Download THE HEART

Cardiac Notes
Human Anatomy & Physiology II
page 1
THE HEART
A. Cardiac Muscle Anatomy
 cardiac muscle is striated, similar to skeletal
 also uses sliding filament mechanism
 cardiac fibers short, branched, w/1 or 2 nuclei. Not long like skeletal fibers
 loose connective tissue between cells has many capillaries
 this CT is connected to the so called "fibrous skeleton" of fibrous CT
 cardiac muscle cells are anchored to and pull against this CT "skeleton"
 cardiac cells interlock at intercalated disks
 desmosomes hold them together
 gap junctions allow ions to pass freely (2 functional syncytia, the heart moves as 2
units)
 lots of mitochondria
 25% of the cell volume
 indicative of the high oxygen demand
 bigger T tubules, well developed SR but without a lot of storage in terminal cisternae.
It is still the influx of Ca++ that initiates the contraction.
B. Heart Muscle Contraction - General. An action potential on the muscle cell membranes
starts the process. The AP is initiated by autorhythmic cells which depolarize by
themselves.
1. influx of Na+ ions opens voltage gated fast sodium channels
a. short duration - they inactivate quickly
b. another positive feedback example
2. the membrane (and the T tubules) depolarizes in a wave which causes the SR to
release calcium ions
a. depolarization of membrane also opens "slow calcium channels. These
channels let in Ca++ from outside the cell, and it's this influx that
triggers the SR to dump the rest of the Ca++
b. Ca++ is also positive, so depolarization is maintained for ~ 100 ms
longer
3. Excitation-Contraction coupling occurs. Depolarization is "coupled" to
contraction via Ca++ (binds to troponin...)
4. End of Action Potential / Repolarization
a. sodium channels have already closed
b. Ca++ channels close
c. K+ channels open. K+ goes out, restores RMP
d. Ca++ pumped out to SR
5. Some contrasts to skeletal muscle: (skeletal then cardiac)
• individual cells contract
vs
the whole heart contracts
• each cell has a nerve ending vs
self exciting
• 1-2 ms refractory period
vs
250 ms refractory period
Cardiac Notes
Human Anatomy & Physiology II
page 2
HEART PHYSIOLOGY
I Electrical
A. The Intrinsic Conduction System - a group of non-contractile cardiac cells that initiate
and distribute impulses. These cells have unstable resting potentials known as pacemaker
potentials. These cells are localized in the following areas.
1. Sinoatrial Node, or SA node
a. fastest rate, so it's the pacemaker
b. 90-100 times per minute
2. Atrioventricular Node, or AV node
a. depolarization reaches it through gap junctions
b. delay (0.1 ms) before signaling the rest of the system
c. during delay, atria contract
d. 50 times per minute
3. Atrioventricular Bundle, AV bundle
a. this is the only electrical connection between atria and ventricles (your
book says this occurs at the distal side of the AV node)
b. no gap junctions between atrial cells and ventricular cells
c. 30 times per minute
4. Bundle Branches.
a. They run through the interventricular septum
b. 30 times per minute
5. Purkinje Fibers
a. Responsible for the bulk of ventricular depolarization (via ventricular
suncytium)
b. 30 times minute
B. Modifying the basic rhythm
1. sympathetic nervous system increases rate and force of contractions
2. parasympathetic slows heart rate
C. Electrocardiography - Graphing the electrical changes during heart activity. Typical ECG
shows 3 distinguishable deflection waves (see figure 15.21)
1. P wave represents the depolarization wave across the atria
2. QRS complex results mostly from ventricular depolarization
a. complicated by the two different ventricle shapes and sizes
b. atrial repolarization wave is obscured by the QRS complex
3. T wave - ventricular repolarization
II Mechanical Events. The heart contracts and expands. Systole = contraction. Diastole =
relaxation.
A. The cardiac cycle includes pressure and volume changes within the heart. Look at figure
B. Heart Sounds. Lub-dup pause, lub-dup pause
1. 1st sound is the AV valves slamming shut at the onset of ventricular systole.
Blood squirts out of the ventricle, opening the semi lunar valves
2. 2nd sound is semi lunars shutting at the onset of ventricular diastole
III Cardiac Output
CO = Cardiac Output (ml/min)
SV = Stroke Volume (ml/beat)
Cardiac Notes
Human Anatomy & Physiology II
page 3
HR = Heart Rate (beats/min)
Cardiac output is variable. Cardiac reserve is the difference between resting CO and maximum
CO. Max CO can be 4-5 times resting CO in non-athletes, 7 times in people who train. CO
changes with changes in SV and HR.
A. Stroke volume is the difference between EDV (end diastolic volume) and ESV (end
systolic volume). 3 things affect SV: Preload, Contractility, and Afterload
1. Preload is the degree of stretch of cardiac muscles
a. more stretch = more forceful contraction
b. increased EDV leads to increased stretch
1) slow heart rate = more ventricular filling time
2) exercise squeezes venous blood back, increasing fill rate
3) rapid heart rate (not accompanied by exercise) can lower EDV
and lower preload
2. Contractility is an increase in contraction strength resulting from increased
Ca++ influx
a. more complete emptying of the ventricles which lowers ESV
b. results from sympathetic stimulation of the heart - norepinephrine
increases Ca++ entry
c. others chemicals affect contractility
1) hormones
2) ions
3) drugs
3. Afterload is the backpressure in the arteries
a. normally not a problem
b. high blood pressure (increased afterload) increases ESV and therefore
lowers SV
B. Heart Rate. Cardiac output can be altered by altering heart rate. Heart rate can be altered
neurally, chemically, and physically.
1. Autonomic nervous system
a. sympathetic stimulation increases rate and contractility
b. parasympathetic stimulation decreases the rate
c. both act simultaneously, parasympathetic dominates. "Vagal Tone" is
the constant parasympathetic stimulation of the heart rate slowing the SA
node to about 75 beats/minute from its intrinsic rate of about 100 bpm
2. Chemical regulation
a. hormones - epinephrine from adrenal medulla, and thyroxine increase
heart rate
b. ions - hypocalcemia decreases heart rate, hypercalcemia leads to
spasms. Obviously levels of sodium and potassium are important.
3. Other (physical) factors influence heart rate
a. age - HR decreases with age
b. gender - faster in females
c. body temperature - high temp increases heart rate by increasing the
metabolic rates of cardiac cells