1. Lecture: Heart Phys iol o g y
I. Cardiac Muscl e (comp ar e to Skel e t al Muscl e )
Cardiac Muscle Cells Skelet al Muscle Cells
fairly short very long
semi- spindle shap e cylindrical shap e
branch e d, interconn e c t e d side- by- side
conne c t e d (intercal at e d discs) no tight binding
electrical link (gap junction) no gap junctions
commo n contraction (syncytium) indepe n d e n t contrac t
1 or 2 central nuclei multinucle a t e d
dens e "endomy sium" light "endomy sium"
high vasculatur e medium vasculatur e
MANY mitochon dri a (25% spac e) less mitochon dri a (2%)
almos t all AEROBIC (oxygen) aerobic & ana e robic
myofiber s fuse at ends myofiber s not fused
T tubules wider, fewer T tubules at A/I spot
II. Mechani sm of Contrac t i on of Contrac t i l e Cardiac Muscl e Fiber s
1. Na + influx from extrac ellular spac e, caus e s positive feedb a ck opening of
voltage- gate d Na + chann el s ;membr a n e potential
quickly depolarize s (-90 to +30); Na + chann el s close within 3 ms
of opening.
2. Depolarization caus e s relea s e of Ca ++ from sarcopl a smic reticulum (as in
skelet al muscle), allowing sliding actin and myosin to proce e d.
3. Depolarization ALSO caus e s opening of slow Ca ++ chann el s on the membr a n e
(special to cardiac muscl e), further increa sing Ca ++ influx and activation of
filame nt s . This caus e s more prolonge d
depolarization than in skelet al muscl e, resulting in a plate a u action
potential, rather than a "spiked" action potenti al (as in skelet al muscl e cells).
Differenc e s Betwe e n Skelet al & Cardiac MUSCLE Contraction
1. All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked
electroch emi c ally, so that activation of a small group of cells spre a d s like a wave
througho u t the entire hear t. This is esse nti al for
"synchroni s tic" contraction of the hear t as oppos e d to skelet al muscle.
2. Automicity (Autorhythmicity) - some skelet al cardiac cells are "self- excitabl e" (see
below, allowing for rhythmic waves of contraction to adjac e nt cells throughout
the hear t. Skelet al muscle cells mus t be stimulat e d by
indepe n d e n t motor neurons as part of a motor unit.
3. Length of Absolute Refractory Period - The absolut e refractory period of cardiac
muscle cells is much longer than skelet al muscle cells (250 ms vs. 2- 3 ms),
preventing wave summa t ion and tet anic
contractions which would caus e the hear t to stop pumping rhythmic ally.

2. III. Internal Conduc t i on (Stimul a t i o n) Sys t em of the Heart
A. Gener al Proper tie s of Conduction
1. hear t can beat rhythmic ally without nervous input
2. nodal system (cardiac conduction syst em) - special aut orhy thmi c cell s of
hear t that initiate impulse s for wave- like
contraction of entire hear t (no nervous stimulation need e d for thes e)
3. gap junctions - electrically couple all cardiac muscle cells so that depol arization
sweep s acros s hear t in seque nt i al fashion from atria to ventricles
B. "Pacema k e r " Featur e s of Autorhythmic Cells
1. pacema k e r potenti al s - "autorhythmi c cells" of hear t muscl e creat e action
potential s in rhythmic fashion; this is due to
unst a bl e resting potenti al s which slowly drift back toward
threshold voltage after repolarization from a previous cycle.
Theoretic al Mechanism of Pacemak e r Potential :
a. K + leak chann el s allow K+ OUT of the cell more slowly than in skelet al muscl e
b. Na + slowly leaks into cell, causing membr a n e potenti al to slowly drift up to
the threshold to trigger Ca ++ influx from outside (-40 mv)
c. when threshold for voltage- gat e d Ca ++ chann el s is reache d (-40 mv), fast

3. calcium chann el s open, permit ting explosive entry of Ca ++ from of the
cell, causing sharp rise in level of
depolarization
d. when peak depol arization is achieve d, voltage- gat ed K+ chann el s open,
causing repolarization to the "unst a bl e resting pot enti al"
e. cycle begins again at step a.
C. Anatomical Seque n c e of Excitation of the Hear t
1. Autorhythmi c Cell Location & Order of Impulse s
(right atrium) sinoatrial node (SA) ->
(right AV valve) atriovent ricular node (AV)
->
atriovent ricular bundle (bundle of His) ->
right & left bundle of His branch e s ->
Purkinje fibers of ventricular walls
(from SA through compl et e hear t contraction = 220 ms = 0.22 s)
a. sinoatrial node (SA node) "the pacema k e r " - has the faste s t autorhythmic rate
(70- 80 per minut e), and set s the pac e for the entire hear t; this rhythm is
called the sinus rhythm ; locat ed in
right atrial wall, just inferior to the superior vena cava
b. atriovent ricular node (AV node) - impulse s pas s from SA via gap junctions in
about 40 ms.; impulse s are delaye d about 100 ms to allow comple tion of the
contraction of both atria; locat ed just
above tricuspid valve (betwe e n right atrium & ventricle)
c. atriovent ricular bundle (bundle of His) - in the interATRIAL septum (conne c t s L
and R atria)

4. d. L and R bundl e of His branch e s - within the interVENTRICULAR septum (betwe e n
L and R ventricles)
e. Purkinje fibers - within the lateral walls of both the L and R ventricles; since left
ventricle much larger, Purkinjes more elabor a t e here; Purkinje fibers
innervat e "papillary muscles" before
ventricle walls so AV can valves preve nt backflow
D. Special Consider a tions of Wave of Excitation
1. initial SA node excitation caus e s contraction of both the R and L atria
2. contraction of R and L ventricles begins at APEX of hear t (inferior point), ejecting
blood superiorly to aorta and pulmon a ry artery
3. the bundl e of His is the ONLY link betwe e n atrial contr action and ventricular
contraction; AV node and bundl e mus t work for ventricular
contractions
4. since cells in the SA node has the faste s t autorhythmic rate (70- 80 per minut e) ,
it drives all other autorhythmic cent er s in a normal hear t
5. arrhythmi a s - uncoordina t e d hear t contractions
6. fibrillation - rapid and irregular contr actions of the hear t chamb e r s ; reduc e s
efficiency of hear t
7. defibrillation - application of electric shock to hear t in att emp t to retain normal
SA node rate

5. 8. ectopic focus - autorhythmic cells other than SA node take over hear t rhythm
9. nodal rhythm - when AV node takes over pacema k e r function (40- 60 per
minut e)
10. extrasys tole - when outside influenc e (such as drugs) leads to prema tur e
contraction
11. hear t block - when AV node or bundle of His is not transmi t ting sinus rhythm
to ventricles
E. External Innerva tion Regulating Heart Function
1. hear t can beat without external innervation
2. ext ernal innervation is from AUTONOMIC SYSTEM
parasymp a t h e t i c - (acetylcholine) DECREASES rate of contrac tions
cardioinhibitory cent er (medulla) ->
vagus nerve (cranial X) ->
hear t
sympa th e t ic - (norepine p hrine) INCREASES rate of contractions
cardioa cc el er a tory cent er (medulla) ->
lateral horn of spinal cord to prega n glionics T1-T5 ->
postg a nlionics cervical/thor a cic ganglia ->
hear t
IV. Electroc ardi o g r a p h y : Electrical Activity of the Heart

6. A. Deflection Waves of ECG
1. P wave - initial wave, demon s t r a t e s the depolarization from SA Node through
both ATRIA; the ATRIA contract about 0.1 s after start of P Wave
2. QRS compl ex - next series of deflections , demo n s t r a t e s the depolarization of AV
node through both ventricles; the ventricles contract througho ut the period of
the QRS complex, with a short delay after the end of atrial contraction;
repolarization of atria also obscur e d
3. T Wave - repolarization of the ventricles (0.16 s)
4. PR (PQ) Interval - time period from beginning of atrial contrac tion to beginning
of ventricular contraction (0.16 s)
5. QT Interval - the time of ventricular contrac tion (about 0.36 s); from beginning
of ventricular depolarization to end of repolarization
V. The Normal Cardiac Cycle
A. Gener al Concept s
1. systole - period of chamb e r contra ction
2. diastole - period of chamb e r relaxation
3. cardiac cycle - all event s of systole and diastol e during one hear t flow cycle
B. Event s of Cardiac Cycle

7. 1. mid- to- late diastole: ventricles filled
* pres sur e: LOW in chamb e r s ; HIGH in aorta/pulmon a ry trunk
* aortic/pulmo n a ry semilun ar valves CLOSED
* blood flows from vena cavas /pulmo n a ry vein INTO atria
* blood flows through AV valves INTO ventricles (70%)
* atrial systole propels more blood > ventricles (30%)
* atrial dias tole returns through end of cycle
2. ventricular systole: blood eject ed from hear t
* filled ventricles begin to contract, AV valves CLOSE
* isovolume t ric contraction phas e - ventricles CLOSED
* contr action of closed ventricles incre a s e s pres sur e
* ventricular ejection phas e - blood forced out
* semiluna r valves open, blood -> aorta & pulmon a ry trunk
3. isovolume t ric relaxation: early diastole
* ventricles relax, ventricular pres sur e become s LOW
* semiluna r valves close, aorta & pulmon a ry trunk backflow
* dicrotic notch - brief incre a s e in aortic pres sur e
TOTAL CARDIAC CYCLE TIME = 0.8 second
(normal 70 beat s /minut e )
atrial systole (contra ction) = 0.1 second
ventricular systole (contra ction) = 0.3 second
quiesc e nt period (relaxation) = 0.4 second

8. VI. Heart Sound s : St e th o s c o p e List enin g
A. Overview of Heart Sounds
1. lub- dub, - , lub,dub, -
2. lub - closur e of AV valves, onse t of ventricular systole
3. dub - closur e of semiluna r valves, onset of diastole
4. paus e - quiesc e n t period of cardiac cycle
5. tricuspid valve (lub) - RT 5th intercos t al, medial
6. mitral valve (lub) - LT 5th intercos t al, lateral
7. aortic semilunar valve (dub) - RT 2nd intercos t al
8. pulmon a ry semilunar valve (dub) - LT 2nd intercos t al
B. Heart Murmurs
1. murmur - sounds other than the typical "lub- dub"; typically cause d by
disruptions in flow
2. incomp e t e n t valve - swishing sound just AFTER the normal "lub" or "dub"; valve
does not compl et ely close, some regurgit ation of blood
3. stenotic valve - high pitched swishing sound when blood should be flowing
through valve; narrowing of outlet in the open stat e

9. VII. Cardiac Output - Blood Pumpin g of the Heart
A. Gener al Variable s of Cardiac Output
1. Cardiac Output (CO) - blood amount pump e d per minut e
2. Stroke Volume (SV) - ventricle blood pump e d per min.
3. Heart Rate (HR) - cardiac cycles per minut e
CO (ml/min) = HR (beat s /min) X SV (ml/be a t )
normal CO = 75 beat s /min X 70 ml/be a t = 5.25 L/min
B. Regulation of Stroke Volume (SV)
1. end diastolic volume (EDV) - total blood collect ed in ventricle at end of dias tole;
det ermin e d by length of diastol e and venous pres sur e (~120 ml)
2. end systolic volume (ESV) - blood left over in ventricle at end of contrac tion (not
pump e d out); det ermin e d by force of ventricle contraction and arterial
blood pres sur e (~50 ml)
SV (ml/be a t ) = EDV (ml/be a t ) - ESV (ml/be a t )
normal SV = 120 ml/be at - 50 ml/be a t = 70 ml/be a t
3. Frank- Starling Law of the Heart - critical factor for stroke volume is "degre e of
stretch of cardiac muscle cells"; more stretch = more contraction force
a. increa s e d EDV = more contraction force
i. slow hear t rate = more time to fill
ii. exercise = more venous blood return
C. Regulation of Heart Rate (Autonomic, Chemic al, Other)

10. 1. Autonomic Regulation of Heart Rate (HR)
a. symp a t h e t ic - NOREPINEPHRINE (NE) increa s e s hear t rate (maint ains Stroke
Volume)
b. para symp a t h e t i c - ACETYLCHOLINE (ACh) decre a s e s hear t rate
c. vagal tone - parasymp a t h e t ic inhibition of inher ent rate of SA node, allowing
normal HR
d. baror ec e pt or s , pres sor e c e p tor s - monitor chang e s in blood pres sur e and
allow reflex activity with the autonomic nervous syst em
2. Hormon al and Chemic al Regulation of Hear t Rate (HR)
a. epinep hrine - hormon e relea s e d by adren al medulla during stres s ; incre a s e s
hear t rate
b. thyroxine - hormon e relea s e d by thryroid; increa s e s hear t rate in large
quantitie s; amplifies effect of epinephr ine
c. Ca ++ , K + , and Na + levels very import ant ;
* hyperkal emi a - incre a s e d K+ level; KCl used to stop hear t on lethal injection
* hypokal emi a - lower K+ levels; leads to abnormal hear t rate rhythms
* hypoc alc emi a - depr e s s e s hear t function
* hyperc alc emi a - incre a s e s contrac tion phas e
* hypern a t r emi a - HIGH Na + conc ent r a t ion; can block Na + transpor t & muscl e
contraction
3. Other Factors Effecting Heart Rate (HR)
a. normal hear t rate - fetus 140- 160 beat s /minut e
femal e 72- 80 beat s /minut e
male 64- 72 beat s /minut e
b. exercise - lowers resting hear t rate (40- 60)
c. heat - incre a s e s hear t rate significantly
d. cold - decre a s e s hear t rate significantly
e. tachyc ar di a - HIGHER than normal resting hear t rate (over 100); may lead to
fibrillation
f. bradyc ardi a - LOWER than normal resting hear t rate (below 60);
para symp a t h e t i c drug side effect s ;
physical conditioning; sign of pathology in non- healthy patient
VIII. Imbalanc e of Cardiac Output & Heart Pathol o gi e s
A. Imbalanc e of Cardiac Output
1. conge s tive hear t failure - hear t cannot pump sufficiently to me e t needs of the
body
a. coronary atherosclerosi s - leads to gradu al occlusion of hear t ves s el s ,
reducing oxyge n nutrient supply to
cardiac muscle cells; (fat & salt diet, smoking, stres s )
b. high blood pres sur e - when aortic pres sur e get s to large, left ventricle
cannot pump properly, incre a sing ESV, and lowering SV

11. c. myoc ardi al infarct (MI) - "hear t cell death" due to numero u s factors,
including coronary artery occlusion
d. pulmon a ry conge s tion - failure of LEFT hear t; leads to buildup of blood in
the lungs
e. peripher al conge s tion - failure of RIGHT hear t; pools in body, leading to
edema (fluid buildup in are a s such as feet, ankles, finger s)
B. Heart Pathologie s (Disea s e s of the Heart)
1. conge ni t al hear t defect s - hear t problems that are pres e nt at the time of birth
a. pat ent ductus arteriosus - bypa s s hole betwe e n pulmon a ry trunk and aort a
does not close
2. sclerosis of AV valves - fatty deposit s on valves; particularly the mitral valve of
LEFT side; leads to hear t murmur
3. decline in cardiac reserve - hear t efficiency decre a s e s with age
4. fibrosis and conduction problems - node s and conduction fibers become scarred
over time; may lead to arrhythmi a s