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A&P Refresher- Heart
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Heart
Diseases and Disorders
Inflammation of the endocardium; affects the valves more severely than other areas of the endocardium; may lead to
scarring, causing stenosed or incompetent valves
Inflammation of the pericardium; see Clinical Impact, “Pericarditis and Cardiac Tamponade”
Disease of the myocardium of unknown cause or occurring secondarily to other disease; results in weakened cardiac
muscle, causing all chambers of the heart to enlarge; may eventually lead to congestive heart failure
Results from a streptococcal infection in young people; toxin produced by the bacteria can cause rheumatic fever
several weeks after the infection that can result in rheumatic endocarditis
Reduces the amount of blood the coronary arteries can deliver to the myocardium
Formation of blood clot in a coronary artery
Damaged cardiac muscle tissue resulting from lack of blood flow to the myocardium; often referred to as a heart attack;
see Clinical Impact, “Angina, Infarctions, and the Treament of Blocked coronary Arteries”
Hole in the septum between the left and right sides of the heart, allowing blood to flow from one side of the heart to the
other and greatly reducing the heart’s pumping effectiveness
Ductus arteriosus fails to close after birth, allowing blood to flow from the aorta to the pulmonary trunk under a higher
pressure, which damages the lungs; also, the left ventricle must work harder to maintain adequate systemic pressure
Narrowed opening through one or more of the heart valves; aortic or pulmonary semilunar stenosis increases the heart’s
workload; bicuspid valve stenosis causes blood to back up in the left atria and lungs, resulting in edema of the lungs;
tricuspid valve stenosis results in similar blood flow problems and edema in the peripheral tissues
Heart valves do not close correctly, and blood flows through in the reverse direction; see Clinical Impact, “Abnormal
Heart Sounds”
Cyanosis (sı-a-no′sis; cyan,
blue + osis, condition of)
Symptom of inadequate heart function in babies with congenital heart disease; the infant’s skin appears blue because
of low oxygen levels in the blood in peripheral blood vessels
Progressive weakening of the heart muscle, reducing the heart’s pumping action; hypertension leading to heart failure
due to increased afterload; advanced age, malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism,
and hereditary factors can lead to heart failure
Condition Description
Inflammation of Heart Tissue
Endocarditis
Pericarditis
Cardiomyopathy
Rheumatic heart disease
Reduced Blood Flow to Cardiac Muscle
Coronary heart disease
Coronary thrombosis
Myocardial infarction
Congenital Heart Diseases (occur at birth)
Septal defect
Patent ductus arteriosus
Stenosis of the heart valve
Incompetent heart valve
Heart Failure
- - -
20-2
20-3
SA node block
TABLE 20.1 Major Cardiac Arrhythmias
Conditions Symptoms Possible Causes
Abnormal Heart Rhythms
Tachycardia
Paroxysmal atrial
tachycardia
Ventricular tachycardia
Heart rate in excess of 100 beats per minute (bpm)
Sudden increase in heart rate to 95–150 bpm for a few
seconds or even for several hours; P wave precedes
every QRS complex; P wave inverted and superimposed
on T wave
Frequently causes fibrillation
Elevated body temperature; excessive
sympathetic stimulation; toxic conditions
Excessive sympathetic stimulation; abnormally
elevated permeability of slow channels
Often associated with damage to AV node
or ventricular muscle
Abnormal Rhythms Resulting from Ectopic Action Potentials
Atrial flutter
Atrial fibrillation
Ventricular fibrillation
Ectopic action potentials in the atria
Ectopic action potentials in the atria
Ectopic action potentials in the ventricles
300 P waves/min; 125 QRS complexes/min, resulting in two or three P
waves (atrial contraction) for every QRS complex (ventricular contraction)
No P waves; normal QRS complexes; irregular timing; ventricles constantly
stimulated by atria; reduced pumping effectiveness and filling time
No QRS complexes; no rhythmic contraction of the myocardium; many
patches of asynchronously contracting ventricular muscle
Heart rate less than 60 bpm
Heart rate varies 5% during respiratory cycle and up to
30% during deep respiration.
Cessation of P wave; new low heart rate due to AV node
acting as pacemaker; normal QRS complex and T wave
PR interval greater than 0.2 second
First-degree
Second-degree
Third-degree (complete
heart block)
PR interval 0.25–0.45 second; some P waves trigger QRS complexes and
others do not; 2:1, 3:1, and 3:2 P wave/QRS complex ratios may occur
P wave dissociated from QRS complex; atrial rhythm approximately
100 bpm; ventricular rhythm less than 40 bpm
Occasional shortened intervals between contractions;
frequently occurs in healthy people
P wave superimposed on QRS complex
Prolonged QRS complex; exaggerated voltage because
only one ventricle may depolarize; inverted T wave;
increased probability of fibrillation
Elevated stroke volume in athletes; excessive
vagal stimulation; carotid sinus syndrome
Cause not always known; occasionally caused by
ischemia or inflammation or associated with cardiac
failure
Ischemia; tissue damage due to infarction;
causes unknown
Inflammation of AV bundle
Excessive vagal stimulation
Ischemia of AV nodal fibers or compression
of AV bundle
Excessive smoking; lack of sleep; too much
caffeine; alcoholism
Ectopic foci in ventricles; lack of sleep;
too much caffeine, irritability; occasionally
occurs with coronary thrombosis
Abbreviations: SA = sinoatrial; AV = atrioventricular.
Bradycardia
Sinus arrhythmia
AV Node Block
Premature atrial
contractions
Premature ventricular
contractions (PVCs)
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20-4
Functions of the Heart
1. Generating blood pressure
2. Routing blood: separates
pulmonary and systemic
circulations
3. Ensuring one-way blood flow:
valves
4. Regulating blood supply
– Changes in contraction rate and
force match blood delivery to
changing metabolic needs
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Lung
CO2
CO2
O2
O2
CO2
O2
Right side of heart
Pulmonary
circulation
(through
lungs)
Lung
capillaries
Tissue
capillaries Circulation to
tissues of head,
neck, and upper
limbs
Systemic
circulation
(through body)
Left side
of heart
Tissue
capillaries
Circulation to
tissues of
thorax, abdomen,
and lower limbs
20-5
Cardiovascular
Overview
Midclavicular line
2nd intercostal space
Sternum
Apex of heart
5th intercostal space
Larynx
Superior vena cava
Right lung
Right atrium
Right ventricle
Rib
Visceral pleura
Pleural cavity
Parietal pleura
Diaphragm
Trachea
Aortic arch
Base of heart
Pulmonary trunk
Left atrium
Left lung
Left ventricle
Apex of heart
Visceral pericardium
Pericardial cavity
Parietal pericardium
Fibrous pericardium
Left lung
Visceralpleura
Pleural cavity
Parietal pleura
(a) Anterior view
Size, Shape, Location of the Heart
• Size of a closed fist
• Shape
– Apex: Blunt rounded
point of cone
– Base: Flat part at
opposite of end of cone
• Located in thoracic cavity
in mediastinum (central
core of the thoracic
cavity; everything in the
thoracic cavity except
the lungs.)
– Important clinically
when using a
stethoscope,
performing an ECG, or
performing CPR
20-6
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or display.
Esophagus
Right pleural cavity
Right pulmonary artery
Right pulmonary vein
Superior vena cava
Ascending aorta
Right atrium
Right ventricle
Descending aorta
Tissue of mediastinum
Bronchus of lung
Parietal pleura
Left pleural cavity
Visceral pleura
Left pulmonary artery
Left pulmonary vein
Pulmonary trunk
Left atrium
Left ventricle
Visceral pericardium
Pericardial cavity
Parietal pericardium
Fibrous pericardium
Superior view
(b)
Heart Cross Section
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or display.
20-7
Anatomy of the Heart
• Pericardium or pericardial sac
– Fibrous pericardium: tough fibrous outer layer.
Prevents over distention; acts as anchor
– Serous pericardium: thin, transparent, inner layer.
Simple squamous epithelium
• Parietal pericardium: lines the fibrous outer layer
• Visceral pericardium (epicardium): covers heart surface
• The two are continuous and have a pericardial cavity
between them filled with pericardial fluid
20-8
Anatomy of the
Heart
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Fibrous pericardium
Parietal pericardium
Serous pericardium
Pericardium
Anterior view
Visceral pericardium
(or epicardium)
Pericardial cavity
filled with pericardial
fluid
Heart Wall
• Three layers of tissue
– Epicardium: Serous
membrane; smooth outer
surface of heart
– Myocardium: Middle layer
composed of cardiac muscle
cell and responsibility for heart
contracting
– Endocardium: Smooth inner
surface of heart chambers
• Pectinate muscles: muscular
ridges in auricles and right
atrial wall
• Trabeculae carneae:
muscular ridges and columns
on inside walls of ventricles
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or display.
Myocardium
Endocardium
Simple squamous
epithelium
Loose connective
tissue and
adipose tissue
Epicardium
(visceral
pericardium)
Trabeculae
carneae
20-10
External Anatomy
Aortic arch
Superior vena cava
Aorta
Coronary sulcus
Pulmonary trunk
Left pulmonary artery
Left pulmonary veins
Left atrium
Left ventricle
Right pulmonary veins
Right atrium
Right coronary artery
Right ventricle
Inferior vena cava
(a) Anterior view
Aorta
Great cardiac vein
(in interatrial septum)
Left ventricle
Right auricle
Right ventricle
(b) Anterior view
Branches of right
pulmonary artery
Superior
vena cava
Anterior interventricular artery
(in anterior interventricular sulcus)
Left auricle
Branches of left
pulmonary artery
Great cardiac vein
(in anterior interventricular sulcus)
Anterior interventricular artery
(in anterior interventricular sulcus)
20-11
Apex
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Aorta
Left atrium
Left pulmonary veins
Left pulmonary artery
Apex
Left ventricle
Coronary sinus
Superior vena cava
Right pulmonary artery
Right pulmonary veins
Right atrium
Inferior vena cava
Right coronary artery
Small cardiac vein
Right ventricle
Posterior interventricular artery
(in posterior interventricular sulcus)
Middle cardiac vein
(in posterior inter-
ventricular sulcus)
(c) Posterior view
Great cardiac vein
(in coronary sulcus)
20-12
External Anatomy
Coronary Circulation: Arteries
• Right coronary artery exits aorta
just superior to point where aorta
exits heart; lies in coronary sulcus.
Smaller than left. Extends to
posterior aspect of heart
– Right marginal artery to lateral
wall of right ventricle
– Posterior interventricular artery
lies in posterior interventricular
sulcus, supplies posterior and inferior
aspects of heart
• Left coronary artery exits aorta near right coronary.
Branches
– Anterior interventricular artery (left anterior descending
artery) in
anterior interventricular sulcus
– Left marginal artery supplies lateral wall of left ventricle
– Circumflex artery extends to posterior aspect
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Left atrium
Aortic arch
Left ventricle
Superior
vena cava
Aortic
semilunar
valve
Right
atrium
Right
coronary
artery
Posterior
interventricular
artery
Right
marginal
artery
Right ventricle
Left marginal
artery
Pulmonary
trunk
Left coronary
artery
Circumflex
artery
Anterior
interventricular
artery
(a)
20-13
Coronary Circulation: Veins
• Great cardiac
vein and small
cardiac vein drain
right margin of
heart
• Coronary sinus:
veins empty here
then into the right
atrium
• Number of small
veins drain the
rest of the heart
Aortic arch
Left atrium
Right ventricle
Great
cardiac
vein
Left
ventricle
Coronary
sinus
Posterior vein
of left ventricle
Pulmonary
trunk
Superior
vena cava
Right
atrium
Into
right
atrium
Middle
cardiac vein
Small
cardiac
vein
(b)
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or display.
20-14
Heart Chambers
• Atria
– Right atrium: three major openings to receive blood
returning from the body (superior vena cava, inferior
vena cava, coronary sinus)
– Left atrium: four openings that receive blood from
pulmonary veins
– Interatrial septum: wall between the atria. Contains a
depression, the foramen ovale, a remnant of the fetal
opening between the atria
• Ventricles
– Atrioventricular canals: openings between atria and
respective ventricles
– Right ventricle opens to pulmonary trunk
– Left ventricle opens to aorta
– Interventricular septum between the two.
20-15
Aortic arch
Pulmonary trunk
Left pulmonary artery
Left pulmonary veins
Left atrium
Right atrium
Left ventricle
Right ventricle
Right atrioventricular canal
Bicuspid (mitral) valve
Chordae tendineae
Papillary muscles
Papillary muscles Interventricular septum
Superior vena cava
Inferior vena cava
Aortic semilunar valve
Coronary sinus
Right pulmonary veins
Branches of right
pulmonary artery
Pulmonary
semilunar valve
Tricuspid valve
Left atrioventricular
canal
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Heart Chambers
20-17
Structure of the Heart Valves
• Atrioventricular valves (AV valves).
Each valve has leaf-like cusps that are
attached to cone-shaped papillary muscles
by tendons (chordae tendineae). Right has
three cusps (tricuspid). Left has two cusps
(bicuspid, mitral). When valve is open,
canal is atrioventricular canal.
• Semilunar valves. Right (pulmonary); left
(atrial). Each cusp is shaped like a cup.
When cusps are filled, valve is closed; when
cusps are empty, valve is open.
20-18
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b. © McMinn & Hutchings, Color Atlas of Human
Anatomy/Mosby
Superior
vena cava
Ascending
aorta
Right atrium
Anterior cusp
of tricuspid valve
Inferior vena cava
(a) Anterior view
Pulmonary
trunk
Trabeculae on
interventricular
septum
Chordae
tendineae
Papillary
muscles
Pulmonary
trunk
Ascending aorta
Opening of right
coronary artery
Aortic semilunar
valve
Superior vena cava
Right atrium
Posterior
(b) Superior view
Left atrium (cut open)
Bicuspid valve
Opening of left
coronary artery
Pulmonary
semiluna rvalve
Anterior
Heart Chambers
Function of Heart Valves
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Pulmonary veins
Aorta
Left atrium
Pulmonary veins
Left atrium
Aorta
1 2
1
1
2
1
2
Aortic semilunar
valve (closed)
Bicuspid valve
(open)
Chordae tendineae
(tension low)
Papillary muscle
(relaxed)
Aortic semilunar
valve (open)
Cardiac muscle
(relaxed)
Left ventricle
(dilated)
(a) Valve positions when blood is flowing into the
left ventricle.
The bicuspid valve is open. The cusps of the valve are
pushed by the blood into the ventricle.
The aortic semilunar valve is closed. The cusps of the
valve overlap as they are pushed by the blood in the
aorta toward the ventricle.
The bicuspid valve is closed. The cusps of the valves
overlap as they are pushed by the blood toward the
left atrium.
The aortic semilunar valve is open. The cusps of the
valve are pushed by the blood toward the aorta.
(b) Valve positions when blood is flowing out of the left
ventricle.
Left ventricle
(contracted)
Cardiac muscle
(contracted)
Papillary muscle
(contracted)
Chordae tendineae
(tension high)
Bicuspid valve
(closed)
2
20-19
Route of Blood Flow Through Heart
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
8 7 6 5
1 2 3 4
(b)
Papillary muscles
Tricuspid valve
Right atrium
Pulmonary veins
Left atrium
Bicuspid valve
Interventricular septum
Left ventricle
Right ventricle
Pulmonary trunk
Aortic arch
Left pulmonary artery
1
3
2
4
4
5
5
7
6
8
Branches of left pulmonary
arteries
Inferior vena cava
Pulmonary semilunar valve
Pulmonary veins
Aortic semilunar valve
Branches of right
pulmonary arteries
Superior vena cava
Superior and
Inferior vena
cava
Right
atrium
Tricuspid
valve
Right
ventricle
Pulmonary
semilunar
valves
Pulmonary
trunk
Pulmonary
arteries
Aorta
Aortic
semilunar
valves
Left
ventricle
Bicuspid
valve
Left
atrium
Pulmonary
veins
Body tissues
(systemic
circulation)
Heart tissue
(coronary
circulation)
Coronary
arteries
Lung tissue
(pulmonary
circulation)
Coronary sinus
Cardiac veins
(a)
20-20
Histology
• Heart Skeleton
– Consists of plate of
fibrous connective tissue
between atria and
ventricles
– Fibrous rings around
valves to support
– Serves as electrical
insulation between atria
and ventricles
– Provides site for muscle
attachment
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or
display.
Pulmonary semilunar valve
Skeleton of the heart,
including fibrous rings
around valves Aortic
semilunar valve
Tricuspid
valve
Bicuspid
valve
Cardiac muscle
of the right
ventricle
Cardiac muscle
of the left ventricle
20-21
• Elongated, branching cells containing 1-2 centrally located nuclei
• Contains actin and myosin myofilaments
• Intercalated disks: specialized cell-cell contacts.
– Cell membranes interdigitate
– Desmosomes hold cells together
– Gap junctions allow action potentials to move from one cell to the
next.
• Electrically, cardiac muscle of the atria and of the ventricles behaves
as single unit
Connective tissue
Mitochondrion
Sarcomere
T tubule
Myofibrils
Striations
Intercalated disks
LM 400x
(b)
(a)
Branching
muscle fibers
Nucleus of cardiac
muscle cell
Sarcoplasmic
reticulum
Sarcolemma
(plasma membrane)
b: © Ed Reschke
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Cardiac Muscle
20-22
Conducting System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1
2
3
4
Left atrium
Left ventricle
Apex
1
2
3
4
Action potentials originate in the
sinoatrial (SA) node (the pacemaker)
and travel across the wall of the atrium
(arrows) from the SA node to the
atrioventricular (AV) node.
Action potentials pass through the AV
node and along the atrioventricular (AV)
bundle, which extends from the AV
node, through the fibrous skeleton, into
the interventricular septum.
The AV bundle divides into right and left
bundle branches, and action potentials
descend to the apex of each ventricle
along the bundle branches.
Action potentials are carried by the
Purkinje fibers from the bundle
branches to the ventricular walls
and papillary muscles.
Left and right
bundle branches
Atrioventricular
(AV) bundle
Atrioventricular
(AV) node
Sinoatrial
(SA) node
Purkinje
fibers
20-23
20-24
Conducting System
• SA node: sinoatrial node. Medial to opening of superior vena
cava. The pacemaker. Specialized cardiac muscle cells.
Generate spontaneous action potentials. Action potentials
pass to atrial muscle cells and to the AV node
• AV node: atrioventricular node. Medial to the right
atrioventricular valve. Action potentials conducted more
slowly here than in any other part of system. Ensures
ventricles receive signal to contract after atria have
contracted
• AV bundle: passes through hole in cardiac skeleton to reach
interventricular septum
• Right and left bundle branches: extend beneath
endocardium to apices of right and left ventricles
• Purkinje fibers: Large diameter cardiac muscle cells with
few myofibrils. Many gap junctions. Conduct action potential
to ventricular muscle cells
Electrical Properties
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1
1
2
2
3
–85
1 2
0
(mV)
Time (ms)
1 Depolarization phase
•
•
2 Repolarization phase
•
•
•
1 Depolarization phase
•
•
•
2 Early repolarization and plateau phases
•
•
•
3 Final repolarization phase
•
•
(mV)
1 2
Time (ms)
500
–85
0
Permeability changes during an action potential in
cardiac muscle:
Voltage-gated Na+ channels close.
Some voltage-gated K+ channels open, causing
early repolarization.
Voltage-gated Ca2+ channels are open, producing
the plateau by slowing further repolarization.
Voltage-gated Ca2+ channels close.
Many voltage-gated K+ channels open.
Voltage-gated Ca2+ channels begin to open.
Voltage-gated K+ channels close.
Voltage-gated Na+ channels open.
Permeability changes during an action potential in
skeletal muscle:
Voltage-gated Na+ channels open.
Voltage-gated K+ channels begin to open.
Voltage-gated Na+ channels close.
Voltage-gated K+ channels continue to open.
Voltage-gated K+ channels close at the end of
repolarization and return the membrane potential
to its resting value.
Depolarization
phase
Depolarization
phase
Repolarization
phase
Final
repolarization
phase
Plateau
phase
Early
repolarization
phase
20-25
20-26
Differences Between Skeletal and
Cardiac Muscle Physiology
• Cardiac: action potentials conducted from
cell to cell. In skeletal, action potential
conducted along length of single fiber
• Cardiac: rate of action potential propagation
is slow because of gap junctions and small
diameter of fibers. In skeletal it is faster due
to larger diameter fibers.
• Cardiac: calcium-induced calcium release
(CICR). Movement of Ca2+ through plasma
membrane and T tubules into sarcoplasm
stimulates release of Ca2+ from sarcoplasmic
reticulum
Autorhythmicity of Cardiac Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Permeability changes in pacemaker cells
1 Pacemaker potential
•
•
•
2 Depolarization phase
•
•
3 Repolarization phase
•
•
Time (ms)
300
1
0
–60
Threshold
Pacemaker potential
(mV)
3
2
1
Repolarization
phase
Depolarization
phase
A small number of Na+ channels are open.
Voltage-gated Ca2+ channels begin to open.
Voltage-gated K+ channels that opened in the
repolarization phase of the previous action
potential are closing.
Voltage-gated Ca+ channels are open.
Voltage-gated K+ channels are closed.
Voltage-gated Ca2+ channels close.
Voltage-gated K+ channels open.
20-27
20-28
Refractory Period
• Absolute: Cardiac muscle cell
completely insensitive to further
stimulation
• Relative: Cell exhibits reduced
sensitivity to additional stimulation
• Long refractory period prevents tetanic
contractions
Electrocardiogram
• Record of electrical event in the
myocardium that can be correlated
with mechanical events
• P wave: depolarization of atrial
myocardium and signals onset of
atrial contraction
• QRS complex: ventricular
depolarization and signals onset of
ventricular contraction.
Repolarization of atria
simultaneously.
• T wave: repolarization of ventricles;
precedes ventricular relaxation
• PQ interval or PR interval: 0.16 sec; atria contract and begin
to relax, ventricles begin to contract
• QT interval: 0.36 sec; ventricles contract and begin to relax
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(mV)
PQ interval QT interval
Time (seconds)
R
Q
S
QRS complex
(ventricular depolarization)
P
(atrial depolarization)
T
(ventricular repolarization)
20-29
20-30
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Premature ventricular contraction (PVC) (no P waves precede PVCs)
Bundle branch block
Atrial fibrillation (no clear P waves and rapid QRS complexes)
Ventricular fibrillation (no P, QRS, or T waves)
Prolonged QRS complexes
Complete heart block (P waves and QRS complexes are not coordinated)
P P P P P P P P P P
PVC
PVC
Electrocardiogram
20-31
SA node block
TABLE 20.1 Major Cardiac Arrhythmias
Conditions Symptoms Possible Causes
Abnormal Heart Rhythms
Tachycardia
Paroxysmal atrial
tachycardia
Ventricular tachycardia
Heart rate in excess of 100 beats per minute (bpm)
Sudden increase in heart rate to 95–150 bpm for a few
seconds or even for several hours; P wave precedes
every QRS complex; P wave inverted and superimposed
on T wave
Frequently causes fibrillation
Elevated body temperature; excessive
sympathetic stimulation; toxic conditions
Excessive sympathetic stimulation; abnormally
elevated permeability of slow channels
Often associated with damage to AV node
or ventricular muscle
Abnormal Rhythms Resulting from Ectopic Action Potentials
Atrial flutter
Atrial fibrillation
Ventricular fibrillation
Ectopic action potentials in the atria
Ectopic action potentials in the atria
Ectopic action potentials in the ventricles
300 P waves/min; 125 QRS complexes/min, resulting in two or three P
waves (atrial contraction) for every QRS complex (ventricular contraction)
No P waves; normal QRS complexes; irregular timing; ventricles constantly
stimulated by atria; reduced pumping effectiveness and filling time
No QRS complexes; no rhythmic contraction of the myocardium; many
patches of asynchronously contracting ventricular muscle
Heart rate less than 60 bpm
Heart rate varies 5% during respiratory cycle and up to
30% during deep respiration.
Cessation of P wave; new low heart rate due to AV node
acting as pacemaker; normal QRS complex and T wave
PR interval greater than 0.2 second
First-degree
Second-degree
Third-degree (complete
heart block)
PR interval 0.25–0.45 second; some P waves trigger QRS complexes and
others do not; 2:1, 3:1, and 3:2 P wave/QRS complex ratios may occur
P wave dissociated from QRS complex; atrial rhythm approximately
100 bpm; ventricular rhythm less than 40 bpm
Occasional shortened intervals between contractions;
frequently occurs in healthy people
P wave superimposed on QRS complex
Prolonged QRS complex; exaggerated voltage because
only one ventricle may depolarize; inverted T wave;
increased probability of fibrillation
Elevated stroke volume in athletes; excessive
vagal stimulation; carotid sinus syndrome
Cause not always known; occasionally caused by
ischemia or inflammation or associated with cardiac
failure
Ischemia; tissue damage due to infarction;
causes unknown
Inflammation of AV bundle
Excessive vagal stimulation
Ischemia of AV nodal fibers or compression
of AV bundle
Excessive smoking; lack of sleep; too much
caffeine; alcoholism
Ectopic foci in ventricles; lack of sleep;
too much caffeine, irritability; occasionally
occurs with coronary thrombosis
Abbreviations: SA = sinoatrial; AV = atrioventricular.
Bradycardia
Sinus arrhythmia
AV Node Block
Premature atrial
contractions
Premature ventricular
contractions (PVCs)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
20-32
Cardiac Cycle
• Heart is two pumps that work together,
right and left half
• Repetitive contraction (systole) and
relaxation (diastole) of heart chambers
• Blood moves through circulatory system
from areas of higher to lower pressure.
– Contraction of heart produces the pressure
20-33
Period of Isovolumetric Contraction
• Begins at the completion of the QRS complex.
• Ventricular muscles start to contract, increasing
the pressure inside the ventricles. This causes
the AV valves to close, which is the beginning of
ventricular systole. The semilunar valves were
closed in the previous diastole and remain closed
during this event.
• 120-130 mL of blood are in the ventricles, left
from the last diastole when the atria emptied into
the ventricles. This is referred to as the end
diastolic volume.
20-34
Period of Ejection
• Pressure in the ventricle has increased to the point
where it is greater than the pressure in the
pulmonary trunk/aorta. This pushes the cusps of
the semilunar valves against the walls of the
vessels, opening the valve.
• Blood is ejected from the ventricles.
• The pressures in the two ventricles are different:
120 mm Hg in the left ventricle; 25 mm Hg in the
right ventricle. Remember: blood in the left
ventricle must be pumped to the whole body; blood
in the right ventricle is pumped to the lungs.
• After the first initial spurt, pressure starts to drop.
• At the end of the period of ejection, 50-60 mL
remain: end-systolic volume.
20-35
Period of Isovolumetric Relaxation
• Completion of T wave results in ventricular
repolarization and relaxation.
• Ventricular pressure falls very rapidly.
• Pulmonary trunk/aorta pressure is higher than
ventricular pressure.
• Elastic recoil of the arteries causes blood to flow
back toward the relaxed ventricles: the
semilunar valves close, which is the beginning of
ventricular diastole.
• Note that the AV valves are also closed.
20-36
Passive Ventricular Filling
• While the ventricles were in systole, the
atria were filling with blood.
• Atrial pressure rises above ventricular
pressure and the AV valves open.
• Blood flows into the relaxed ventricles,
accounting for most of the ventricular
filling (70%).
20-37
Active Ventricular Filling
• Depolarization of the SA node generates
action potentials that spread over the atria (P
wave) and the atria contract. This completes
ventricular filling.
• At rest, contraction of atria not necessary for
heart function.
• During exercise, atrial contraction necessary
for function as heart pumps 300-400%.
Cardiac Cycle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
2
3
4
5
1
Semilunar
valves closed
AV valves
closed
Semilunar
valves closed
Semilunar
valves opened
AV valves
closed
Atrial systole: active ventricular filling. The atria contract,
Increasing atrial pressure and completing ventricular
filling while the ventricles are relaxed.
Semilunar
valves closed
AV valves
opened
Ventricular diastole: passive ventricular filling. As
ventricular relaxation continues, the AV valves open, and
blood flows from the atria Into the relaxing ventricles,
accounting for most of the ventricular filling.
Ventricular systole: period of isovolumetric contraction. The
atria are relaxed, and blood flows into them from the veins.
ventricular contraction causes ventricular pressure to
increase and causes the AV valves to close, which is the
beginning of ventricular systole. The semilunar valves were
closed in the previous diastole and remain closed during
this period
AV valves
opened
Ventricular systole: period of ejection. Continued
ventricular contraction causes a greater increase
interventricular pressure, which pushes blood out of the
ventricles, causing the semilunar valves to open.
Semilunar
valves closed
AV valves
closed
Ventricular diastole: period of isovolumetric relaxation. As the
ventricles begin to relax at the beginning of ventricular
diastole, blood flowing back from the aorta and pulmonary
trunk toward the relaxing ventricles causes the semilunar
valves to close. Note that the AV valves are closed also. 20-38
20-39
Events Occurring During the Cardiac Cycle
Q
S
R
T
T
P
Q
S
R
P
Time periods:
Passive
ventricular
filling
Period of
isovolumetric
relaxation
Period of
ejection
Period of
isovolumetric
contraction
Active
ventricular
filling
(mV)
Pressure
(mm
Hg)
Left
ventricular
volume
(mL)
"Sound“
frequency
(cycles/second)
120
100
80
60
40
20
0
125
90
55
Atrial
systole
Ventricular
systole
Ventricular
diastole
Semilunar
valves
close.
AV valves
open.
Second
heart
sound
End-systolic volume
End-diastolic volume
First
heart
sound
Systolic
pressure
Semilunar
valves
open.
AV valves
close.
End-systolic volume
First
heart
sound
Second
heart
sound
Third
heart
sound
End-diastolic
volume
AV valves
open.
Dicrotic
notch
Semilunar
valves
close.
Semilunar
valves open.
Diastolic
pressure
AV valves
close.
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
20-40
Summary of the Events of the Cardiac Cycle
Atrial Systole Atrial Diastole
Ventricular Diastole Ventricular Systole
Active Ventricular Filling Period of Isovolumetric Contraction
Time Period Contraction of the atria pumps blood into the ventricles. The ventricles begin to contract, but ventricular volume
does not change.
Condition of Valves The semilunar valves are closed; the AV valves are
opened (figure 20.18, step 1 ).
The semilunar valves are closed; the AV valves are closed
(figure 20.18, step 2).
ECG The P wave is completed and the atria are stimulated to
contract. Action potentials are delayed in the AV node
for 0.11 second, allowing time for the atria to contract.
The QRS complex is completed, and the ventricles are
depolarized. As a result, the ventricles begin to contract.
The QRS complex begins as action potentials are
propagated from the AV node to the ventricles.
Atrial Pressure Graph Atrial contraction (systole) causes an increase in atrial
pressure, and blood is forced to flow from the atria into
the ventricles.
Atrial repolarization is masked by the QRS complex.
The atria are relaxed (atrial diastole).
Atrial pressure decreases in the relaxed atria. When atrial
pressure is less than venous pressure, blood flows into
the atria.
Atrial pressure increases briefly as the contracting ventricles
push blood back toward the atria.
Ventricular Pressure
Graph
Atrial contraction (systole) and the movement of blood
into the ventricles cause a slight increase in ventricular
pressure.
Ventricular contraction causes an increase in ventricular
pressure, which causes blood to flow toward the atria,
closing the AV valves.
Ventricular pressure increases rapidly.
Aortic Pressure Graph Aortic pressure gradually decreases as blood runs out
of the aorta into other systemic blood vessels.
Just before the semilunar valves open, pressure in the
aorta decreases to its lowest value, called the diastolic
pressure (approximately 80 mm Hg).
Volume Graph Atrial contraction (systole) completes ventricular filling
during the last one-third of diastole. The amount of
blood in a ventricle at the end of ventricular diastole
is called the end-diastolic volume.
During the period of isovolumetric contraction, ventricular
volume does not change because the semilunar and AV
valves are closed.
Sound Graph Blood flowing from the ventricles toward the atria closes
the AV valves. Vibrations of the valves and the turbulent
flow of blood produce the first heart sound, which marks
the beginning of ventricular systole
Abbreviation: AV = atrioventricular.
20-41
Atrial Diastole
Ventricular Diastole
Period of Isovolumetric Relaxation Passive Ventricular Filling
The ventricles relax, but ventricular volume
does not change.
Blood flows into the ventricles because blood
pressure is higher in the veins and atria than in
the relaxed ventricles.
The semilunar valves are closed; the AV valves
are closed (figure 20.18, step 4).
The semilunar valves are closed; the AV valves
are opened (see figure 20.18, step 5).
The T wave is completed, and the ventricles
are repolarized. The ventricles relax.
The P wave is produced when the SA node generates
action potentials and a wave of depolarization
begins to propagate across the atria.
Atrial pressure continues to increase gradually
as blood flows from the veins into the relaxed
atria
After the AV valves open, atrial pressure
decreases as blood flows out of the atria into the
relaxed ventricles.
Elastic recoil of the aorta pushes blood back
toward the heart, causing the semilunar
valves to close.
No significant change occurs in ventricular pressure
during this time period.
After the semilunar valves close, elastic recoil
of the aorta causes a slight increase in aortic
pressure, producing the dicrotic notch and
dicrotic wave.
Aortic pressure gradually decreases as blood
runs out of the aorta into other systemic blood
vessels.
During the period of isovolumetric relaxation,
ventricular volume does not change because
the semilunar and AV valves are closed.
After the AV valves open, blood flows from the
atria and veins into the ventricles because of
pressure differences. Most ventricular filling
occurs during the first one-third of diastole.
Sometimes the turbulent flow of blood into the
ventricles produces a third heart sound.
Ventricular Systole
Period of Ejection
The ventricles continue to contract, and blood
is pumped out of the ventricles.
The semilunar valves are opened; the AV valves
are closed (figure 20.18, step 3).
The T wave results from ventricular repolarization.
Atrial pressure increases gradually as blood
flows from the veins into the relaxed atria.
Ventricular pressure becomes greater than
pressure in the aorta as the ventricles continue
to contract. The semilunar valves are pushed
open as blood flows out of the ventricles.
As ventricular contraction forces blood into
the aorta, pressure in the aorta increases to
its highest value, called the systolic pressure
(approximately 120 mm Hg).
After the semilunar valves open, blood volume
decreases as blood flows out of the ventricles
during the period of ejection.
Ventricular pressure peaks as the ventricles
contract maximally; then pressure decreases
as blood flow out of the ventricles decreases
The amount of blood left in a ventricle at the
end of the period of ejection is called the
end-systolic volume.
After closure of the semilunar valves, the
pressure in the relaxing ventricles rapidly
decreases.
Little ventricular filling occurs during the middle
one-third of diastole.
Blood flowing from the ventricles toward the
aorta and pulmonary trunk closes the semilunar
valves. Vibrations of the valves and the
turbulent flow of blood produce the second
heart sound, which marks the beginning of
ventricular diastole.
20-42
Heart Sounds
• First heart sound or “lubb”
– Atrioventricular valves and surrounding fluid
vibrations as valves close at beginning of ventricular
systole
• Second heart sound or “dupp”
– Results from closure of aortic and pulmonary
semilunar valves at beginning of ventricular diastole,
lasts longer
• Third heart sound (occasional)
– Caused by turbulent blood flow into ventricles and
detected near end of first one-third of diastole
20-43
Aortic Pressure Curve
• Dicrotic notch (incisura): when the
aortic semilunar valve closes, pressure
within the aorta increases slightly
• Blood pressure measurement taken in
the arm is a reflection of aortic
pressures, not ventricular
20-44
20.8 Mean Arterial Pressure
• Average blood pressure in aorta
• MAP = CO x PR
– CO is amount of blood pumped by heart per
minute
• CO = SV x HR
– SV: Stroke volume (blood pumped during each heart
beat)
– HR: Heart rate (number of times heart beats per
minute)
• Cardiac reserve: Difference between CO at rest and
maximum CO
– PR is total resistance against which blood must
be pumped
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Factors Affecting Cardiac Output Factors Affecting Peripheral Resistance
Increased vasoconstriction
Increased heart rate
Increased cardiac output
Increased stroke volume
Increased peripheral resistance
Increased mean arterial pressure
Decreased blood pressure, decreased blood
pH, increased blood carbon dioxide, decreased
blood oxygen, exercise, and emotions
Increased blood volume, exercise,
change from a standing to a lying
down position
Increased sympathetic stimulation,
decreased parasympathetic stimulation, and
increased epinephrine and norepinephrine
secretion from the adrenal medulla
Increased venous return increases
end-diastolic volume and preload.
Decreased blood pressure,
decreased blood pH, increased
blood carbon dioxide, and
decreased blood oxygen
(see chapter 21)
Increased force of contraction
(Starling law of the heart)
ejects increased end-diastolic
volume.
Increased force
of contraction
decreases end-
systolic volume.
Factors Affecting MAP
20-45
20-46
20.9 Regulation of the Heart
• Intrinsic regulation: Results from normal
functional characteristics, not on neural or
hormonal regulation
– Preload: Starling’s law of the heart
• Preload is the amount of stretch of the
ventricular walls. The greater the stretch
(preload), the greater the force of
contraction.
– Afterload: pressure the contracting
ventricles must produce to overcome the
pressure in the aorta and move blood into
the aorta. Heart not as sensitive to this as it
is to changes in preload.
• Extrinsic regulation: Involves neural and hormonal control
– Parasympathetic stimulation
• Supplied by vagus nerve, decreases heart rate, acetylcholine
is secreted and hyperpolarizes the heart
– Sympathetic stimulation
• Supplied by cardiac nerves. Innervate the SA and AV nodes,
coronary vessels and the atrial and ventricular myocardium.
Increases heart rate and force of contraction. Epinephrine
and norepinephrine released.
• Increased heart beat causes increased cardiac output.
Increased force of contraction causes a lower end-systolic
volume; heart empties to a greater extent. Limitations:
heart has to have time to fill.
– Hormonal Control. Epinephrine and norepinephrine from the
adrenal medulla. Occurs in response to increased physical
activity, emotional excitement, stress
20-47
Regulation of the Heart
20-48
Heart and Homeostasis
• Effect of blood pressure
– Baroreceptors monitor blood pressure; in walls of internal
carotids and aorta. This sensory information goes to centers in
the medulla oblongata
• Effect of pH, carbon dioxide, oxygen
– Receptors that measure pH and carbon dioxide levels found in
hypothalamus
– Chemoreceptors monitoring oxygen levels found in aorta and
internal carotids. Prolonged lowered oxygen levels causes
increased heart rate, which increases blood pressure and can
thus deliver more oxygen to the tissues.
• Effect of extracellular ion concentration
– Increase or decrease in extracellular K+ decreases heart rate
• Effect of body temperature
– Heart rate increases when body temperature increases, heart
rate decreases when body temperature decreases
Baroreceptor and Chemoreceptor Reflexes
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Heart
Circulation
Epinephrine and norepinephrine
Adrenal medulla
1
2
3
4
1
2
3
4
Sympathetic
nerve fibers to
adrenal gland
Sensory neurons (green) carry
action potentials from baroreceptors
and carotid body chemoreceptors
to the cardioregulatory center.
Chemoreceptors in the medulla
oblongata also influence the
cardioregulatory center.
The cardioregulatory center
controls the frequency of action
potentials in the parasympathetic
neurons (red) extending to the
heart through the vagus nerves.
The parasympathetic neurons
decrease the heart rate.
The cardioregulatory center
controls the frequency of action
potentials in the sympathetic
neurons (blue). The sympathetic
neurons extend through the
cardiac nerves and increase the
heart rate and the stroke volume.
The cardioregulatory center
influences the frequency of action
potentials in the sympathetic
neurons (blue) extending to the
adrenal medulla. The sympathetic
neurons increase the secretion of
epinephrine and some
norepinephrine into the systemic
circulation. Epinephrine and
Norepinephrine increase the heart
Rate and stroke volume.
SA node
Sensory
nerve
fibers
Cardioregulatory center and
chemoreceptors in medulla oblongata
Sensory nerve
fibers
Baroreceptors
in wall of internal
carotid artery
Carotid body
chemoreceptors
Baroreceptors
in aorta
Parasympathetic nerve fibers
Vagus nerves
Sympathetic nerve fibers
20-49
Cardiac nerves
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Heart rate and stroke volume increase.
Heart rate and stroke volume decrease.
Start here
Actions
Actions
Response
Response
Baroreceptors in the carotid
arteries and aorta detect an
increase in blood pressure.
The cardioregulatory center increases
parasympathetic and decreases
sympathetic stimulation of the heart.
Blood pressure increases:
Homeostasis Disturbed
Blood
pressure
(normal
range)
Blood
pressure
(normal
range)
Blood pressure decreases:
Homeostasis Disturbed
Baroreceptors in the carotid arteries and
aorta detect a decrease in blood pressure.
The cardioregulatory center decreases
parasympathetic and increases
sympathetic stimulation of the heart;
adrenal medulla secretion of epinephrine
and norepinephrine increases.
Blood pressure increases:
Homeostasis Restored
Blood pressure decreases:
Homeostasis Restored
6
5
1
2
3 4
The effectors (SA node and cardiac
muscle) respond:
The effectors (SA node and cardiac
muscle) respond:
20-50
Baroreceptor
Reflex
Blood
pH
(normal
range)
Reactions
Actions
Actions Reactions
Heart rate and stroke volume decrease,
reducing blood flow to the lungs. Blood
CO2 levels increase.
Chemoreceptors in the medulla
oblongata detect an increase in blood
pH (often caused by a decrease in
blood CO2). Cardioregulatory center
increases parasympathetic and
decreases sympathetic stimulation
of the heart.
Blood
pH
(normal
range)
Chemoreceptors in the medulla
oblongata detect a decrease in blood pH
(often caused by an increase in blood
CO2). Cardioregulatory center decreases
parasympathetic and increases
sympathetic stimulation of the heart
Heart rate and stroke volume increase,
increasing blood flow to the lungs.
Blood CO2 levels decrease.
6
5
1
2
3 4
5
The effectors (SA node and cardiac
muscle) respond:
The effectors (SA node and cardiac
muscle) respond:
Blood pH decreases:
Homeostasis Restored
Blood pH increases:
Homeostasis Restored
Blood pH increases:
Homeostasis Disturbed
Blood pH decreases:
Homeostasis Disturbed
Start here
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
20-51
Chemoreceptor
Reflex
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Heart
Diseases and Disorders
Inflammation of the endocardium; affects the valves more severely than other areas of the endocardium; may lead to
scarring, causing stenosed or incompetent valves
Inflammation of the pericardium; see Clinical Impact, “Pericarditis and Cardiac Tamponade”
Disease of the myocardium of unknown cause or occurring secondarily to other disease; results in weakened cardiac
muscle, causing all chambers of the heart to enlarge; may eventually lead to congestive heart failure
Results from a streptococcal infection in young people; toxin produced by the bacteria can cause rheumatic fever
several weeks after the infection that can result in rheumatic endocarditis
Reduces the amount of blood the coronary arteries can deliver to the myocardium
Formation of blood clot in a coronary artery
Damaged cardiac muscle tissue resulting from lack of blood flow to the myocardium; often referred to as a heart attack;
see Clinical Impact, “Angina, Infarctions, and the Treament of Blocked coronary Arteries”
Hole in the septum between the left and right sides of the heart, allowing blood to flow from one side of the heart to the
other and greatly reducing the heart’s pumping effectiveness
Ductus arteriosus fails to close after birth, allowing blood to flow from the aorta to the pulmonary trunk under a higher
pressure, which damages the lungs; also, the left ventricle must work harder to maintain adequate systemic pressure
Narrowed opening through one or more of the heart valves; aortic or pulmonary semilunar stenosis increases the heart’s
workload; bicuspid valve stenosis causes blood to back up in the left atria and lungs, resulting in edema of the lungs;
tricuspid valve stenosis results in similar blood flow problems and edema in the peripheral tissues
Heart valves do not close correctly, and blood flows through in the reverse direction; see Clinical Impact, “Abnormal
Heart Sounds”
Cyanosis (sı-a-no′sis; cyan,
blue + osis, condition of)
Symptom of inadequate heart function in babies with congenital heart disease; the infant’s skin appears blue because
of low oxygen levels in the blood in peripheral blood vessels
Progressive weakening of the heart muscle, reducing the heart’s pumping action; hypertension leading to heart failure
due to increased afterload; advanced age, malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism,
and hereditary factors can lead to heart failure
Condition Description
Inflammation of Heart Tissue
Endocarditis
Pericarditis
Cardiomyopathy
Rheumatic heart disease
Reduced Blood Flow to Cardiac Muscle
Coronary heart disease
Coronary thrombosis
Myocardial infarction
Congenital Heart Diseases (occur at birth)
Septal defect
Patent ductus arteriosus
Stenosis of the heart valve
Incompetent heart valve
Heart Failure
- - -
20-52

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AP-Refresher-1--Heart-Physiology.pptx

  • 1. A&P Refresher- Heart Note: Not all slides will be covered - Goal is to provide quick background/review to hopefully begin to understand some of the pathologies on first 2 slides 20-1
  • 2. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Heart Diseases and Disorders Inflammation of the endocardium; affects the valves more severely than other areas of the endocardium; may lead to scarring, causing stenosed or incompetent valves Inflammation of the pericardium; see Clinical Impact, “Pericarditis and Cardiac Tamponade” Disease of the myocardium of unknown cause or occurring secondarily to other disease; results in weakened cardiac muscle, causing all chambers of the heart to enlarge; may eventually lead to congestive heart failure Results from a streptococcal infection in young people; toxin produced by the bacteria can cause rheumatic fever several weeks after the infection that can result in rheumatic endocarditis Reduces the amount of blood the coronary arteries can deliver to the myocardium Formation of blood clot in a coronary artery Damaged cardiac muscle tissue resulting from lack of blood flow to the myocardium; often referred to as a heart attack; see Clinical Impact, “Angina, Infarctions, and the Treament of Blocked coronary Arteries” Hole in the septum between the left and right sides of the heart, allowing blood to flow from one side of the heart to the other and greatly reducing the heart’s pumping effectiveness Ductus arteriosus fails to close after birth, allowing blood to flow from the aorta to the pulmonary trunk under a higher pressure, which damages the lungs; also, the left ventricle must work harder to maintain adequate systemic pressure Narrowed opening through one or more of the heart valves; aortic or pulmonary semilunar stenosis increases the heart’s workload; bicuspid valve stenosis causes blood to back up in the left atria and lungs, resulting in edema of the lungs; tricuspid valve stenosis results in similar blood flow problems and edema in the peripheral tissues Heart valves do not close correctly, and blood flows through in the reverse direction; see Clinical Impact, “Abnormal Heart Sounds” Cyanosis (sı-a-no′sis; cyan, blue + osis, condition of) Symptom of inadequate heart function in babies with congenital heart disease; the infant’s skin appears blue because of low oxygen levels in the blood in peripheral blood vessels Progressive weakening of the heart muscle, reducing the heart’s pumping action; hypertension leading to heart failure due to increased afterload; advanced age, malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism, and hereditary factors can lead to heart failure Condition Description Inflammation of Heart Tissue Endocarditis Pericarditis Cardiomyopathy Rheumatic heart disease Reduced Blood Flow to Cardiac Muscle Coronary heart disease Coronary thrombosis Myocardial infarction Congenital Heart Diseases (occur at birth) Septal defect Patent ductus arteriosus Stenosis of the heart valve Incompetent heart valve Heart Failure - - - 20-2
  • 3. 20-3 SA node block TABLE 20.1 Major Cardiac Arrhythmias Conditions Symptoms Possible Causes Abnormal Heart Rhythms Tachycardia Paroxysmal atrial tachycardia Ventricular tachycardia Heart rate in excess of 100 beats per minute (bpm) Sudden increase in heart rate to 95–150 bpm for a few seconds or even for several hours; P wave precedes every QRS complex; P wave inverted and superimposed on T wave Frequently causes fibrillation Elevated body temperature; excessive sympathetic stimulation; toxic conditions Excessive sympathetic stimulation; abnormally elevated permeability of slow channels Often associated with damage to AV node or ventricular muscle Abnormal Rhythms Resulting from Ectopic Action Potentials Atrial flutter Atrial fibrillation Ventricular fibrillation Ectopic action potentials in the atria Ectopic action potentials in the atria Ectopic action potentials in the ventricles 300 P waves/min; 125 QRS complexes/min, resulting in two or three P waves (atrial contraction) for every QRS complex (ventricular contraction) No P waves; normal QRS complexes; irregular timing; ventricles constantly stimulated by atria; reduced pumping effectiveness and filling time No QRS complexes; no rhythmic contraction of the myocardium; many patches of asynchronously contracting ventricular muscle Heart rate less than 60 bpm Heart rate varies 5% during respiratory cycle and up to 30% during deep respiration. Cessation of P wave; new low heart rate due to AV node acting as pacemaker; normal QRS complex and T wave PR interval greater than 0.2 second First-degree Second-degree Third-degree (complete heart block) PR interval 0.25–0.45 second; some P waves trigger QRS complexes and others do not; 2:1, 3:1, and 3:2 P wave/QRS complex ratios may occur P wave dissociated from QRS complex; atrial rhythm approximately 100 bpm; ventricular rhythm less than 40 bpm Occasional shortened intervals between contractions; frequently occurs in healthy people P wave superimposed on QRS complex Prolonged QRS complex; exaggerated voltage because only one ventricle may depolarize; inverted T wave; increased probability of fibrillation Elevated stroke volume in athletes; excessive vagal stimulation; carotid sinus syndrome Cause not always known; occasionally caused by ischemia or inflammation or associated with cardiac failure Ischemia; tissue damage due to infarction; causes unknown Inflammation of AV bundle Excessive vagal stimulation Ischemia of AV nodal fibers or compression of AV bundle Excessive smoking; lack of sleep; too much caffeine; alcoholism Ectopic foci in ventricles; lack of sleep; too much caffeine, irritability; occasionally occurs with coronary thrombosis Abbreviations: SA = sinoatrial; AV = atrioventricular. Bradycardia Sinus arrhythmia AV Node Block Premature atrial contractions Premature ventricular contractions (PVCs) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  • 4. 20-4 Functions of the Heart 1. Generating blood pressure 2. Routing blood: separates pulmonary and systemic circulations 3. Ensuring one-way blood flow: valves 4. Regulating blood supply – Changes in contraction rate and force match blood delivery to changing metabolic needs
  • 5. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lung CO2 CO2 O2 O2 CO2 O2 Right side of heart Pulmonary circulation (through lungs) Lung capillaries Tissue capillaries Circulation to tissues of head, neck, and upper limbs Systemic circulation (through body) Left side of heart Tissue capillaries Circulation to tissues of thorax, abdomen, and lower limbs 20-5 Cardiovascular Overview
  • 6. Midclavicular line 2nd intercostal space Sternum Apex of heart 5th intercostal space Larynx Superior vena cava Right lung Right atrium Right ventricle Rib Visceral pleura Pleural cavity Parietal pleura Diaphragm Trachea Aortic arch Base of heart Pulmonary trunk Left atrium Left lung Left ventricle Apex of heart Visceral pericardium Pericardial cavity Parietal pericardium Fibrous pericardium Left lung Visceralpleura Pleural cavity Parietal pleura (a) Anterior view Size, Shape, Location of the Heart • Size of a closed fist • Shape – Apex: Blunt rounded point of cone – Base: Flat part at opposite of end of cone • Located in thoracic cavity in mediastinum (central core of the thoracic cavity; everything in the thoracic cavity except the lungs.) – Important clinically when using a stethoscope, performing an ECG, or performing CPR 20-6 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  • 7. Esophagus Right pleural cavity Right pulmonary artery Right pulmonary vein Superior vena cava Ascending aorta Right atrium Right ventricle Descending aorta Tissue of mediastinum Bronchus of lung Parietal pleura Left pleural cavity Visceral pleura Left pulmonary artery Left pulmonary vein Pulmonary trunk Left atrium Left ventricle Visceral pericardium Pericardial cavity Parietal pericardium Fibrous pericardium Superior view (b) Heart Cross Section Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 20-7
  • 8. Anatomy of the Heart • Pericardium or pericardial sac – Fibrous pericardium: tough fibrous outer layer. Prevents over distention; acts as anchor – Serous pericardium: thin, transparent, inner layer. Simple squamous epithelium • Parietal pericardium: lines the fibrous outer layer • Visceral pericardium (epicardium): covers heart surface • The two are continuous and have a pericardial cavity between them filled with pericardial fluid 20-8
  • 9. Anatomy of the Heart Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fibrous pericardium Parietal pericardium Serous pericardium Pericardium Anterior view Visceral pericardium (or epicardium) Pericardial cavity filled with pericardial fluid
  • 10. Heart Wall • Three layers of tissue – Epicardium: Serous membrane; smooth outer surface of heart – Myocardium: Middle layer composed of cardiac muscle cell and responsibility for heart contracting – Endocardium: Smooth inner surface of heart chambers • Pectinate muscles: muscular ridges in auricles and right atrial wall • Trabeculae carneae: muscular ridges and columns on inside walls of ventricles Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Myocardium Endocardium Simple squamous epithelium Loose connective tissue and adipose tissue Epicardium (visceral pericardium) Trabeculae carneae 20-10
  • 11. External Anatomy Aortic arch Superior vena cava Aorta Coronary sulcus Pulmonary trunk Left pulmonary artery Left pulmonary veins Left atrium Left ventricle Right pulmonary veins Right atrium Right coronary artery Right ventricle Inferior vena cava (a) Anterior view Aorta Great cardiac vein (in interatrial septum) Left ventricle Right auricle Right ventricle (b) Anterior view Branches of right pulmonary artery Superior vena cava Anterior interventricular artery (in anterior interventricular sulcus) Left auricle Branches of left pulmonary artery Great cardiac vein (in anterior interventricular sulcus) Anterior interventricular artery (in anterior interventricular sulcus) 20-11 Apex
  • 12. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Aorta Left atrium Left pulmonary veins Left pulmonary artery Apex Left ventricle Coronary sinus Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium Inferior vena cava Right coronary artery Small cardiac vein Right ventricle Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein (in posterior inter- ventricular sulcus) (c) Posterior view Great cardiac vein (in coronary sulcus) 20-12 External Anatomy
  • 13. Coronary Circulation: Arteries • Right coronary artery exits aorta just superior to point where aorta exits heart; lies in coronary sulcus. Smaller than left. Extends to posterior aspect of heart – Right marginal artery to lateral wall of right ventricle – Posterior interventricular artery lies in posterior interventricular sulcus, supplies posterior and inferior aspects of heart • Left coronary artery exits aorta near right coronary. Branches – Anterior interventricular artery (left anterior descending artery) in anterior interventricular sulcus – Left marginal artery supplies lateral wall of left ventricle – Circumflex artery extends to posterior aspect Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Left atrium Aortic arch Left ventricle Superior vena cava Aortic semilunar valve Right atrium Right coronary artery Posterior interventricular artery Right marginal artery Right ventricle Left marginal artery Pulmonary trunk Left coronary artery Circumflex artery Anterior interventricular artery (a) 20-13
  • 14. Coronary Circulation: Veins • Great cardiac vein and small cardiac vein drain right margin of heart • Coronary sinus: veins empty here then into the right atrium • Number of small veins drain the rest of the heart Aortic arch Left atrium Right ventricle Great cardiac vein Left ventricle Coronary sinus Posterior vein of left ventricle Pulmonary trunk Superior vena cava Right atrium Into right atrium Middle cardiac vein Small cardiac vein (b) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 20-14
  • 15. Heart Chambers • Atria – Right atrium: three major openings to receive blood returning from the body (superior vena cava, inferior vena cava, coronary sinus) – Left atrium: four openings that receive blood from pulmonary veins – Interatrial septum: wall between the atria. Contains a depression, the foramen ovale, a remnant of the fetal opening between the atria • Ventricles – Atrioventricular canals: openings between atria and respective ventricles – Right ventricle opens to pulmonary trunk – Left ventricle opens to aorta – Interventricular septum between the two. 20-15
  • 16. Aortic arch Pulmonary trunk Left pulmonary artery Left pulmonary veins Left atrium Right atrium Left ventricle Right ventricle Right atrioventricular canal Bicuspid (mitral) valve Chordae tendineae Papillary muscles Papillary muscles Interventricular septum Superior vena cava Inferior vena cava Aortic semilunar valve Coronary sinus Right pulmonary veins Branches of right pulmonary artery Pulmonary semilunar valve Tricuspid valve Left atrioventricular canal Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Heart Chambers
  • 17. 20-17 Structure of the Heart Valves • Atrioventricular valves (AV valves). Each valve has leaf-like cusps that are attached to cone-shaped papillary muscles by tendons (chordae tendineae). Right has three cusps (tricuspid). Left has two cusps (bicuspid, mitral). When valve is open, canal is atrioventricular canal. • Semilunar valves. Right (pulmonary); left (atrial). Each cusp is shaped like a cup. When cusps are filled, valve is closed; when cusps are empty, valve is open.
  • 18. 20-18 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. b. © McMinn & Hutchings, Color Atlas of Human Anatomy/Mosby Superior vena cava Ascending aorta Right atrium Anterior cusp of tricuspid valve Inferior vena cava (a) Anterior view Pulmonary trunk Trabeculae on interventricular septum Chordae tendineae Papillary muscles Pulmonary trunk Ascending aorta Opening of right coronary artery Aortic semilunar valve Superior vena cava Right atrium Posterior (b) Superior view Left atrium (cut open) Bicuspid valve Opening of left coronary artery Pulmonary semiluna rvalve Anterior Heart Chambers
  • 19. Function of Heart Valves Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pulmonary veins Aorta Left atrium Pulmonary veins Left atrium Aorta 1 2 1 1 2 1 2 Aortic semilunar valve (closed) Bicuspid valve (open) Chordae tendineae (tension low) Papillary muscle (relaxed) Aortic semilunar valve (open) Cardiac muscle (relaxed) Left ventricle (dilated) (a) Valve positions when blood is flowing into the left ventricle. The bicuspid valve is open. The cusps of the valve are pushed by the blood into the ventricle. The aortic semilunar valve is closed. The cusps of the valve overlap as they are pushed by the blood in the aorta toward the ventricle. The bicuspid valve is closed. The cusps of the valves overlap as they are pushed by the blood toward the left atrium. The aortic semilunar valve is open. The cusps of the valve are pushed by the blood toward the aorta. (b) Valve positions when blood is flowing out of the left ventricle. Left ventricle (contracted) Cardiac muscle (contracted) Papillary muscle (contracted) Chordae tendineae (tension high) Bicuspid valve (closed) 2 20-19
  • 20. Route of Blood Flow Through Heart Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 8 7 6 5 1 2 3 4 (b) Papillary muscles Tricuspid valve Right atrium Pulmonary veins Left atrium Bicuspid valve Interventricular septum Left ventricle Right ventricle Pulmonary trunk Aortic arch Left pulmonary artery 1 3 2 4 4 5 5 7 6 8 Branches of left pulmonary arteries Inferior vena cava Pulmonary semilunar valve Pulmonary veins Aortic semilunar valve Branches of right pulmonary arteries Superior vena cava Superior and Inferior vena cava Right atrium Tricuspid valve Right ventricle Pulmonary semilunar valves Pulmonary trunk Pulmonary arteries Aorta Aortic semilunar valves Left ventricle Bicuspid valve Left atrium Pulmonary veins Body tissues (systemic circulation) Heart tissue (coronary circulation) Coronary arteries Lung tissue (pulmonary circulation) Coronary sinus Cardiac veins (a) 20-20
  • 21. Histology • Heart Skeleton – Consists of plate of fibrous connective tissue between atria and ventricles – Fibrous rings around valves to support – Serves as electrical insulation between atria and ventricles – Provides site for muscle attachment Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pulmonary semilunar valve Skeleton of the heart, including fibrous rings around valves Aortic semilunar valve Tricuspid valve Bicuspid valve Cardiac muscle of the right ventricle Cardiac muscle of the left ventricle 20-21
  • 22. • Elongated, branching cells containing 1-2 centrally located nuclei • Contains actin and myosin myofilaments • Intercalated disks: specialized cell-cell contacts. – Cell membranes interdigitate – Desmosomes hold cells together – Gap junctions allow action potentials to move from one cell to the next. • Electrically, cardiac muscle of the atria and of the ventricles behaves as single unit Connective tissue Mitochondrion Sarcomere T tubule Myofibrils Striations Intercalated disks LM 400x (b) (a) Branching muscle fibers Nucleus of cardiac muscle cell Sarcoplasmic reticulum Sarcolemma (plasma membrane) b: © Ed Reschke Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Cardiac Muscle 20-22
  • 23. Conducting System Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 2 3 4 Left atrium Left ventricle Apex 1 2 3 4 Action potentials originate in the sinoatrial (SA) node (the pacemaker) and travel across the wall of the atrium (arrows) from the SA node to the atrioventricular (AV) node. Action potentials pass through the AV node and along the atrioventricular (AV) bundle, which extends from the AV node, through the fibrous skeleton, into the interventricular septum. The AV bundle divides into right and left bundle branches, and action potentials descend to the apex of each ventricle along the bundle branches. Action potentials are carried by the Purkinje fibers from the bundle branches to the ventricular walls and papillary muscles. Left and right bundle branches Atrioventricular (AV) bundle Atrioventricular (AV) node Sinoatrial (SA) node Purkinje fibers 20-23
  • 24. 20-24 Conducting System • SA node: sinoatrial node. Medial to opening of superior vena cava. The pacemaker. Specialized cardiac muscle cells. Generate spontaneous action potentials. Action potentials pass to atrial muscle cells and to the AV node • AV node: atrioventricular node. Medial to the right atrioventricular valve. Action potentials conducted more slowly here than in any other part of system. Ensures ventricles receive signal to contract after atria have contracted • AV bundle: passes through hole in cardiac skeleton to reach interventricular septum • Right and left bundle branches: extend beneath endocardium to apices of right and left ventricles • Purkinje fibers: Large diameter cardiac muscle cells with few myofibrils. Many gap junctions. Conduct action potential to ventricular muscle cells
  • 25. Electrical Properties Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 1 2 2 3 –85 1 2 0 (mV) Time (ms) 1 Depolarization phase • • 2 Repolarization phase • • • 1 Depolarization phase • • • 2 Early repolarization and plateau phases • • • 3 Final repolarization phase • • (mV) 1 2 Time (ms) 500 –85 0 Permeability changes during an action potential in cardiac muscle: Voltage-gated Na+ channels close. Some voltage-gated K+ channels open, causing early repolarization. Voltage-gated Ca2+ channels are open, producing the plateau by slowing further repolarization. Voltage-gated Ca2+ channels close. Many voltage-gated K+ channels open. Voltage-gated Ca2+ channels begin to open. Voltage-gated K+ channels close. Voltage-gated Na+ channels open. Permeability changes during an action potential in skeletal muscle: Voltage-gated Na+ channels open. Voltage-gated K+ channels begin to open. Voltage-gated Na+ channels close. Voltage-gated K+ channels continue to open. Voltage-gated K+ channels close at the end of repolarization and return the membrane potential to its resting value. Depolarization phase Depolarization phase Repolarization phase Final repolarization phase Plateau phase Early repolarization phase 20-25
  • 26. 20-26 Differences Between Skeletal and Cardiac Muscle Physiology • Cardiac: action potentials conducted from cell to cell. In skeletal, action potential conducted along length of single fiber • Cardiac: rate of action potential propagation is slow because of gap junctions and small diameter of fibers. In skeletal it is faster due to larger diameter fibers. • Cardiac: calcium-induced calcium release (CICR). Movement of Ca2+ through plasma membrane and T tubules into sarcoplasm stimulates release of Ca2+ from sarcoplasmic reticulum
  • 27. Autorhythmicity of Cardiac Muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Permeability changes in pacemaker cells 1 Pacemaker potential • • • 2 Depolarization phase • • 3 Repolarization phase • • Time (ms) 300 1 0 –60 Threshold Pacemaker potential (mV) 3 2 1 Repolarization phase Depolarization phase A small number of Na+ channels are open. Voltage-gated Ca2+ channels begin to open. Voltage-gated K+ channels that opened in the repolarization phase of the previous action potential are closing. Voltage-gated Ca+ channels are open. Voltage-gated K+ channels are closed. Voltage-gated Ca2+ channels close. Voltage-gated K+ channels open. 20-27
  • 28. 20-28 Refractory Period • Absolute: Cardiac muscle cell completely insensitive to further stimulation • Relative: Cell exhibits reduced sensitivity to additional stimulation • Long refractory period prevents tetanic contractions
  • 29. Electrocardiogram • Record of electrical event in the myocardium that can be correlated with mechanical events • P wave: depolarization of atrial myocardium and signals onset of atrial contraction • QRS complex: ventricular depolarization and signals onset of ventricular contraction. Repolarization of atria simultaneously. • T wave: repolarization of ventricles; precedes ventricular relaxation • PQ interval or PR interval: 0.16 sec; atria contract and begin to relax, ventricles begin to contract • QT interval: 0.36 sec; ventricles contract and begin to relax Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. (mV) PQ interval QT interval Time (seconds) R Q S QRS complex (ventricular depolarization) P (atrial depolarization) T (ventricular repolarization) 20-29
  • 30. 20-30 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Premature ventricular contraction (PVC) (no P waves precede PVCs) Bundle branch block Atrial fibrillation (no clear P waves and rapid QRS complexes) Ventricular fibrillation (no P, QRS, or T waves) Prolonged QRS complexes Complete heart block (P waves and QRS complexes are not coordinated) P P P P P P P P P P PVC PVC Electrocardiogram
  • 31. 20-31 SA node block TABLE 20.1 Major Cardiac Arrhythmias Conditions Symptoms Possible Causes Abnormal Heart Rhythms Tachycardia Paroxysmal atrial tachycardia Ventricular tachycardia Heart rate in excess of 100 beats per minute (bpm) Sudden increase in heart rate to 95–150 bpm for a few seconds or even for several hours; P wave precedes every QRS complex; P wave inverted and superimposed on T wave Frequently causes fibrillation Elevated body temperature; excessive sympathetic stimulation; toxic conditions Excessive sympathetic stimulation; abnormally elevated permeability of slow channels Often associated with damage to AV node or ventricular muscle Abnormal Rhythms Resulting from Ectopic Action Potentials Atrial flutter Atrial fibrillation Ventricular fibrillation Ectopic action potentials in the atria Ectopic action potentials in the atria Ectopic action potentials in the ventricles 300 P waves/min; 125 QRS complexes/min, resulting in two or three P waves (atrial contraction) for every QRS complex (ventricular contraction) No P waves; normal QRS complexes; irregular timing; ventricles constantly stimulated by atria; reduced pumping effectiveness and filling time No QRS complexes; no rhythmic contraction of the myocardium; many patches of asynchronously contracting ventricular muscle Heart rate less than 60 bpm Heart rate varies 5% during respiratory cycle and up to 30% during deep respiration. Cessation of P wave; new low heart rate due to AV node acting as pacemaker; normal QRS complex and T wave PR interval greater than 0.2 second First-degree Second-degree Third-degree (complete heart block) PR interval 0.25–0.45 second; some P waves trigger QRS complexes and others do not; 2:1, 3:1, and 3:2 P wave/QRS complex ratios may occur P wave dissociated from QRS complex; atrial rhythm approximately 100 bpm; ventricular rhythm less than 40 bpm Occasional shortened intervals between contractions; frequently occurs in healthy people P wave superimposed on QRS complex Prolonged QRS complex; exaggerated voltage because only one ventricle may depolarize; inverted T wave; increased probability of fibrillation Elevated stroke volume in athletes; excessive vagal stimulation; carotid sinus syndrome Cause not always known; occasionally caused by ischemia or inflammation or associated with cardiac failure Ischemia; tissue damage due to infarction; causes unknown Inflammation of AV bundle Excessive vagal stimulation Ischemia of AV nodal fibers or compression of AV bundle Excessive smoking; lack of sleep; too much caffeine; alcoholism Ectopic foci in ventricles; lack of sleep; too much caffeine, irritability; occasionally occurs with coronary thrombosis Abbreviations: SA = sinoatrial; AV = atrioventricular. Bradycardia Sinus arrhythmia AV Node Block Premature atrial contractions Premature ventricular contractions (PVCs) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  • 32. 20-32 Cardiac Cycle • Heart is two pumps that work together, right and left half • Repetitive contraction (systole) and relaxation (diastole) of heart chambers • Blood moves through circulatory system from areas of higher to lower pressure. – Contraction of heart produces the pressure
  • 33. 20-33 Period of Isovolumetric Contraction • Begins at the completion of the QRS complex. • Ventricular muscles start to contract, increasing the pressure inside the ventricles. This causes the AV valves to close, which is the beginning of ventricular systole. The semilunar valves were closed in the previous diastole and remain closed during this event. • 120-130 mL of blood are in the ventricles, left from the last diastole when the atria emptied into the ventricles. This is referred to as the end diastolic volume.
  • 34. 20-34 Period of Ejection • Pressure in the ventricle has increased to the point where it is greater than the pressure in the pulmonary trunk/aorta. This pushes the cusps of the semilunar valves against the walls of the vessels, opening the valve. • Blood is ejected from the ventricles. • The pressures in the two ventricles are different: 120 mm Hg in the left ventricle; 25 mm Hg in the right ventricle. Remember: blood in the left ventricle must be pumped to the whole body; blood in the right ventricle is pumped to the lungs. • After the first initial spurt, pressure starts to drop. • At the end of the period of ejection, 50-60 mL remain: end-systolic volume.
  • 35. 20-35 Period of Isovolumetric Relaxation • Completion of T wave results in ventricular repolarization and relaxation. • Ventricular pressure falls very rapidly. • Pulmonary trunk/aorta pressure is higher than ventricular pressure. • Elastic recoil of the arteries causes blood to flow back toward the relaxed ventricles: the semilunar valves close, which is the beginning of ventricular diastole. • Note that the AV valves are also closed.
  • 36. 20-36 Passive Ventricular Filling • While the ventricles were in systole, the atria were filling with blood. • Atrial pressure rises above ventricular pressure and the AV valves open. • Blood flows into the relaxed ventricles, accounting for most of the ventricular filling (70%).
  • 37. 20-37 Active Ventricular Filling • Depolarization of the SA node generates action potentials that spread over the atria (P wave) and the atria contract. This completes ventricular filling. • At rest, contraction of atria not necessary for heart function. • During exercise, atrial contraction necessary for function as heart pumps 300-400%.
  • 38. Cardiac Cycle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 2 3 4 5 1 Semilunar valves closed AV valves closed Semilunar valves closed Semilunar valves opened AV valves closed Atrial systole: active ventricular filling. The atria contract, Increasing atrial pressure and completing ventricular filling while the ventricles are relaxed. Semilunar valves closed AV valves opened Ventricular diastole: passive ventricular filling. As ventricular relaxation continues, the AV valves open, and blood flows from the atria Into the relaxing ventricles, accounting for most of the ventricular filling. Ventricular systole: period of isovolumetric contraction. The atria are relaxed, and blood flows into them from the veins. ventricular contraction causes ventricular pressure to increase and causes the AV valves to close, which is the beginning of ventricular systole. The semilunar valves were closed in the previous diastole and remain closed during this period AV valves opened Ventricular systole: period of ejection. Continued ventricular contraction causes a greater increase interventricular pressure, which pushes blood out of the ventricles, causing the semilunar valves to open. Semilunar valves closed AV valves closed Ventricular diastole: period of isovolumetric relaxation. As the ventricles begin to relax at the beginning of ventricular diastole, blood flowing back from the aorta and pulmonary trunk toward the relaxing ventricles causes the semilunar valves to close. Note that the AV valves are closed also. 20-38
  • 39. 20-39 Events Occurring During the Cardiac Cycle Q S R T T P Q S R P Time periods: Passive ventricular filling Period of isovolumetric relaxation Period of ejection Period of isovolumetric contraction Active ventricular filling (mV) Pressure (mm Hg) Left ventricular volume (mL) "Sound“ frequency (cycles/second) 120 100 80 60 40 20 0 125 90 55 Atrial systole Ventricular systole Ventricular diastole Semilunar valves close. AV valves open. Second heart sound End-systolic volume End-diastolic volume First heart sound Systolic pressure Semilunar valves open. AV valves close. End-systolic volume First heart sound Second heart sound Third heart sound End-diastolic volume AV valves open. Dicrotic notch Semilunar valves close. Semilunar valves open. Diastolic pressure AV valves close. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  • 40. 20-40 Summary of the Events of the Cardiac Cycle Atrial Systole Atrial Diastole Ventricular Diastole Ventricular Systole Active Ventricular Filling Period of Isovolumetric Contraction Time Period Contraction of the atria pumps blood into the ventricles. The ventricles begin to contract, but ventricular volume does not change. Condition of Valves The semilunar valves are closed; the AV valves are opened (figure 20.18, step 1 ). The semilunar valves are closed; the AV valves are closed (figure 20.18, step 2). ECG The P wave is completed and the atria are stimulated to contract. Action potentials are delayed in the AV node for 0.11 second, allowing time for the atria to contract. The QRS complex is completed, and the ventricles are depolarized. As a result, the ventricles begin to contract. The QRS complex begins as action potentials are propagated from the AV node to the ventricles. Atrial Pressure Graph Atrial contraction (systole) causes an increase in atrial pressure, and blood is forced to flow from the atria into the ventricles. Atrial repolarization is masked by the QRS complex. The atria are relaxed (atrial diastole). Atrial pressure decreases in the relaxed atria. When atrial pressure is less than venous pressure, blood flows into the atria. Atrial pressure increases briefly as the contracting ventricles push blood back toward the atria. Ventricular Pressure Graph Atrial contraction (systole) and the movement of blood into the ventricles cause a slight increase in ventricular pressure. Ventricular contraction causes an increase in ventricular pressure, which causes blood to flow toward the atria, closing the AV valves. Ventricular pressure increases rapidly. Aortic Pressure Graph Aortic pressure gradually decreases as blood runs out of the aorta into other systemic blood vessels. Just before the semilunar valves open, pressure in the aorta decreases to its lowest value, called the diastolic pressure (approximately 80 mm Hg). Volume Graph Atrial contraction (systole) completes ventricular filling during the last one-third of diastole. The amount of blood in a ventricle at the end of ventricular diastole is called the end-diastolic volume. During the period of isovolumetric contraction, ventricular volume does not change because the semilunar and AV valves are closed. Sound Graph Blood flowing from the ventricles toward the atria closes the AV valves. Vibrations of the valves and the turbulent flow of blood produce the first heart sound, which marks the beginning of ventricular systole Abbreviation: AV = atrioventricular.
  • 41. 20-41 Atrial Diastole Ventricular Diastole Period of Isovolumetric Relaxation Passive Ventricular Filling The ventricles relax, but ventricular volume does not change. Blood flows into the ventricles because blood pressure is higher in the veins and atria than in the relaxed ventricles. The semilunar valves are closed; the AV valves are closed (figure 20.18, step 4). The semilunar valves are closed; the AV valves are opened (see figure 20.18, step 5). The T wave is completed, and the ventricles are repolarized. The ventricles relax. The P wave is produced when the SA node generates action potentials and a wave of depolarization begins to propagate across the atria. Atrial pressure continues to increase gradually as blood flows from the veins into the relaxed atria After the AV valves open, atrial pressure decreases as blood flows out of the atria into the relaxed ventricles. Elastic recoil of the aorta pushes blood back toward the heart, causing the semilunar valves to close. No significant change occurs in ventricular pressure during this time period. After the semilunar valves close, elastic recoil of the aorta causes a slight increase in aortic pressure, producing the dicrotic notch and dicrotic wave. Aortic pressure gradually decreases as blood runs out of the aorta into other systemic blood vessels. During the period of isovolumetric relaxation, ventricular volume does not change because the semilunar and AV valves are closed. After the AV valves open, blood flows from the atria and veins into the ventricles because of pressure differences. Most ventricular filling occurs during the first one-third of diastole. Sometimes the turbulent flow of blood into the ventricles produces a third heart sound. Ventricular Systole Period of Ejection The ventricles continue to contract, and blood is pumped out of the ventricles. The semilunar valves are opened; the AV valves are closed (figure 20.18, step 3). The T wave results from ventricular repolarization. Atrial pressure increases gradually as blood flows from the veins into the relaxed atria. Ventricular pressure becomes greater than pressure in the aorta as the ventricles continue to contract. The semilunar valves are pushed open as blood flows out of the ventricles. As ventricular contraction forces blood into the aorta, pressure in the aorta increases to its highest value, called the systolic pressure (approximately 120 mm Hg). After the semilunar valves open, blood volume decreases as blood flows out of the ventricles during the period of ejection. Ventricular pressure peaks as the ventricles contract maximally; then pressure decreases as blood flow out of the ventricles decreases The amount of blood left in a ventricle at the end of the period of ejection is called the end-systolic volume. After closure of the semilunar valves, the pressure in the relaxing ventricles rapidly decreases. Little ventricular filling occurs during the middle one-third of diastole. Blood flowing from the ventricles toward the aorta and pulmonary trunk closes the semilunar valves. Vibrations of the valves and the turbulent flow of blood produce the second heart sound, which marks the beginning of ventricular diastole.
  • 42. 20-42 Heart Sounds • First heart sound or “lubb” – Atrioventricular valves and surrounding fluid vibrations as valves close at beginning of ventricular systole • Second heart sound or “dupp” – Results from closure of aortic and pulmonary semilunar valves at beginning of ventricular diastole, lasts longer • Third heart sound (occasional) – Caused by turbulent blood flow into ventricles and detected near end of first one-third of diastole
  • 43. 20-43 Aortic Pressure Curve • Dicrotic notch (incisura): when the aortic semilunar valve closes, pressure within the aorta increases slightly • Blood pressure measurement taken in the arm is a reflection of aortic pressures, not ventricular
  • 44. 20-44 20.8 Mean Arterial Pressure • Average blood pressure in aorta • MAP = CO x PR – CO is amount of blood pumped by heart per minute • CO = SV x HR – SV: Stroke volume (blood pumped during each heart beat) – HR: Heart rate (number of times heart beats per minute) • Cardiac reserve: Difference between CO at rest and maximum CO – PR is total resistance against which blood must be pumped
  • 45. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Factors Affecting Cardiac Output Factors Affecting Peripheral Resistance Increased vasoconstriction Increased heart rate Increased cardiac output Increased stroke volume Increased peripheral resistance Increased mean arterial pressure Decreased blood pressure, decreased blood pH, increased blood carbon dioxide, decreased blood oxygen, exercise, and emotions Increased blood volume, exercise, change from a standing to a lying down position Increased sympathetic stimulation, decreased parasympathetic stimulation, and increased epinephrine and norepinephrine secretion from the adrenal medulla Increased venous return increases end-diastolic volume and preload. Decreased blood pressure, decreased blood pH, increased blood carbon dioxide, and decreased blood oxygen (see chapter 21) Increased force of contraction (Starling law of the heart) ejects increased end-diastolic volume. Increased force of contraction decreases end- systolic volume. Factors Affecting MAP 20-45
  • 46. 20-46 20.9 Regulation of the Heart • Intrinsic regulation: Results from normal functional characteristics, not on neural or hormonal regulation – Preload: Starling’s law of the heart • Preload is the amount of stretch of the ventricular walls. The greater the stretch (preload), the greater the force of contraction. – Afterload: pressure the contracting ventricles must produce to overcome the pressure in the aorta and move blood into the aorta. Heart not as sensitive to this as it is to changes in preload.
  • 47. • Extrinsic regulation: Involves neural and hormonal control – Parasympathetic stimulation • Supplied by vagus nerve, decreases heart rate, acetylcholine is secreted and hyperpolarizes the heart – Sympathetic stimulation • Supplied by cardiac nerves. Innervate the SA and AV nodes, coronary vessels and the atrial and ventricular myocardium. Increases heart rate and force of contraction. Epinephrine and norepinephrine released. • Increased heart beat causes increased cardiac output. Increased force of contraction causes a lower end-systolic volume; heart empties to a greater extent. Limitations: heart has to have time to fill. – Hormonal Control. Epinephrine and norepinephrine from the adrenal medulla. Occurs in response to increased physical activity, emotional excitement, stress 20-47 Regulation of the Heart
  • 48. 20-48 Heart and Homeostasis • Effect of blood pressure – Baroreceptors monitor blood pressure; in walls of internal carotids and aorta. This sensory information goes to centers in the medulla oblongata • Effect of pH, carbon dioxide, oxygen – Receptors that measure pH and carbon dioxide levels found in hypothalamus – Chemoreceptors monitoring oxygen levels found in aorta and internal carotids. Prolonged lowered oxygen levels causes increased heart rate, which increases blood pressure and can thus deliver more oxygen to the tissues. • Effect of extracellular ion concentration – Increase or decrease in extracellular K+ decreases heart rate • Effect of body temperature – Heart rate increases when body temperature increases, heart rate decreases when body temperature decreases
  • 49. Baroreceptor and Chemoreceptor Reflexes Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Heart Circulation Epinephrine and norepinephrine Adrenal medulla 1 2 3 4 1 2 3 4 Sympathetic nerve fibers to adrenal gland Sensory neurons (green) carry action potentials from baroreceptors and carotid body chemoreceptors to the cardioregulatory center. Chemoreceptors in the medulla oblongata also influence the cardioregulatory center. The cardioregulatory center controls the frequency of action potentials in the parasympathetic neurons (red) extending to the heart through the vagus nerves. The parasympathetic neurons decrease the heart rate. The cardioregulatory center controls the frequency of action potentials in the sympathetic neurons (blue). The sympathetic neurons extend through the cardiac nerves and increase the heart rate and the stroke volume. The cardioregulatory center influences the frequency of action potentials in the sympathetic neurons (blue) extending to the adrenal medulla. The sympathetic neurons increase the secretion of epinephrine and some norepinephrine into the systemic circulation. Epinephrine and Norepinephrine increase the heart Rate and stroke volume. SA node Sensory nerve fibers Cardioregulatory center and chemoreceptors in medulla oblongata Sensory nerve fibers Baroreceptors in wall of internal carotid artery Carotid body chemoreceptors Baroreceptors in aorta Parasympathetic nerve fibers Vagus nerves Sympathetic nerve fibers 20-49 Cardiac nerves
  • 50. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Heart rate and stroke volume increase. Heart rate and stroke volume decrease. Start here Actions Actions Response Response Baroreceptors in the carotid arteries and aorta detect an increase in blood pressure. The cardioregulatory center increases parasympathetic and decreases sympathetic stimulation of the heart. Blood pressure increases: Homeostasis Disturbed Blood pressure (normal range) Blood pressure (normal range) Blood pressure decreases: Homeostasis Disturbed Baroreceptors in the carotid arteries and aorta detect a decrease in blood pressure. The cardioregulatory center decreases parasympathetic and increases sympathetic stimulation of the heart; adrenal medulla secretion of epinephrine and norepinephrine increases. Blood pressure increases: Homeostasis Restored Blood pressure decreases: Homeostasis Restored 6 5 1 2 3 4 The effectors (SA node and cardiac muscle) respond: The effectors (SA node and cardiac muscle) respond: 20-50 Baroreceptor Reflex
  • 51. Blood pH (normal range) Reactions Actions Actions Reactions Heart rate and stroke volume decrease, reducing blood flow to the lungs. Blood CO2 levels increase. Chemoreceptors in the medulla oblongata detect an increase in blood pH (often caused by a decrease in blood CO2). Cardioregulatory center increases parasympathetic and decreases sympathetic stimulation of the heart. Blood pH (normal range) Chemoreceptors in the medulla oblongata detect a decrease in blood pH (often caused by an increase in blood CO2). Cardioregulatory center decreases parasympathetic and increases sympathetic stimulation of the heart Heart rate and stroke volume increase, increasing blood flow to the lungs. Blood CO2 levels decrease. 6 5 1 2 3 4 5 The effectors (SA node and cardiac muscle) respond: The effectors (SA node and cardiac muscle) respond: Blood pH decreases: Homeostasis Restored Blood pH increases: Homeostasis Restored Blood pH increases: Homeostasis Disturbed Blood pH decreases: Homeostasis Disturbed Start here Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 20-51 Chemoreceptor Reflex
  • 52. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Heart Diseases and Disorders Inflammation of the endocardium; affects the valves more severely than other areas of the endocardium; may lead to scarring, causing stenosed or incompetent valves Inflammation of the pericardium; see Clinical Impact, “Pericarditis and Cardiac Tamponade” Disease of the myocardium of unknown cause or occurring secondarily to other disease; results in weakened cardiac muscle, causing all chambers of the heart to enlarge; may eventually lead to congestive heart failure Results from a streptococcal infection in young people; toxin produced by the bacteria can cause rheumatic fever several weeks after the infection that can result in rheumatic endocarditis Reduces the amount of blood the coronary arteries can deliver to the myocardium Formation of blood clot in a coronary artery Damaged cardiac muscle tissue resulting from lack of blood flow to the myocardium; often referred to as a heart attack; see Clinical Impact, “Angina, Infarctions, and the Treament of Blocked coronary Arteries” Hole in the septum between the left and right sides of the heart, allowing blood to flow from one side of the heart to the other and greatly reducing the heart’s pumping effectiveness Ductus arteriosus fails to close after birth, allowing blood to flow from the aorta to the pulmonary trunk under a higher pressure, which damages the lungs; also, the left ventricle must work harder to maintain adequate systemic pressure Narrowed opening through one or more of the heart valves; aortic or pulmonary semilunar stenosis increases the heart’s workload; bicuspid valve stenosis causes blood to back up in the left atria and lungs, resulting in edema of the lungs; tricuspid valve stenosis results in similar blood flow problems and edema in the peripheral tissues Heart valves do not close correctly, and blood flows through in the reverse direction; see Clinical Impact, “Abnormal Heart Sounds” Cyanosis (sı-a-no′sis; cyan, blue + osis, condition of) Symptom of inadequate heart function in babies with congenital heart disease; the infant’s skin appears blue because of low oxygen levels in the blood in peripheral blood vessels Progressive weakening of the heart muscle, reducing the heart’s pumping action; hypertension leading to heart failure due to increased afterload; advanced age, malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism, and hereditary factors can lead to heart failure Condition Description Inflammation of Heart Tissue Endocarditis Pericarditis Cardiomyopathy Rheumatic heart disease Reduced Blood Flow to Cardiac Muscle Coronary heart disease Coronary thrombosis Myocardial infarction Congenital Heart Diseases (occur at birth) Septal defect Patent ductus arteriosus Stenosis of the heart valve Incompetent heart valve Heart Failure - - - 20-52