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Transcript
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
The Cardiovascular System Defined
 What it is:
• A closed system of the
heart and blood vessels
o The heart pumps blood
o Blood vessels allow
blood to circulate to all
parts of the body
 Function:
• Deliver oxygen and
nutrients and to remove
carbon dioxide and
other waste products
Heart Gross Anatomy
•
Location: Mediastinum of the thorax
•
Size: As big as your fist
•
Serous Membrane Coverings:
1.
Epicardium (= visceral pericardium) innermost
2.
Parietal pericardium outermost
3.
Mediastinal pleura outside that
The Heart Wall: Three Layers
Visceral
Parietal
Myocardium
Endocardium
Pericardium
Pericardium
(Epicardium)
Parietal
= visceral
pericardium
Exception: In the heart layers, peri- is outside of epi-
Coronal Section of Human Heart
Flow of Blood Through the Heart
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Operation of Heart Valves
AV valves
Semilunar
valves
Stenotic and Regurgitant Valve Conditions
Heart sounds movie online
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Coronary Circulation: Blood Feeding the Heart
Superior
vena cava
Anastomosis
(junction of
vessels)
Right
atrium
Aorta
Pulmonary
trunk
Left atrium
Left
coronary
artery
Circumflex
artery
Right
coronary
Left
artery
ventricle
Right
ventricle
Anterior
Right
interventricular
marginal Posterior
artery
artery
interventricular
artery
Posterior View of Heart
Circumfle
x artery
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Homeostatic Imbalances
 Angina pectoris
• Thoracic pain caused by a fleeting
deficiency in blood delivery to the
myocardium
• Cells are weakened
• Erythrocyte sedimentation rate (ESR)
is normal in patients who experience
only angina.
 Myocardial infarction (heart attack)
• Prolonged coronary blockage due to, e.g.
cardiac embolism or throbus
o
Causes ischemia (lack of O2) leading to
muscle death
• Areas of cell death are repaired with noncontractile scar tissue
• ESR is elevated after an MI; can be used for
diagnosis
Heart Muscle, Compared
Intercalated disks
Cardiac Muscle Behaves as a Single Unit
Nucleus
Intercalated discs
Cardiac muscle cell
Gap junctions between
cardiac cells provide
electrical coupling
between cells, making the
myocardium behave as a
single coordinated unit.
Gap junctions
Desmosomes
In smooth and skeletal
muscles, depolarization
sweeps across the surface
of cells. In cardiac
muscle, depolarization
occurs from within
through gap junctions.
Cardiac Cells Have Simpler T-Tubules
Cardiac
muscle cell
Mitochondrion
Intercalated
disc
Nucleus
T tubule
Mitochondrion
Sarcoplasmic
reticulum
Z disc
Nucleus
Sarcolemma
(b)
I band
A band
I band
Figure 18.11b
Four Step Power Cycle or “Cross Bridge Cycle”
Thin filament
Actin
Ca2+
Myosin
cross bridge
ADP
Pi
Thick
filament
Myosin
Cross
bridge
formation.
1
ADP
ADP
Pi
Pi
ATP
hydrolysis
2 The power (working)
stroke.
4 Cocking of myosin head.
ATP
ATP
3 Cross bridge
detachment.
Figure 9.12
The Power Cycle
A. Masking protein complex (tropomyosin) binds Ca++ released from the
SR moves aside to expose head-binding sites
B. Steps of the Power Cycle
1. "Cocked" myosin head binds to actin myofilament site
2. Head bends towards the M line (sarcomere center-line), pulling
thin filament along and releasing ADP and P (broken ATP) for
the power stroke
3. ATP binds to the myosin head, causing it to detach
4. Myosin head “recocks” as ATP broken down to ADP and P
Longer Refractory Period in Cardiac Cells Prevents Tetanic Contractions
1 Depolarization is
due to Na+ influx through
fast voltage-gated Na+
channels. A positive
feedback cycle rapidly
opens many Na+
Long-lasting
channels, reversing the
tension
membrane potential.
inactivation ends
Briefdevelopment
tension developmentChannel
(contraction)
(contraction)
this phase.
Stimulus of a skeletal
muscle
2
3
1
-60
Long absolute
refractory
period
Short refractory period
Time (ms)
Ca+2
About 20% of the
needed for the calcium pulse enters
from the extracellular fluid, triggering large Ca+2 release from
the SR.
Tension (g)
Membrane potential (mV)
Action
potential
Plateau
2 Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
3 Repolarization is
due to Ca2+ channels
inactivating and K+
channels opening. This
allows K+ efflux, which
brings the membrane
potential back to its
resting voltage.
Figure 18.12
Cardiac Stimulation and Contraction is Different
Cell
type
Resting
potential
Stability of
resting
potential
Source of Ca+2
for binding
totroponin
Main
trigger of
contraction
cycle
Range of
depolarization
in action
potential
Duration
of action
potential
Duration of
contraction
Skeletal
muscle
-60 mV
Stable, no
leaks
All from
sarcoplasmic
reticulum;
released only by
depolarization
Neurally
stimulated
depolarization to
single cells
100 mV (-70
mV to +30 mv)
1-2 ms;
short
refractory
period
15-100 ms;
brief
contraction
Cardiac
muscle
-80 mV
Most stable
but
pacemaker
cells drift
towards 0
mV due to
some open
Na+
channels
10-20%
extracellular
Ca+2 through
slow Ca+2
channels,
dramatically
increasing total
Ca+2 release
from SR
Depolarization of
neighboring
cells
120 mV (-90
mV to +30
mV)
200+ ms;
long
refractory
period
200+ ms;
longer
sustained
contraction
Longer Refractory Period in Cardiac Cells Prevents Tetanic Contractions
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
The Heart: Conduction System

Intrinsic conduction system
(nodal system)
•

Heart muscle cells
contract, without nerve
impulses, in a regular,
continuous way
Special tissue sets the pace
1.
Sinoatrial node
(pacemaker)
2.
Atrioventricular node
3.
Atrioventricular bundle
4.
Bundle branches
5.
Purkinje fibers

Contraction is initiated by the
sinoatrial node

Sequential stimulation occurs at
other autorhythmic cells
Pacemaker with electrode in right ventricle
Exterior conduction
Homeostatic Imbalances

Defects in the intrinsic conduction system
may result in
1. Arrhythmias: irregular heart rhythms
2. Uncoordinated atrial and ventricular
contractions
3. Fibrillation: rapid, irregular contractions;
useless for pumping blood
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhymic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Filling of Heart Chambers – the Cardiac Cycle
 1. Atria contract simultaneously
 2. Atria relax, then ventricles contract
 Systole = contraction (can be subdivided into atrial and ventricular contraction
but otherwise refers to ventricular systole)
 Diastole = relaxation (ventricular)
Figure 11.6
Medulla Oblongata Cardiac Centers Accelerated and Decelerate Heart Beat
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Medulla oblongata
Cardioacceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15
Electrocardiograph - A chart Showing Heart Electrical Activity
QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
Figure 18.16
Heart Voltages and the ECG
Pressure, ECG, and Heart
online
EKG, Heart contractions,
conduction online
Ventricular systole occurs
Ventricular
systole
occurs
in T
(a) Normal sinus rhythm.
(b) Junctional rhythm. The SA
node is nonfunctional, P waves
are absent, and heart is paced by
the AV node at 40 - 60 beats/min.
(c) Second-degree heart block. (d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
Some P waves are not conducted
deflections are seen in acute
through the AV node; hence more
heart attack and electrical shock.
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
Figure 18.18
The Heart: Cardiac Cycle
lub (S1)
PCG: Phonocardiograph
dup (S2)
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Cells of the S/A Pacemaker Are Autorhythmic
 About 1% of cardiac cells are self-excitable
• Pacemaker cells have unstable resting potential
due to open slow Na+ channels
• As potential drifts towards neutrality, action
potential initiates at threshold Ca2+ channels open
• Explosive Ca+2 influx produces the rising phase of
the action potential
• Repolarization results from inactivation of Ca2+
channels and opening of voltage-gated K+
channels
Action Potential of Autorhythmic Cells Like at the Pacemaker
Threshold
Action
potential
2
2
3
1
1
Pacemaker
potential
1 Pacemaker potential
2 Depolarization The
3 Repolarization is due to
This slow depolarization is
due to both opening of Na+
channels and closing of K+
channels. Notice that the
membrane potential is
never a flat line.
action potential begins when
the pacemaker potential
reaches threshold.
Depolarization is due to Ca2+
influx through Ca2+ channels.
Ca2+ channels inactivating and
K+ channels opening. This
allows K+ efflux, which brings
the membrane potential back
to its most negative voltage.
Figure 18.13
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects
Looking at Ventricular Volumes: End Diastolic Volume, End Systolic Volume, and
Stroke Volume
Left heart
QRS
P
Electrocardiogram
T
1st
Heart sounds
P
2nd
Pressure (mm Hg)
Dicrotic notch
Aorta
SV = end diastolic
volume (EDV) –
end systolic
volume (ESV)
Left ventricle
Ventricular
volume (ml)
Atrial systole
Left atrium
Example: SV =
120ml/beat50ml/beat = 70
ml/beat
EDV
SV
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Open
Closed
Open
Closed
Open
Closed
1
2a
2b
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Early diastole
Ventricular
filling
Figure 18.20
Regulation of Stroke Volume

Three main factors affect SV: Preload, Contractility, and Afterload
1.
Preload
o
Degree to which the cardiac muscle cells are stretched before
contraction

At a certain cell length, active cross-bridges are maximized
and force of contraction is maximal

Cardiac cells normally shorter than optimal length

Therefore, according to the Frank-Starling Law of the
heart, increasing stretching (greater venous return)
increases contractile force
Regulation of Stroke Volume
2.
Contractility
•
Defined as: contractile strength at a given muscle length
o
Contractile strength is independent of muscle stretch and EDV
o
Enhanced contractility causes more blood to be ejected, increasing stroke volume
and decreasing ESV
•
Factors increasing contractility
o
Increased Ca2+ influx due to sympathetic stimulation
o
Hormones (thyroxine, glucagon, and epinephrine)
o
Digitalis
•
Factors decreasing contractility
o
Acidosis (H+ interferes with Ca+2 binding to myofilaments)
o
Increased extracellular K+
o
Calcium channel blockers drugs (CCBs) like amlodipine
Regulation of Stroke Volume
3.
Afterload

Defined as: pressure that must be overcome for ventricles to eject
blood
•

Same as “back pressure” exerted on aortic and pulmonary valves
Factor increasing afterload
•
Hypertension increases afterload
•
More blood remains in heart after systole, increasing ESV and
decreasing stroke volume
Heart Rate Affected by Sympathetic and Parasympathetic Systems
 Heart Rate increased by sympathetic nervous system
• Activated by emotional or physical stressors
• Activated by increased venous return (the atrial reflex) as SA node
stimulated by stretch receptors
• Epinephrine from adrenal medulla enhances heart rate and contractility
• Thyroxine increases heart rate and enhances the effects of
norepinephrine and epinephrine
 Heart rate decreased by parasympathetic nervous system
opposes sympathetic effects
 Other factors include age, gender, exercise, body temperature
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Problems and Defects
Homeostatic Imbalances
 Tachycardia: abnormally fast heart rate (>100 bpm)
• If persistent, may lead to fibrillation
 Bradycardia: heart rate slower than 60 bpm
• May result in grossly inadequate blood
circulation
• May be desirable result of endurance training
Ductus Arteriosus and Foramen Ovale of the Fetus
Handling of collapsed lungs
Modif 1
Modif 2
Developmental Aspects of the Heart
 Congenital heart defects
• Lead to mixing of systemic and pulmonary blood
• Involve narrowed valves or vessels that increase the workload on the heart
Narrowed
aorta
“Stenotic”
Occurs in
about 1 in
every
500 births
(a)Ventricular septal
defect.
(b) Coarctation
of the
aorta.
(c) Tetralogy of
Fallot.
Multiple defects
Age-Related Changes Affecting the Heart
 Sclerosis and thickening of valve flaps
 Decline in cardiac reserve
 Fibrosis of cardiac muscle
 Atherosclerosis
Congestive Heart Failure (CHF)
 Progressive condition where the CO is
so low that blood circulation is
inadequate to meet tissue needs
 Caused by
• Coronary atherosclerosis
• Persistent high blood pressure
• Multiple myocardial infarcts
• Dilated cardiomyopathy (DCM)
Cardiovascular System I: Heart Anatomy and Physiology
 Cardiovascular System Defined
 Gross Anatomy of the Heart
 Operation of Heart Valves
 Systemic and Coronary Circulation
 Cardiac Muscle Cell Anatomy and Stimulation
 Electrical Conduction in the Heart
 Cardiac Cycle and the EKG
 Autorhythmic Cells of the Pacemaker
 Stroke Volume and Contributing Factors
 Heart Defects