Transcript Chapter 20 - Martini

The Heart
Chapter 20
Function of the Heart
• Pumping the red stuff
Anatomy of the Heart
• Location – mediastinum, slightly to the left
of center
• Size – about that of your fist
• Mass – 250 – 300 g
Organization of
the
Cardiovascular
System
Location
Tissues of
the Heart
Coverings of the Heart: Anatomy
• Pericardium – a double-walled sac around
the heart composed of:
– A superficial fibrous pericardium
– A deep two-layer serous pericardium
• The parietal layer lines the internal surface of the
fibrous pericardium
• The visceral layer or epicardium lines the surface of
the heart
• They are separated by the fluid-filled pericardial
cavity
Coverings of the Heart:
Physiology
• The pericardium:
– Protects and anchors the heart
– Prevents overfilling of the heart with blood
– Allows for the heart to work in a relatively
friction-free environment
Serous pericardium
General
Anatomy
• Epicardium – visceral layer of the serous
pericardium
• Myocardium – cardiac muscle layer forming the
bulk of the heart
• Fibrous skeleton of the heart – crisscrossing,
interlacing layer of connective tissue
• Endocardium – endothelial layer of the inner
myocardial surface
Heart Wall
• Vessels returning blood to the heart include:
– Superior and inferior venae cavae
– Right and left pulmonary veins
• Vessels conveying blood away from the heart
include:
– Pulmonary trunk, which splits into right and left
pulmonary arteries
– Ascending aorta (three branches) – brachiocephalic,
left common carotid, and subclavian arteries
External Heart: Major Vessels of the
Heart (Anterior View)
• Arteries – right and left coronary (in
atrioventricular groove), marginal,
circumflex, and anterior interventricular
arteries
• Veins – small cardiac, anterior cardiac, and
great cardiac veins
External Heart: Vessels that
Supply/Drain the Heart (Anterior View)
Surface features of the heart
Cardiac Muscle Cells
Figure 20–5
• Vessels returning blood to the heart include:
– Right and left pulmonary veins
– Superior and inferior venae cavae
• Vessels conveying blood away from the heart
include:
– Aorta
– Right and left pulmonary arteries
External Heart: Major Vessels of the
Heart (Posterior View)
Posterior view
Atria of the Heart
• Atria are the receiving chambers of the
heart
• Each atrium has a protruding auricle
• Pectinate muscles mark atrial walls
• Blood enters right atria from superior and
inferior venae cavae and coronary sinus
• Blood enters left atria from pulmonary
veins
Deep in your heart of hearts…
Ventricles of the Heart
• Ventricles are the discharging chambers of
the heart
• Papillary muscles and trabeculae carneae
muscles mark ventricular walls
• Right ventricle pumps blood into the
pulmonary trunk
• Left ventricle pumps blood into the aorta
Note the differences in wall thickness
• Heart valves ensure unidirectional blood flow
through the heart
• Atrioventricular (AV) valves lie between the atria
and the ventricles
• AV valves prevent backflow into the atria when
ventricles contract
• Chordae tendineae anchor AV valves to papillary
muscles
Heart Valves
Heart Valves
• Aortic semilunar valve lies between the left
ventricle and the aorta
• Pulmonary semilunar valve lies between the
right ventricle and pulmonary trunk
• Semilunar valves prevent backflow of blood
into the ventricles
The heart valves
Function of the bicuspid valve
Valve functions
Heart Sounds
Where to go to listen to heart sounds
Some heart valve disorders
• Stenosis (narrowing) – the inability of a valve to
open fully
• Insufficiency (incompetence) – failure of the
valve to prevent back flow or close properly
– Mitral valve prolapse – one or both of the flaps
blows back into the atrium during systole
(contraction) of the ventricle allowing backflow into
the atrium.
– The aortic semilunar valves can also suffer from
stenosis or insufficiency, allowing backflow into the
ventricle.
• Right atrium  tricuspid valve  right
ventricle
• Right ventricle  pulmonary semilunar
valve  pulmonary arteries  lungs
• Lungs  pulmonary veins  left atrium
• Left atrium  bicuspid valve  left
ventricle
• Left ventricle  aortic semilunar valve 
aorta
• Aorta  systemic circulation
Pathway of Blood Through the Heart and Lungs
Systemic & pulmonary circuits
Blood flow
Coronary Circulation
• Coronary circulation is the functional blood
supply to the heart muscle itself
• Collateral routes ensure blood delivery to
heart even if major vessels are occluded
Coronary
Circulation
(arterial)
Coronary
Circulation
(venous)
Cardiac histology & physiology
• Cardiac muscle is made of short, branched
fibers
• Striated
• Uninucleate
• There is now some evidence that it has limited
mitotic capability (it is likely that regeneration
is from migration of stem cells from the
blood)
• 99% are contractile
• 1% are “autorhythmic” or “pacemaker” cells
Cardiac Muscle Tissue
Cardiac Muscle Cells
• Intercalated discs:
–
–
–
–
–
interconnect cardiac muscle cells
secured by desmosomes
linked by gap junctions
convey force of contraction
propagate action potentials
Characteristics of
Cardiac Muscle Cells
1.
2.
3.
4.
Small size
Single, central nucleus
Branching interconnections between cells
Intercalated discs
Cardiac Cells vs. Skeletal Fibers
Table 20-1
The intrinsic conduction system
• Sinoatrial node: the primary pacemaker – has an
intrinsic firing rate of about 100 bpm but kept at
60 – 80 by parasympathetic tone
• Generates pacemaker potentials from leakage of
Ca++
• Depolarization spreads via gap junctions in
intercalated disks
• Rate can be adjusted by ANS
Intrinsic conduction system
• Signals from SA node travel to the
Atrioventricular Node via the internodal
pathway
• The AV node has its own intrinsic firing rate of
40 – 60 bpm. In absence of SA node function it
can establish a “junctional rhythm” that keeps
the ventricles working
The conducting pathways
• The signal is delayed about 0.1 s and then
transmitted down the …
• Bundle of His or AV bundle and the left &
right bundle branches to the apex
• And from there the depolarization is
distributed by the Purkinje fibers
Fig. 20.10a
Contraction of cardiac muscle fibers
and the cardiac cycle
The Electrocardiogram
Figure 20–14b
NSR:
Normal
Sinus
Rhythm
Prolonged contraction of cardiac muscle
Features of an ECG
• P wave:
– atria depolarize
• QRS complex:
– ventricles depolarize
• T wave:
– ventricles repolarize
Resting Potential
• Of a ventricular cell:
–about —90 mV
• Of an atrial cell:
–about —80 mV
3 Steps of
Cardiac Action Potential
1.Rapid depolarization:
» voltage-regulated sodium
channels (fast channels) open
3 Steps of
Cardiac Action Potential
2. As sodium channels close:
– voltage-regulated calcium channels
(slow channels) open
+
– balance Na ions pumped out
– hold membrane at 0 mV plateau
3 Steps of
Cardiac Action Potential
3. Repolarization:
– plateau continues
– slow calcium channels close
– slow potassium channels open
– rapid repolarization restores resting
potential
The Refractory Periods
• Absolute refractory period:
– long
– cardiac muscle cells cannot respond
• Relative refractory period:
– short
– response depends on degree of
stimulus
Timing of Refractory Periods
• Length of cardiac action potential in
ventricular cell:
– 250–300 msecs
• 30 times longer than skeletal muscle fiber
• long refractory period prevents summation
and tetany
Electrical
Activity
and the
Cardiac
Cycle
Calcium and Contraction
• Contraction of a cardiac muscle cell is
produced by an increase in calcium ion
concentration around myofibrils
2 Steps of Calcium
Ion Concentration
1. 20% of calcium ions required for a
contraction:
–
calcium ions enter cell membrane during
plateau phase
2 Steps of Calcium
Ion Concentration
2. Arrival of extracellular Ca2+:
–
triggers release of calcium ion reserves from
sarcoplasmic reticulum
Intracellular and
Extracellular Calcium
• As slow calcium channels close:
– intracellular Ca2+ is absorbed by the SR
– or pumped out of cell
• Cardiac muscle tissue:
– very sensitive to extracellular Ca2+
concentrations
• CO is the amount of blood pumped by each
ventricle in one minute
• CO is the product of heart rate (HR) and
stroke volume (SV)
• HR is the number of heart beats per minute
• SV is the amount of blood pumped out by a
ventricle with each beat
• Cardiac reserve is the difference between
resting and maximal CO
The Cardiac Cycle
Phases of the Cardiac Cycle
Figure 20–16
Cardiac output
• CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
• CO = 5250 ml/min (5.25 L/min)
Cardiac output
• SV = end diastolic volume (EDV) minus
end systolic volume (ESV)
• EDV = amount of blood collected in a
ventricle during diastole
• ESV = amount of blood remaining in a
ventricle after contraction
Pressure
and
Volume
in the
Cardiac
Cycle
Figure 20–17
Factors Affecting Stroke Volume
• Preload – amount ventricles are stretched by
contained blood
• Contractility – cardiac cell contractile force
due to factors other than EDV
• Afterload – back pressure exerted by blood in
the large arteries leaving the heart
• Changes in EDV or ESV
Factors Affecting Stroke Volume
Figure 20–23 (Navigator)
Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac
muscle cells before they contract is the
critical factor controlling stroke volume
• Slow heartbeat and exercise increase
venous return to the heart, increasing SV
• Blood loss and extremely rapid heartbeat
decrease SV
Extrinsic Factors Influencing
Stroke Volume
• Contractility is the increase in contractile
strength, independent of stretch and
EDV
• Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
Factors Affecting Heart Rate and Stroke Volume
Extrinsic Factors Influencing
Stroke Volume
• Agents/factors that decrease
contractility include:
– Acidosis
– Increased extracellular K+
– Calcium channel blockers
Contractility and Norepinephrine
• Sympathetic
stimulation
releases
norepinephrin
e and initiates
a cyclic AMP
secondmessenger
system
Figure 18.22
Regulation of Heart Rate
• Positive chronotropic factors increase
heart rate
• Negative chronotropic factors decrease
heart rate
• Sympathetic nervous system (SNS)
stimulation is activated by stress, anxiety,
excitement, or exercise
• Parasympathetic nervous system (PNS)
stimulation is mediated by acetylcholine
and opposes the SNS
• PNS dominates the autonomic stimulation,
slowing heart rate and causing vagal tone
Regulation of Heart Rate: Autonomic
Nervous System
Autonomic Innervation
Autonomic
Pacemaker
Regulation
Autonomic Pacemaker
Regulation (1 of 3)
• Sympathetic and parasympathetic
stimulation:
– greatest at SA node (heart rate)
• Membrane potential of pacemaker cells:
– lower than other cardiac cells
Autonomic Pacemaker
Regulation (2 of 3)
• Rate of spontaneous depolarization depends
on:
– resting membrane potential
– rate of depolarization
Autonomic Pacemaker
Regulation (3 of 3)
• ACh (parasympathetic stimulation):
– slows the heart
• NE (sympathetic stimulation):
– speeds the heart
Atrial (Bainbridge) Reflex
• Atrial (Bainbridge) reflex – a
sympathetic reflex initiated by increased
blood in the atria
– Causes stimulation of the SA node
– Stimulates baroreceptors in the atria,
causing increased SNS stimulation
CNS and ANS controls of Cardiac output
Chemical Regulation of the Heart
• The hormones epinephrine and
thyroxine increase heart rate
• Intra- and extracellular ion
concentrations must be maintained for
normal heart function
PLAY
InterActive Physiology®:
Cardiovascular System: Cardiac Output
Factors Involved in Regulation of Cardiac Output
How the heart starts
Examples of Congenital Heart
Defects
Congestive Heart Failure (CHF)
• Congestive heart failure (CHF) is caused
by:
–
–
–
–
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)
Arteriosclerosis
Fig. 20.20
Age-Related Changes Affecting
the Heart
•
•
•
•
Sclerosis and thickening of valve flaps
Decline in cardiac reserve
Fibrosis of cardiac muscle
Atherosclerosis