Download File

QUIZ/TEST REVIEW NOTES
SECTION 1 CARDIAC MYOCYTE PHYSIOLOGY
[CARDIOLOGY]
Learning Objectives:
 Describe the ionic basis of action
potentials in cardiac contractile
and autorhythmic cells
 Explain the relationship between
refractory periods and the absence
of summation in cardiac muscle
contraction
I. TWO TYPES OF ELECTRICAL SIGNALS
a. Structure of cardiac myocytes
Appearance under microscope:
Fiber arrangement:
Fiber proteins:
Control:
Nervous control:
Hormonal influence:
Location:
Morphology:
Internal structure:
Contraction speed:
Contraction force of single fiber twitch:
Initiation of contraction:
Striated
Sarcomeres
Actin, myosin: troponin/tropomyosin
Involuntary/Ca2+ and troponin/Fibers electrically
linked via gap junctions
Autonomic neurons
Epinephrine
Heart muscle
Uninucleate; branch fibers
T-tubule and Sarcoplasmic reticulum
Intermediate
Graded
Autorhythmic
MAJOR POINTS
- Single nucleus per fiber
- Individual cardiac cells branch and join neighboring cells end-to-end creating complex
of networks formed through cell junctions known as intercalated disks
Intercalated Disks components:
(1) Desmosomes: tie cell together allowing contractile force to
be transfer cell to cell
(2) Gap Junctions: Electrically connect cardiac cells together
- T-tubules branch inside the myocardial cells
- Sarcoplasmic reticulum is smaller because Extracellular Ca2+ is needed to initiate
contraction; not a adjacent protein
- Mitochondria occupy about 1/3 the cell volume of a contractile fiber
TWO FORMS OF MYOCYTES
- Contractile Cardiac Muscle Cells (myocardium)
[Organized sarcomeres/99% of heart]
- Autorhythmic Myocytes (pacemakers)
[Unorganized sarcomeres/1% of heart/generate A.P. spontaneously]
INSERT FIGURE 14-10 CARDIAC MUSCLE
1
II. MYOCARDIAL CONTRACTION
a. Depolarization
- A.P. enters contractile cell moving across the sarcolemma into the t-tubes
- A.P. then opens voltage-gated Ca2+ channels in the t-tubules, allowing Ca2+ to open up
ryanodine receptor channels (RyR) in the Sarcoplasmic reticulum
[RyR operated by Ca2+ binding unlike mechanical linkage of RyR found in
skeletal muscle]
- Ca2+ Induced Ca2+ Release: RyR opening caused by calcium, which leads to the flow of stored
calcium out into the cytosol to meet with troponin and initiate the cycle of cross-bridge formation
and movement
REUPTAKE: Cytoplasmic Ca2+ concentrations decrease, Ca2+ unbinds from troponin,
myosin releases actin, and contractile filaments slide back to relaxed position
(1) Ca2+ transported back to Sarcoplasmic reticulum with Ca2+-ATPase
(2) Ca2+ removed via Na+-Ca2+ antiport protein [3 Na+ in for 1 Ca2+ out]
[Na is later removed by Na+-K+-ATPase]
GRADED CONTRACTIONS: Force generated by cardiac muscle is proportional to the
number of cross-bridges that are active; number of active cross-bridges is determined by
how much Ca2+ is bound to troponin
b. Action Potential of contractile Myocytes
1. Membrane Potential Changes
- Resting potential -90mV [skeletal muscle -70mV]
- Depolarization: Na+ influx
- Repolarization: K+ efflux
- Longer action potential caused by Ca2+ entry
2. Role of Calcium
- Ca2+ influx at the plateau lengthens total duration of A.P, slowing down
repolarization; causing the cell to stay positive for longer period of time
2
3. Increased length of refractory period
- Longer A.P. helps prevent tetanus or sustained contraction which is important because
muscles must relax between contractions so ventricles can fill with blood
- Tetanus cannot occur in cardiac muscle because the longer A.P. means the refractory
period and the contraction end almost simultaneously
Phase 4: Resting Membrane Potential [resting potential of -90mV]
Phase 0: Depolarization [Depolarization spreads through gap junctions, membrane becomes more positive.
Voltage gated Na+ channels open allowing Na+ to enter cell and rapidly depolarize; potential reaches about +20mV
then double-gated Na+ channels close]
Phase 1: Initial Repolarization: Na+ channels close; cell begins to repolarize by efflux of K+ through K+
channels
Phase 2: The Plateau: Decrease in K+ permeability and increase in Ca2+ permeability; Ca2+ channels slowly
opening since phases 0 and 1; When Ca2+ channels open some K+ channels close, a influx of Ca2+ and decreased
efflux of Na+ causes A.P. to flatten out into plateau [extending refractory period/action potential]
Phase 3: Rapid Repolarization: Plateau ends with Ca2+ channels close and K+ permeability increase; K+
channels are activated during depolarization but are slow to open; Once K+ channels open K+ efflux occurs rapidly
returning cell to resting potential
III. AUTORHYTHMIC CELLS [pacemakers]
a. Characteristics
- Fulfill 1% of cardiac myocytes
- Unstable membrane potential
- No organized sarcomeres
- Generated spontaneous action potentials
3
- Pacemaker cells found toward apex of the heart are faster then pacemaker cells found toward the
base of the heart (slow)
- Speed with which pacemaker cells depolarizes determines the rate at which heart contracts (bpm)
b. Instability
- If Channels: Permeable to both K+ and Na+
> Allow current (I) to flow
> Subscript (f) stands for funny current because scientists did not understand them
- If Channel opens at negative membrane potential:
> Na+ influx exceeds K+ efflux
> Net influx of positive charge depolarizes autorhythmic cell
> As membrane becomes more, If channels close and Ca2+ channels open
> Ca2+ channels close at peak of A.P, slow K+ channels now open
> Repolarization phase autorhythmic action due to efflux K+
c. Pacemaker Autonomic Cardiac myocytes
- SA node [Sinoatrial]
- Internodal pathway
- AV node [atrioventricular]
- AV bundle
- AV branch
- Perkinje fibers
Populations of cells and not neurons
d. Action Potentials of autorhythmic cells
(1) Unstable Membrane Potential
> Membrane potential never “rests” at a constant value and is thus called a pacemaker
potential rather then a resting membrane potential
(2) Depolarization to threshold
Unstable pacemaker potential usually starts at -60mV
(3) Depolarization
NO REFRACTORY PERIOD
Na+ influx through If channels and Ca2+ influx
(4) Repolarization
K+ efflux
e. Autonomic Neurotransmitters Modulate Heart Rate
- Sympathetic stimulation of pacemaker cells increase heart rate
> The catecholamines Norepinephrine (from sympathetic neurons) and epinephrine (from
adrenal medulla) increase ion flow through both If and Ca2+ channels
> Catecholamines bind to B1-adrenergic receptors on autorhythmic cells
4
- Parasympathetic stimulation of pacemaker cells decrease heart rate
> Acetylcholine (ACh) activates Muscarinic cholinergic receptors that influence K+ and
Ca2+ channels in pacemaker cell
> K+ permeability increases, hyperpolarizing cell so pacemaker potential begins at more
negative value
> Ca2+ permeability of pacemaker decreases, slowing the rate at which the pacemaker
potential depolarizes
IV. CARDIAC CYCLE
a. Anatomy
(1) General Information
- Heart is found at the center of thoracic cavity
- Pointed apex of heart angles down to left side of the body
- The base lies just behind the sternum
- Incased with a tough membranous sac pericardium
5
(2) Chambers
(3) Valves
a. General Information
>
b. Atrioventricular Valves
> Opening between each atrium and its ventricles
> Formed by thin flaps that are anchored to ventricular side to collagenous
tendons, chordae tendineae (prevent valve from being pushed back into atrium;
prolapse)
> Chordae tendineae connect to papillary muscles in ventricular chamber to
provide stability
[Neither Chordae or Papillary muscles open/close the AV valves]
Tricuspid Valve (Right AV)
- Three flaps
- Separates right atrium and right ventricle
Mitral Valve (Left AV; Bicuspid)
- Two flaps
- Separates left atrium and left ventricle
c. Semilunar Valves
> Between the ventricles and the arteries
> Prevent backward flow of blood
Pulmonary Semilunar Valve
- Lies between right ventricle and the pulmonary trunk
Aortic Semilunar Valve
- Lies between left ventricle and the aorta
6
(4) Blood flow
Right Atrium
Tricuspid Valve
Right Ventricle
Pulmonary Semilunar Valve
Pulmonary Trunk / Pulmonary Arties
Lungs
Left Atrium
Bicuspid/Left AV/Mitral Valve
Left Ventricle
Aortic Semilunar Valve
Aorta
Systematic Circuit
7
(5) Contractions
Diastole: Time during cardiac muscles relaxes
Systole: Time during which muscle is contracting
[Contractions of Atria and ventricles do not contract and relax at same time]
a. Atrial Diastole
Atrial Relaxation (both Atrium/Ventricle chambers fill passively)
b. Atrial Systole
Atrial contraction forces a small amount of additional blood into ventricles;
c. Ventricular Systole
(Part 1 Isovumic) Contraction closes AV valves but not enough pressure to open
semilunar valves
(Part 2 Ejection) Pressure rises, opening semilunar valves to eject blood
d. Ventricular Diastole
Ventricles relax, pressure falls, blood flows back into cups of semilunar valves
and snaps them closed
(6) Intrinsic Conducting System
> Electrical communication in heart begins with A.P. in autorhythmic cell;
depolarization spreads through gap junctions in intercalated disks;
depolarization wave followed by wave of contraction that passes across atria,
then moves into the ventricles
a. Sinoatrial SA node
> Autorhythmic cells in the right atrium
> Serve as pacemaker to heart
> Sets the pace for the entire heart
> P-Waves in ECG
[Internodal Pathway: Link between SA and AV nodes]
8
b. Atrioventircular AV node
> Near the floor of the Atrium
> Delay occurs at AV node while atria contract
c. AV Bundle (of His)
> Found in superior atrioventricular septum
> Link between atria and ventricles
d. Bilateral Bundle branches
> Convey impulse down right and left ventricles to the hearts apex
e. Purkinje fibers
>Convey impulse throughout the ventricular walls
[Ejection of blood aided by spiral arrangement of muscles/during
contractions muscle pull the apex and base close together squeezing
blood out the openings at the top of the ventricles]
V. ELECTROCARDIOGRAM (ECG)
1. Background
- ECG tracing shows the summed electrical potentials generated by all cells of the heart
- ECG reflects depolarization and repolarizations of atria and ventricles
- Contraction Cycle: Single contraction-relaxation cycle
9
- Heart rate is normally timed from the beginning of one P wave to the beginning of the next P
wave or from peak of one R wave to peak of next R wave
Waves: Deflections above or below the baseline
Segments: Sections of baseline between two waves
Intervals: Combinations of waves and segments
NOTE: Cannot tell if ECG
recording represents
depolarization or
repolarization by looking
at the shape of wave
relative to the baseline
(example: P represents
depolarization and T
represents repolarization;
even though both are
above the baseline)
a. Atrial Depolarization
> P Wave
b. Atrial systole
> PR interval
c. Atrial repolarization/relaxtion
> Not represented by special wave but incorporated into QRS complex
d. Atrial diastole
> Later drop of QRS complex (S) to prefix of P wave
e. Ventricular depolarization
> QRS complex
f. Ventricular systole
> QT interval
g. Ventricular repolarization
> T wave
h. Ventricular diastole
> End of T wave to the first drop of QRS complex (Q)
i. U-wave
10
11
b. Arrhythmias
a. Sinus Rhythm
> NORMAL
> 60-100 bpm adults
> 90-110 bpm older children
> 100-120 bpm small children
> 120-160 bpm infants
b. Bradycardia
> Slower then normal heart rate
c. Trachycardia
> Faster then normal heart rate
d. Fluter
> Coordinated fast heart rate
> In Atrium
> Little blood flow
> Usually above 200 bpm
> Light headed/dizziness/pass-out
e. Fibrillation
> Non-coordinated fast heart fate
> “Circus Rhythms”
> No blood flow
[Fibulator repolarizes (resets) intrinsic conducting system to base]
f. AV Heart Block
> Slow conduction through AV node
> Independence of atrial and ventricular rhythms
12
13