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Difference between cardiac contraction and skeletal muscle contraction
cardiac contraction lasts for a much longer duration
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What separates individual muscle fibers
intercalate disk, specialized cell membranes with gap junctions that present small amounts of resistance to electrical impulses
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cardiac muscle contracts as a
- syncytium
- when one becomes excited they all become excited
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milivolts of a ventricular AP
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Plateau phase
- allows cardiac muscle contraction to last 15x longer then skeletal muscle
- last about 0.2 seconds
- immediately after the onset of the AP the cardiac muscle membrane permeability for K decreases, can occur due to Ca influx, prevents early depolarization
- K permeability returns to normal when the Ca channels close
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Cause of cardiac muscle action potentials
- opening of fast Na channels and slow calcium channels (calcium-sodium channels)
- slow channels are slower to open and remain open for a longer duration, these cause the plateau phase
- the entering calcium ions are what cause the contraction of cardiac muscle
- The SA node's fast channels are inactivated because of its less negative resting state, The AP here is slower.
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Length of the normal ventricular refractory period
.25 - .3
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Relative refractory period
- about .05 seconds in cardiac muscle
- muscle can be excited but it takes a much larger stimulus
- the atrial muscle is mush shorts refractory period then ventricular muscle, about .15 sec
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How does the AP spread to the interior of cardiac muscle
- T tubules
- also release Ca ions into the muscle, determines the strength of contraction
- 5 times larger in cardiac muscle then in skeletal muscle
- calcium is made available in the T tubules by a large quantity of mucopolysaccharides that bind and store calcium
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Storage of calcium in different muscle tissues
- in skeletal muscle it is stored in the cistern of SR
- on cardiac muscle calcium is in the extracellular fluid
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length of time for ventricular muscle contraction
0.2-0.3
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Atrial pressure waves; A, V, C
- A is atrial contraction
- V is the passive flow of fluid into the atria while the AV valve is closed
- C is ventricular contraction causing a slight back flow of blood before the AV valves close increasing the pressure of the atria
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The ventricle contraction is over after the T wave
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Priming feature of atrial contraction
- about 80% of blood passively flows from the atria to the ventricle
- the remaining 20% is forced into the ventricle by atrial contraction
- The body can function without this priming action while at rest, during exercise it can become pathological
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Period of rapid ventricular filling
- as soon as ventricular contraction is over the AV valves open
- flow is due to the amount of blood that has accumulated in the atria while the AV valve is closed
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Isovolemic contraction
period of ventricular contraction when the AV valves have closed and the ventricle must build up enough pressure the open the Ao valve
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period of slow and fast ejection
- fast ejection is during the first third of ventricular contraction, 70% of volume
- slow ejection is last two thirds, 30% of volume
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calculation of mean BP
- systolic + 2x diostolic divided by 3
- diostolic + 1/3 pulse pressure
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volume of ventricle
- 110-120 ml
- end diastolic volume
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other name for moderator band
septomarginal trabeculea
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semilunar valves lack
chordae tendineae
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Incisura
- occurs in the aortic pressure wave when the aortic valve closes
- dicrotic notch
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First heart sound
- when the ventricles contract the AV valves close causing the sound
- low in pitch and long lasting
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second heart sound
- closing of the semilunar valves
- rapid snap
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Stroke work output of the heart
- the amount of energy that the heart converts to work during each heartbeat
- Minute work output is how much energy is converted each minute, stroke work times heart rate
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Volume pressure work, external work
work done to move the volume from the veins to the arteries
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Kinetic energy of blood flow
- work done to propel the blood
- increases during aortic stenosis
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Amount of blood in the LV before diastolic pressure rises greatly
- 150ml
- fibrous tissue can not stretch much more
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max pressure that can be generated by LV
250-300
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Phases of the volume pressure loop
- phase 1: period of filling, volume of LV increases by about 70ml and pressure rises from 0 to ~5
- Phase 2: isovolemic contraction; no volume change but pressure rises to equal the diastolic pressure of the aorta
- Phase 3: ejection; systolic pressure open Ao valve, volume of LV decreases, pressure continues to rise but then peaks and falls
- Phase 4: isovolemic relaxation; Ao valve closes, pressure falls to level of atrial pressure and mitral valve opens
- area within this loop is external work, this will increase when the heart pumps more volume
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Preload
end diastolic pressure
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Afterload
the pressure of the aorta
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MAin energy sources for cardiac muscle
oxidation of fatty acids
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efficiency of contraction
- ratio of energy converted to heat to energy converted to work
- normal heart this is 20-25%
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Two system that regulate heart pumping
- intrinsic, heart pumps out what it receives,
- control by the autonomic nervous system
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Frank starling mechanism
- the greater the heart muscle is stretched during filling the greater the force of contraction and the greater the quantity of blood pumped into the aorta
- actin and myosin filiments are brought to a more optimal length
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Stretch of the rt atrial wall
- directly increases heart rate 10-20 percent
- bainbridge reflex
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sympathetic stimulation
- increase heart rate as well as contractile strength
- normal conditions has 30% stimulation
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distribution of parasympathetic fibers
SA and AV nodes and atrial muscle
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Excess potassium ions in the extracellular fluid
- causes the heart to become dilated
- can block conduction
- decreases the resting membrane potential
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Excess calcium ions
spastic contractions
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Effects of body temp on the heart
increase rate
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cardiac output os mainly controlled by
- the ease of flow through organs, venous return
- arterial pressure does not diminish CO until mean rises above 160
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