CHAPTER 9 | CARDIAC PHYSIOLOGY

HEART • What causes AP in cardiac ms?

 Functions to pump blood towards the different parts • Fast opening of Na channels
of the body. • Slow closing of Ca channels → Ca-Na Channels
• Permeability of cardiac muscle membrane for K
RECAP ON CARDIAC MUSCLE ions decreases
 Involuntary about fivefold
 Striated
 Consists of the atrial, ventricular, and conductive ATRIUM
fibers  Primer pumps for the ventricles
 Action potential includes a plateau due to the Ca  When the atrial fail to function, the difference is
channels unlikely to be noticed unless a person exercise
 Calcium is released from both SR and T-tubules
VENTRICLES
FLOW OF BLOOD IN THE HEART  Main heart pumps
 Upper extremity--> superior vena cava--> right  Fill with blood during diastole
atrium
 Lower extremity--> inferior vena cava--> right atrium ANTRIOVENTICULAR SEMILUNAR VALVES
 Right atrium--> right ventricle--> pulmonary artery-- VALVES
> lungs--> pulmonary vein--> left atrium--> left  Tricuspid and bicuspid  Aortic and
ventricle--> aorta (mitral valves pulmonary valves
 Prevent backflow of  Prevent backflow of
blood to the atria blood to the
 Thin and filmy ventricles
 Papillary muscle: pull  Snap closed due to
the valves during high pressures and
systole has smaller
 Chordae tendineae: openings
attaches papillary  Constructed with a
muscle to valves strong and pliable
 Related to the 1st fibrous tissue
heart sound (S1)  Related to the 2nd
heart sound (S2)
CARDIAC MUSCLE AS SYNCYTIUM
 Intercalated disc- cell membranes that separates  AV- in between left and right atrium
individual cardiac muscle cells from one another.
 Heart is composed of 2 syncytiums: CARDIAC CYCLE
 Atrial- constitutes walls of 2 atrium. ▪ Events that occur from the beginning of the
 Ventricular- constitutes walls of 2 ventricles heartbeat the beginning of the next
▪ Diastole: period of relaxation
▪ Systole: period of contraction
▪ Duration: reciprocal of the heart rate (HR)
▪ (Increased HR = decreased Cardiac Cycle)

▪ Phase I (Period of filling)

ACTION POTENTIAL IN CARDIAC MUSCLE
• AP in ventricular ms fiber : 105 mV
• Intracellular potential rises from a very negative
value - -85 mV
• Increases +20 mV during each beat
• After initial spike, membrane depolarizes for about 0.2
sec
→ this causes the plateau → this eventually cause
prolonged ventricular contraction (15x longer than
skeletal ms)
• blood flow into the ventricles
➢ Rapid filling: due to AV valve opening. 1st
third of diastole
➢ Slow filling: middle third diastolic relaxation
➢ Atrial kick/systole: 20% of the filling cycle
➢ AV valves open, SL valves close
▪ Phase II (Isovolumic/metric contraction)
• contraction occurring in the ventricles, but no
emptying occurs
➢ Both valves closed

▪ Phase III (Period of ejection): when the pressure rises
high enough, it pushes the SL valves and the blood
pours out
➢ Rapid ejection: 70% of blood pours out. 1st third
➢ Slow ejection: Remaining 30% pours out.
Last 2/3
➢ AV valves close, SL valves open
▪ Phase IV (Isovolumic/metric relaxation)
• ventricular relaxation while the ventricular
volume does not change
➢ Rapid ejection: 70% of blood pours out. 1st
third
➢ Slow ejection: Remaining 30% pours out.
Last ⅔
➢ Both valves closed
HEMODYNAMICS
 Systolic blood pressure (SBP): highest arterial
pressure (90-120 mmHg)
 Diastolic blood pressure (DBP): lowest arterial
pressure (60-80 mmHg)
 Pulse pressure (PP): difference between Systolic BP
& Diastolic BP (40mmHg)
 (SBP-DBP)
 Mean Arterial Pressure: Arterial pressure with
respect to time (93mmHg)
 (DBP + 1/3 PP)
 End diastolic volume (EDV): Amount of blood left in
the ventricles after diastole (120 mL)
 End systolic volume (ESV): Amount of blood left
after systole (50mL)
 Stroke volume (SV): Amount of blood pumped by
the ventricles per contraction (70 mL)
 SV = EDV - ESV
 Ejection fraction: fraction of the end-diastolic
volume that is ejected (60%)
 (SV/EDV) *100
 Heart rate: Amount of beats per minute by the heart
(60-100 bpm)
 Cardiac output: Amount of blood pumped by the
ventricles per minute (Avg. 4-6 L)
 CO = SV x HR
CHAPTER 9 | CARDIAC PHYSIOLOGY
 Preload: degree of tension on the muscle when it
begins to contract
 Afterload: also called Vascular resistance; the
pressure that the heart must overcome to eject
blood during contraction. Load against which the
muscle exerts its contractile force.
 Cardiac Index: Cardiac output per square
meter of body surface area (2.5-4)
 CO/BSA
 Pulse deficit: Apical pulse - radial pulse
REGULATION OF HEART PIMPING
▪ FRANK-STARLING MECHANISM
➢ The greater the heart muscle is stretched
during filling, the greater is the force of
contraction and the greater the quantity of
blood pumped into the aorta
▪ AUTONOMIC CONTROL
➢ Sympathetic nervous control: (increases
the heart rate and force of heart
contraction)
➢ Parasympathetic (vagal) stimulation:
(can stop the heartbeat for a few seconds)
▪ EFFECT OF IONS
➢ Potassium: causes the heart to become
dilated and flaccid and also slows the heart
rate. (Can also block conduction of the
cardiac impulse from the atria to the
ventricles)
• Partially depolarizes the
cell
membrane, causing the membrane
potential to be less negative
 Calcium: causes the heart to move
toward spastic contraction. (Caused by a
direct effect of calcium ions to initiate the
cardiac contractile process)
▪ EFFECT OF TEMPERATURE
➢ Increased body temperature greatly
increases the heart rate and temporarily
enhances contractile strength of the heart
➢ (Results from increased permeability of the
cardiac muscle membrane to ions that
control heart rate)
➢ Dilation of blood vessels, faster movement
of blood
CARDIAC CONDUCTION
HEMODYNAMICS
▪ The human heart has a special system for
rhythmic self-excitation and repetitive
contraction approximately 100,000 times each

day, or 3 billion times in the average human
lifetime.
SINUS (SINOATRIAL) NODE: MAIN
PACEMAKER OF THE HEART
▪ A small, flattened, ellipsoid strip of specialized
cardiac muscle
▪ Located in the right atrium below the opening of
the superior vena cava
▪ Controls the beat of the heart because its rate of
rhythmical discharge is the fastest
▪ RMP: -55 to -60 mV
▪ Connect directly with the atria so the action
potential spreads immediately into the atrial
muscle wall
▪ Discharge at 70 to 80 times per minute
SELF-EXCITATION
▪ Sodium tends to leak inside the sinus fibers.
Therefore, between heart beats, influx of
positively charged sodium ions causes a slow rise
in the resting membrane potential in the positive
direction
▪ When the potential reaches a threshold voltage at
about -40 millivolts, the L-type calcium channels
become “activated”, thus causing the action
potential
▪ L-type calcium channels become inactivated
within about 100 to 150 ms after opening
▪ At about the same time, greatly increased number
of potassium channels open
INTERNODAL AND INTERATRIAL
PATHWAY
▪ The ends of the sinus nodal fibers connect
directly with surrounding atrial muscle fibers.
(Therefore, action potentials originating in the
sinus node travel outward into this atrial muscle
fibers)
ATRIOVENTRICULAR NODE
CHAPTER 9 | CARDIAC PHYSIOLOGY
▪ Delays impulse conduction from the atria to
the ventricles so that the cardiac impulse does
not travel to the ventricles too rapid
▪ (Allows time for the atrial to empty their blood
into the ventricles before ventricular
contraction begins)
▪ Located in the posterior wall of the right
atrium immediately behind the tricuspid valve.
▪ (Slow conduction is caused by diminished
number of gap junctions between successive
cells in the conducting pathways
▪ Discharge at 40 to 60 times per minute)
ATRIOVENTRICULAR BUNDLE (BUNDLE
OF HIS)
▪ One-way conduction only
▪ Prevents the re-entry of cardiac impulses by
the route from the ventricles to the atria
▪ Everywhere, except at the A-V bundle, the
atrial muscle is separated from the ventricular
muscle by a continuous fibrous barrier
VENTRICULAR PURKINJE SYSTEM
▪ Lead from the A-V nodes through the A-V
bundle into the ventricle
▪ Very large fibers and allows almost
instantaneous transmission of the cardiac
impulse to the ventricular muscle
▪ Caused by a very high level of permeability of
the gap junctions at the intercalated discs
between the successive cells that make up the
Purkinje fibers
▪ Discharge at 15 and 40 times per minute
BUNDLE BRANCHES
▪ After penetrating the fibrous tissue between
the atrial and ventricular muscle, the distal
portion of the A-V bundle passes downward in
the ventricular septum then the bundle divides
into left and right bundle branches
▪ Each branch spreads downward toward the
apex of the ventricle, progressively dividing
into smaller branches
▪ The ends of the Purkinje fibers penetrate
about one-third of the way into the muscle
mass and finally become continuous with the
cardiac muscle fibers
▪ Once the cardiac impulse enters the
ventricular Purkinje conductive system, it is
spreads almost immediately to the entire
ventricular muscle mass
ABNORMAL PACEMAKER
CHAPTER 9 | CARDIAC PHYSIOLOGY
 CHAPTER 9 | CARDIAC PHYSIOLOGY

▪ Ectopic pacemaker CONTROL OF CORONARY BLOOD FLOW

➢ pacemaker elsewhere than the sinus node
➢ Blockage of transmission of the cardiac
impulse from the sinus node to the other
parts of the heart
➢ Occasionally some other part of the heart
develops rhythmical discharge rate that is
more rapid than that of the sinus node
▪ Ventricular escape:
➢ When A-V block occurs, atria continued to
beat at the normal rate of rhythm of the
sinus node, while a new pacemaker usually
develops in the Purkinje system of the
ventricles
▪ Overdrive suppression
➢ Ventricular excitability is at first suppressed
because the ventricles have been driven by
the atria
AUTONOMIC CONTROL
▪ PARASYMPATHETIC NERVES
➢ Distributed to the SA and AV nodes
➢ Related to the acetylcholine released at the
vagal endings
➢ Decreases the rate of rhythm of the sinus
node and the excitability of the A-V
junctional fibers
▪ SYMPATHETIC NERVES
➢ Distributed all throughout the heart
➢ Related to the norepinephrine release at
sympathetic nerve endings
➢ Increases the rate of sinus nodal discharge
and increases the rate of conduction
➢ Increases greatly the force of contraction of
all the cardiac musculature
▪ Local muscle metabolism: primary controller.
Regulation in response to the nutritional needs
of cardiac muscle
▪ Oxygen demand: major factor. Regulated
almost exactly in proportion to the need of the
cardiac musculature for oxygen
▪ Nervous control: Acetylcholine and the vagal
nerves. Norepinephrine on the sympathetic
nerve endings
ISCHEMIC HEART DISEASE
▪ Most common cause of death in Western culture
▪ ATHEROSCLEROSIS: hardening of the
blood vessel walls
▪ ACUTE CORONARY OCCLUSION:
➢ Thrombus: caused by atherosclerotic
plaque
➢ Embolus
▪ SECONDARY THROMBOSIS: coronary
artery spasm
MYOCARDIAL INFARCTION
▪ Area of muscle that has either zero flow or little
flow that it cannot sustain cardiac function is
said to be infarcted
▪ Heart attack
▪ Angina pectoris (Cardiac Pain)
➢ begins to appear whenever the load on the
heart become too great
➢ Coronary heart disease

CORONARY CIRCULATION

CORONARY ARTERIES
▪ Blood supply of the heart
➢ Left coronary artery: supplies mainly the
anterior and left lateral portions of the left
ventricle
➢ Right coronary artery: supplies most of the
right ventricle, as well as the posterior part
of the left ventricle

VENOUS DRAINAGE

▪ Left ventricle: coronary sinus, (here are the

major vessels mostly drained)
▪ Right ventricle: anterior cardiac veins
 CHAPTER 9 | CARDIAC PHYSIOLOGY
ELECTROCARDIOGRAM (ECG)

NORMAL ECG
▪ P wave: atrial depolarization
▪ QRS wave: ventricular depolarization
▪ T wave: ventricular repolarization
▪ The atria repolarize 0.15 to 0.20 sec after
termination of the P wave, which is also when the
QRS complex is being recorded in the ECG.
Therefore, the atrial repolarization wave (atrial
T wave) is usually obscured by the much larger
QRS complex
▪ P-Q or P-R Interval: interval between the
beginning of electrical excitation of the atria and
the beginning of excitation of the ventricle
➢ Normal: 0.16 second
▪ Q-T Interval: Beginning of the Q wave to the CHEST LEADS (PRECORDIAL LEADS)
end of the T wave
➢ Normal: 0.35 second ▪ V1 (red): 4th intercostal space to the right of
the sternum
▪ V2 (yellow): 4th intercostal space to the left of
the sternum
▪ V3 (green): Between V2 and V4
▪ V4 (blue): 5th intercostal space at the
midclavicular line
▪ V5 (orange): Anterior axillary line at the same
level as V4
▪ V6 (violet): Midaxillary line at the same level
as V4 and V5

DETERMINING HEARTBEAT AUGMENTED UNIPOLAR LIMB LEADS

▪ The normal interval between two successive QRS ▪ Two of the limbs are connected through
complexes in an adult is about 0.83 second, electrical resistances to the negative terminal
which is a heart rate of 60/0.83 times per minute, of the electrocardiogram, and the third limb is
or 72 beats/min connected to the positive terminal
▪ aVL: (+) terminal is under right arm, the lead
ECG LEADS is known
▪ THREE BIPOLAR LIMB LEADS: ▪ aVR: (+) terminal on the left arm
➢ Electrocardiogram is recorded from two ▪ aVF: (+) Terminal on the left leg
electrodes located on different sides of the
heart
➢ Einthoven’s Triangle: Illustrates that the 2
arms and the left leg form a triangle
surrounding the heart
➢ Einthoven’s Law: Lead I potential + Lead III
potential = Lead II potential
▪ Lead I - Negative terminal: right arm, Positive
terminal: left arm
▪ Lead II - Negative terminal: right arm, Positive
terminal: left leg
▪ Lead III - Negative terminal: left arm, Positive
terminal: left leg

ABNORMAL SINUS RHYTHMS
▪ Tachycardia: fast heartbeat
▪ Bradycardia: slow heart rate
▪ Sinus arrhythmia: irregular heart rate
CONDUCTION BLOCKS
▪ SA block: impulse from the sinus node is
blocked before it enters the atrial muscle
➢ Sudden cessation of P wave
▪ AV block: impulses from the atrium into the
ventricle are blocked
➢ 1st degree: Prolonged PR interval
➢ 2nd degree: (+) atrial P wave but no QRST
wave (dropped beats)
• Type I (Wenckebach periodicity):
prolongation of the PR interval until a
ventricular beat is dropped
• Type II: fixed number of non-conductive
P wave for every QRS complex
➢ 3rd degree (Complete): the P waves become
dissociated from the QRS-T complex
➢ Strokes-Adams Syndrome: Total block
comes and goes
• 5 to 20 seconds delay wherein the
ventricles failed to pump blood, and the
person faints after the first 4 to 5 seconds
because of lack of blood flow to the brain
▪ Electrical alternans: partial intraventricular
block every other heartbeat
CHAPTER 9 | CARDIAC PHYSIOLOGY
PREMATURE CONTRACTIONS
▪ Premature atrial contractions: single
premature atrial contraction. The P waves of
this b occurred too soon and the P-R interval
is shortened
▪ AV nodal/bundle premature contractions: P-
waves is superimposed into the QRS-T
complex because cardiac impulse traveled
backward
▪ Premature ventricular contractions:
prolonged and high voltage QRS and a T wave
with an opposite electrical potential polarity
FIBRILATION
▪ Ventricular fibrillation: cardiac impulses
that have gone berserk within the ventricular
muscle mass
➢ Mysterious of all cardiac arrhythmias
➢ Due to increased pathway, decreased
speed of conduction or a shortened
refractory period
▪ Atrial fibrillation: cardiac impulses gone
berserk in the atrial muscle mass
▪ Atrial flutter: electrical signal travels as a
single large wave
▪ Cardiac arrest: cessation of all electrical
control signals in the heart
CURRENT OF INJURY
▪Current flows between the pathologically
depolarized and the normally polarized area, even
between heartbeats
▪J point: reference potential for analyzing current
of injury
▪Myocardial ischemia:
➢ST segment depression
➢T wave inversion
▪Myocardial infarction:
➢ST segment elevation
➢Q wave abnormality
 CHAPTER 9 | CARDIAC PHYSIOLOGY

HEART SOUNDS

NORMAL HEART SOUNDS

▪ When listening to a normal heart rate with a

stethoscope, one hears a sound usually described
as “lub, dub, lub, dub.”
▪ First heart sound (“lub”/S1): closure of the AV
Valves
▪ Second heart sound (“dub”/S2): closure of the
SL Valves
▪ Third heart sound (S3): occurs at the middle
third of diastole
➢ Due to oscillation of blood back and forth
between the walls of the ventricles
➢ Maybe normally present in children,
adolescents, and young adults
➢ Indicates systolic heart failure in older adults
▪ Atrial contractions sound (Fourth heart
sound/S4): can almost never be heard with a
stethoscope and occurs when the atria contract
➢ Common in persons who derive benefit from
atrial contraction for ventricular filling
VULVULAR LESIONS

▪ Rheumatic fever: greatest number of valvular

lesions results from this condition
➢ Stenosis: valve in which the leaflets
adhere to one another so extensively that
blood cannot flow through it normally
➢ Regurgitation: when the valve edges are
so destroyed by scar tissue that they cannot
close

PHONOCARDIOGRAM
▪ Recording from a microphone specially designed
to detect low-frequency sound placed at the chest
for heart sounds
HEART MURMURS
▪ SYSTOLIC MURMURS
➢ Aortic stenosis: blood is injected from the
left ventricle through only a small fibrous
opening of the aortic valve. Harsh and
loud sound
➢ Mitral regurgitation: blood flows
backward through the mitral valve into the
left atrium. High-frequency blowing
▪ DIASTOLIC MURMURS
➢ Aortic regurgitation: blood flows
backward from the high-pressure aorta into
the left ventricle
➢ Mitral stenosis: blood passes with
difficulty through thestenosed mitral valve
from the left atrium to the left ventricle
➢
CONGENITAL ABNORMALITIES
▪ During fetal life, the lungs are collapsed.
Therefore, resistance to blood flow to the

lungs is great and pulmonary artery pressure is
high while aortic pressure is low.
▪ Ductus arteriosus: a special artery present in the
fetus that connects the pulmonary artery with the
aorta
➢ Closest after birth and becomes the
ligamentous arteriosum
CHAPTER 9 | CARDIAC PHYSIOLOGY
excessively weekend heart pump a normal
cardiac output
▪Fluid continues to be retained, the person
develops more and more edema, and this state
of events eventually lead to death.

▪ Foramen ovale: a special passageway of blood

from the right atria to the left atria
➢ Closest after birth and becomes the fossa
ovale
▪ LEFT TO RIGHT SHUNT
➢ Patent ductus arteriosus: increase in
backward flow of blood from the aorta into
the pulmonary artery, here opens the major
blood vessel
➢ Patent foramen ovale: increase in backward
flow of blood from the left atria into the right
atria
▪ RIGHT TO LEFT SHUNT
➢ Tetralogy of Fallot: most common cause of
blue baby
• Overriding of the aorta to the right
• Pulmonary artery stenosis
• Ventricular septal defect
• Right ventricular hypertrophy
CARDIAC FAILURE
▪ Can result from any heart condition that reduces
the heart's ability to pump enough blood
▪ Two main effects:
➢
Reduced cardiac output
➢ Damming of blood in veins
▪ Compensation:
➢ Autonomic response:
• Baroreceptor reflex
• Chemoreceptor reflex
▪ Chronic response:
➢ Retention of fluid by the kidneys
➢ Varying degrees of recovery of the heart itself
over a period of weeks to months
LEFT CHRONIC HEART FAILURE
▪Blood continues to be pumped into the lungs
with usual right heart vigor, whereas it is not
pumped adequately out of the lungs by the left
heart into the systemic circulation
▪Pulmonary edema
▪Pulmonary vascular congestion
▪Lung congestion
▪Dyspnea
RIGHT CHRONIC HEART FAILURE
 Blood continues to be pumped into the system
with usual left heart vigor, whereas it is not
pumped adequately into the lungs by the right
heart
 Peripheral edema
 Ascites
 Jugular vein distention
 Weight gain
CARDIOGENIC SHOCK
▪
Circulatory shock syndrome caused by
inadequate cardiac pumping
▪ Happens because the heart becomes incapable
of pumping even the minimal amount of blood
flow required to keep the body alive causing
the body tissues begin to suffer and
deteriorate, leading the death within a few
hours to a few days

COMPENSATED CARDIAC FAILURE

▪ Return of the cardiac output to almost normal

after several days to several weeks of partial
cardiac recovery and fluid retention

DECOMPENSATED CARDIAC FAILURE

▪If the heart becomes severely damaged, no
amount of compensation can make the