Download Document

PowerPoint® Lecture Slides
prepared by
Janice Meeking,
Mount Royal College
CHAPTER
18
The
Cardiovascular
System: The
Heart: Part B
Copyright © 2010 Pearson Education, Inc.
The conductive system
• The heart is an autonomic system that can work
without neural stimuli – an intrinsic conduction
system.
• The autonomic function of the heart results from:
• The pacemaker function – Autorhythmic cells
• The conductive system that transfer those impulses
throughout the heart
• Two types of cardiac muscle cells that are involved in
a normal heartbeat:
• Specialized muscle cells of the conducting system
• Contractile cells
Copyright © 2010 Pearson Education, Inc.
Cardiac Muscle Contraction
• Depolarization opens voltage-gated fast Na+ channels
in the sarcolemma
• Reversal of membrane potential from –90 mV to +30
mV
• Depolarization wave causes release Ca2+ that causes the
cell contraction
• Depolarization wave also opens slow Ca2+ channels in
the sarcolemma
• Ca2+ surge prolongs the depolarization phase (plateau)
Copyright © 2010 Pearson Education, Inc.
Contractile Cells
• In skeletal muscle and neurons, an action potential falls back to
Resting Membrane Potential (RMP) within 1-2 msec, but in
cardiac muscle, slow calcium channels remain open longer (after
sodium channels close), prolonging the depolarization of the
cell.
• As long as the action potential is in its plateau and calcium
is entering the myocytes, the myocytes contract.
• These plateaus are more pronounced in the ventricles.
• Cardiac muscle has an absolute refractory period of 250 msec,
compared with 1–2 msec in skeletal muscle.
• The cardiac muscle must return completely to resting
potential before it can be contracted again.
• As a result, the heart can not go through tetanus contraction.
Copyright © 2010 Pearson Education, Inc.
Action potential in contractile cardiac muscle cells
Copyright © 2010 Pearson Education, Inc.
Heart Physiology: Electrical Events
• Intrinsic cardiac conduction system
• A network of noncontractile (autorhythmic) cells that initiate
and distribute impulses to coordinate the depolarization and
contraction of the heart
• Have unstable resting potentials/ pacemaker potentials (they
constantly
depolarized
slowly
towards
AP
–
hyperpolarization closes K+ and opens Na+)
• At threshold, Ca2+ channels open
• Ca2+ influx produces the rising phase of the action potential
• Repolarization results from inactivation of Ca2+ channels and
opening of voltage-gated K+ channels
Copyright © 2010 Pearson Education, Inc.
Heart Physiology: Sequence of Excitation
1. Sinoatrial (SA) node (pacemaker)
•
Generates impulses about 75 times/minute (sinus
rhythm)
•
Depolarizes faster
myocardium
than
any
other part
of
the
2. Atrioventricular (AV) node
•
Smaller diameter fibers; fewer gap junctions
•
Delays impulses approximately 0.1 second
•
Depolarizes 50 times per minute in absence of SA node
input
Copyright © 2010 Pearson Education, Inc.
Heart Physiology: Sequence of Excitation
3. Atrioventricular (AV) bundle (bundle of His)
•
Only electrical connection between the atria and
ventricles
4. Right and left bundle branches
•
Two pathways in the interventricular septum that
carry the impulses toward the apex of the heart
5. Purkinje fibers
•
Complete the pathway into the apex and ventricular
walls
•
AV bundle and Purkinje fibers depolarize only
30 times per minute in absence of AV node input
Copyright © 2010 Pearson Education, Inc.
• The upper part of the heart (the 2 atria) is insulated from the lower part
• Electrical excitation can pass from the atria to the ventricles only at the
AV node
Copyright © 2010 Pearson Education, Inc.
Extrinsic Innervation of the Heart
• Heartbeat is modified by the ANS
• Cardiac centers are located in the medulla oblongata
• Cardioacceleratory center innervates SA and AV
nodes, heart muscle, and coronary arteries through
sympathetic neurons
• Cardioinhibitory center inhibits SA and AV nodes
through parasympathetic fibers in the vagus nerves
Copyright © 2010 Pearson Education, Inc.
Electrocardiography (ECG or EKG)
• Body fluids are good conductors which allows the
record of the myocardial action potential extracellularly
• EKG pairs of electrodes (leads) one serve as positive
side of the lead and one as the negative
• Potentials (voltage) are being measured between the 2
electrodes
• EKG is the summed electrical potentials generated by
all cells of the heart and gives electrical “view” of 3D
object (different from one action potential)
• EKG shows depolarization and repolarization
Copyright © 2010 Pearson Education, Inc.
Electrocardiography
• EKG is made of waves and segments
• Waves are deflections above or below baseline
• Three waves
1.P wave: depolarization of SA node
2.QRS complex: ventricular depolarization (Atrial
repolarization record is masked by the larger
QRS complex)
3.T wave: ventricular repolarization
• Segments are sections of baseline between waves
Copyright © 2010 Pearson Education, Inc.
Homeostatic Imbalances
•
Defects in the intrinsic conduction system may
result in
1. Arrhythmias: irregular heart rhythms
2. Uncoordinated atrial and ventricular contractions
3. Fibrillation: rapid, irregular contractions; useless
for pumping blood
Copyright © 2010 Pearson Education, Inc.
Homeostatic Imbalances
• Defective SA node may result in
• Ectopic focus: abnormal pacemaker takes over
• If AV node takes over, there will be a junctional
rhythm (40–60 bpm)
• Defective AV node may result in
• Partial or total heart block
• Few or no impulses from SA node reach the
ventricles
Copyright © 2010 Pearson Education, Inc.
Autorythmic cells - ectopic pacemakers
• Autorythmic cells of the SA node (pacemaker) may be replaced
by ectopic pacemakers
• Ectopic pacemakers – other parts in the heart that can
induce beating
• The ectopic pacemakers may become dominant:
• If their rythmicity increased
• The pacemaker is inhibited/blocked
• The conduction system pathways are blocked
• First to take over will be the AV node
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Heart Sounds
• Two sounds (lub-dup) associated with closing of
heart valves
• First sound occurs as AV valves close and signifies
beginning of systole
• Second sound occurs when SL valves close at the
beginning of ventricular diastole
• Heart murmurs: abnormal heart sounds most often
indicative of valve problems
Copyright © 2010 Pearson Education, Inc.
Cardiac Cycle
• Cardiac cycle - The period between the start of one heartbeat and the
beginning of the next.
• refers to all events associated with blood flow through the heart
• During the cycle, each of the four chambers goes through
• Systole – contraction of heart muscle
• Diastole – relaxation of heart muscle
• An average heart beat (HR)/cardiac cycle is 75 bpm. That means that
a cardiac cycle length is about 0.8 second.
• Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation
and ventricular contraction.
• The remaining 0.4 seconds are called the quiescent period which
represent the ventricular relaxation
Copyright © 2010 Pearson Education, Inc.
Phases of the Cardiac Cycle
1. Ventricular filling — takes place in mid-to-late
diastole
•
AV valves are open
•
80% of blood passively flows into ventricles
•
Atrial systole occurs, delivering the remaining
20%
•
End diastolic volume (EDV): volume of blood in
each ventricle at the end of ventricular diastole
Copyright © 2010 Pearson Education, Inc.
Phases of the Cardiac Cycle
2. Ventricular systole
• Atria relax and ventricles begin to contract
• Rising ventricular pressure results in closing of AV
valves
• Isovolumetric contraction phase (all valves are
closed)
• In ejection phase, ventricular pressure exceeds
pressure in the large arteries, forcing the SL valves
open
• End systolic volume (ESV): volume of blood
remaining in each ventricle
Copyright © 2010 Pearson Education, Inc.
Phases of the Cardiac Cycle
3. Isovolumetric relaxation occurs in early diastole
•
Ventricles relax
•
Backflow of blood in aorta and pulmonary trunk
closes SL valves and causes dicrotic notch (brief
rise in aortic pressure)
Copyright © 2010 Pearson Education, Inc.
Cardiodynamics
• Movements and forces generated during cardiac contractions
• End-diastolic volume (EDV) – the amount of blood in each
ventricle at the end of ventricular diastole (before contraction
begins)
• End-systolic volume (ESV) - the amount of blood remains in
each ventricle at the end of ventricular systole
Copyright © 2010 Pearson Education, Inc.
Cardiodynamics
• Stroke volume (SV) – The amount of blood that leaves the
heart with each beat or ventricular contraction; EDV-ESV=SV
• Not all blood ejected
• Normal Adult 70 ml / beat
• Ejection fraction – The percentage of end-diastole blood
actually ejected with each beat or ventricular contraction.
• Normal adult 55-70% (healthy heart)
Copyright © 2010 Pearson Education, Inc.
Stroke Volume and Cardiac Output
• Cardiac output (CO) – the amount of blood pumped by
each ventricle in one minute.
• Physiologically, CO is an indication of blood flow through
peripheral tissues
• Cardiac output equals heart rate times stroke volume;
Normal CO: Approximately 4-8 liters/minute
CO
Cardiac output
(ml/min)
Copyright © 2010 Pearson Education, Inc.
SV
HR
=
Heart rate
(beats/min)
X
Stroke
volume
(ml/beat)
Factors Affecting Cardiac Output
Figure 20.20
Copyright © 2010 Pearson Education, Inc.
• Effect inotropy – effect on contractility of the heart
• Effect chronotropy – effect on HR
• Effect dromotropy – effect on the conductive velocity
• Sympathetic stimuli has a positive effect (increase) all
• Parasympathetic stimuli has a negative effect (decrease)
all
Copyright © 2010 Pearson Education, Inc.
Autonomic Nervous System Regulation
• In healthy conditions, parasympathetic effects dominate and slows
the rate of the pacemaker from 80-100 bpm to a 70-80 bpm.
• The binding of Ach to muscarinic receptors (M2) inhibit NE
release (mechanism by which vagal stimulation override
sympathetic stimulation)
• Sympathetic nervous system is activated by emotional or physical
stressors
• Norepinephrine causes the pacemaker to fire more rapidly (and
at the same time increases contractility)
• Parasympathetic nervous system opposes sympathetic effects
• Acetylcholine hyperpolarizes pacemaker cells by opening K+
channels
• The heart at rest exhibits vagal tone (parasympathetic)
Copyright © 2010 Pearson Education, Inc.
Autonomic Nervous System Regulation
• Atrial (Bainbridge) reflex: a sympathetic reflex
initiated by increased venous return
• Stretch of the atrial walls stimulates the SA node
• Also stimulates atrial stretch receptors activating
sympathetic reflexes
Copyright © 2010 Pearson Education, Inc.
Effects on SA node
• The effect of the ANS on the heart is by changing the
permeability of the conducting system cells.
• Ach released by the parasympathetic neurons slow the
depolarization rate and extend slightly the repolarization.
• This decreases the HR
• The NE released by the sympathetic neurons binds to beta–1
receptors, leading to the opening of calcium ion channels.
• That increases the depolarization rate and shortens the
repolarization period. Threshold is reached more quickly and
HR increases
Copyright © 2010 Pearson Education, Inc.
Pacemaker Function
Figure 20.22
Copyright © 2010 Pearson Education, Inc.
Chemical Regulation of Heart Rate
1. Hormones
•
Epinephrine from adrenal medulla enhances heart
rate and contractility
•
Thyroxine increases heart rate and enhances the
effects of norepinephrine and epinephrine
2. Intra- and extracellular ion concentrations (e.g.,
Ca2+ and K+) must be maintained for normal heart
function
Copyright © 2010 Pearson Education, Inc.
Homeostatic Imbalances
• Tachycardia: abnormally fast heart rate (>100 bpm)
• If persistent, may lead to fibrillation
• Bradycardia: heart rate slower than 60 bpm
• May result in grossly inadequate blood circulation
• May be desirable result of endurance training
Copyright © 2010 Pearson Education, Inc.
Factors Affecting Stroke Volume
Figure 20.23
Copyright © 2010 Pearson Education, Inc.
Regulation of Stroke Volume
• SV = EDV – ESV
• Three main factors affect SV
• Preload
• Contractility
• Afterload
Copyright © 2010 Pearson Education, Inc.
Regulation of Stroke Volume
• Preload
• The amount of tension on a muscle before it begins to
contract. The preload of the heart is determined by
the EDV.
• In general, the greater the EDV the larger is the stroke
volume : EDV-ESV=SV
• These relationships is known as the FrankStarling principle/Sterling’s law of the heart :
• The force of cardiac muscle contraction is
proportional to its initial length
• The greater the EDV the larger the preload
Copyright © 2010 Pearson Education, Inc.
 Preload =  Contractility (to a point)
Copyright © 2010 Pearson Education, Inc.
Factors Affecting stroke volume - Preload/EDV
• Stroke volume is the difference between the EDV and ESV.
Changes in either one can change the stroke volume and
cardiac output:
• The EDV volume is affected by 2 factors:
• The filling time – duration of ventricular diastole;
depends on HR – the faster the HR the shorter is the
available filing time
• The venous return – changes in response to several
changes: cardiac output, blood volume, peripheral
circulation etc.
Copyright © 2010 Pearson Education, Inc.
Diastolic filling increased
EDV increase (preload increased)
Cardiac muscle stretch increased
Force of contraction increased
Ejection volume increased
Copyright © 2010 Pearson Education, Inc.
Regulation of Stroke Volume
• Contractility
• Force of ventricular contraction (systole) regardless of
EDV
• Positive inotropic agents increase contractility
• Increased Ca2+ influx due to sympathetic
stimulation
• Hormones (thyroxine and epinephrine)
• Negative inotropic agents decrease contractility
• Increased extracellular K+
• Calcium channel blockers
Copyright © 2010 Pearson Education, Inc.
Regulation of Stroke Volume
• Afterload
• The amount of resistance the ventricular wall must
overcome to eject blood during systole (influenced by
arterial pressure).
• The greater is the afterload, the longer is the period of
isovolumetric contraction (ventricles are contracting
but there is no blood flow), the shorter the duration of
ventricular ejection and the larger the ESV – afterload
increase – stroke volume decrease
• Hypertension increases afterload, resulting in increased
ESV and reduced SV
Copyright © 2010 Pearson Education, Inc.
Congestive Heart Failure (CHF)
• Progressive condition where the CO is so low that blood
circulation is inadequate to meet tissue needs
• Caused by
• Coronary atherosclerosis
• Persistent high blood pressure
• Multiple myocardial infarcts (decreased blood supply
and myocardial cell death)
• Dilated cardiomyopathy (DCM) – heart wall weakens
and can not contract efficiently. Causes are unknown but
sometimes associated with toxins (ex. Chemotherapy),
viral infections, tachycardia and more
Copyright © 2010 Pearson Education, Inc.