BIOL- 2305
Cardiac Physiology
Anatomy Review
Functions of the Heart
Generating blood pressure
Routing blood
Heart separates pulmonary and systemic circulations
Ensuring one-way blood flow
Regulating blood supply
Changes in contraction rate and force match blood delivery to changing metabolic needs
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Blood Flow Through Blood Flow Through Heart
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Cardiac Cell Histology
Intercalated discs – allow branching of the myocardium
Desmosomes in intercalated discs transfer force
Gap Junctions in intercalated discs allow fast cell-to-cell signaling
Replace the roll of synapses
Allow APs to spread between cardiac cells by permitting the passage of ions between
cells that lead to depolarization
Many mitochondria – for ATP synthesis
Large T-tubes – allow APs to quickly reach the center of cardiac muscle fibers
Electrical Activity of Heart
Heart beats rhythmically as result of action potentials it generates by itself (autorhythmicity)
Two specialized types of cardiac muscle cells:
Contractile cells
99% of cardiac muscle cells
Perform mechanical work of
pumping
Normally do not initiate own action
potentials
Autorhythmic cells
Do not contract
Make up the electrical conduction
system of the heart
Specialized for initiating and
conducting action potentials
responsible for contraction of
working cells
Intrinsic Cardiac Conduction System
Made up of autorhythmic cells that initiate and distribute electrical impulses (action potentials)
throughout the heart
SA Node 70-80 bpm
Sets the pace of the heartbeat
Located within wall of rt. atrium, below superior vena cava
AV Node 40-60 bpm
Delays the transmission of action potentials
Located within wall of rt. atrium, above tricuspid valve
Purkinje fibers 20-30 bpm
Can act as pacemakers under some conditions
Located within walls of left & right ventricles
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Electrical Signal Flow - Conduction Pathway
Cardiac impulse originates at SA node, just inferior to
the entrance of the superior vena cava into the right
atrium
Action potential spreads throughout right and
left atria
Impulse passes from atria into ventricles through AV
node, just above the tricuspid valve in the lower part
of the right atrium
AV node is the only point of electrical contact
between chambers
AV node briefly delays action potential. This
ensures atrial contraction precedes ventricular
contraction to allow complete ventricular
filling.
Impulse travels rapidly down interventricular septum
by means of bundle of His
Impulse rapidly disperses throughout ventricular
myocardium by means of Purkinje fibers
Myocardial cells not immediately adjacent to
autorhythmic cells are activated by cell-to-cell spread
of impulse through gap junctions in intercalated discs
Electrical Conduction in Heart
Atria contract as single unit followed after brief delay by a synchronized ventricular contraction
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Intrinsic Conduction System
Autorhythmic cells:
Initiate action potentials
Have “drifting” resting potentials called pacemaker potentials
Pacemaker potential - membrane slowly depolarizes “drifts” to threshold, initiates action
potential, membrane repolarizes to -60 mV.
Use calcium influx (rather than sodium) for rising phase of the action potential
Pacemaker Potential of Autorhythmic Cells
K+ channels closed: Decreased efflux of K+
Constant influx of Na+: no voltage-gated Na+ channels
Drifting depolarization: K+ builds up and Na+ flows inward
Voltage-gated Ca2+ T-channels open at ~ -55mV: Small influx of Ca2+ further depolarizes to threshold
(-40 mV) via “Transient Channels”
Voltage-gated Ca2+ L-channels open at Threshold: sharp depolarization due to activation of Ca2+ L
channels allow large influx of Ca2+ via “Long Lasting Channels”
Peak at ~ +20 mV: Ca-L channels close, voltage-gated K channels open, repolarization due to normal
K+ efflux
K+ channels close: at -60mV
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AP of Contractile Cardiac cells
Contractile cells
Rapid depolarization
Rapid, partial early repolarization,
prolonged period of slow repolarization
which is plateau phase
Rapid final repolarization phase
Action potentials of cardiac contractile cells
exhibit prolonged positive phase (plateau)
accompanied by prolonged period of contraction
Ensures adequate ejection time
Plateau primarily due to activation of slow
L-type Ca2+ channels
Why A Longer AP In Cardiac Contractile Fibers?
At no time would we want summation and tetanus in our myocardium
Because long refractory period occurs in conjunction with prolonged plateau phase, summation and
tetanus of cardiac muscle are impossible
Plateau ensures alternate periods of contraction and relaxation which are essential for pumping blood
Refractory period
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Membrane Potentials in Autorhythmic and Contractile cells
Action Potentials
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Excitation-Contraction Coupling in Cardiac Contractile Cells
Action potential from Autorhythmic cells is passed to contractile cells,
propagating down T-tubules, causing a small influx of Ca2+ via Ca2+ Lchannels
Ca2+ entry through L-type channels in T tubules triggers larger release
of Ca2+ from sarcoplasmic reticulum
Ca2+ induced Ca2+ release leads to cross-bridge cycling and
contraction
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Electrocardiogram (ECG)
Record of overall spread of electrical activity through heart
Represents:
Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body
surface
Recording of overall spread of activity throughout heart during depolarization and repolarization
Not direct recording of actual electrical activity of heart
Not a recording of a single action potential in a single cell at a single point in time
Comparisons in voltage detected by electrodes at two different points on body surface, not the
actual potential
Does not record potential at all when ventricular muscle is either completely depolarized or
completely repolarized
Electrocardiogram (ECG)
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Electrocardiogram (ECG)
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ECG Information Gained
Non-invasive
Heart Rate
Signal conduction
Heart tissue
Conditions
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Intrinsic Cardiac Conduction System
Cardiac Cycle - Filling of Heart Chambers
Heart is two pumps that work together, right and left halves
Repetitive systole (contraction) and diastole (relaxation) of heart chambers
Blood moves through circulatory system from areas of higher to lower pressure
Contraction of heart ventricles produces the pressure
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Cardiac Cycle - Mechanical Events
Cardiac Cycle - Mechanical Events
2 Phases of Ventricular Systole:
Isovolumic Contraction Phase:
First phase of ventricular contraction
Ventricles begin to contract, pushing AV valves close, SL valves still closed, pressure in
ventricles rises
Pressure in ventricles is not enough to open semilunar valves
Therefore, All Valves Are Closed
Ventricular Ejection Phase:
Second (and last) phase of ventricular contraction
Pressure in ventricles rises and forces semilunar valves open. Blood is ejected into
arteries.
Ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves
open and blood is ejected.
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Wiggers Diagram
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Heart Sounds
First heart sound or “lubb”
AV valves close causing surrounding fluid turbulence
Second heart sound or “dupp”
Aortic and pulmonary semilunar valves at close causing surrounding fluid turbulence; lasts
longer
Left Ventricular Volume
EDV = ~135 mL The blood volume in the heart before ventricular ejection, about 135 mL, is called the
end diastolic volume
ESV = ~ 65 mL The blood volume remaining in the heart after ventricular ejection, about 65 mL, is
called the end systolic volume
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Cardiac Output (CO) and Reserve
Cardiac Output (CO) is the amount of blood pumped by each ventricle in one minute (usually referring
to the left ventricle)
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute (bpm)
SV is the amount of blood pumped out by the left ventricle with each beat; measured in milliliters
per beat
Cardiac reserve is the difference between resting CO and maximal CO
Maximal cardiac output – the maximum amount of blood that can be pumped by the heart per minute
Maximal cardiac output can be 4-5 times that of a individual’s resting cardiac output (may be
higher in athletes)
Cardiac Output = Heart Rate X Stroke Volume
Cardiac Output ≈ 5 liters/min (resting, on average)
HR beats/min x SV mL/beat = CO
70 beats/min x 70 mL/beat = 4900 mL/min
SV = EDV – ESV
Residual blood in left ventricle after systole = about 50%
Formulas to know:
CO = HR X SV
SV = EDV – ESV
Calculating Cardiac Reserve
Maximal cardiac output can be 4-5 times that of the resting cardiac output (in non-athletes)
If an non-athletic individual’s resting CO is 5000 mL/min (5 L/min), then multiplying their CO by
4 and 5 gives us the range that can expected for that individual’s maximal cardiac output:
20,000-25,000 mL/min (20-25 L/min) during intense exercise
Since the cardiac reserve is the difference between the resting and maximal COs, then the cardiac
reserve for this individual is 15,000-20,000 mL/min (15-20 L/min)
This means that this individual’s heart can pump 15-20 L/min more than that required under the
normal circumstances of daily life
If expressed in percentages, this individual’s heart can increase activity by 300-400% during
intense exercise, reaching a maximum CO that is 400-500% of their resting CO
Since maximal cardiac output is calculated by HR times SV, then this individual’s HR can be measured
and their approximate SV can then be calculated.
If during intense exercise, they measure their HR to be 195 bpm, then their SV would be
approximately 102-128 mL/beat.
A trained athlete’s heart pumps more blood per beat (a greater SV), and therefore needs to
pump less frequently, both at rest and during intense exercise. Therefore, their max HR would
be substantially lower than a sedentary person’s max HR.
Factors Affecting Cardiac Output
Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)
Heart rate
Autonomic innervation
Hormones - Epinephrine (E), norepinephrine(NE), and thyroid hormone (T3)
Cardiac reflexes
Stroke volume
Starlings law
Venous return
Cardiac reflexes
Factors Influencing Cardiac Output
Intrinsic: results from normal functional characteristics of heart - contractility, HR, preload stretch
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Extrinsic: involves neural and hormonal control – Autonomic Nervous system
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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
Intrinsic Factors Affecting SV
Stroke Volume Factors:
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
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
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Extrinsic Factors Influencing SV
Contractility is the increase in contractile strength (force of contraction), 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 second-messenger system
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Modulation of Cardiac Contractions
Factors that Affect Cardiac Output
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Medulla Oblongata Centers Affect Autonomic Innervation
Cardio-acceleratory center activates sympathetic neurons
Cardio-inhibitory center controls parasympathetic neurons
Receives input from higher centers, monitoring blood pressure (baroreceptors) and dissolved gas
concentrations (chemoreceptors)
Reflex Control of Heart Rate
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Establishing Normal Heart Rate
SA node establishes baseline
Modified by ANS
Sympathetic stimulation
Supplied by cardiac plexus, stemming from the sympathetic trunk
Epinephrine and norepinephrine released
Positive chronotropic (HR) and inotropic (force) effect
Parasympathetic stimulation - Dominates
Supplied by cardiac plexus, stemming from vagus nerve
Acetylcholine secreted
Negative chronotropic (HR) and inotropic (force) effect
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Regulation of Cardiac Output
Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)
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