Download Chapter 21: Blood Vessels and Circulation

Chapter 20: The Heart
BIO 211 Lecture
Instructor: Dr. Gollwitzer
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• Today in class we will discuss:
– The heart and the heartbeat
• The 2 types of cardiocytes (heart muscle cells) involved
– The structure and characteristics of contractile cells
– Structures of cardiac muscle tissue
– The events of an action potential (AP) in cardiac
muscle
• AP of cardiac muscle compared to skeletal muscle
– The role of calcium (Ca2+) ions in the contractile
process
– The components and functions of the conducting
system of the heart
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Heart
• Main function is to:
– Receive blood from veins at low pressure,
– Pump it through arteries at pressure high enough
to get it through blood vessels and
– Back to heart again
• Heartbeat = single contraction of the heart
• Entire heart contracts in specific sequence
so that blood flows in right direction at
right time
– First the atria
– Then the ventricles
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Heart and the Heartbeat
• Contraction of atria first and then ventricles
occurs because contractions of individual
cardiac muscle cells that make up heart
chambers occur in a specific sequence
• Involves 2 types of cardiac muscle cells
– Contractile cells
• Produce contractions that move blood through heart
– Conducting system cells
• Control and coordinate contractile cells
• Control and coordinate heartbeat
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Contractile Cells
• Cardiocytes
• 99% of muscle cells in heart
• Make up most of atria and ventricle walls
(myocardium)
• Form branched network
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Cardiac Muscle Tissue
• Myofibrils  striations
– Thin filaments (actin)
– Thick filaments (myosin)
• Intercalated discs
– Region in muscle tissue where membranes of
adjacent cardiac muscle cells are interconnected
– Transfer force of contraction from cell to cell
– Have 2 types of cell junctions
• Gap junctions
– Allow ions and small molecules to move easily between
cells
– Form direct electrical connection between cardiocytes
• Desmosomes
– Interlock adjacent cardiac cells together to prevent cells
from separating during contraction
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Fig. 10-3
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Fig. 20-5
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Review: Action Potential in a Neuron
Table 12-3
8th Edition
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Contraction of Cardiac Muscle
• Action potential (AP)
– = Electrical impulse conducted by muscle fiber
– Leads to appearance of Ca2+ among myofibrils
• Ca2+ binds to troponin (muscle protein) on
actin (thin filaments)
– Initiates contraction
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Origin of AP in Cardiac Muscle
• Resting membrane potential of ventricular
contractile cell = -90 mV
• Stimulus = excitation of cardiac muscle cell
• Membrane of muscle cell brought to
threshold (-75 mV)
– Usually reached next to intercalated disc
– AP begins
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Action Potential in Cardiac Muscle
Fig. 20-15a
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Action Potential in Cardiac Muscle
• Proceeds in 3 steps
– Depolarization
• Voltage-regulated fast Na+ channels open, Na+ rushes into cell
• Na+ channels close when transmembrane potential reaches +30 mV
– Plateau
• As Na+ channels close, voltage-regulated slow Ca2+ channels open, Ca2+
enters cell
• Provides 20% of Ca2+ required for contraction; 80% from SR
• Transmembrane potential remains at 0 mV for extended period of time
(during Ca2+ entry)
• Ends with closure of slow Ca2+ channels
– Repolarization
• As Ca2+ channels close, slow K+ channels open
• K+ leaves cells
• Restores resting potential to -90mV
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Refractory Period
• = Time after action potential begins when muscle will
not respond normally to a second stimulus
• Absolute refractory period
– Time after AP when membrane absolutely cannot respond
because Na+ channels opened/closed
– Long in length
– Lasts thru plateau and initial part of repolarization (approx.
200 msec)
• Relative refractory period
– = time following absolute refractory period when muscle
can respond to stronger-than-normal stimulus
– Shorter than absolute refractory period
– Lasts thru repolarization (approx. 50 msec)
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Action Potentials in
Cardiac and Skeletal Muscle
Figure 20–15a, b
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Conducting System
• Cardiac muscle contracts on its own
– Autorhythmicity or automaticity
– vs. neural/hormonal stimulation for skeletal
muscle
• System of specialized cardiac muscle cells
– Initiate and distribute electrical impulses that
stimulate contractions
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Conducting System
• 3 Components to cardiac conduction
(nodal) system
– Sinoatrial (SA) node
– Atrioventricular (AV) node
– Conducting cells
• From SA node to
– Atrial myocardium
– AV node along internodal pathways
• From AV node to ventricular myocardium
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Figure 20-11a The Conducting System of the Heart
Sinoatrial
(SA) node
Internodal
pathways
Atrioventricular
(AV) node
AV bundle
Bundle
branches
Purkinje
fibers
Components of the conducting
system
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Sinoatrial (SA) Node
• In posterior wall of R atrium near entrance to superior
vena cava
• Contains cardiac pacemaker cells
– Originate/generate action potential
– Reach threshold first
– Establish heart rate
• Abnormal function
– Tachycardia = heart rate faster than normal
(>100 bpm)
– Bradycardia = heart rate slower than normal
(<50 bpm)
• Connected to AV node by internodal pathways in atrial
walls
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Atrioventricular Node
• Larger than SA node
• In floor of R atrium near opening of coronary
sinus
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Conducting Cells
• Smaller than contractile cells
• Connect SA and AV nodes
• Distribute contractile stimulus throughout
myocardium
– Atrial conducting cells
• In internodal pathways in atrial walls
• Distribute contractile stimulus to atrial muscle cells as
impulse travels from SA node to AV node
– Ventricular conducting cells
• In IV septum
• In AV bundle (bundle of His), L & R bundle branches and
Purkinje fibers that distribute stimulus to ventricular
myocardium
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Path of an Impulse from Initiation at SA
Node to AV node
• As AP passes from SA to AV node, conducting cells
pass stimulus to contractile cells of both atria
• AP then spreads across entire atria via cell-to-cell
contact
• Rate of propagation slows as impulse leaves
internodal pathway
– Nodal cells smaller in diameter than conducting cells
– Connections between nodal cells less efficient
• Results in delay at AV node
– Important because atria must contract before ventricles
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Fig. 20-13, Step 1
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Fig. 20-13, Step 2
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Fig. 20-13, Step 3,
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AV Bundle, Bundle Branches, and
Purkinje Fibers
• Connection between AV node and AV bundle (aka Bundle of
His) is only electrical connection between atria and ventricles
– Fibrous skeleton around valves “insulates” other AV connections
• When impulse enters AV bundle, it:
– Travels to the interventricular septum
– Enters the R and L bundle branches
• Both bundle branches extend toward the apex of the heart
and fan out deep into the endocardial surface
• As branches diverge, they conduct impulse to:
– Purkinje fibers
– Papillary muscles of right ventricle
• Purkinje fibers radiate from apex to base
– Contraction of ventricles occurs as a wave that begins at the apex and
spreads toward the base
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Fig. 20-13, Step 4
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Fig. 20-13, Step 5
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Summary of Cardiac Conduction
• Before each heart beat (contraction)
– Action potential initiated spontaneously at SA
node
– Wave of depolarization radiates from SA node
– Spreads through contractile cells of atrial
myocardium
– To AV node
– Travels down IV septum to apex
– Turns and spreads through contractile cells of
ventricular myocardium to the base
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• Today in class we will discuss:
– The electrocardiogram
• Important features of an electrocardiogram recording
• The electrical events associated with an electrocardiogram
– The cardiac cycle
• The events that occur during the cardiac cycle
• How different heart sounds are related to specific events in
the cardiac cycle
• Cardiac arrhythmias
– Cardiac output and describe factors that influence it
– Age related changes in the heart
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Figure 20-13a An Electrocardiogram
Electrode placement for
recording a standard ECG.
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Electrocardiogram (ECG, EKG)
• = Record of electrical events in heart
• Associated with conduction/propagation of
heart beat
– Strong enough to be detected on body surface
• Can monitor electrical activity of heart by
comparing info from electrodes at specific
body locations
• ECGs reveal abnormal patterns of impulse
conduction
– When portion of heart is damaged, those cells
no longer conduct AP
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Figure 20-13b An Electrocardiogram
800 msec
R
P wave
(atria
depolarize)
R
T wave
(ventricles repolarize)
P–R segment
S–T
segment
Millivolts
QS
P–R
interval
S–T
interval
Q–T
interval
QRS interval
(ventricles depolarize)
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Electrocardiogram
• Important features of an ECG
– P wave = atrial depolarization
• Small wave
• Atria start contracting about 100 msec after start of Pwave
– QRS complex = ventricular depolarization and atrial
repolarization
• Strong signal because ventricular muscle more massive
than atrial muscle
• Complex because also includes atrial repolarization
• Ventricles start contracting shortly after peak of R wave
– T wave = ventricular repolarization
• Small, like P wave
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ECG Analysis
• Measure:
– Size of voltage changes: usually focused on
amount of depolarization occurring during P
wave and QRS complex
• Small P wave = mass of heart muscle decreased
• Large QRS = heart has become enlarged
• Small T wave = affected by anything that slows
ventricular repolarization
– e.g., starvation, low cardiac energy reserves, coronary
ischemia, abnormal ion concentration
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ECG Analysis
• Measure:
– Duration and temporal relationships of various
components
– Reported as intervals
• P-R interval
– = From start of P wave to start of QRS complex
– Extension may indicate damage to atrial conducting pathways
or AV node
• Q-T interval
– = From end of P-R interval to end of T wave
– Extension may indicate conduction problems, coronary
ischemia, myocardial damage, congenital heart defect
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Cardiac Arrhythmias
• = Abnormal patterns of electrical activity
• Normal if transient
• Clinical problems may develop and reduce
pumping efficiency of heart
• May indicate:
–
–
–
–
Damage to myocardium
Injury to pacemaker or conducting pathways
Exposure to drugs
Variation in electrolyte concentration
• Asystole = flatline
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Cardiac Cycle
Figure 20–11
9th Edition
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Cardiac Cycle
• = Period between start of one heartbeat and
beginning of next
– Includes electrical events and associated blood
flow
– Lasts approx. 0.8 sec in resting adult (72/min)
• Involves alternating periods of contraction and
relaxation of atria and ventricles
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Cardiac Cycle
• Systole = contraction (squeezing) of chambers
–
–
–
–
Pressure in chambers rises (systolic pressure)
In RV=30 mm Hg (only pumps blood through pulmonary circuit)
In LV=120 mm Hg (pumps blood through systemic circuit)
Pushes blood into adjacent chamber or arterial trunks
• Diastole = relaxation (dilation) of chambers
– Pressure in chambers drops
– Chambers fill with blood and prepare for next cardiac cycle
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Cardiac Cycle
• Blood flows from one chamber to another only
if pressure in first exceeds that of second
– Controlled by timing of contractions
– Directed by 1-way valves
• Phases of cardiac cycle
– Atrial systole
– Atrial diastole
– Ventricular systole
– Ventricular diastole
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Figure 20-16a Phases of the Cardiac Cycle
Start
Atrial systole begins:
Atrial contraction forces a small amount of
additional blood into relaxed ventricles.
0
800 msec
msec
100
msec
Cardiac
cycle
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Figure 20-16b Phases of the Cardiac Cycle
Atrial systole ends,
atrial diastole
begins
100
msec
Cardiac
cycle
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Figure 20-16c Phases of the Cardiac Cycle
Cardiac
cycle
Ventricular systole—
first phase: Ventricular
contraction pushes AV
valves closed but does
not create enough
pressure to open
semilunar valves.
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Figure 20-16d Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular systole—
second phase: As
ventricular pressure rises
and exceeds pressure
in the arteries, the
semilunar valves
open and blood
is ejected.
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Figure 20-16e Phases of the Cardiac Cycle
Cardiac
cycle
370
msec
Ventricular diastole—early:
As ventricles relax, pressure in
ventricles drops; blood flows back
against cusps of semilunar valves
and forces them closed. Blood
flows into the relaxed atria.
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Figure 20-16f Phases of the Cardiac Cycle
800
msec
Ventricular
diastole—late:
All chambers are
relaxed.
Ventricles fill
passively.
Cardiac
cycle
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Cardiac Cycle
• People can usually survive with severe atrial
damage
– Because atrial systole makes relatively minor
contribution to ventricular volume
• Damage to one or both ventricles leads to heart
failure
– Lack of adequate blood flow to peripheral
tissues/organs
• Although both atria and ventricles undergo
systole and diastole, terms usually refer to
ventricular contraction and relaxation
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Heart Sounds
• Closing of valves and rushing of blood through
heart  characteristic heart sounds heard
during auscultation with stethoscope
– AV valves close = “lubb” (S1)
– Semilunar valves close = “dubb” (S2)
– S3 and S4 are sounds of blood flowing through
heart
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Figure 20-18 Heart Sounds
Sounds heard
Valve location
Aortic
valve
Semilunar
valves open
Pulmonary
valve
Pressure
(mm Hg)
Valve location
Sounds heard
Semilunar
valves close
Left
ventricle
Left
atrium
Sounds heard
Valve location
Valve location
Sounds heard
Placements of a stethoscope for
listening to the different sounds
produced by individual valves
Left
AV
valve
Right
AV
valve
S4
AV valves
open
AV valves
close
S1
S2
Heart sounds
“Lubb”
S3
S4
“Dubb”
The relationship between heart sounds and key events in the
cardiac cycle
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Figure 20-17 Pressure and Volume Relationships in the Cardiac Cycle
ONE CARDIAC CYCLE
QRS
complex
QRS
complex
Electrocardiogram
(ECG)
T
P
ATRIAL
ATRIAL
DIASTOLE SYSTOLE
VENTRICULAR
DIASTOLE
P
ATRIAL
SYSTOLE
ATRIAL DIASTOLE
VENTRICULAR
SYSTOLE
VENTRICULAR DIASTOLE
Aortic valve
closes
Aortic valve
opens
Aorta
Dicrotic
notch
Pressure
(mm Hg)
Atrial contraction begins.
Atria eject blood into ventricles.
Atrial systole ends; AV valves close.
Left
ventricle
Isovolumetric ventricular contraction.
Ventricular ejection occurs.
Semilunar valves close.
Left AV
valve opens
Left AV
valve closes
Left atrium
Isovolumetric relaxation occurs.
AV valves open; passive ventricular
filling occurs.
Left
ventricular
volume (mL)
End-diastolic
volume
Stroke
volume
End-systolic
volume
Time (msec)
51
Cardiodynamics
• Stroke volume (SV)
– = Amount of blood ejected by ventricle during
single beat
• Cardiac output (CO)
– = Amount of blood pumped by L ventricle
/minute
– CO = SV (stroke volume) x HR
– e.g. 80 mL/heartbeat x 72 beats/min = 5,760
mL/min (approx. 1.5 gallons!)
– Adjusted by change in SV or HR
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Figure 20-20 Factors Affecting Cardiac Output
Factors Affecting
Heart Rate (HR)
Autonomic
innervation
Hormones
HEART RATE (HR)
Factors Affecting
Stroke Volume (SV)
End-diastolic
volume
End-systolic
volume
STROKE VOLUME (SV) = EDV – ESV
CARDIAC OUTPUT (CO) = HR  SV
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Factors Affecting Heart Rate
• Autonomic innervation (by ANS)
– To SA and AV nodes and atrial muscle cells
• Sympathetic accelerates HR
• Parasympathetic slows HR
– Controlled by cardiac centers in medulla oblongata
• Monitor chemoreceptors and baroreceptors
• e.g. when walls of right atrium stretch b/c of increased venous
return, atrial (Bainbridge) reflex triggered  increased
sympathetic activity  increased heart rate
• Hormones
– Thyroid hormone and epinephrine/norepinephrine increase
heart rate
– Stimulate SA node
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Cardiovascular Pathology
• Valvular heart disease
– = When valve deteriorates and can’t maintain
adequate blood flow
– Cause
• Congenital malformations
• Carditis (inflammation of the heart)
– Rheumatic fever
55
Cardiovascular Pathology
• Mitral valve prolapse
– Cusps do not close properly
• Abnormally long or short chordae tendineae
• Malfunctioning papillary muscles
– Regurgitation occurs
• Detected by auscultation as a heart murmur (rushing,
gurgling sound)
56
Cardiovascular Pathology
• Coronary artery disease (CAD)
– = Areas of partial or complete blockage of coronary circulation
(usually arteries)  coronary ischemia (reduced blood supply to
heart)
– Causes
• Formation of fatty plaque in wall of vessel
• Thrombus (clot)
• Spasm of smooth muscle in walls of vessel
– Symptoms
• Early: angina pectori (chest pain)
• Exertion or emotional stress  pressure, chest constriction, pain radiating
from sternal area to arms, back, and neck
– Treatment
•
•
•
•
Diet, exercise, no smoking
Medication
Balloon angioplasty
Coronary artery bypass graft (CABG), e.g., quadruple bypass)
57
Cardiovascular Pathology
• Myocardial infarction (MI) (heart attack)
– Coronary circulation becomes blocked (occluded)
– “Coronary thrombosis” if blockage due to thrombus at
plaque in coronary artery
– Result
• Cardiac muscle cells die from lack of O2
• Tissue degenerate creating “infarct” (nonfunctional area)
– Consequences: Depend on site and nature of blockage
• If near start of coronary artery widespread damage, often fatal
• If in smaller arterial branch, may survive with complications
– 25% mortality prior to medical assistance
– If >50 y.o. = 65% die within 1 hour after initial infarct
58
Damaged Cells vs. Normal Cells
• Cells more dependent on anaerobic metabolism
to meet energy needs (due to lack of O2)
• Accumulate large numbers of enzymes for
anaerobic metabolism (in cytoplasm)
• As cell membranes deteriorate, enzymes enter
surrounding intercellular fluids and circulatory
system
– Measurable and diagnostic
• LDH = lactate dehydrogenase
• CPK or CK = creatine phosphokinase
• CK-MB = special creatine phosphokinase found only in
cardiac muscle
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Abnormal Conditions Affecting Cardiac
Output
• Abnormal Ca
– Hypocalcemia
• Contractions weaken and may cease
– Hypercalcemia
• Cardiac muscle cells very excitable
• Have powerful, prolonged contractions
• Extreme case: heart goes into extended state of
contraction that is usually fatal
60
Abnormal Conditions Affecting Cardiac
Output
• Abnormal K
– Hypokalemia
• Cells less responsive to stimulation and heart rate
decreases
• Blood pressure falls
• Heart eventually stops
– Hyperkalemia
• Muscle cells depolarize, repolarization inhibited
• Contractions weak and irregular
• In severe cases, heart stops
61
Abnormal Conditions Affecting Cardiac
Output
• Abnormal body temperature
– Reduced body temperature
• Slows rate of depolarization at SA node, lowers
heart rate, reduces strength of cardiac contractions
• In open heart surgery, heart chilled until it stops
beating
– Elevated body temperature
• Accelerates heart rate and contractile force
• Pounding and racing heart during high fever
62
Age-related Changes
•
•
•
•
Reduction in maximum cardiac output
Changed activity of nodal and conducting cells
Reduced elasticity
Progressive atherosclerosis that restricts
coronary circulation
• Replacement of damaged cardiac muscle cells
by scar tissue
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