Ch 12 Heart and Circulatory
System
The Body’s Transport System
4 Chambered Heart – size of clenched fist
•2 Atria
•2 Ventricles
Arteries (efferent vessels)
Veins (afferent vessels)
Layers of the Heart
• Epicardium – outmost layer;
covers surface of heart
•Myocardium – muscle layer;
contains cardiac muscle, blood
vessels and nerves
•Endocardium – lines heart’s
chambers and valves; composed
of simple squamous tissue
Two Circuits for Blood
• Pulmonary Circuit:
right side of heart;
receives blood and
transports de-oxygenated
blood to lungs.
• Systemic Circuit:
left side of heart;
supplies body with
oxygenated blood.
Pericardium is the
shiny covering around
the heart.
Function:
•To reduce friction
between surrounding
surfaces as heart beats
• Protect the heart
• Anchor the
surrounding structures
Characteristics of Heart Muscle
Intercalated discs – allows heart to beat as one unit
Involuntary
Striated
One nuclei per cell
Location of Heart
Structure of the Heart
• Main Veins into heart
–
–
–
–
5
Coronary Sinus
Superior Vena Cava
Inferior Vena Cava
Pulmonary Vein
• Main Arteries
– Coronary Artery
– Pulmonary Artery
– Aorta
1
2
6
Blood flow through the Heart
• De-oxygenated blood
from the body enters the
R atrium and is pumped
to the R ventricle. From
the R ventricle deO2
blood is sent to the lungs
where gas exchange
occurs.
• Oxygenated blood enters
the L atria and is sent to
the L ventricle where it
is sent to the body via
the aorta.
Flow of blood through heart
A
B
C
9
1
5
6
7
3
4
2
8
1.
2.
3.
4.
5.
6.
7.
8.
9.
Superior Vena Cava
Inferior Vena Cava
R. atrium
R. ventricle
Pulmonary trunk (artery)
Pulmonary vein
L. atrium
L. ventricle
Aorta
A.
B.
C.
Brachiocephalic
L. Common Carotid
L. Subclavian
• Difference in
myocardium thickness
between R. ventricle
and L. ventricle.
• Why?
Valves of the Heart
Atrioventricular Valves
- one way valves; prevent back
flow of blood
-chordae tendineae
- papillary muscles
• Tricuspid – 3 flaps
– Found between R atrium and R.
ventricle
• Bicuspid (mitral) – 2 flaps
– Found between L atrium and L.
ventricle
Anatomy of AV valves
One-way valves
Atrioventricular valves
• Chordae tendineae
• Papillary muscles
Semilunar Valves
• Located in
Pulmonary Artery
and Aortic Artery
• 3 flaps
• Prevents blood from
flowing back into
ventricles
Valve position when ventricles
relaxed
Valve position when ventricles
contract
Heart Sounds
• Two sounds (lubb-dupp) associated with
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 murmurs: abnormal heart sounds
most often indicative of valve problems
Aortic valve sounds heard
in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
Figure 18.19
Cardiac Muscle Contraction
Rapid Depolarization: Threshold is reached along the
membrane.
• Causes Na+ channels in the sarcolemma to open
• Na+ enters cell reversing membrane potential from –90
mV to +30 mV (Na+ gates close)
Plateau: Calcium channels open and Ca+2 enters
sarcoplasm
• Ca+2 also is released from SR
• Ca+2 surge prolongs the depolarization phase and delays
repolarization (excess + ions in cell)
Repolarization: Ca+2 begin to close; K+ channels open and
K+ leaves the cell.
In Cardiac muscle, depolarization lasts
longer. Thus cardiac muscle can’t
increase tension with another impulse;
tetanus doesn’t occur.
Why is this important?
Heart Physiology: Electrical
Events
• Intrinsic cardiac conduction system
– A network of noncontractile (autorhythmic) cells
that initiate and distribute impulses to coordinate
the depolarization and contraction of the heart
– Nodes – cells that are responsible for starting the
impulse
– Conducting cells – distribute the impulse to the
myocardium
– 1 % of the heart’s cardiac cells have this capability
5
• Internal
Conduction System
• 1. Sinoatrial node
• 2. AV node
• 3. AV bundle or
Bundle of HIS
• 4. R and L bundle
branches
• 5. Purkinge fibers
Nodes – cluster of
nervous tissue that
begins an impulse.
1. Sinoatrial (SA) node (pacemaker)
Generates impulses about 70-80 times/minute (sinus rhythm)
Depolarizes faster than any other part of the myocardium
2. Atrioventricular (AV) node
–
Delays impulses approximately 0.1 second
•
–
Allows for Atria to contract
Depolarizes 40-60 times per minute in absence
of SA node input
Conducting Cells
3. Atrioventricular (AV) bundle
(bundle of His)
4. Right and left bundle branches
–
Two pathways in the
interventricular septum that carry
the impulses toward the apex of
the heart
5. Purkinje fibers
–
Complete the pathway into the apex and
ventricular walls
Superior vena cava
Right atrium
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
Internodal pathway
2 The impulses
pause (0.1 s) at the
atrioventricular
(AV) node.
3 The atrioventricular
(AV) bundle
connects the atria
to the ventricles.
Left atrium
Purkinje
fibers
4 The bundle branches
conduct the impulses
through the
interventricular septum.
5 The Purkinje fibers
Interventricular
septum
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
Figure 18.14a
Electrocardiography
•
•
Electrocardiogram (ECG or EKG): a
composite of all the action potentials
generated by nodal and contractile cells at a
given time.
Three waves
1. P wave: depolarization of SA node
2. QRS complex: ventricular depolarization (AV
node)
3. T wave: ventricular repolarization
Normal EKG has 3 distinct
waves.st
1 wave (P) - SA node
fires
- Natural Pacemaker
- fires around 70-80
times/minute
The atria depolarize
Impulse is being
generated across R and
L atria via diffusion.
.1s after P wave, atria
contract.
AV node – back up pacemaker
- Beats 40-60 times/minute
- Impulse is delayed at bundle
of HIS until Atria contract.
• 2nd wave (QRS)
• AV Node fires;
depolarization of
ventricles.
• Q-R interval represents
beginning of atrial
repolarization and AV
node firing; ventricles
depolarize
• R-S interval represents
beginning of ventricle
contractions
• S-T End of Ventricular
depolarization
• 3rd Wave (T)
• T wave repolarization
of ventricles
• Ventricles return to
normal relaxed state.
• In a healthy heart,
size, duration and
timing of waves is
consistent. Changes
reveal a damage or
diseased heart.
QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
Figure 18.16
SA node
Depolarization
R
Repolarization
R
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
R
AV node
T
P
Q
Q
S
4 Ventricular depolarization
is complete.
R
T
P
T
P
Q
S
2 With atrial depolarization
complete, the impulse is
delayed at the AV node.
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
T
P
T
P
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
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
Problems with Sinus Rhythms
• Tachycardia: Heart rate in excess of 100 bpm
when at rest
– If persistent, may lead to fibrillation
• Bradycardia: Heart rate less than 60 bpm when
at rest
– May result in grossly inadequate blood circulation
– May be desirable result of endurance training
Homeostatic Imbalances
• Defective SA node may result
– Ectopic focus: abnormal pacemaker takes over
– No P waves; If AV node takes over, there will be a
slower rhythm (40–60 bpm)
• Defective AV node may result in
– Partial or total heart block
– Longer delay at AV node than normal
– No all impulses from SA node reach the ventricles
• Ventricular fibrillation:
– cardiac muscle cells are overly sensitive to
stimulation; no normal rhythm is established
Problems with Sinus Rhythms
• 2nd degree heart block; Missed QRS complex
• SA node is sending impulses, but the AV node is not
sending the impulses along the bundle branches
• 1st degree is represented by a longer delay between P &
QRS
(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
Pacemaker
• Used to correct nodes
that are no longer are
in rhythm.
• Becomes the new
heart’s pacemaker.
Myocardial Infarction
• A Heart Attack is
caused by oxygen
not getting to the
heart muscle
usually by
blockages in the
coronary arteries
Stopping a Heart Attack
• Breaking apart the
blockage is done
with:
–
–
–
–
Medication
Angioplasty
Stents
Coronary bypass
surgery (CABG)
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
Mechanical Events: The Cardiac
Cycle
• Cardiac cycle: all events associated with
blood flow through the heart during one
complete heartbeat
– Systole—contraction
– Diastole—relaxation
Phases of the Cardiac Cycle
1. Ventricular filling—takes place in mid-tolate diastole
–
–
–
–
AV valves are open
80% of blood passively flows into ventricles
Atrial systole occurs, delivering the remaining
20%
End diastolic volume (EDV): volume of blood
in each ventricle at the end of ventricular
diastole
Phases of the Cardiac Cycle
2. Ventricular systole
– Atria relax and ventricles begin to contract
– Rising ventricular pressure results in closing of
AV valves
– In ejection phase, ventricular pressure exceeds
pressure in the large arteries, forcing the
Semilunar valves open
– End systolic volume (ESV): volume of blood
remaining in each ventricle
Phases of the Cardiac Cycle
3. Ventricles relax
–
–
Decrease in pressure causes blood to flow
backward
Backflow of blood in aorta and pulmonary
trunk closes SL valves
EKG and One Cardiac Cycle
Cardiac Cycle = events during one heart beat
Cardiac Cycle & BP
describes the contracting and relaxing stages of the heart.
• Includes all events that
occur in the heart
during one complete
heart beat.
• Blood Pressure
• Systolic pressure: (top
number) measurement
of the force on the
arterial walls when the
L ventricle contracts.
• Diastolic pressure:
(bottom number)
measurement of the force
on the arterial walls
when the L ventricle is
relaxed.
• Normal BP = 120/80
• Hypertension
• Hypotension
Cardiac Output
• Volume of blood pumped by each ventricle in
1 minute.
• CO = Heart rate (HR) x Stroke volume (SV)
– Heart Rate (beats/minute)
– Stroke Volume – volume of blood pumped out of
the L. ventricle with each beat. Why Left
ventricle?
• SV = EDV(end diastolic volume) – ESV (end systolic
volume)
• Stroke volume can be determined by subtracting
systolic BP volume from diastolic BP volume
• Stroke volume/pulse pressure = SBP – DBP
• Cardiac Output in a normal adult is 4.5 – 5
Liters of blood per minute
– At rest: CO (ml/min) = HR (75 beats/min)  SV (70
ml/beat) = 5.25 L/min
• Varies with body’s demands
– Change in HR or force of contraction
• Cardiac Reserve – the heart’s ability to push
cardiac output above normal limits
– difference between resting and maximal CO
– Healthier hearts can have a large increase in C.R.
• Athlete 7X C.O. = 35L/minute
• Nonathlete 4X C.O. = 20L/minute
Factors that Influence Heart Rate
•
•
•
•
Age
Gender
Exercise
Body temperature
Regulation of Stroke Volume
• Contractility: contractile strength at a given muscle
length, independent of muscle stretch and EDV
• Factors which increase contractility
– Increased Ca2+ influx due to sympathetic stimulation
– Hormones (thyroxine and epinephrine)
• Factors which decrease contractility
– Increased extracellular K+
– Calcium channel blockers
Factors that Control Cardiac Output
• Blood volume reflexes
• Autonomic Nervous System with assistance
from neurotransmitters and hormones
– Norepinephrine
– Acethylcholine
– Thyroxine
• Ions
• Temperature
Blood Volume Reflexes
• Frank Starling Law of the Heart
– Stroke volume is controlled by Preload - the degree to
which cardiac muscles are stretched just before they
contract.
• “More blood in = More blood out”
– Increase in stretch is caused by an Increase in the
venous return to the right atrium which causes the walls
of the right atrium to stretch.
• Increase in stretch causes SA node to depolarize faster;
increasing HR
• Increase in stretch also increases force of contraction; Stroke
volume
• At rest heart walls are not overstretched; ventricles
don’t need forceful contractions
Autonomic Nervous System
• Controlled by Medulla oblongata
• Parasympathetic (Resting and Digesting)
– Stimulates Vagus nerve (CN X) – decreases SV and
HR; decreasing CO
– Acetylcholine – decreases HR and SV; opposite action
on cardiac muscle then on skeletal muscle (stimulates)
• Sympathetic (Fight or Flight) – prepares the body
for stress
– Secretes Norephinephrine and epinephrine – increases
HR and SV; increasing CO
– Increasing HR causes overstretch (Frank S. law)
– Beta blockers-
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
Ions
Calcium
Hypercalcemia
•Excess Ca ions in
muscle cell
•Extended state of
contraction; fatal
Hypocalcemia
•Low Ca levels;
results in no/weak
contractions
Potassium
Hyperkalemia
•High levels of K
•Interferes with
depolarization of
SA and AV nodes
•Results in heart
block
Sodium
Increase in Na
•Blocks Ca
•No Ca; no T&T
moving out of way
•No/weak
contractions
Temperature
Hyperthermia
Hypothermia
Temp > 98.6°F
Temperature < 95° F
•Increases HR and
SV
•Slows
depolarization
•Increase CO
•Slows contraction
•Decrease CO
Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Venous
return
Contractility
EDV
(preload)
ESV
Exercise,
fright, anxiety
Sympathetic
activity
Parasympathetic
activity
Heart
rate
Stroke
volume
Cardiac
output
Initial stimulus
Physiological response
Result
Figure 18.22