve
Pulmonary valve
Cardiac
skeleton
Anterior
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Figure 18.6b Heart valves.
Pulmonary valve
Aortic valve
Area of cutaway
Mitral valve
Tricuspid valve
Myocardium
Mitral
(left atrioventricular)
valve
Tricuspid
(right atrioventricular)
valve
Aortic valve
Pulmonary valve
Area of cutaway
Mitral valve
Tricuspid valve
Pulmonary valve
Aortic valve
Area of cutaway
Mitral valve
Tricuspid valve
Myocardium
of right
ventricle
Interventricular
septum
Papillary Myocardium
muscles of left ventricle
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Homeostatic Imbalance
Pulmonary circuit
Right atrium tricuspid valve right
ventricle
Right ventricle pulmonary semilunar valve
pulmonary trunk pulmonary arteries
lungs
Lungs pulmonary veins left atrium
Systemic circuit
Left atrium mitral valve left ventricle
Left ventricle aortic semilunar valve
aorta
Aorta systemic circulation
Systemic Pulmonary
capillaries capillaries
Aorta Pulmonary
veins
Mitral Left
Aortic
semilunar valve atrium
valve Left
ventricle
Aortic
Semilunar Mitral
Left valve Left Four
valve
Aorta ventricle atrium pulmonary
2013 Pearson Education, Inc. veins
Figure 18.9 The heart is a double pump, each side supplying its own circuit. Slide 2
SVC
Coronary
sinus
IVC
SVC
Coronary
sinus
Right
atrium
IVC
Tricuspid
Superior vena cava (SVC) Right valve Right Oxygen-poor blood
Inferior vena cava (IVC)
Coronary sinus atrium ventricle
Oxygen-rich blood
SVC Tricuspid
Coronary
valve
sinus
Right
atrium
Right
IVC ventricle
Pulmonary
Tricuspid Semilunar
Superior vena cava (SVC) Right valve Right valve Pulmonary Oxygen-poor blood
Inferior vena cava (IVC) trunk
atrium ventricle Oxygen-rich blood
Coronary sinus
Pulmonary
arteries
SVC Tricuspid
Coronary
sinus valve Pulmonary
trunk
Right
atrium
Pulmonary
Right semilunar
ventricle valve
IVC
Pulmonary
arteries
SVC Tricuspid
Coronary
sinus valve Pulmonary
trunk
Right
atrium
Pulmonary
semilunar
Right
valve
IVC ventricle
Pulmonary
capillaries
veins
Four
pulmonary
veins
2013 Pearson Education, Inc.
Figure 18.9 The heart is a double pump, each side supplying its own circuit. Oxygen-poor blood Slide 8
Pulmonary
Right
veins ventricle
Left
atrium
Left Four
atrium pulmonary
veins
2013 Pearson Education, Inc.
Figure 18.9 The heart is a double pump, each side supplying its own circuit. Slide 9
Oxygen-poor blood
Oxygen-rich blood
Pulmonary
veins
Mitral Left
valve atrium
Left
ventricle
Mitral
Left Left Four
valve
ventricle atrium pulmonary
veins
Oxygen-poor blood
Oxygen-rich blood
Right
ventricle
Aorta Pulmonary
veins
Aortic
Semilunar Mitral
valve Left Left Four
valve
Aorta ventricle atrium pulmonary
veins
Systemic
capillaries
Oxygen-rich blood is
delivered to the body
To body
tissues (systemic
circuit).
Aorta Pulmonary
veins
Aortic
Semilunar Mitral
valve Left Left Four
valve
Aorta ventricle atrium pulmonary
veins
2013 Pearson Education, Inc.
Figure 18.9 The heart is a double pump, each side supplying its own circuit. Slide 12
Both sides of the heart pump at the same time, but lets Oxygen-poor blood
follow one spurt of blood all the way through the Oxygen-rich blood
system. Pulmonary
Tricuspid Semilunar
Superior vena cava (SVC) Right valve Right valve Pulmonary
Inferior vena cava (IVC)
Coronary sinus atrium ventricle trunk
Pulmonary
Tricuspid arteries
SVC Coronary valve Pulmonary
sinus trunk
Right
atrium Pulmonary
Right semilunar
IVC ventricle valve
Oxygen-poor blood is carried
Oxygen-poor blood
To heart in two pulmonary arteries to To lungs
returns from the body
the lungs (pulmonary circuit)
tissues back to the heart.
to be oxygenated.
Systemic Pulmonary
capillaries capillaries
Aorta Pulmonary
veins
Mitral Left
Aortic
semilunar valve atrium
valve Left
ventricle
Aortic
Semilunar Mitral
Left valve Left Four
valve
Aorta ventricle atrium pulmonary
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Pathway of Blood Through the Heart
Left
ventricle
Right
ventricle
Interventricular
septum
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Coronary Circulation
Superior
vena cava
Anterior Great
cardiac cardiac
veins vein
Coronary
sinus
Small
cardiac vein Middle cardiac vein
Angina pectoris
Thoracic pain caused by fleeting deficiency in
blood delivery to myocardium
Cells weakened
Myocardial infarction (heart attack)
Prolonged coronary blockage
Areas of cell death repaired with
noncontractile scar tissue
Intercalated Cardiac
Nucleus discs muscle cell Gap junctions Desmosomes
Cardiac muscle
cell
Mitochondrion Nucleus
Intercalated
disc
Mitochondrion
T tubule
Sarcoplasmic
reticulum Z disc
Nucleus
Sarcolemma
I band A band I band
More differences
Depolarization wave also opens slow Ca2+
channels in sarcolemma SR to release its
Ca2+
Ca2+ surge prolongs the depolarization phase
(plateau)
More differences
Action potential and contractile phase last
much longer than a neuron.
Allow blood ejection from heart
Repolarization result of inactivation of Ca2+
channels and opening of voltage-gated K+
channels
Ca2+ pumped back to SR and extracellularly
Tension (g)
(contraction) Channel inactivation ends this phase.
20
1 3 2 Plateau phase is due to Ca2+
40 influx through slow Ca2+ channels.
This keeps the cell depolarized
60 because few K+ channels are open.
Absolute
80
refractory 3 Repolarization is due to Ca2+
period channels inactivating and K+
channels opening. This allows K+
0 150 300 efflux, which brings the membrane
Time (ms) potential back to its resting voltage.
Tension (g)
(contraction) Channel inactivation ends this phase.
20
1
40
60
Absolute
refractory
80 period
0 150 300
Time (ms)
Tension (g)
(contraction) Channel inactivation ends this phase.
20
1 2 Plateau phase is due to Ca2+
40 influx through slow Ca2+ channels.
This keeps the cell depolarized
60 because few K+ channels are open.
Absolute
refractory
80 period
0 150 300
Time (ms)
Tension (g)
(contraction) Channel inactivation ends this phase.
20
1 3 2 Plateau phase is due to Ca2+
40 influx through slow Ca2+ channels.
This keeps the cell depolarized
60 because few K+ channels are open.
Absolute
80
refractory 3 Repolarization is due to Ca2+
period channels inactivating and K+
channels opening. This allows K+
0 150 300 efflux, which brings the membrane
Time (ms) potential back to its resting voltage.
Cardiac muscle
Has many mitochondria
Great dependence on aerobic respiration
Little anaerobic respiration ability
Readily switches fuel source for respiration
Even uses lactic acid from skeletal muscles
Internodal pathway
3 The Subendocardial
atrioventricular conducting
(AV) bundle network
connects the atria (Purkinje fibers)
to the ventricles.
4 The bundle branches
conduct the impulses Inter-
through the ventricular
interventricular septum. septum
5 The subendocardial
conducting network
depolarizes the contractile
cells of both ventricles.
Pacemaker potential
SA node
Atrial muscle
AV node
Pacemaker Ventricular
potential muscle
Plateau
AV
node
SA
node
Sinoatrial
node
Atrioventricular
node
QRS complex
R
Ventricular
depolarization
Atrial Ventricular
depolarization repolarization
P T
Q
P-R S-T
Interval Segment
S
Q-T
Interval
0 0.2 0.4 0.6 0.8
2013 Pearson Education, Inc. Time (s)
Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 1
waves of an ECG tracing.
SA node R
R
P T
P T
Q
S Q
S
1 Atrial depolarization, initiated by 4 Ventricular depolarization is
the SA node, causes the P wave. complete.
R
AV node R
T P T
P
Q Q
S S
2 With atrial depolarization 5 Ventricular repolarization begins
complete, the impulse is delayed at at apex, causing the T wave.
the AV node.
R
R
P T
P T
Q
Q S
S 6
Ventricular repolarization is complete.
3 Ventricular depolarization begins at
apex, causing the QRS complex. Atrial
repolarization occurs. Depolarization Repolarization
P-R interval
Beginning of atrial excitation to beginning of
ventricular excitation
S-T segment
Entire ventricular myocardium depolarized
Q-T interval
Beginning of ventricular depolarization
through ventricular repolarization
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Cardiac cycle
Blood flow through heart during one complete
heartbeat: atrial systole and diastole followed
by ventricular systole and diastole
Systolecontraction
Diastolerelaxation
Series of pressure and blood volume changes
2. Ventricular systole
Atria relax; ventricles begin to contract
Rising ventricular pressure closing of AV
valves
Isovolumetric contraction phase (all valves
are closed)
In ejection phase, ventricular pressure
exceeds pressure in large arteries, forcing SL
valves open
End systolic volume (ESV): volume of blood
remaining in each ventricle after systole
Left heart
QRS
P T P
Electrocardiogram
1st 2nd
Heart sounds
Dicrotic notch
120
Left ventricle
40
Atrial systole Left atrium
0
120
volume (ml)
Ventricular
EDV
SV
50 ESV
Left atrium
Right atrium
Left ventricle
Right ventricle
At rest
CO (ml/min) = HR (75 beats/min) SV (70 ml/beat)
= 5.25 L/min
CO increases if either/both SV or HR increased
Maximal CO is 45 times resting CO in nonathletic
people
Maximal CO may reach 35 L/min in trained athletes
Cardiac reserve - difference between resting and
maximal CO
SV = EDV ESV
EDV affected by length of ventricular diastole
and venous pressure
ESV affected by arterial BP and force of
ventricular contraction
Three main factors affect SV:
Preload
Contractility
Afterload
Extracellular fluid
Norepinephrine
Adenylate cyclase Ca2+
Ca2+
1-Adrenergic channel
receptor G protein (Gs)
ATP is converted
Cytoplasm
to cAMP
a Phosphorylates plasma
GDP membrane Ca2+
channels, increasing
extracellular Ca2+ entry
Inactive protein Active protein
kinase kinase
SR Ca2+ Sarcoplasmic
channel reticulum (SR)
Cardiac muscle
force and velocity
EDV
ESV
(preload)
Result Cardiac
output
Hormones
Epinephrine from adrenal medulla increases
heart rate and contractility
Thyroxine increases heart rate; enhances
effects of norepinephrine and epinephrine
Intra- and extracellular ion concentrations
(e.g., Ca2+ and K+) must be maintained for
normal heart function
Age
Fetus has fastest HR
Gender
Females faster than males
Exercise
Increases HR
Body temperature
Increases with increased temperature
Pulmonary congestion
Left side fails blood backs up in lungs
Peripheral congestion
Right side fails blood pools in body organs
edema
Failure of either side ultimately weakens
other
Treat by removing fluid, reducing afterload,
increasing contractility
Day 20: Day 22: Day 24: Heart Day 28: Bending Day 35: Bending is
Endothelial Heart starts continues to continues as ventricle complete.
tubes begin pumping. elongate and moves caudally and
to fuse. starts to bend. atrium moves cranially.
Ductus arteriosus
Foramen
ovale
Ductus venosus
Sounds
Normal
http://www.easyauscultation.com/
cases-listing-details.aspx?caseID=7
The human heart begins beating at a rate near the mothers, about
75-80 BPM.
The embryonic heart rate (EHR) then accelerates linearly for the first
month of beating, peaking at 165-185 BPM during the early 7th week.
This acceleration is approximately 3.3 BPM per day, or about 10 BPM
every three days
( increase of 100 BPM in the first month).
After peaking at about 9.2 weeks after the normal menstrual period
(LMP), it decelerates to about 150 BPM (+/-25 BPM) during the 15th
week after the LMP.
Terry J. DuBose, M.S., RDMS; Director Diagnostic Medical
Congenital Heart Diseases: Neonate &
Young Infant
Significant congenital heart disease (CHD) may be
diagnosed at virtually any age.
Perry et al. 2010. Maternal Child Nursing Care, 4th Edition. Chapter 48
Septal defects
Na+
K+
Brugada syndrome : Genetic disease, abnormal ECG sudden cardiac death (Sudden Unexpected
Death Syndrome -SUDS). First described in 1992, ventricular fibrillation mutation in Na+ ion channel
Ion channels