The Heart as a Pump
Cardiac Muscle
Striated
Actin Myosin
Intercalated disc Syncitium
Membrane Potentials in SA Node and Ventricle
Action Potentials
Refractory period
Effect of Heart Rate on Duration of Contraction
Heart rate increase Duration systole & diastole decrease
Diastole > Systole in decrease
At normal heart rate (72/mnt): Period of systole = 0.4 of entire cycle At 3 times normal heart rate: Period of systole = 0.65 of entire cycle At a very fast heart beat doesnt remain relaxed long enough to allow complete filling.
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
Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each ventricle 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 between resting and maximal CO
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%)
Factors Influencing Cardiac Output
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
Intrinsic Factors Affecting SV
Contractility cardiac cell contractile force due to factors other than EDV Preload amount ventricles are stretched by contained blood - EDV Venous return - skeletal, respiratory pumping Afterload back pressure exerted by blood in the large arteries leaving the heart
Stroke volume
Strength of cardiac contraction
End-diastolic volume
Venous return
Frank-Starling Law
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Frank-Starling Law
Slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV
Extrinsic Factors Influencing SV
Contractility is the increase in contractile strength, 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
Contractility and Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cAMP secondmessenger system
Figure 18.22
Modulation of Cardiac Contractions
Figure 14-30
Factors that Affect Cardiac Output
Figure 14-31
Cardio-acceleratory center activates sympathetic neurons Cardio-inhibitory center controls parasympathetic neurons Receives input from higher centers, monitoring blood pressure and dissolved gas concentrations
Medulla Oblongata Centers Affect Autonomic Innervation
Reflex Control of Heart Rate
Figure 14-27
Modulation of Heart Rate by the Nervous System
Figure 14-16
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
Regulation of Cardiac Output
Figure 18.23
