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 Cardiac Physiology

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 and Pump Action of the Heart

Blood Flow Through Heart

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Cardiac Muscle Cells
• Myocardial Autorhythmic Cells
• Membrane potential “never rests” pacemaker potential.
• Myocardial Contractile Cells
• Have a different looking action potential due to calcium channels.
• Cardiac cell histology
• Intercalated discs allow branching of the myocardium
• Gap Junctions (instead of synapses) fast Cell to cell signals
• Many mitochondria
• Large T tubes

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
• Do mechanical work of pumping
• Normally do not initiate own action potentials
• Autorhythmic cells
• Do not contract
• Specialized for initiating and conducting action potentials responsible for contraction of
working cells

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Intrinsic Cardiac Conduction System
• SA Node 70-80 bpm
• Sets the pace of the heartbeat
• AV Node 40-60 bpm
• Delays the transmission of action potentials
• Purkinje fibers 20-30 bpm
• Can act as pacemakers under some conditions

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

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Pacemaker Potential
• 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

AP of Contractile Cardiac cells

• Contractile cells
• Rapid depolarization
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 • 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

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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+ L-
channels
• 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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Electrical Signal Flow - Conduction Pathway
• Cardiac impulse originates at SA node
• Action potential spreads throughout right and left
atria
• Impulse passes from atria into ventricles through
AV node (only point of electrical contact between
chambers)
• Action potential briefly delayed at AV node
(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 myocardium
by means of Purkinje fibers
• Rest of ventricular cells activated by cell-to-cell
spread of impulse through gap junctions

Electrical Conduction in Heart

• Atria contract as single unit followed after brief delay by a synchronized ventricular 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)

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 half
• Repetitive contraction (systole) and relaxation (diastole) 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 and surrounding fluid vibrations at systole
• Second heart sound or “dupp”
• Results from closure of aortic and pulmonary semilunar valves at diastole, 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
• 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

• 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
• HR Rate: beats per minute
• Stroke Volume: ml per beat
• SV = EDV – ESVs
• Residual (about 50%)
Formulas:
CO = HR X SV
SV = EDV – ESV

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
• 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

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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 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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