Chapter17 Class25

1
Human Anatomy & Physiology

Second Edition
Chapter 17
The Cardiovascular
System I:The Heart
Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
PowerPoint® Lectures created by Suzanne Pundt, University of Texas at Tyler
MODULE 17.1 OVERVIEW OF

THE HEART
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The Cardiovascular System

• Cardiovascular system:
– Consists of heart, blood vessels, and blood
Location and Basic Structure of the Heart

• Chambers and external anatomical features (Figure 17.1b and 17.2):
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Functions of the Heart

• Heart helps maintain homeostasis of pressure that blood exerts on blood vessels
(blood pressure)
– rate and force of heart’s contraction are major factors that influence blood
pressure and blood flow to organs
– produces atrial natriuretic peptide (ANP)
 ANP lowers blood pressure by decreasing sodium ion retention in kidneys
– reduces osmotic water reabsorption and volume and pressure of blood in
blood vessels
MODULE 17.2 HEART ANATOMY

AND BLOOD FLOW PATHWAY
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The Pericardium, Heart Wall, and Heart

Skeleton
– Pericardial cavity—between parietal and visceral pericardia
 Visceral pericardium rests on top of thin layer of areolar connective tissue;
contains large fat deposits
– Epicardium
The Pericardium, Heart Wall, and Heart

Skeleton
• Myocardium components: cardiac muscle tissue and fibrous skeleton
– Cardiac muscle tissue consists of cardiac muscle cells (myocytes) and their
surrounding extracellular matrix
– Cardiac muscle cells are attached to and woven through fibrous skeleton
 Providing structural support
 Acting as insulator for heart’s
electrical activity
• Endocardium: continuous with lining

of blood vessels
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The Heart’s Great Vessels, Chambers, and Valves

Great vessels—bring blood to and away from heart; largest in body (Figure 17.5):
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The Heart’s Chambers,and Valves
Pectinate
muscles
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Figure 17.8 The Big Picture of Blood Flow through the Heart.
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Figure 17.8 The Big Picture of Blood Flow through the Heart.
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Module 17.3 Cardiac Muscle

Tissue Anatomy and
Electrophysiology
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Histology of Cardiac Muscle Tissue and

Cells
• Heart does not require conscious intervention to elicit cardiac muscle to contract;
cardiac muscle exhibits autorhythmicity: pacemaker cells vs contractile cells
– Intercalated discs contain

 Desmosomes
 Gap junctions
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Histology of Cardiac Muscle Tissue and

Cells
• Like skeletal muscle fibers and other excitable cells, cardiac muscle cells contain
selective gated ion channels in sarcolemma
• Types of gated ion channels:

– Voltage-gated sodium ion channels—open in response to voltage changes
across membrane; in all cardiac muscle cells except certain pacemaker cells
– Calcium ion channels—demonstrate voltage-gated opening but time-gated
closing; close after certain period regardless of voltage
– All types of cardiac muscle cells have one or more types of potassium ion
channels; some ligand-gated; others voltage-gated
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Revisiting Electrophysiology
Terminology:
• Voltage—difference in electrical potential between two points
• Membrane potential—voltage (charge) difference that exists across membranes of all

cells, including excitable cells
• Resting membrane potential—membrane potential of excitable cell at rest (not being

stimulated); averages between −60 and −90 mV: difference in concentration of ions
across plasma membrane
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Revisiting Electrophysiology
Terminology (continued):
• Current—flow of ions or electrons with chemical or electrical gradient
• Depolarization—change in resting membrane potential to value less negative than

when at rest; occurs when positive charges (generally, sodium and/or calcium ions) rush
into cell
• Repolarization—return of cell to its negative resting membrane potential; occurs when

positive charges (potassium ions) leave cell
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Electrophysiology of Cardiac Muscle Tissue

• Pacemaker cells undergo rhythmic, spontaneous depolarizations that lead to action
potentials; spread quickly through heart by cardiac conduction system (group of
interconnected pacemaker cells) (Figures 17.11–7.12)
• Action potentials are transmitted from pacemaker cells to contractile cells through
intercalated discs that unite them
– produce coordinated heartbeat: functional syncytium (term for large,
multinucleated cell)
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• Pacemaker potential—much different from that of contractile cell (Figure 17.11):
– Depolarization in pacemaker cell occurs much more slowly
– Pacemaker cell action potentials lack plateau phase and membrane potential
oscillates—never remains at resting level; instead occurs in cycle, with last event
triggering first
– Occurs because of nonspecific cation channels; unique to pacemaker cells
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• Pacemaker potential (continued)
– Slow initial depolarization phase—pacemaker potential starts with plasma
membrane in hyperpolarized state—at minimum membrane potential
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– Full depolarization phase—when membrane reaches threshold
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– Repolarization phase—calcium ion channels are time-gated for closing; after
certain time (about 100–150 msec), as voltage-gated potassium ion channels
begin to open
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– Minimum potential phase—potassium ion channels remain open until membrane

reaches its minimum potential (membrane is hyperpolarized)
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• Pacing Heart: Sinus rhythm--SA node is normal pacemaker of entire heart
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• Sequence of events of contractile cell action potential proceeds as follows (Figure
17.13):
– Rapid depolarization phase—pacemaker cell action potentials cause voltage
changes in adjacent cells
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• Sequence of events of contractile cell action potential proceeds as follows (Figure
17.13):
– Initial repolarization phase—small, initial repolarization immediately after
depolarization spike
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• Sequence of events (continued):
– Plateau phase—depolarization is sustained at about 0 mV in plateau phase
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• Sequence of events (continued):
– Repolarization phase—final phase of action potential; both sodium and calcium
ion channels return to resting states
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• Sequence of events of contractile cell action potential resembles that of skeletal muscle
fiber action potential with one important exception: plateau phase
– Plateau phase prevents tetany in heart by lengthening
refractory period
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• Electrocardiogram (ECG)—important clinical tool for examining health of heart;
graphic depiction of electrical activity occurring in all cardiac muscle cells over period of
time (Figure 17.14)
– Recorded by placing electrodes on surface of patient’s skin: six on chest and two
on each extremity
– Electrical changes are shown on ECG as deflections (waves)
– One of most obvious changes in heart revealed by ECG is disturbance in electrical
rhythm (dysrhythmia or arrhythmia)
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Figure 17.14 A normal electrocardiogram (ECG) tracing.

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Figure 17.14 A normal electrocardiogram (ECG) tracing.

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Dysrhythmias
Cardiac dysrhythmias have three basic patterns:
• Disturbances in heart rate:

– Bradycardia—heart rate under 60 beats per minute
– Tachycardia—heart rate over 100 beats per minute
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Dysrhythmias
• Disturbances in conduction pathways—normal conduction pathway may be disrupted
by accessory pathways between atria and ventricles or by blockage along conduction
system (heart block)
– at AV node:
 P-R interval is longer than normal
 Extra P waves present
– along right or left bundle branch:
 Wider QRS complex
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Dysrhythmias
• In fibrillation
– parts of heart to depolarize and contract while others are repolarizing and not
contracting
– Atrial fibrillation
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Dysrhythmias
– Ventricular fibrillation—immediately life-threatening and manifests on ECG with
chaotic activity
 Treated with defibrillation (electric shock to heart); depolarizes all ventricular
muscle cells simultaneously and throws cells into their refractory periods
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Module 17.4 Mechanical

Physiology of the Heart: The
Cardiac Cycle
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Introduction to Mechanical Physiology

• Mechanical physiology—actual processes by which blood fills cardiac chambers and
is pumped out of them
– Cardiac muscle cells contract as unit to produce one coordinated contraction
(heartbeat); muscle cells are arranged in spiral pattern, producing “wringing”
action in heart when it contracts
– Cardiac cycle—sequence of events within heart from one heartbeat to next
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Pressure Changes, Blood Flow, and Valve

Function
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Function
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Function
• Each cardiac cycle consists of one period of relaxation (diastole) and one period of
contraction (systole) for each chamber of heart (Figures 17.17, 17.18)
– Atrial and ventricular diastoles and systoles occur at different times as result of AV
node delay; both sides of heart are working to pump blood into their respective
circuits simultaneously
– Cycle is divided into four main phases; defined by actions of ventricles and
positions of valves: filling, contraction, ejection, and relaxation
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Function
Figure 17.17 Events of the cardiac cycle.

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Function

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Function

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Function
Approximately 70 ml of blood
pumped from each ventricle;
about 50 ml of blood remains in
each ventricle (end-systolic
volume (ESV))

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Figure 17.18 Comparison of pressure changes in left and right ventricles during the
cardiac cycle.
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Figure 17.19 Cardiac cycle diagram showing an overview of electrical and mechanical
events in the heart during the cardiac cycle.
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Module 17.5 Cardiac Output

and Regulation
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Introduction to Cardiac Output and

Regulation
• Heart undergoes average of 60–80 cardiac cycles (beats) per minute; value known as
heart rate (HR)
– HR is one determinant of cardiac output (CO); amount of blood pumped into
pulmonary and systemic circuits in 1 minute
– CO is also determined by amount of blood pumped in one heartbeat (stroke
volume (SV))
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Determination of Cardiac Output

• Stroke volume (SV) and heart rate (HR) must be known to calculate cardiac output for
ventricle:
– SV can be calculated by subtracting amount of blood in ventricle at end of
contraction (end-systolic volume, or ESV) from amount of blood in ventricle after it
has filled during diastole (end-diastolic volume, or EDV)
– In average heart, resting stroke volume is equal to about 70 ml:
120 ml (EDV) −50 ml (ESV) = 70 ml (SV)
• To find cardiac output, multiply heart rate by stroke volume:
72 beats/min (HR) × 70 ml/beat (SV) = 5040 ml/min ~5 liters/min (CO)
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Factors that Influence Stroke Volume

Stroke volume averages about 70 ml per beat; may range from 50 to 120 ml; exact stroke
volume may be difficult to measure directly; often measurement called ejection fraction is
used in its place
• Ejection fraction—percentage of blood (out of total amount) that is ejected with each
ventricular systole; equal to stroke volume divided by EDV; normal ejection fraction is
about 50–65%, and this value should be equal for each ventricle
• Three factors that influence stroke volume: preload, heart contractility, and afterload
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– Preload refers to length or degree of stretch of sarcomeres in ventricular cells
before they contract; largely determined by EDV
 Two factors influence EDV:
– Length of time ventricle spends in diastole
– venous return
– Afterload refers to force that right and left ventricles must overcome in order to
eject blood into their respective arteries
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– Relationship between preload and stroke volume is explained by mechanism
known as Frank-Starling law
 increased ventricular muscle cells stretch, leads to more forceful contraction
 optimal overlap of actin and myosin filaments in muscle cells; enables
stronger contraction and higher stroke volume
 Ensures that volume of blood discharged from heart is equal to volume that
enters it
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– Contractility—heart’s intrinsic pumping ability, or ability to generate tension;
 Increasing contractility will increase SV and therefore decrease ESV
 Decreasing contractility will do opposite: decreasing SV and increasing ESV
(assuming that preload and afterload remain constant)
 Agents that affect contractility are known as inotropic agents
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– Afterload refers to force that right and left ventricles must overcome in order to
eject blood into their respective arteries
 determined by blood pressure in arteries of both pulmonary and systemic
circuits
 As afterload increases, ventricular pressure must be greater to exceed
pressure in arterial pulmonary and systemic vessels and open SL valves
 Increase in afterload therefore generally causes decrease in SV and rise in
ESV of ventricles; conversely, decrease in afterload generally corresponds to
higher SV and lower ESV
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Factors that determine stroke volume—preload, contractility, and afterload—illustrated

using only the left ventricle for simplicity.
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How Changes in Preload, Contractility, and Afterload Affect

Stroke Volume
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How Changes in Preload, Contractility, and Afterload

Affect Stroke Volume
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Factors that Influence Heart Rate

Other determinant of cardiac output is heart rate:
• Chronotropic agents
 positive chronotropic agent
– include sympathetic nervous system, certain hormones, and elevated
body temperature
 Negative chronotropic agent
– include parasympathetic nervous system and decreased body
temperature
• Inotropic agents
– positive inotropes
 strengthen the force of the heartbeat
– negative inotropes
 weaken the force of the heartbeat
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Regulated primarily by
nervous and endocrine
systems, which
influence both heart
rate and stroke volume
(Figure 17.21)
Figure 17.21 Innervation and nervous regulation of the heart.

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ANP
Figure 17.22 Regulation of cardiac output.

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ADH/Aldosterone
EPI/NE TH GLUCAGON
Figure 17.22 Regulation of cardiac output.

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1

Human Anatomy & Physiology

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

PowerPoint® Lectures created by Suzanne Pundt, University of Texas at Tyler

MODULE 17.1 OVERVIEW OF

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

The Cardiovascular System

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Location and Basic Structure of the Heart

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Functions of the Heart

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

MODULE 17.2 HEART ANATOMY

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

The Pericardium, Heart Wall, and Heart

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

The Pericardium, Heart Wall, and Heart

• Endocardium: continuous with lining

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

The Heart’s Great Vessels, Chambers, and Valves

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The Heart’s Chambers,and Valves

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Module 17.3 Cardiac Muscle

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Histology of Cardiac Muscle Tissue and

– Intercalated discs contain

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Histology of Cardiac Muscle Tissue and

• Types of gated ion channels:

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

• Voltage—difference in electrical potential between two points

• Membrane potential—voltage (charge) difference that exists across membranes of all

• Resting membrane potential—membrane potential of excitable cell at rest (not being

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

• Current—flow of ions or electrons with chemical or electrical gradient

• Depolarization—change in resting membrane potential to value less negative than

• Repolarization—return of cell to its negative resting membrane potential; occurs when

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

– Full depolarization phase—when membrane reaches threshold

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

– Minimum potential phase—potassium ion channels remain open until membrane

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved

Electrophysiology of Cardiac Muscle Tissue

Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved