Biology 221
Anatomy & Physiology II
TOPIC 2
Circulatory System – The Heart
Chapter 18
pp. 675-710
E. Lathrop-Davis / E. Gorski / S. Kabrhel
Interactive Physiology: Cardiovascular System
1
Function & Size
N
• Function: provide pressure for movement of
blood through blood vessels by alternately
contracting (systole) and relaxing (diastole)
• Size
– 250 – 350 grams
– extends from 2nd rib to 5th intercostal
space
2
Location
• within the pericardial cavity in mediastinum of
the thoracic cavity
• directly posterior to the sternum, ~2/3 lies
left of midline
Fig. 18.1, p. 677
3
Pericardium & Pericardial Cavity
N
• Fibrous pericardium
– outer layer of pericardial sac
– stabilizes heart in mediastinum
• Serous pericardium
– parietal layer
– visceral layer = epicardium
http://www.cyber-nurse.com/veetac/horrorctam.htm
4
Pericardium & Pericardial Cavity
N
• Pericardial cavity
– pericardial fluid
– Pericarditis – inflammation of the
pericardium
° normally hinders production of serous fluid
° cardiac tamponade – fluid in pericardial
cavity increases
http://www.cyber-nurse.com/veetac/horrorctam.htm
http://www.cyber-nurse.com/veetac/horrorctam.htm
5
Chambers of the Heart
N
• 2 Atria – receive blood from veins
– auricles – fill with blood from venae cavae
– coronary sulcus = atrioventricular groove
– interatrial septum
– fossa ovalis – remnant of foramen ovale
– pectinate muscles
• Base
Fig. 18.4b p. 679
6
Chambers of the Heart
N
• 2 Ventricles pump blood into arteries
– anterior interventricular groove
– posterior interventricular groove
– interventricular septum
– papillary muscles attach to chordae
tendineae
– trabeculae carneae
• Apex
Fig. 18.4b p. 679
7
Structure of the Heart Wall
Composed of 3 layers:
• Epicardium = visceral pericardium
• Myocardium
• Endocardium
Fig. 18.2, p. 677
http://www.cyber-nurse.com/veetac/horrorctam.htm
8
Structure of the Heart Wall
N
• Epicardium = visceral pericardium
– serous membrane
° mesothelium
° areolar connective tissue
– adipose accumulates in grooves
• Myocardium
– cardiac muscle, blood vessels and nerves
– fibrous skeleton
• Endocardium – endothelium
– What is the importance of lining the
chambers with epithelial tissue?
Fig. 18.2, p. 677
9
Great Vessels of Heart
N
Arteries – carry blood away from heart
(ventricles) to lungs or rest of body.
• pulmonary artery (trunk) – pulmonary circ.
• aorta – systemic circulation
• Bearing in mind that the lungs are the sites of
gas exchange between blood and air, which of
these would you expect to be high in oxygen?
Low in oxygen? Explain.
Fig. 18.4, p. 679-680
10
Great Vessels of Heart
N
Veins – return blood to heart (atria)
• pulmonary veins – pulmonary circulation
• superior & inferior venae cavae – systemic
circulation
• coronary sinus and other coronary veins coronary circulation
• Bearing in mind that the lungs are the sites of
gas exchange between blood and air, which of
these would you expect to be high in oxygen?
Low in oxygen? Explain.
Fig. 18.4, p. 679-680
11
Atrioventricular (AV) Valves
N
• allow blood to flow from atria to ventricles
when latter are relaxing
• prevent flow from ventricles to atria when
ventricles are contracting*
– mitral (bicuspid)
– tricuspid
Fig. 18.8, p. 685
Return to cardiac cycle
12
Semilunar (SL) Valves
N
• allow blood to flow from ventricles to arteries
when ventricles are contracting
• prevent back flow from arteries to ventricles
when ventricles relax*
Fig. 18.8, p. 685
Fig. 18.4, p. 681
Return to cardiac cycle
13
Heart Sounds
N
• Normal sounds - closure of valves
– “lub” – closure of AV valves
– “dup” –closure of semilunar valves
Fig. 18.19, p. 695
14
Valve Disorders
N
• Rheumatic heart disease (RHD) – strep
(Streptococcus pyogenes) infection leads to
inflammation of heart and valves; heart valves
become stiffened into partially closed
position
• Murmur – abnormal heart sound associated
with bad valves
– incompetence – damaged valve allows
backflow of blood
– stenosis – narrowing of passageway through
valve
15
Fibrous Skeleton
• Internal connective tissue framework
• Functions include:
– stabilizes positions of muscle cells and
valves
– supports muscle cells, blood vessels, nerves
– helps spread force of contraction through
heart
– prevents over-distention
– helps maintain shape of heart
– physically and electrically separates atrial
and ventricular musculatures
16
Cardiac Anatomy Review, pp. 8-9
N
Microanatomy of the Myocardium
• Cardiac muscle
– short, branching, uninucleate cells
– striated – sliding filament movement
• Connected by intercalated discs
http://www.usc.edu/hsc
– gap junctions
/dental/ghisto/musc/c_
° functional syncytium
20.html
– desmosomes
• Numerous large mitochondria
– aerobic respiration
Fig. 18.11, p. 688
– high O2 demand
– myoglobin
17
Cardiac Anatomy Review, pp. 6-7
Blood Flow Through the Heart
• Pulmonary circulation goes to and from
capillary beds associated with alveoli of
lungs
– brings deoxygenated blood to lungs;
returns oxygenated blood to heart
• Systemic circulation goes to and from
capillary beds of the tissues of the body
– brings oxygenated blood to tissues;
returns deoxygenated blood to heart
Fig. 18.5 p. 682
18
Coronary Blood Supply
N
• Anastomoses – provide collateral circulation
• Blood enters coronary vessels during diastole,
empties during systole
• Autoregulation – coronary arteries dilate
when demand for nutrients and oxygen
increases
• Capillaries present in endomysium (endo =
within; mysium = muscle), which is:
– areolar CT within intracellular space
between muscle cells
– connected to fibrous skeleton
19
Coronary Blood Supply: Arteries
• Branches of aorta
• Supply oxygen-rich blood to myocardium
• Right coronary artery
– branches serve right atrium and right
ventricle, SA and AV nodes, and posterior
walls of both ventricles
Fig. 18.7, p. 683
20
Coronary Blood Supply: Arteries
• Left coronary artery
– branches serve interventricular septum and
anterior walls of both ventricles, left
atrium and posterior wall of left ventricle
– branches into anterior interventricular
artery and circumflex artery
Fig. 18.7, p. 683
21
Coronary Circulation: Veins
N
• Coronary Sinus
– great cardiac vein - drains area supplied by
anterior interventricular artery
– other left and posterior coronary veins drain left side and posterior of heart
• Anterior cardiac veins – drain anterior
surface of right ventricle
Fig. 18.7, p. 683
Fig. 18.4, p. 679
22
Coronary Circulation: Disorders
• Occlusion – blockage; in a vessel, tissue
downstream will be deprived of oxygen and
nutrients
• Ischemia – transient state of oxygen deficit
leading to reversible changes in cell structure
and function
• Infarction – localized area of cell death
(necrosis) resulting from anoxia; causes
include
– disruption of arterial circulation serving
the area
– disruption of venous drainage
23
Comparison with Skeletal Muscle
N
• All-or-none law - either an event occurs
completely (e.g., contraction) or it does not
(no partial contraction)
– in skeletal muscle, applies to motor units
– in cardiac muscle, applies to entire organ
• Length of absolute refractory period
– skeletal muscle – 1-2 ms  allows tetanus
– cardiac muscle ~ 250 ms  prevents
tetanus
° Why is it important to prevent tetanus in
the heart?
Fig. 18.12, p. 689
24
Comparison with Skeletal Muscle
Means of stimulation
• skeletal muscle – only contracts in response to
stimulation by somatic motor neuron
– What happens when nerve is cut?
• cardiac muscle
– certain cells are self-excitatory =
autorhythmicity
– autonomic innervation changes rate of
depolarization
° sympathetic innervation increases rate
- What happens when nerve is cut?
° parasympathetic innervation decreases rate
- What happens when nerve is cut?
– also responds to epinephrine
N
25
Cardiac Action Potential, p. 3
Types of Cardiac Muscle Cells
Autorhythmic cardiac muscle cells
• capable of spontaneously depolarizing to
produce pacemaker potentials
• conduct action potentials through myocardium
• not contractile
• form intrinsic conduction system
26
Cardiac Action Potential, p. 4
Types of Cardiac Muscle Cells
Contractile cardiac muscle cells
• depolarization spreads from autorhythmic
cells via gap junctions
• action potential leads to contraction as
myofilaments slide past each other
• responsible for alternating contraction
(systole) and relaxation (diastole) that
creates pressure on blood
27
Cardiac Action Potential, p. 5
Conduction Through the Heart
• Action potential spreads rapidly through
conduction system and contractile cells via
gap junctions
• Atria and ventricles functionally separated by
fibrous skeleton
• Time to total depolarization ~ 220 ms
(~0.22s) in a healthy heart
28
Cardiac Action Potential, p. 6-10
AP: Autorhythmic Cells - Overview
N
• Ion channels allow ion movements
– Na+ ( Na+/K+) leakage channels
– Voltage-gated K+ channels
– Voltage-gated Ca2+ channels
• Ion movements affect membrane potential
• Resting membrane potential is negative
• Given the ionic conditions inside and outside
of the cell (see Chapter 3), which way will
each of the ions move?
Fig. 18.13, p. 690
29
Cardiac Action Potential, p. 6-10
AP: Autorhythmic Cells - Steps
1. Pacemaker potential
2. Action potential depolarization
3. Action potential repolarization
Fig. 18.13, p. 690
30
Cardiac Action Potential, p. 6-10
Autorhythmic AP:
Pacemaker Potential
N
• gradual change in membrane potential from
resting (- 60 to -70 mV) toward threshold
• Na+ channels open  net gain of + charge 
slow depolarization = pacemaker potential
• closure of voltage-gated K+ channels
contributes to slow depolarization
Fig. 18.13, p. 690
31
Cardiac Action Potential, p. 6-10
Autorhythmic AP: Depolarization
N
• at threshold (~ -40 mV), voltage-gated Ca2+
channels open  Ca2+ enters from
extracellular fluid  rapid depolarization of
action potential
• Differentiate between the roles of Na+ and
Ca2+ in the depolarization of autorhythmic
cells.
Fig. 18.13, p. 690
32
Cardiac Action Potential, p. 6-10
Autorhythmic AP: Repolarization
N
• depolarization causes voltage-gated K+
channels to open  K+ leaves  cell
repolarizes
– decrease in voltage causes Ca2+ channels to
close, aids repolarization
• after a while, K+ channels start to close, Na+
channels open; cycle starts over
• Na+/K+ pump
Fig. 18.13, p. 690
33
Cardiac Action Potential, p. 11
AP: Contractile Cells
• Connected to autorhythmic cells by gap
junctions
• Ion channels allow ion movements
– Voltage-gated Na+ channels
– Voltage-gated K+ channels
– Voltage-gated Ca2+ channels
• Resting membrane potential is negative
Fig. 18.12, p. 689
34
Cardiac Action Potential, p. 12-17
AP: Contractile Cells - Steps
• Depolarization
• Plateau
• Repolarization
Fig. 18.12, p. 689
35
Cardiac Action Potential, p. 12-17
Contractile AP: Depolarization
N
• Sodium (and calcium) ions pass from
autorhythmic cells via gap junctions
• Contractile cell depolarizes from resting to
threshold
• At threshold, fast voltage-gated sodium
channels open  Na+ rushes in 
depolarization to ~ +30 mV
Fig. 18.12, p. 689
36
Cardiac Action Potential, p. 12-17
Contractile AP: Plateau
N
• After a short time, Na+ channels close and
voltage-gated K+ channels open  membrane
potential begins to fall
• Voltage-gated Ca2+ channels also open and
allow Ca2+ influx
• Ca2+ influx balances K+ efflux (channels close
temporarily) resulting in plateau
Fig. 18.12, p. 689
37
Cardiac Action Potential, p. 12-17
Contractile AP: Plateau
N
• combination of Ca2+ influx and inactivation of
K+ channels results in plateau, coupled with
slow return of Na+ channels to ready position
results in long absolute refractory period
– Why would this be important to heart
function?
• Ca2+ influx causes contraction
Fig. 18.12, p. 689
38
Cardiac Action Potential, p. 12-17
Contractile AP: Repolarization
• rapid repolarization occurs as Ca2+ channels
close and K+ channels reopen
• K+ efflux returns membrane to resting
potential
• Ca2+ actively transported out of cell and into
sarcoplasmic reticulum
• Na+/K+ pump restores ion levels to resting
Fig. 18.12, p. 689
39
Intrinsic Conduction System, pp. 3-4
Electrical Conduction - Overview
sinoatrial (SA) node  internodal pathway to
atrioventricular (AV) node & atria 
atrioventricular (AV) bundle (bundle of His)
 right and left bundle branches  Purkinje
fibers  ventricles (starting at apex)
Fig. 18.14, p. 691
40
Intrinsic Conduction System, pp. 3-4
Conduction Pathway: SA Node
• Sinoatrial (SA) Node
• located in right atrial wall, inferior to opening
of superior vena cava
• acts as normal pacemaker  sinus rhythm
• intrinsic rate ~ 100 APs/min
– ~ 75 APs / min at rest under normal
hormonal and neural control
– resting HR varies; more fit, slower heart
rate
• AP spreads to atria and to AV node via
internodal pathway
Fig. 18.14, p. 691
41
Intrinsic Conduction System, pp. 3-4
Conduction Pathway: AV Node
N
• Atrioventricular (AV) Node
• located in inferior interatrial septum above
tricuspid valve
• connects atria and ventricles electrically
• short delay (~ 0.1 s)
– Why is this delay important?
42
Intrinsic Conduction System, pp. 3-4
Conduction Pathway: AV Bundle
• Atrioventricular (AV) Bundle (bundle of His)
• Right and Left Bundle Branches
– run through interventricular septum toward
apex of heart
Fig. 18.14, p. 691
Fig. 18.17, p. 694
43
Intrinsic Conduction System, pp. 3-4
Conduction Pathway:
Purkinje Fibers
N
• run through interventricular septum to apex
of heart where they turn and run superiorly
through outer wall of ventricles
• supply papillary muscles before rest of
ventricular wall
– Why would this be important?
Fig. 18.14, p. 691
Fig. 18.17, p. 694
44
Electrocardiograph (ECG)
N
• Measures electrical changes in heart
• Electrocardiograph – instrument used to
measure changes
• Leads
– combinations of electrodes used to detect
changes
– 12 standard leads
° I – right arm (-) -> left arm (+)
° II – right arm (-) -> left leg (+)
° III – left arm (-) -> left leg (+)
° Chest leads
http://www.cardioliving.com/consumer/Heart/Electrocardiogram.shtm
45
Electrocardiogram (ECG)
N
• Electrocardiogram – recording of the changes
in membrane potential
– Series of deflections from baseline –
correspond to spread of action potential
through myocardium
• Analysis – ECG shows:
– overall heart rate
– wave shape, height and duration
– deviations from normal
46
Intrinsic Conduction System, pp. 5-6
ECG Waves - Overview
• P Wave
– PR Interval
• QRS complex
– QT segment
• T wave
Fig. 18.16, p. 694
47
Intrinsic Conduction System, pp. 5-6
ECG : P wave, PR Interval
N
• P wave - depolarization of SA node followed
by atrial depolarization
• P-R (P-Q) interval
– time from beginning of atrial
depolarization to onset of ventricular
depolarization;
– includes spread of AP through atria and
conducting system
Fig. 18.16, p. 694
48
ECG Analysis: QRS and T
N
• QRS complex – spread of depolarization
through system and both ventricles
– Q-T segment – time from onset of
ventricular depolarization to end of
repolarization
• T wave – repolarization of ventricles
Fig. 18.16, p. 694
http://www.emergencynurse.com/resource/clipart/clipart9.htm
49
Common Cardiac Arrhythmias
• Sinus bradycardia – impulses arise at SA node
at slower than normal rate (<60 per minute)
http://www.rnceus.com/ekg/ekgsb.html
• Sinus tachycardia – impulses arise at SA node
at faster than normal rate (>100 per minute at
rest)
http://home.earthlink.net/~avdoc/infocntr/htrhythm/hrstachy.htm
50
Common Cardiac Arrhythmias
• Atrial flutter – single ectopic pacemaker causes
200-300 atrial APs per minute
http://www.emergencynurse.com/resource/clipart/clipart9.htm
• Atrial fibrillation – several ectopic foci in atria
cause rate of 450-600 per minute; transmission
to ventricles is erratic
http://www.emergencynurse.com/resource/clipart/clipart9.htm
51
Common Cardiac Arrhythmias
N
• Ventricular fibrillation – several ectopic foci in
ventricles fire independently resulting in
asynchronous and ineffective contraction  no
pulse
http://www.emergency-nurse.com/resource/clipart/clipart9.htm
52
Common Cardiac Arrhythmias
N
• Atrioventricular block – impaired conduction
from SA node through AV node
– 1st degree block – all impulses pass through
but with greater than normal delay
° What segment is longer?
– 2nd degree block – some, but not all
impulses pass through
° What wave is seen more often?
http://www.nda.ox.ac.uk/wfsa/html/u1
1/u1105f17.htm
Second Degree AV Block
First Degree AV Block
http://www.nda.ox.ac.uk/wfsa/htm
l/u11/u1105f18.htm
53
Common Cardiac Arrhythmias
N
– 3rd degree block = complete block – no
impulses pass through AV node  atria and
ventricles contract independently
http://www.nda.ox.ac.uk/wfsa/html/u11/u1105f20.htm
54
Common Cardiac Arrhythmias
N
• Bundle branch block – impairment in one of the
bundles
right bundle branch block
http://www.emergencynurse.com/resource/ecg/rbbb.htm
55
Intrinsic Conduction System, pp. 6
Cardiac Cycle and ECG
• Wiggers’ Diagram shows changes in
pressure in heart and aorta
• Changes correspond to activity in ventricles
• Activity in heart musculature corresponds
to electrical activity in heart
Fig. 18.19, p.695
56
Cardiac Cycle, p. 4
Cardiac Cycle and ECG: Overview
N
• Alternating systole and diastole results in
different periods of cardiac cycle
• Three main phases (periods):
– Ventricular filling
– Ventricular systole
– Isovolumetric relaxation
• AV and semilunar valves prevent backflow
57
Cardiac Cycle, p. 5-6
Cardiac Cycle: Ventricular Filling
• Ventricular Filling (#1)
– Passive filling occurs as blood flows into
ventricles from atria through open AV
valves (~ 70%); heart is at rest
– Atrial depolarization (P wave)  atrial
systole – moves remaining blood (~30%) into
ventricles
Fig. 18.20, p. 697
58
Cardiac Cycle, p. 7
Cardiac Cycle: Ventricular Systole
• ventricular systole results from ventricular
depolarization (QRS complex)
– period of isovolumetric contraction –
ventricles contract, push blood against AV
valves  AV valves close; pressure rises
without change in volume (#2a)
Fig. 18.20, p. 697
59
Cardiac Cycle, p. 8
Cardiac Cycle: Ventricular Systole
• Ventricular systole
– period of ejection – increased pressure in
ventricles pushes semilunar valves open and
blood forced into elastic arteries (#2b)
– ventricular volume drops as blood is
ejected
Fig. 18.20, p. 697
60
Cardiac Cycle:
Isovolumetric Relaxation
Cardiac Cycle, p. 9
N
• isovolumetric relaxation (#3) occurs as a
result of ventricular repolarization (T wave)
• semilunar valves close
• ventricles relax with both sets of valves
closed; pressure drops but volume stays the
same
Fig. 18.20, p. 697
61
Cardiac Cycle, p. 10
Cardiac Cycle and ECG
• atria have been filling while AV valves have
been closed
• when pressure in ventricles drops below (<)
pressure in atria  AV valves open and filling
begins again
Fig. 18.20, p. 697
62
Cardiac Cycle, p. 11-18
Pressure Changes in Heart
N
• Blood moves through system based on
pressure gradients
• Pressure changes open/close AV and
semilunar (SL) valves
– Increased pressure in ventricles  closes
AV valves and opens SL valves
– Decreased pressure allows SL valves to
close and AV valves to open
• Pressure in aorta (& pulmonary artery)
increases as blood is ejected
– Dicrotic notch
• Ventricular volume drops during ejection
63
Cardiac Output, p. 3-5
Cardiac Output (CO)
N
• Volume of blood ejected from each ventricle
per minute
– at rest, normally 5 L / min
• CO = HR x SV
– Heart rate (HR) – number of beats per
minute
– Stroke volume (SV) – amount of blood
ejected per beat
• HR and SV change to maintain steady CO at
rest and increase to maintain blood flow and
pressure during activity
64
Cardiac Output, p. 6
Cardiac Output (CO): SV
N
• SV = EDV – ESV
– EDV = end diastolic volume (preload) –
amount of blood in the ventricle at the end
of filling
° ave. 120 ml
– ESV = end systolic volume – amount of
blood in the ventricle at the end of
contraction
° ave. 50 ml
Fig. 18.21, p. 698
65
Cardiac Output: Heart Rate
N
• Number of beats per minute
• Intrinsic rate (normally around 100
beats/minute) altered by:
– autonomic innervation
– hormones
– temperature
– ion concentrations
66
Increasing Heart Rate
N
• Increased temperature
• Sympathetic division of the ANS – innervates
SA node, AV node, ventricular myocardium
– increases action potential frequency of SA
node
– increases action potential conduction at AV
node  less delay
– increases strength of contraction (see
stroke volume)
67
Increasing Heart Rate
N
• Hormones
– epinephrine directly increases heart rate
– thyroxine increases metabolic rate
• Altered ion concentrations (see Albasan et al.
for additional information)
– decreased Ca2+ (hypocalcemia)
– slightly increased K+ (hyperkalemia)
68
Decreasing Heart Rate
N
• Parasympathetic division of the ANS –
innervates SA node, AV node
– decreases action potential frequency and
increases delay in conduction pathway
– preganglionic fibers are from Vagus nerve
(CN X)
• Decreased temperature
• Altered ion concentrations (see Albasan et al.)
– increased Ca2+ (hypercalcemia)
– decreased K+ (hypokalemia)
– severe hyperkalemia
69
Neural Control of Heart Rate
N
• Response to arterial or atrial blood pressure
• Cardiac centers in medulla oblongata
– baroreceptors (pressoreceptors) –
stimulated by pressure of blood in aorta,
carotid arteries, right atrium
– Cardioacceleratory Center (CAC) –
increases heart rate through sympathetic
outflow
– Cardioinhibitory Center (CIC) – decreases
heart rate through parasympathetic
outflow
70
Neural Control: Increased BP
N
• Increased blood pressure (BP) stimulates
baroreceptors in aortic sinus and carotid
sinus
 afferent impulses sent through Vagus (from
aorta) and Glossopharyngeal nerves (from
carotids)
 these afferent impulses stimulate
cardioinhibitory center (CIC); inhibit
cardioacceleratory center (CAC)
71
Neural Control: Increased BP
N
 CAC sends fewer sympathetic impulses; CIC
sends parasympathetic impulses through
Vagus
 Vagus releases ACh at SA node and AV node
• What type of ACh receptors are found in
the heart?
 HR decreases
 CO decreases
 blood pressure decreases
72
Neural Control: Decreased BP
N
• Decreased blood pressure results in less
stimulation of baroreceptors
 fewer impulses through Vagus and
Glossopharyngeal nerves
 CIC not stimulated & CAC becomes more
active
 CAC sends impulses through sympathetic
nerves to SA node, AV node, ventricular
myocardium  release of norepinephrine
 heart rate and strength of contraction
increase
 CO and blood pressure increase
73
Neural Control: Bainbridge Reflex
• Bainbridge (Right Atrial) Reflex occurs when
right atrial pressure increases
 afferent impulses via Vagus nerve stimulate
CAC
 increased sympathetic impulses to heart
 increased heart rate and strength of
contraction moves blood more quickly
through atrium
 decreased right atrial pressure
74
Clinical Control of Heart Rate
• Digitalis – Digoxin
– cardiac glycoside
– makes calcium more available  increases
strength of contraction
– used to treat congestive heart failure
(CHF), atrial arrhythmias
• calcium-channel blockers – Verapamil
– inhibit calcium influx into cells  weaker
contractions
– used to treat hypertension, chronic angina
75
Clinical Control of Heart Rate
• beta-blockers (beta-adrenergic blockers) –
Propranolol
– block action of epinephrine and
norepinephrine at beta receptors
– used to treat hypertension, ventricular
arrhythmias
76
N
Factors Affecting SV: EDV
• EDV = “preload”
• amount of blood in ventricle at end of
diastole; normally, 120-130 ml
• EDV is main controller of stroke volume
• Frank-Starling law of the heart – heart
contraction adjusts to match venous inflow
– greater venous return  greater stretch
 stronger contraction
– decreased return  less stretch  weaker
contraction
77
Factors Affecting SV: ESV
N
• amount of blood left in ventricle at end of
contraction
• normally, ~ 50 ml
• affected by afterload – related to pressure
of blood in arteries
– must be overcome for blood to be ejected
from ventricle
– higher afterload  smaller SV
78
SV: Ventricular Contractility
N
• measure of the ventricles’ ability to produce
contraction force
• Positive inotropic agents – increase
contractility
– sympathetic innervation – increases influx
of Ca2+
– hormones
° epinephrine
° glucagon, thyroxine
– Digitalis (cardiac glycoside, Digoxin)
79
SV: Ventricular Contractility
N
• Negative inotropic agents – decrease
contractility
– rising extracellular K+
– calcium channel blockers (e.g., Verapamil)
– acidosis
80
Factors That Increase SV
• Increased contractility
• Increased EDV
– increased time for filling
– increased venous return
° increased skeletal muscle activity
° inspiration
° venoconstriction
° increased blood volume
• Decreased afterload
– decreased mean arterial pressure (MAP)
• Why/how does each of these increase SV?
N
81
Factors That Decrease SV
N
• Decreased contractility
• Decreased EDV
– decreased time for filling
– decreased venous return
° decreased skeletal muscle activity
° expiration
° decreased venous pressure
° decreased blood volume
• Increased afterload
– increased mean arterial pressure
• Why/how does each of these decrease SV?
82
Cardiac Output, p. 8 can be used to review
Summary of Autonomic Control
Fig. 18.23, p. 701
83
Congestive Heart Failure
N
• Results from failure to balance venous return
and stroke volume
• Pumping action of heart insufficient to meet
needs of body
• Form of positive feedback
• Left ventricular failure  pulmonary
congestion  pulmonary edema
• Right ventricular failure  peripheral
congestion
84
CHF: Causes
• Intrinsic causes – weaken contractions
– myocardial infarction, cardiomyopathy
• Extrinsic causes – make it more difficult to
eject blood into aorta
– systemic hypertension
– coronary atherosclerosis
– aortic stenosis
85
CHF: Mechanism
Increased systemic resistance
Increased force of left ventricular contraction
Increased left ventricular oxygen demand
Decreased
Increased left ventricular hypoxia
oxygen
supply
Decreased left ventricular contraction
Decreased
arterial
pressure
Increased left ventricular end diastolic pressure
Increased left atrial pressure
Pulmonary congestion & pulmonary edema
Increased pulmonary vascular resistance
Right ventricular failure
86
CHF: Treatments
N
• Decrease HR while increasing strength –
digitalis derivatives (Digoxin)
• Decrease edema and afterload with diuretics
• Decrease afterload with vasodilators (ACE
inhibitors)
87