The Heart as a Pump.ppt
Transcript of The Heart as a Pump.ppt
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The Heart as a Pump
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Cardiac Muscle
Striated
Actin
Myosin
Intercalated disc
Syncitium
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Membrane Potentials in SA Node and Ventricle
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Action Potentials
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Refractory period
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Effect of Heart Rate on Duration of
Contraction
Heart rate increaseDuration systole &diastole decrease
Diastole > Systole in decrease
At normal heart rate (72/mnt): Period ofsystole = 0.4 of entire cycle
At 3 times normal heart rate: Period of
systole = 0.65 of entire cycleAt a very fast heart beat doesnt remain
relaxed long enough to allow completefilling.
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Effect of Potassium & Calcium
Potassium:
Excess Heart dilated & flaccid & slows rate
Elevation 2 or 3 times normal death
Calcium: Excess spastic contraction
Deficiency flaccid
Temperature: Increase increase heart ate
Decrease decrease heart rate
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Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by eachventricle 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 betweenresting and maximal CO
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Cardiac Output = Heart Rate X Stroke
Volume
Around 5L :
(70 beats/m 70 ml/beat = 4900 ml)
Rate: beats per minute Volume: ml per beat
SV = EDV - ESV
Residual (about 50%)
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Factors Influencing Cardiac Output
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Stroke Volume (SV) Determined by extent of venous return and by
sympathetic activity
Influenced by two types of controls
Intrinsic control
Extrinsic control
Both controls increase stroke volume by
increasing strength of heart contraction
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Intrinsic Factors Affecting SV
Contractility cardiac cellcontractile force due to factors
other than EDV
Preload amount ventricles
are stretched by containedblood - EDV
Venous return - skeletal,
respiratory pumping
Afterload back pressureexerted by blood in the large
arteries leaving the heart
Stroke volume
Strength of
cardiac contraction
End-diastolic
volume
Venous return
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Frank-Starling Law Preload, or degree of stretch, of cardiac muscle cells before
they contract is the critical factor controlling stroke volume
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Frank-Starling Law Slow heartbeat and exercise increase venous return to
the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV
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Extrinsic Factors Influencing SV
Contractility is the increase in contractilestrength, independent of stretch and EDV
Increase in contractility comes from
Increased sympathetic stimuli
Hormones - epinephrine and thyroxine
Ca2+ and some drugs
Intra- and extracellular ion concentrations must be
maintained for normal heart function
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Contractility and Norepinephrine
Sympatheticstimulation
releases
norepinephrineand initiates a
cAMP second-
messengersystem
Figure 18.22
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Modulation of Cardiac Contractions
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Figure 14-31
Factors that Affect Cardiac Output
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Medulla Oblongata Centers Affect
Autonomic Innervation
Cardio-acceleratorycenter activatessympathetic neurons
Cardio-inhibitory center
controlsparasympatheticneurons
Receives input from
higher centers,monitoring bloodpressure and dissolvedgas concentrations
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Figure 14-27
Reflex Control of Heart Rate
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Figure 14-16
Modulation of Heart Rate by the Nervous System
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Establishing Normal Heart Rate SA node establishes baseline
Modified by ANS
Sympathetic stimulation
Supplied by cardiac nerves
Epinephrine and norepinephrine
released
Positive inotropic effect Increases heart rate
(chronotropic) and force of
contraction (inotropic)
Parasympathetic stimulation -
Dominates
Supplied by vagus nerve
Acetylcholine secreted
Negative inotropic and
chronotropic effect
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Regulation of Cardiac Output
Figure 18.23