Chapter 20: The Heart
Biol 141 A& P
R.L. Brashear-Kaulfers
How are the cardiovascular
system and heart organized?
Organization of the
Cardiovascular System
PLAY
The Heart: Anatomy
Figure 20–1
The Pulmonary Circuit
• Carries blood to and from gas exchange
surfaces of lungs
The Systemic Circuit
• Carries blood to and from the body
Alternating Circuits
• Blood alternates between pulmonary
circuit and systemic circuit
3 Types of Blood Vessels
• Arteries:
– carry blood away from heart
• Veins:
– carry blood to heart
• Capillaries:
– networks between arteries and veins
Capillaries
• Also called exchange vessels
• Exchange materials between blood and
tissues
• Dissolved gases, nutrients, wastes
4 Chambers of the Heart
• 2 for each circuit:
– left and right: ventricles and atria
• Right atrium:
– collects blood from systemic circuit
• Right ventricle:
– pumps blood to pulmonary circuit
4 Chambers of the Heart
• Left atrium:
– collects blood from pulmonary circuit
• Left ventricle:
– pumps blood to systemic circuit
Anatomy of the Heart
• Located directly behind sternum
PLA
Y
Figure 20–2a
Anatomy of the Heart
• Great veins and arteries at the base
• Pointed tip is apex
Figure 20–2c
Relation to Thoracic Cavity
Surrounded
by
pericardial
sac
Between 2
pleural
cavities
In the
mediastinum
Figure 20–2b
The Pericardium
• Double lining of the pericardial cavity
Figure 20–2c
2 Layers of Pericardium
1. Parietal pericardium:
–
–
outer layer
forms inner layer of pericardial sac
2. Visceral pericardium:
–
inner layer of pericardium
Structures of Pericardium
• Pericardial cavity:
– Is between parietal and visceral layers
– contains pericardial fluid
• Pericardial sac:
– fibrous tissue
– surrounds and stabilizes heart
Pericarditis
An infection of the pericardium
Superficial Anatomy of the Heart
• 4 cardiac chambers
• Atria - Thin-walled
• Expandable outer auricle
• Coronary sulcus:
– divides atria and ventricles
• Anterior and posterior
interventricular sulci:
– separate left and right
ventricles
– contain blood vessels of
cardiac muscle
Figure 20–3
The Heart Wall
Figure 20–4
3 Layers of the Heart Wall
• Epicardium:- outer layer
• Visceral pericardium , Covers the heart
•
•
•
•
Myocardium: middle layer, Muscular wall
Concentric layers of cardiac muscle tissue
Atrial myocardium wraps around great vessels
2 divisions of ventricular myocardium
• Endocardium: inner layer
Cardiac Muscle Cells
Intercalated discs:
interconnect
cardiac muscle cells
secured by
desmosomes
linked by gap
junctions
convey force of
contraction
propagate action
potentials
Figure 20–5
Characteristics of
Cardiac Muscle Cells
1. Small size
2. Single, central nucleus
3. Branching interconnections between
cells
4. Intercalated discs
Cardiac Cells vs. Skeletal Fibers
Table 20-1
What is the path of blood flow
through the heart, and what
are the major blood vessels,
chambers, and heart valves?
Internal Anatomy
PLAY
3D Panorama of the Heart
Figure 20–6a
Atrioventricular (AV) Valves
• Connect right atrium to right ventricle and left
atrium to left ventricle
• Permit blood flow in 1 direction:
– atria to ventricles
Septa –
• Interatrial septum:
– separates atria
• Interventricular septum:
– separates ventricles
The Vena Cava
• Delivers systemic circulation to right atrium
• Superior vena cava:
– receives blood from head, neck, upper limbs, and
chest
• Inferior vena cava:
– receives blood from trunk, and viscera, lower limbs
Coronary Sinus
• Cardiac veins return blood to coronary sinus
• Coronary sinus opens into right atrium
Foramen Ovale
• Before birth, is an opening through
interatrial septum
• Connects the 2 atria
• Seals off at birth, forming fossa ovalis
Cusps - Fibrous flaps that form
bicuspid (2) and tricuspid (3) valvesPrevent valve from opening
backward
Right Atrioventricular (AV) Valve
• Also called tricuspid valve
• Opening from right atrium to right
ventricle
• Has 3 cusps
• Prevents backflow
The Pulmonary Circuit
• Conus arteriosus (superior right
ventricle) leads to pulmonary trunk
• Pulmonary trunk divides into left and
right pulmonary arteries
• Blood flows from right ventricle to
pulmonary trunk through pulmonary
valve
• Pulmonary valve has 3 semilunar cusps
Return from Pulmonary Circuit
• Blood gathers into left and right
pulmonary veins
• Pulmonary veins deliver to left atrium
• Blood from left atrium passes to left
ventricle through left atrioventricular
(AV) valve
• 2-cusp bicuspid valve or mitral valve
The Left Ventricle
• Holds same volume as right ventricle
• Is larger; muscle is thicker, and more
powerful
• Similar internally to right ventricle, but
does not have moderator band
Systemic circulation:
– blood leaves left ventricle through aortic
valve into ascending aorta
– ascending aorta turns (aortic arch) and
becomes descending aorta
Left and Right Ventricles
• Have significant
structural differences
• Right ventricle wall is
thinner, develops less
pressure than left
ventricle
• Right ventricle is
pouch-shaped, left
ventricle is round
Figure 20–7
The Heart Valves
• One-way valves prevent
backflow during contraction
• (AV) Valves- between atria
and ventricles
• Blood pressure closes valve
cusps during ventricular
contraction
• Papillary muscles tense
chordae tendineae:
– prevent valves from swinging
into atria
• Regurgitation -Failure of
valves
• Causes backflow of blood into
atria
Figure 20–8
Semilunar Valves
• Pulmonary and aortic tricuspid valves
• Prevent backflow from pulmonary
trunk and aorta into ventricles
• Have no muscular support
• 3 cusps support like tripod
• Aortic Sinuses - at base of ascending
aorta
• Prevent valve cusps from sticking to
aorta
• Origin of right and left coronary arteries
Carditis - An inflammation of the heart
• Can result in valvular heart disease
(VHD): e.g., rheumatic fever
KEY CONCEPT
• The heart has 4 chambers:
– 2 for pulmonary circuit:
• right atrium and right ventricle
– 2 for systemic circuit:
• left atrium and left ventricle
• Left ventricle has a greater workload
• Is much more massive than right ventricle, but
the two chambers pump equal amounts of
blood
• AV valves prevent backflow from ventricles into
atria
• Semilunar valves prevent backflow from aortic
and pulmonary trunks into ventricles
Connective Tissue
Fibers of the Heart
1. Physically support cardiac muscle
fibers
2. Distribute forces of contraction
3. Add strength and prevent
overexpansion of heart
4. Elastic fibers return heart to original
shape after contraction
Blood Supply to the Heart
• Coronary circulation
Figure 20–9
Coronary Circulation
• Coronary arteries-Left and right
Originate at aortic sinuses
• High blood pressure, elastic rebound force
blood through coronary arteries between
contractions
• cardiac veins
• Supplies blood to muscle tissue of heart
Right Coronary Artery
• Supplies blood to:
– right atrium
– portions of both ventricles
– cells of sinoatrial (SA) and atrioventricular
nodes
– marginal arteries (surface of right
ventricle)
– posterior interventricular artery
Left Coronary Artery
• Supplies blood to:
– left ventricle
– left atrium
– interventricular septum
• 2 main branches:
– circumflex artery
– anterior interventricular artery
Cardiac Veins
• Great cardiac vein:
– drains blood from area of anterior
interventricular artery into coronary sinus
• Anterior cardiac vein:
– empties into right atrium
• Posterior cardiac vein, middle cardiac
vein, and small cardiac vein:
– empty into great cardiac vein or coronary
sinus
The Cardiac Cycle
The Heartbeat
A single
contraction of
the heart
The entire heart
contracts in
series:
first the atria
then the
ventricles
Figure 20–11
2 Types of Cardiac Muscle Cells
• Conducting system:
– controls and coordinates heartbeat
• Contractile cells:
– produce contractions
* The Cardiac Cycle begins with action potential
at SA node
– transmitted through conducting system
– produces action potentials in cardiac muscle cells
(contractile cells)
• Electrical events in the cardiac cycle can be
recorded on an electrocardiogram (ECG)
The Conducting System
Figure 20–12
The Conducting System
• A system of specialized cardiac muscle
cells:
– initiates and distributes electrical
impulses that stimulate contraction
• Automaticity:
– cardiac muscle tissue contracts
automatically
Structures of the
Conducting System
• Sinoatrial (SA) node
• Atrioventricular (AV) node
• Conducting cells
Conducting Cells
• Interconnect SA and AV nodes
• Distribute stimulus through
myocardium
• In the atrium:
– internodal pathways
• In the ventricles:
– AV bundle and bundle branches
Prepotential
• Also called pacemaker potential
• Resting potential of conducting cells:
– gradually depolarizes toward threshold
• SA node depolarizes first, establishing
heart rate
Heart Rate
• SA node generates 80–100 action
potentials per minute
• Parasympathetic stimulation slows
heart rate
• AV node generates 40–60 action
potentials per minute
Impulse Conduction
through the Heart
Figure 20–13
The Sinoatrial (SA) Node
• In posterior wall of right atrium
• Contains pacemaker cells
• Connected to AV node by internodal
pathways
• Begins atrial activation (Step 1)
The Atrioventricular (AV) Node
•
•
•
•
In floor of right atrium
Receives impulse from SA node (Step 2)
Delays impulse (Step 3)
Atrial contraction begins
The AV Bundle
• In the septum
• Carries impulse to left and right bundle
branches:
– which conduct to Purkinje fibers (Step 4)
• And to the moderator band:
– which conducts to papillary muscles
4. The Purkinje Fibers
• Distribute impulse through ventricles (Step 5)
• Atrial contraction is completed
• Ventricular contraction begins
Abnormal Pacemaker Function
• Bradycardia:
– abnormally slow heart rate
• Tachycardia:
– abnormally fast heart rate
Ectopic Pacemaker:
•
•
•
•
Abnormal cells
Generate high rate of action potentials
Bypass conducting system
Disrupt ventricular contractions
The Electrocardiogram
Figure 20–14b
Electrocardiogram (ECG or EKG)
• A recording of electrical events in the
heart
• Obtained by electrodes at specific body
locations
• Abnormal patterns diagnose damage
Features of an ECG :
• P wave: atria depolarize
• QRS complex: ventricles depolarize
• T wave: ventricles repolarize
Time Intervals
• P–R interval:
– from start of atrial depolarization
– to start of QRS complex
• Q–T interval:
– from ventricular depolarization
– to ventricular repolarization
Cardiac Arrhythmias –
Abnormal patterns of cardiac electrical
activity
KEY CONCEPT
• Heart rate is normally established by cells of SA
node
• Rate can be modified by autonomic activity,
hormones, and other factors
• From the SA node, stimulus is conducted to AV
node, AV bundle, bundle branches, and Purkinje
fibers before reaching ventricular muscle cells
• Electrical events associated with the heartbeat
can be monitored in an electrocardiogram
(ECG)
What events take
place during an action
potential in cardiac muscle?
Action Potentials in
Skeletal and Cardiac Muscle
Figure 20–15
Resting Potential
• Of a ventricular cell:
– about —90 mV
• Of an atrial cell:
– about —80 mV
3 Steps of
Cardiac Action Potential
1. Rapid depolarization:
–
voltage-regulated sodium channels (fast
channels) open
3 Steps of
Cardiac Action Potential
2. As sodium channels close:
–
–
–
voltage-regulated calcium channels
(slow channels) open
balance Na+ ions pumped out
hold membrane at 0 mV plateau
3 Steps of
Cardiac Action Potential
3. Repolarization:
–
–
–
–
plateau continues
slow calcium channels close
slow potassium channels open
rapid repolarization restores resting
potential
The Refractory Periods
• Absolute refractory period:
– long
– cardiac muscle cells cannot respond
• Relative refractory period:
– short
– response depends on degree of stimulus
Timing of Refractory Periods
• Length of cardiac action potential in
ventricular cell:
– 250–300 msecs
• 30 times longer than skeletal muscle fiber
• long refractory period prevents summation
and tetany
Contraction of a cardiac muscle
cell is produced by an increase in
calcium ion concentration around
myofibrils
1. 20% of calcium ions required for a
contraction:
–
calcium ions enter cell membrane during
plateau phase
2. Arrival of extracellular Ca2+:
–
triggers release of calcium ion reserves
from sarcoplasmic reticulum
Intracellular and
Extracellular Calcium
• As slow calcium channels close:
– intracellular Ca2+ is absorbed by the SR
– or pumped out of cell
• Cardiac muscle tissue:
– very sensitive to extracellular Ca2+
concentrations
The Cardiac Cycle
• The period between the start of 1
heartbeat and the beginning of the
next
• Includes both contraction and
relaxation
2 Phases of the Cardiac Cycle:
• Within any 1 chamber:
– systole (contraction)
– diastole (relaxation)
Blood Pressure
• In any chamber:
– rises during systole
– falls during diastole
• Blood flows from high to low pressure:
– controlled by timing of contractions
– directed by one-way valves
Phases of the Cardiac Cycle
Figure 20–16
4 Phases of the Cardiac Cycle
1.
2.
3.
4.
Atrial systole
Atrial diastole
Ventricular systole
Ventricular diastole
Cardiac Cycle and Heart Rate
• At 75 beats per minute:
– cardiac cycle lasts about 800 msecs
• When heart rate increases:
– all phases of cardiac cycle shorten,
particularly diastole
Pressure and Volume
in the Cardiac Cycle
• 8 steps in the cardiac cycle
Figure 20–17
8 Steps in the Cardiac Cycle
1. Atrial systole:
–
–
atrial contraction begins
right and left AV valves are open
2. Atria eject blood into ventricles:
–
filling ventricles
3. Atrial systole ends:
–
–
–
AV valves close
ventricles contain maximum volume
end-diastolic volume (EDV)
4. Ventricular systole:
–
–
–
isovolemic ventricular contraction
pressure in ventricles rises
AV valves shut
8 Steps in the Cardiac Cycle
5. Ventricular ejection:
–
–
semilunar valves open
blood flows into pulmonary and aortic trunks
• Stroke volume (SV) = 60% of end-diastolic
volume
6. Ventricular pressure falls:
–
–
semilunar valves close
ventricles contain end-systolic volume (ESV),
about 40% of end-diastolic volume
8 Steps in the Cardiac Cycle
7. Ventricular diastole:
–
–
–
ventricular pressure is higher than atrial
pressure
all heart valves are closed
ventricles relax (isovolumetric relaxation)
8. Atrial pressure is higher than ventricular
pressure:
–
–
–
–
AV valves open
passive atrial filling
passive ventricular filling
cardiac cycle ends
Heart Failure
• Lack of adequate blood flow to
peripheral tissues and organs due to
ventricular damage
How do heart sounds relate to specific
events in the cardiac cycle?
Heart Sounds
Figure 20–18b
4 Heart Sounds
• S1:
– loud sounds
– produced by AV valves
• S2:
– loud sounds
– produced by semilunar valves
• S3, S4:
– soft sounds
– blood flow into ventricles and atrial contraction
Positioning the Stethoscope
• To detect sounds of
each valve
• Heart Murmur• Sounds produced
by regurgitation
through valves
Figure 20–18a
Aerobic Energy of Heart
• From mitochondrial breakdown of fatty
acids and glucose
• Oxygen from circulating hemoglobin
• Cardiac muscles store oxygen in
myoglobin
Stroke Volume
• Volume (ml) of blood ejected per beat
Figure 20–19
Cardiac Output
• Cardiac output (CO) ml/min =
• Heart rate (HR) beats/min 
• Stroke volume (SV) ml/beat
Overview: Control
of Cardiac Output
Figure 20–20 (Navigator)
Adjusting to Conditions
• Cardiac output:
– adjusted by changes in heart rate or
stroke volume
• Heart rate:
– adjusted by autonomic nervous system or
hormones
• Stroke volume:
– adjusted by changing EDV or ESV
What variables
influence heart rate?
Autonomic Innervation
Figure 20–21 (Navigator)
Autonomic Pacemaker
Regulation
Figure 20–22
Autonomic Pacemaker
Regulation
• Sympathetic and parasympathetic stimulation:
– greatest at SA node (heart rate)
• Membrane potential of pacemaker cells:lower
than other cardiac cells
• Rate of spontaneous depolarization depends on:
– resting membrane potential
– rate of depolarization
• ACh (parasympathetic stimulation):
– slows the heart
• NE (sympathetic stimulation):
– speeds the heart
Atrial Reflex
• Also called Bainbridge reflex
• Adjusts heart rate in response to
venous return
• Stretch receptors in right atrium:
– trigger increase in heart rate
– through increased sympathetic activity
Hormonal Effects on Heart Rate
• Increase heart rate (by sympathetic
stimulation of SA node):
– epinephrine (E)
– norepinephrine (NE)
– thyroid hormone
What variables influence stroke volume?
Factors Affecting Stroke Volume
• Changes in EDV or ESV
2 Factors Affect
EDV1. Filling time:
duration of
ventricular
diastole
2. Venous return:
rate of blood
flow during
ventricular
diastole
Figure 20–23 (Navigator)
Preload
• The degree of ventricular stretching
during ventricular diastole
• Directly proportional to EDV
• Affects ability of muscle cells to
produce tension
EDV, Preload, and Stroke Volume
• At rest:
– EDV is low
– myocardium stretches less
– stroke volume is low
• With exercise:
– EDV increases
– myocardium stretches more
– stroke volume increases
• As EDV increases, stroke volume increases
Physical Limits
• Ventricular expansion is limited by:
– myocardial connective tissue
– the fibrous skeleton
– the pericardial sac
End-Systolic Volume (ESV)
• The amount of blood that remains in
the ventricle at the end of ventricular
systole is the ESV
3 Factors that Affect ESV
1. Preload:
–
ventricular stretching during diastole
2. Contractility:
–
force produced during contraction, at a
given preload
3. Afterload:
–
tension the ventricle produces to open
the semilunar valve and eject blood
Contractility is affected by:
autonomic activity &
hormones :
• Sympathetic stimulation:
– NE released by postganglionic fibers of cardiac
nerves
– epinephrine and NE released by adrenal
medullae
– causes ventricles to contract with more force
– increases ejection fraction and decreases ESV
• Parasympathetic activity:
– acetylcholine released by vagus nerves
– reduces force of cardiac contractions
Hormones and Contractility
• Many hormones affect heart
contraction
• Pharmaceutical drugs mimic hormone
actions:
– stimulate or block beta receptors
– affect calcium ions e.g., calcium channel
blockers
Afterload
• Is increased by any factor that restricts
arterial blood flow
• As afterload increases, stroke volume
decreases
Factors Affecting Heart
Rate and Stroke Volume
Autonomic
nervous
system:
sympathetic
and
parasymp
athetic
Circulating
hormones
Venous return
and stretch
receptors
Figure 20–24
Stroke Volume Control Factors
• EDV:
– filling time
– rate of venous return
• ESV:
– preload
– contractility
– Afterload
Cardiac Reserve• The difference between resting and maximal
cardiac output
KEY CONCEPT
• Cardiac output:
– the amount of blood pumped by the left
ventricle each minute
– adjusted by the ANS in response to:
• circulating hormones
• changes in blood volume
• alterations in venous return
• Most healthy people can increase
cardiac output by 300–500%
The Heart and
Cardiovascular System
• Cardiovascular regulation:
– ensures adequate circulation to body
tissues
• Cardiovascular centers:
– control heart and peripheral blood vessels
• Cardiovascular system responds to:
– changing activity patterns
– circulatory emergencies
SUMMARY (1)
• Organization of cardiovascular system:
– pulmonary and systemic circuits
• 3 types of blood vessels:
– arteries, veins, and capillaries
• 4 chambers of the heart:
– left and right atria
– left and right ventricles
• Pericardium, mediastinum, and pericardial sac
• Coronary sulcus and superficial anatomy of the
heart
• Structures and cells of the heart wall
SUMMARY (2)
• Internal anatomy and structures of the
heart:
– septa, muscles, and blood vessels
• Valves of the heart and direction of blood
flow
• Connective tissues of the heart
• Coronary blood supply
• Contractile cells and the conducting
system:
– pacemaker calls, nodes, bundles, and Purkinje
fibers
SUMMARY (3)
• Electrocardiogram and its wave forms
• Refractory period of cardiac cells
• Cardiac cycle:
– atrial and ventricular
– systole and diastole
• Cardiodynamics:
– stroke volume and cardiac output
• Control of cardiac output