the heart as a pump.ppt

7/30/2019 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

the heart as a pump.ppt

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