University of Baghdad
College of Nursing
Department of Basic Medical Sciences
Overview of
Anatomy and Physioloy –II
Second Year Students
Asaad Ismail Ahmad , Ph.D.
Electrolyte and Mineral Physiology
asaad50.2011@gmail.com
2012 - 2013
ANATOMY AND PHYSIOLOGY - II
Brief Contents
1- Cardiovascular System
2- Blood
3- Lymphatic System
4- Urinary System
5- Male Reproductive System
6- Female Reproductive System
7- Sensory Function
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
Text book
Martini FH. Fundamentals of Anatomy and
Physiology, 5th ed. Prentice Hall, New Jersey,
2001.
References:
1.Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical
Physiology, 23rd ed. McGraw Hill, Boston, 2010.
2.Drake RL, Vogl W, Mitchell AWM. Gray's Anatomy for Students. Elsevier,
Philadelphia, 2005.
3.Goldberger ,E. 1975.A Primer of Water Electrolyte and Acid-Base Syndromes. 5th ed.,
Lea and Febiger ,Philadelphia.
4. Martini, FH and Welch K. Applications Manual Fundamentals of Anatomy and
Physiology,4th ed., Prentice Hall, NewJersey, 1998.
5.Maxwell, MH and Kleeman CR. 1980.Clinical Disorders of Fluid and
Electrolyte Metabolism. McGraw-Hill Book Company, New York.
6.McKinley M, and O'Loughlin VD. Human Anatomy, McGraw Hill, Boston,
2006.
7.Nutrition Foundation.1984.Present Knowledge in Nutrition. 5th ed.,
Nutrition Foundation, Inc , Washington, D.C.
8.Vander A, Sherman J, Luciano D., Human Physiology, 7th ed., McGraw Hill,
Boston, 1998.
Contents:
CARDIOVASCULAR
SYSTEM
I- ANATOMY OF THE HEART
II- ANATOMY OF BLOOD VESSELS
III- PHYSIOLOGY OF THE HEART
IV- PHYSIOLOGY BLOOD VESSELS
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
THIRD LECTURE
Physiology of the Heart
1. Functional Properties of CardiacMuscle
2. Action Potential and Conducting System
3. Cardiac Cycle
4. Electrocardiogram
5. Arrhythmia
6. Cardiodynemic
Asaad Ismail Ahmad, Ph.D in Electrolyte and Mineral Physiology
College of Nursing – University of Baghdad / 2012 – 2013
asaad50.2011@gmail.com
PHYSIOLOGY OF HEART AND BLOOD VESSELS
Maintaining Blood Flow
( Tissue Perfusion )
Contents:
1- Functional Properties of
CardiacMuscle
FUNCTIONAL PROPERTIES OF
CARDIAC MUSCLE
IIIIIIIV-
EXCITABILITY
CONDUCTIVITY
RHYTHMICITY
CONTRACTILITY
I- EXCITABILITY
I- EXCITABILITY
Response of the tissue to stimuli,
are created and conducted by
development action potential
( example of excitable cells are
nerve cell and muscle cell)
Action Potential of
Cardiac Muscle
Voltmeter for Measuring Potentials
STEPS OF ACTION POTENTIAL IN CARDIAC
MUSCLE FIBER 668-669
1- DEPOLARIZATION (Na+ entry)
2- PLATEAU (Ca++ entry)
3- REPOLARIZATION (K+ loss)
ACTION POTENTIAL OF CARDIAC MUSCLE 669
Action Potential of Nerve Cell (Neuron)
II- CONDUCTIVITY
II- CONDUCTIVITY
670-671
Ability of cardiac muscle to transmit
electrical signal (impulse) produce by
SA node to all cardiac muscle cell by
special conducting system
CONDUCTING SYSTEM 670
A network of specialized cardiac muscle
cells that initiates and distributes
electrical impulses
STRUCTURES OF
CONDUCTING SYSTEM 670
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SA node
Internodal fiber
AV node
AV bundle
Bundle branches
Purkinje fiber
RESTING MEMBRANE POTENTIAL
1- Cardiac muscle fiber = - 90 mV
2- SA node
= - 60 mV
3- Perkinje fiber
= - 95 mV
Threshold membrane potential
Membrane potential at which an action
potential (electrical signal) begins
CONDUCTION PATHWAY
Sinus nodal action potential is compared with
that of a ventricular muscle fiber 670
III- RHYTHMICITY
III- RHYTHMICITY
Ability of the tissue to produce its own
impulses regularly, also called
autorhythmicity or self excitation
RHYTHMICITY OF DIFFERENT PART OF
THE HEART
SA node
75 / minute
AV node
50 / minute
Atrial muscle
50 / minute
Ventricular muscle 30 / minute
PACEMAKER
Cardiac pacemaker
is part of the heart which impulses for the
heart beat are produced normally.
SA node is the cardiac pacemaker where the
electrical activity start first.
AUTONOMIC INNERVATION OF SA node
(PACEMAKER) 684
1- Parasympathetic stimulation releases
Acetylcholine which extends repolarization and
decrease the rate of spontaneous
depolarization. (Slow the heart rate )
2- Sympathetic stimulation release
norepinephrine which shortens repolarization
And increased the rate of spontaneous
depolarization, as a result,
(Increase heart rate )
AUTONOMIC INERVATION OF THE HEART 684
CONTROL of PACEMAKER FUNCTION
685
IMPLANTED PACEMAKERS
When there is marked bradycardia
in patients implanted pacemaker
are useful in patients with sinus
node dysfunction, AV block and
third-degree heart block.
ARTIFICIAL PACEMAKER
An electronic cardiac pacemaker that
generates an extrinsic electrical impulse,
which cause the heart muscle to depolarize
and then contract.
Its rate is preset regardless of the heart
intrinsic activity, it can be either temporary
(transcutaneous, transvenous, or epicardial)
or implantated
IV- CONTRACTILITY
Ability of the tissue to contract after
receiving a stimulus (action potential).
REFRECTORY PERIOD 669
Period in which the muscle does not show
any response to stimulus. There are two
types of refractory period:
a- Absolute refractory period
b- Relative refractory period
PHYSIOLOGICAL HEART PARAMETERS
Normal Range
Heart rate (pulse):
60–80 bpm
Stroke volume:
60–80 mL/beat
Description
Generated by the SA node, propagated through
the conduction pathway; parasympathetic
impulses (vagus nerves) decrease the rate;
sympathetic impulses increase the rate
The amount of blood pumped by a ventricle in one beat
Cardiac output:
5–6 L/min
The volume of blood pumped by a ventricle in
one minute = stroke volume x pulse
Ejection fraction:
60%–70%
The percentage of blood within a ventricle that is pumped out
per one beat
Cardiac reserve:
15 liters or more
The difference between resting cardiac out put
and maximum cardiac output during exercise
ECG
ELECTROCARDIOGRAM , Recorded or graphical registration of
electrical activities of the heart
Echo
HEART RATE (PULSE) 668
Number of heart contraction per minute.
Both sympathetic and parasympathetic
From cardiac plexus innervate SA node
And AV nodes, atrial and ventricular
muscle cells.
CHRONOTROPIC ACTION: Effect on heart rate
either a- Tachycardia (+ chro.trop)
b- Bradycardia (- chro.trop)
CONTROL
HEART
RATE
FACTRS AFFECTING HEART RATE 683
I- AUTONOMIC INNERVATION
1- Sympathetic release NE bind to beta-1 receptor,
lead to opening Ca++ influx, Ca++ influx increase
rate of depolarization and shortens period of
repolarization. SA node reach the threshold more
quickly, this result in increase heart rate.
2- Parasympathetic release Ach lead to opening
K+ efflex channels which prolonge repolarization
and slow spontaneous depolarization, and thise
result in decrease heart rate.
II- HORMONES
1- Epinephrine
2- Norepinephrine
3- Thyroxine
CARDIAC CYCLE 674
One complete heartbeat, include atrial
and ventriculars systole and diastole
lasting for 0.8 second (800 msec).
SYSTOLE: period of cardiac contraction
lasting for 0.3 second (300 msec).
DIASTOLE: period of cardiac relaxation
lasting for 0.5 second (500 msec).
HEART SOUND 677
Sound produce during mechanical
activity of each cardiac cycle (systole
and diastole). These are:
LUBB: The first sound due to sudden
closure of atrioventricular valves
DUPP: The second sound due to sudden closure
of semilunar valves in aorta and pulmonary
artery
CARDIAC MURMUR
ABNORMAL HEART SOUND
1- Systolic murmur
2- Diastolic murmur
3- Continuous murmur
Contents:
4. Electrocardiogram
(ECG)
ELECTROCARDIOGRAM
“ ECG “ 673
Recorded or graphical registration of
electrical activities of the heart (the sum
of extracellular electrical activity of all
cardiac muscle cells
ELECTROCARDIOGRAPH
Machine used in ECG
ELECTROCARDIOGRAM 673
LEADS IN ECG “electrocardiogram”
Lead is a pair of electrodes used in recording
changes in electric potential ( action potential)
of the heart (electrocardiography) or the brain
(electroencephalography).
TYPES OF LEAD
1- Lead I (between two arms)
2- Lead II (btween right arm and left leg)
3- Lead III (between left arm and left leg)
4- Leads V 1-6 (over the heart)
5- Others
Normal Electrocardiogram (ECG)
WAVES, SEGMENT AND INTERVAL OF
NORMAL “ECG”
P
wave :
QRS complex :
T
wave :
P-R interval :
QRS duration:
QT interval :
S-T interval :
Atrial depolarization
Ventricular depolarization
Ventricular repolarization
Atr.depo. = 0.18 second
Ven.depo. = 0.1 second
Ven,Elec.Act.=0.4 second
Ven.Repo. =0.08 second
Basic ECG Assessment
Follow these steps for basic electrocardiogram
interpretation.
1. Determine ventricular rate.
2. Determine QRS duration and shape.
3. Identify P waves and determine if a P wave precedes every
QRS complex.
4. If more than 1 P wave precedes a QRS complex, determine
the ratio of P waves to QRS complex (ex., 4:1, 3:1, 2:1).
5. Is P wave shape consistent?
6. Determine atrial rate and rhythm.
7. Determine P-R intervals and if they are consistent.
Contents:
5. Arrhythmia
CARDIAC ARRHYTHMIA
Abnormal or irregular heartbeat
CAUSES OF CARDIAC ARRHYTHMIA
1- Electrolyte imbalance
2- Hypoxia
3- Trauma
4- Inflammation
5- Drugs
TYPES OF ARRHYTHMIA
I- NORMOTROPIC ARRHYTHMIA
Abnormality in SA node (the normal
cardiac pacemaker)
1- Sinus tachycardia
2- Sinus brady cardia
3- Sinus arrhythmia
Continue: TYPES OF ARRHYTHMIA
II- ECTOPIC ARRHYTHMIA
(ECTOPIC BEATS)
In this abnormalities, the cardiac
pacemaker is any cardiac tissue other
than SA node.
1- Extrasystole
2- Paroxysmal tachycardia
3- Heart block
4- Atrial fibrillation
5- Atrial flutter
6- Ventricular fibrillation
ECTOPIC FOCI OF EXCITATION
(ECTOPIC BEATS)
Normally myocardial cells, his bundle and purkinje system
are low spontaneously discharge, becaus the normal
pacemaker discharge of SA node is more rapid than their
rate of spontaneous discharge. In excited ectopic focus, the
abnormal dischrge of cardiac muscle cells and purkinje
system occur before the expected next normal beat and
transiently interrupts the cardiac rhythm (atrial nodal or
ventricular extrasystole or premature beat). If the focus
discharges are higher rate than SA node produce ( atrial,
ventricular, or nodal paroxysmal tachycardia or atrial flutter)
Application of electrical current to the chest
to stop ventricular fibrillation
CARDIODYNAMICS
STROKE VOLUME
CARDIAC OUTPUT
CARDIAC RESERVE
( productivity of the heart)
CARDIODYNAMICS 680
Movements and forces generated during cardiac
contraction.
End-diastolic volume (EDV): volume of blood
in each ventricle at the end of ventricular diastol
End-systolic volume (ESV): volume of blood
remaining in each ventricle at the end of ventricular systole
Stroke volume (SV): volume of blood pumped
of each ventricle during single beat,
expressed as: SV = EDV - ESV
Note: stroke volume is the most important factor
in an examination of a single cardiac cycle
CARDIAC OUTPUT
Blood volume pumped by each ventricle in
one minute
(ventricular efficiency).
CO = SV X HR
CARDIAC STROKE
HEART
OUTPUT VOLUME
RATE
ml / min. ml / beat
beats / min.
FACTORS AFFECTING CARDIAC
OUTPUT 681
FACTORS AFFECTING CARDIAC OUTPUT
686
FACTORS AFFECTING CARDIAC OUTPUT 681
1234-
Autonomic innervation
Heart
Hormones
Rate
End-diastolic volume (EDV) Stroke
End –systolic volume (ESV)
Volume
CONDITION INCREASE
CARDIAC OUTPUT
1- Fever ( oxidative process )
2- Anemia ( hypoxia )
3- Hypothyroidism ( BMR )
CONDITION DECREASED
CARDIAC OUTPUT
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Hypothyroidism
Atrial fibrilation
Coronary stenosis
Myocardial infarction (MI)
Congestive heart failure
Incomplete heart block
Shock
Hemorrhage
ABNORMAL ELECROLYTE DISORDERS
AFFECTING CARDIAC OUTPUT 686
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Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Abnormal body temperature
FACTORS AFFECTING STROKE VOLUME “EDV
and ESV” 681
Factors affecting EDV
1- Filling time
2- Venous return
Factors affecting ESV
1- Preload
2- Contractility of ventricle
3- After load
FACTORS INFLUENCE “ESV” 681
Definitions:
Preload: degree of stretching experience
during ventricular diastole
Contractility ( inotropic ): amount of force
produced during a contraction at a given
preload
Afterload: amount of tension (force) the
contracting ventricle must produce to force
open the semilunar valve and eject blood
CARDIAC RESERVE
The difference between resting and
Maximal cardiac outputs during heavy
exercise (increase SV and HR). Heavy
exercise can raise CO by 300 – 500 %
to 18 – 30 liters / minute. Trained athlets
with maximum exercise increase CO
by 700 % to 40 liters / minute.
FACTORS AFFECTING FORCE OF
CONTRACTILITY (INOTROPIC)
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Autonomic innervation
Hormones
Drugs
Change in ion concentration
in ECF
TYPES OF IONTROPICS
Positive inotroic
1- Sympathetic stimulation
2- Epinephrine and norepinephrine
3- Thyroid hormones
4- Glucagon
5- Agents stimulate influx of Ca++
into cardiac muscle cells
CONTINUE:
TYPES OF INOTROPIC
Negative inotropic
1- Parasympathetic (Ach)
2- Agents block Ca++ channels
( e.g. verapamil – antiarhythmia )
3- Drugs block alpha and beta
receptors ( drugs used for treat
hypertension e.g. propranolol,
atenolol, timolol,metoprolol …