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02 B215 Heart

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Daniel Howell

on 9 November 2018

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Transcript of 02 B215 Heart

Factors Affecting Cardiac Output
Heart Sounds
Timing of the Cardiac Cycle
The resting membrane potential of cardiac myocytes (contractile cells) =
-90mV

Cardiac action potentials proceed in 3 steps:
Rapid membrane depolarization
Prolonged depolarization unique to cardiac muscle, called the
plateau phase
Slow repolarization

A refractory period follows depolarization
Absolute refractory
period during plateau phase
Relative refractory
period during repolarization
Cardiac Resting & Action Potentials
Coronary Circulation
Valves of the Heart
The Pericardium
Next time… Peripheral Blood Vessels
The Heart Is Part of the Cardiovascular System
The goal of the cardiovascular system is to maintain adequate blood flow to all body tissues

Blood transports nutrients & wastes

The heart is a pump that moves the blood

Blood is pumped through peripheral blood vessels
Sympathetic stimulation
increases
heart rate

Parasympathetic stimulation
decreases
heart rate

Circulating hormones, specifically E, NE, and T3,
increase
heart rate

Increased venous return
increases
heart rate

EDV
is determined by available filling time and rate of venous return

ESV
is determined by preload, degree of contractility, and afterload
Summary: Regulation of Heart Rate and Stroke Volume
Factors Affecting Stroke Volume
Recall the E and NE function in close association with sympathetic ANS (sympathetic nerves stimulate adrenal medulla)
Hormones
Epinephrine (E), norepinephrine (NE) and thyroid hormone (T3) affect heart rate
All affect the SA node
All increase cardiac output by increasing speed of contraction
Hormonal Factors Affecting Heart Rate
Hormonal Factors Affecting Heart Rate
Increased venous return increases atrial pressures

Stretched atrial cells send afferent signals through the vagus nerve to the medulla oblongata

Efferent signals from medulla return via vagus and sympathetic nerves to increase heart rate and strength of contraction
Result ->
arterial output increased to match venous input
Cardiac output may be increased by up to 60% by the atrial reflex
The Atrial Reflex
Cardioacceleratory
center activates sympathetic neurons

Cardioinhibitory
center controls parasympathetic neurons

Both receive input from higher centers (hypothalamus) monitoring blood pressure and dissolved gas concentrations

Parasympathetic
mediated via cranial nerves (CN X)

Sympathetic
mediated via spinal nerves (sympathetic chain ganglia)
Medulla Oblongata Innervates the Heart
Nervous Factors Affecting Heart Rate
Autonomic Innervation of the Heart
SV = EDV – ESV
= 130mL – 50mL
= 80mL
A Simple Model of Stroke Volume
Atrial Systole: Pressure & Volume Changes
Rising atrial pressures push blood into the ventricles
The
end-diastolic volume (EDV)
is the volume of blood in the ventricles at the end of ventricular diastole just before ventricular contraction (~130 mL)
Other Irregular Heartbeats
All LQT genes encode subunits of ion channels expressed in cardiac tissue
Genes Associated with LQTS
The Electrocardiogram (ECG, or EKG)
A recording of the electrical events occurring during the cardiac cycle

Probes distributed along the body detect electrical currents from the heart
Arteries
right & left coronary arteries (RCA & LCA)
marginal arteries
anterior and posterior interventricular arteries
circumflex artery

Veins
great cardiac vein
anterior & posterior cardiac veins
middle cardiac vein
small cardiac vein
Coronary veins empty into the right atrium via the coronary sinus
Blood Supply to the Heart:
Coronary Circuit
Valves of the Heart
Valves of the Heart
Keep the blood flowing in ONE direction !
Heart Chambers and Valves
Structural Differences in heart chambers:
The left side of the heart is more muscular than the right side
Why?

Functions of valves
AV valves prevent backflow of blood from the ventricles to the atria
Semilunar valves prevent backflow into the ventricles from the pulmonary trunk and aorta
The Sectional Anatomy of the Heart
The Sectional Anatomy of the Heart
Internal Anatomy and Organization
Atria
Thin walled chambers that receive blood from the
venae cavae
(right) or
pulmonary veins
(left)

Ventricles
Thick walled chambers separated from the atria by
AV valves
(atrioventricular)

Chordae tendineae (
"heart strings"
)
Tendinous fibers attached to the AV valves

Papillary muscle and trabeculae carneae
Muscular projections on the inner wall of ventricles
Superficial Anatomy of the Heart
The Pericardium & Heart Wall
Body Cavities Review
Body Cavities Review
Summary of Factors Affecting Cardiac Output
Factors Affecting Stroke Volume
SA node establishes baseline heart rate

SA node activity modified by ANS (autonomic nervous system)

ACh
released by parasympathetic stimulation opens
K+
channels, slows spontaneous depolarization -> slows heart rate

NE
released by sympathetic stimulation opens
Ca++
channels, speeds up depolarization -> faster heart rate
Stroke Volume and Cardiac Output
Cardiac output = the amount of blood pumped by each
ventricle
in one minute

Cardiac output = heart rate x stroke volume
Ventricular Systole: Pressure & Volume Changes
Isovolumetric contraction
of the ventricles: ventricles are contracting but there is no blood flow

Ventricular ejection:
ventricular pressure increases beyond arterial pressure on semilunar valves, forcing blood through the valves and into arteries
The Cardiac Cycle
Cardiac Cycle = The period between the start of one heartbeat and the beginning of the next

During a cardiac cycle
Each heart chamber goes through
systole
(contraction) and
diastole
(relaxation)
Proper timing of chamber contractions is critical to efficiently propel blood
Correct pressure relationships are dependent on careful timing of contractions
Used by cardiologist to diagnose heart conditions

Abnormal wave intervals are indicative of specific conditions

For example, long QT syndrome
The Electrocardiogram (ECG)
(Atrial repolarization is masked by QRS complex)
The Electrocardiogram (ECG)
A plot of volt vs time is called a
trace
The
P wave
accompanies the depolarization of the
atria
The
QRS complex
reflects depolarize of
ventricles
The T wave indicates ventricular repolarization

Physically
&
electrically
isolates heart chambers
The Fibrous Skeleton of the Heart
Steps for impulse conduction through the heart:
Impulse Conduction through the Heart
SA node begins the action potential
Automaticity
Stimulus spreads to the AV node
Impulse is delayed at the AV node
Impulse then travels through ventricular conducting cells
Impulse distributed to ventricles by Purkinje fibers
Sinoatrial (SA) node
Atrioventricular (AV) node

Conducting cells
Atrial conducting cells found in internodal pathways
Ventricular conducting cells in AV bundle, bundle branches & Purkinje fibers
The Conducting System of the Heart
Two classes of cardiac muscle cells:
Cardiac Physiology
Specialized muscle cells of the
conducting system
control & coordinate heartbeat

Contractile cells
produce forceful contractions to propel blood
99% of cardiac cells
Valves of the Heart
Tricupsid --> 3 cusps

Bicuspid --> 2 cusps

Semilunars --> 3 cups
Valves of the Heart
Differences Between The Left & Right Ventricles
Blood Flow Through The Heart
Blood Flow Through The Heart
Vena cava
Right atrium
Tricuspid valve
Right ventricle
Pulmonary valve
Pulmonary artery
Pulmonary circuit
(lungs)
Pulmonary vein
Left atrium
Bicuspid valve
Left ventricle
Aortic valve
Aorta
Systemic circuit
Functional Syncytium
Cardiac Myocytes
Superficial Anatomy of the Heart
The Pericardium
Visceral pericardium (or epicardium)
Parietal pericardium
Percardial cavity filled with pericardial fluid (10-20 mL)
The Location of the Heart
The heart is located in the
mediastinum
(middle portion) of thoracic cavity within the
pericardial cavity

The heart is flanked
anteriorly by the
sternum
posteriorly by the
esophagus
laterally by the
lungs
inferiorly by the
diaphragm
The Location of the Heart
Divisions of the Cardiovascular System
Increases in cardiac output limited by filling time; at rates >180 bpm the heart cannot be filled between contractions.
Exercise and Cardiac Output
Heavy exercise can increase output by 300-500 % (18–30 L/min)
Trained athletes may increase cardiac output by 700% (40 L/min)!

Cardiac reserve = The difference between resting and maximal cardiac output
Factors Affecting Stroke Volume
EDV
Frank-Starling principle (“
more in, more out
”)
increased ventricular stretching = increase contractile force

ESV
Preload - degree of ventricular
stretching
Contractility - the force produced by contraction
Afterload - the amount of arterial
resistance
Additional Ca2+ ions are released from reserves in the sarcoplasmic reticulum
Repolarization achieved by the efflux of K+ ions
Recall: Ions & Cardiac Contraction
Depolarization is achieved by an influx of Na+ ions
Plateau phase is maintained by influx of Ca2+ ions
Ca2+ enters the cell membranes during the plateau phase
CO = 75 bpm x 80 mL/beat = 6000 mL/min = 6 L/min
normal heart sound
mitral regurgitation (systolic murmur)
acute rheumatic fever
http://www.bioscience.org/atlases/heart/
Heart Sounds
Auscultation – listening to body sounds
Heart sounds heard using a
stethoscope

Heart sounds are generated by the valves
S1 – “lubb” caused by the closing of the
AV valves
S2 – “dupp” caused by the closing of the
semilunar valves
In the past 10 minutes, your heart went through this cycle
~700
times!
Pressure & Volume Relationships in the Cardiac Cycle
Early ventricular diastole: A period of isovolumetric relaxation when all heart valves are
closed

Late ventricular diastole: Rising atrial pressures force the AV valves open, ventricles fill passively
Ventricular Diastole: Pressure / Volume Changes
Ca2+ enters the cell membranes during the plateau phase

Additional Ca2+ ions are released from reserves in the sarcoplasmic reticulum

Repolarization achieved by the efflux of
K+ ions
Ions & Cardiac Contraction
Depolarization is achieved by an influx of
Na+ ions
Plateau phase is maintained by influx of
Ca2+ ions
Characterized by longer-than-normal QT interval
QT interval measures time for depolarization & repolarization of ventricles to occur (normally ~440 ms)






Mutant ion channels result in excessive influx of cations into myocardial cells during depolarization
Myocytes take longer to “reset” for next depolarization
Leads to arrhythmia, sudden loss of consciousness, cardiac arrest
Long QT Syndrome (LQTS)
SA = 90 bpm (pacemaker)
AV = 50 bpm (max = 230 bpm)
Nodal cells cannot maintain a stable resting potential
“leak” channels leak ions into the muscle cells
Depolarization occurs once enough ions have leaked into the cell to reach threshold
The Conducting System Automaticity
Major blood vessels of the heart
Inferior and superior vena cavae
Aorta
Pulmonary arteries
Pulmonary veins
Organization of the Heart
The heart consists of
four
chambers
Two
atria and
two
ventricles
An Overview of the Cardiovascular System
Phases of the Cardiac Cycle
Due to slow contraction & plateauing action potential, cardiac myocytes cannot enter
tetanus
Skeletal vs Cardiac Muscle
Connective tissue fibers of the heart
Provide physical support and elasticity
Distribute the force of contraction
Prevent overexpansion
Connective Tissues of the Heart
The Fibrous Skeleton
Stabilizes the heart valves
Physically
isolates atrial from ventricular cells
Electrically
isolates atrial from ventricular cells
Epicardium
Myocardium
Endocardium
The Heart Wall
Components of the heart wall include
All valves closed
All valves closed
The Heart
The Heartbeat
Organization of the Cardiovascular System
Cardiodynamics
The heart & Cardiovascular System
http://www.heartcenteronline.com/myheartdr/common/articles.cfm?ARTID=225

http://www.bioscience.org/atlases/heart/
Extras
Daniel Howell, PhD
Liberty University

Upside-down pyramid
base at top (superior)
apex at bottom (inferior)
Recall Skeletal Muscle Contraction / Nerve Impulse
Pulmonary circuit
blood to and from the
lungs
Systemic circuit
blood to and from the
rest of the body
Vessels carry the blood through the circuits
Arteries
(efferent vessels) carry blood away from the heart
Veins
(afferent vessels) carry blood to the heart
Capillaries
permit exchange & connect arteries to veins
Cardiodynamics
BIOL 215
Made possible by the fibrous skeleton
Resting potential maintained by Na-K ATPase

Slight depolarization by graded potentiials or (in the heart) leak channels

Rapid depolarization at threshold

Rapid repolarization

Hyperpolarization and re-establish resting potential
CO = HR x SV
Full transcript