Lecture: Heart Physiology

I. Cardiac Muscle (compare to Skeletal Muscle)

Cardiac Muscle Cells Skeletal Muscle Cells

fairly short very long

semi-spindle shape cylindrical shape
branched, interconnected side-by-side
connected (intercalated discs) no tight binding
electrical link (gap junction) no gap junctions
common contraction (syncytium) independent contract
1 or 2 central nuclei multinucleated
dense "endomysium" light "endomysium"
high vasculature medium vasculature
MANY mitochondria (25% space) less mitochondria (2%)
almost all AEROBIC (oxygen) aerobic & anaerobic
myofibers fuse at ends myofibers not fused
T tubules wider, fewer T tubules at A/I spot

II. Mechanism of Contraction of Contractile Cardiac Muscle Fibers

1. Na+ influx from extracellular space, causes positive feedback opening of

voltage-gated Na+ channels;membrane potential
quickly depolarizes (-90 to +30); Na+ channels close within 3 ms
of opening.

2. Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in

skeletal muscle), allowing sliding actin and myosin to proceed.

3. Depolarization ALSO causes opening of slow Ca++ channels on the membrane

(special to cardiac muscle), further increasing Ca++ influx and activation of
filaments. This causes more prolonged
depolarization than in skeletal muscle, resulting in a plateau action
potential, rather than a "spiked" action potential (as in skeletal muscle cells).

Differences Between Skeletal & Cardiac MUSCLE Contraction

1. All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked
electrochemically, so that activation of a small group of cells spreads like a wave
throughout the entire heart. This is essential for
"synchronistic" contraction of the heart as opposed to skeletal muscle.

2. Automicity (Autorhythmicity) - some skeletal muscle cells are "self-excitable" (see

below, allowing for rhythmic waves of contraction to adjacent cells throughout
the heart. Skeletal muscle cells must be stimulated by
independent motor neurons as part of a motor unit.

3. Length of Absolute Refractory Period - The absolute refractory period of cardiac

muscle cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms),
preventing wave summation and tetanic
contractions which would cause the heart to stop pumping rhythmically.
III. Internal Conduction (Stimulation) System of the Heart
A. General Properties of Conduction

1. heart can beat rhythmically without nervous input

2. nodal system (cardiac conduction system) - special autorhythmic cells of
heart that initiate impulses for wave-like
contraction of entire heart (no nervous stimulation needed for these)
3. gap junctions - electrically couple all cardiac muscle cells so that depolarization
sweeps across heart in sequential fashion from atria to ventricles

B. "Pacemaker" Features of Autorhythmic Cells

1. pacemaker potentials - "autorhythmic cells" of heart muscle create action

potentials in rhythmic fashion; this is due to
unstable resting potentials which slowly drift back toward
threshold voltage after repolarization from a previous cycle.

Theoretical Mechanism of Pacemaker Potential:

a. K+ leak channels allow K+ OUT of the cell more slowly than in skeletal muscle

b. Na+ slowly leaks into cell, causing membrane potential to slowly drift up to
the threshold to trigger Ca++ influx from outside (-40 mv)

c. when threshold for voltage-gated Ca++ channels is reached (-40 mv), fast
calcium channels open, permitting explosive entry of Ca++ from of the
cell, causing sharp rise in level of
depolarization

d. when peak depolarization is achieved, voltage-gated K+ channels open,

causing repolarization to the "unstable resting potential"

e. cycle begins again at step a.

C. Anatomical Sequence of Excitation of the Heart

1. Autorhythmic Cell Location & Order of Impulses

(right atrium) sinoatrial node (SA) ->

(right AV valve) atrioventricular node (AV)
->
atrioventricular bundle (bundle of His) ->
right & left bundle of His branches ->
Purkinje fibers of ventricular walls

(from SA through complete heart contraction = 220 ms = 0.22 s)

a. sinoatrial node (SA node) "the pacemaker" - has the fastest autorhythmic rate
(70-80 per minute), and sets the pace for the entire heart; this rhythm is
called the sinus rhythm; located in
right atrial wall, just inferior to the superior vena cava

b. atrioventricular node (AV node) - impulses pass from SA via gap junctions in
about 40 ms.; impulses are delayed about 100 ms to allow completion of the
contraction of both atria; located just
above tricuspid valve (between right atrium & ventricle)

c. atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L

and R atria)
 d. L and R bundle of His branches - within the interVENTRICULAR septum (between
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 elaborate here; Purkinje fibers
innervate "papillary muscles" before
ventricle walls so AV can valves prevent backflow

D. Special Considerations of Wave of Excitation

1. initial SA node excitation causes contraction of both the R and L atria

2. contraction of R and L ventricles begins at APEX of heart (inferior point), ejecting
blood superiorly to aorta and pulmonary artery
3. the bundle of His is the ONLY link between atrial contraction and ventricular
contraction; AV node and bundle must work for ventricular
contractions
4. since cells in the SA node has the fastest autorhythmic rate (70-80 per minute),
it drives all other autorhythmic centers in a normal heart

5. arrhythmias - uncoordinated heart contractions

6. fibrillation - rapid and irregular contractions of the heart chambers; reduces
efficiency of heart
7. defibrillation - application of electric shock to heart in attempt to retain normal
SA node rate
 8. ectopic focus - autorhythmic cells other than SA node take over heart rhythm
9. nodal rhythm - when AV node takes over pacemaker function (40-60 per
minute)
10. extrasystole - when outside influence (such as drugs) leads to premature
contraction
11. heart block - when AV node or bundle of His is not transmitting sinus rhythm
to ventricles

E. External Innervation Regulating Heart Function

1. heart can beat without external innervation

2. external innervation is from AUTONOMIC SYSTEM

parasympathetic - (acetylcholine) DECREASES rate of contractions

cardioinhibitory center (medulla) ->
vagus nerve (cranial X) ->
heart

sympathetic - (norepinephrine) INCREASES rate of contractions

cardioacceleratory center (medulla) ->
lateral horn of spinal cord to preganglionics T1-T5 ->
postganlionics cervical/thoracic ganglia ->
heart

IV. Electrocardiography: Electrical Activity of the Heart

 A. Deflection Waves of ECG

1. P wave - initial wave, demonstrates the depolarization from SA Node through

both ATRIA; the ATRIA contract about 0.1 s after start of P Wave

2. QRS complex - next series of deflections, demonstrates the depolarization of AV

node through both ventricles; the ventricles contract throughout the period of
the QRS complex, with a short delay after the end of atrial contraction;
repolarization of atria also obscured

3. T Wave - repolarization of the ventricles (0.16 s)

4. PR (PQ) Interval - time period from beginning of atrial contraction to beginning

of ventricular contraction (0.16 s)

5. QT Interval - the time of ventricular contraction (about 0.36 s); from beginning
of ventricular depolarization to end of repolarization

V. The Normal Cardiac Cycle

A. General Concepts

1. systole - period of chamber contraction

2. diastole - period of chamber relaxation
3. cardiac cycle - all events of systole and diastole during one heart flow cycle

B. Events of Cardiac Cycle

1. mid-to-late diastole: ventricles filled

* pressure: LOW in chambers; HIGH in aorta/pulmonary trunk

* aortic/pulmonary semilunar valves CLOSED
* blood flows from vena cavas/pulmonary vein INTO atria
* blood flows through AV valves INTO ventricles (70%)

* atrial systole propels more blood > ventricles (30%)

* atrial diastole returns through end of cycle

2. ventricular systole: blood ejected from heart

* filled ventricles begin to contract, AV valves CLOSE

* isovolumetric contraction phase - ventricles CLOSED
* contraction of closed ventricles increases pressure
* ventricular ejection phase - blood forced out
* semilunar valves open, blood -> aorta & pulmonary trunk

3. isovolumetric relaxation: early diastole

* ventricles relax, ventricular pressure becomes LOW

* semilunar valves close, aorta & pulmonary trunk backflow
* dicrotic notch - brief increase in aortic pressure

TOTAL CARDIAC CYCLE TIME = 0.8 second

(normal 70 beats/minute)

atrial systole (contraction) = 0.1 second

ventricular systole (contraction) = 0.3 second
quiescent period (relaxation) = 0.4 second
VI. Heart Sounds: Stethoscope Listening
A. Overview of Heart Sounds

1. lub-dub, - , lub,dub, -
2. lub - closure of AV valves, onset of ventricular systole
3. dub - closure of semilunar valves, onset of diastole
4. pause - quiescent period of cardiac cycle

5. tricuspid valve (lub) - RT 5th intercostal, medial

6. mitral valve (lub) - LT 5th intercostal, lateral

7. aortic semilunar valve (dub) - RT 2nd intercostal

8. pulmonary semilunar valve (dub) - LT 2nd intercostal

B. Heart Murmurs

1. murmur - sounds other than the typical "lub-dub"; typically caused by

disruptions in flow
2. incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve
does not completely close, some regurgitation of blood
3. stenotic valve - high pitched swishing sound when blood should be flowing
through valve; narrowing of outlet in the open state
VII. Cardiac Output - Blood Pumping of the Heart

A. General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute

2. Stroke Volume (SV) - ventricle blood pumped per min.
3. Heart Rate (HR) - cardiac cycles per minute

CO (ml/min) = HR (beats/min) X SV (ml/beat)

normalCO = 75 beats/min X 70 ml/beat = 5.25 L/min

B. Regulation of Stroke Volume (SV)

1. end diastolic volume (EDV) - total blood collected in ventricle at end of diastole;
determined by length of diastole and venous pressure (~120 ml)
2. end systolic volume (ESV) - blood left over in ventricle at end of contraction (not
pumped out); determined by force of ventricle contraction and arterial
blood pressure (~50 ml)

SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)

normalSV = 120 ml/beat - 50 ml/beat = 70 ml/beat

3. Frank-Starling Law of the Heart - critical factor for stroke volume is "degree of
stretch of cardiac muscle cells"; more stretch = more contraction force

a. increased EDV = more contraction force

i. slow heart rate = more time to fill

ii. exercise = more venous blood return

C. Regulation of Heart Rate (Autonomic, Chemical, Other)

 1. Autonomic Regulation of Heart Rate (HR)

a. sympathetic - NOREPINEPHRINE (NE) increases heart rate (maintains Stroke

Volume)
b. parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate
c. vagal tone - parasympathetic inhibition of inherent rate of SA node, allowing
normal HR
d. baroreceptors, pressoreceptors - monitor changes in blood pressure and
allow reflex activity with the autonomic nervous system

2. Hormonal and Chemical Regulation of Heart Rate (HR)

a. epinephrine - hormone released by adrenal medulla during stress; increases

heart rate
b. thyroxine - hormone released by thryroid; increases heart rate in large
quantities; amplifies effect of epinephrine
c. Ca++, K+, and Na+ levels very important;

* hyperkalemia - increased K+ level; KCl used to stop heart on lethal injection

* hypokalemia - lower K+ levels; leads to abnormal heart rate rhythms
* hypocalcemia - depresses heart function
* hypercalcemia - increases contraction phase
* hypernatremia - HIGH Na+ concentration; can block Na+ transport & muscle
contraction

3. Other Factors Effecting Heart Rate (HR)

a. normal heart rate - fetus 140-160 beats/minute

female 72- 80 beats/minute
male 64- 72 beats/minute

b. exercise - lowers resting heart rate (40-60)

c. heat - increases heart rate significantly
d. cold - decreases heart rate significantly

e. tachycardia - HIGHER than normal resting heart rate (over 100); may lead to
fibrillation
f. bradycardia - LOWER than normal resting heart rate (below 60);
parasympathetic drug side effects;
physical conditioning; sign of pathology in non-healthy patient

VIII. Imbalance of Cardiac Output & Heart Pathologies

A. Imbalance of Cardiac Output

1. congestive heart failure - heart cannot pump sufficiently to meet needs of the
body

a. coronary atherosclerosis - leads to gradual occlusion of heart vessels,

reducing oxygen nutrient supply to
cardiac muscle cells; (fat & salt diet, smoking, stress)
b. high blood pressure - when aortic pressure gets to large, left ventricle
cannot pump properly, increasing ESV, and lowering SV
 c. myocardial infarct (MI) - "heart cell death" due to numerous factors,
including coronary artery occlusion
d. pulmonary congestion - failure of LEFT heart; leads to buildup of blood in
the lungs
e. peripheral congestion - failure of RIGHT heart; pools in body, leading to
edema (fluid buildup in areas such as feet, ankles, fingers)

B. Heart Pathologies (Diseases of the Heart)

1. congenital heart defects - heart problems that are present at the time of birth

a. patent ductus arteriosus - bypass hole between pulmonary trunk and aorta
does not close

2. sclerosis of AV valves - fatty deposits on valves; particularly the mitral valve of

LEFT side; leads to heart murmur

3. decline in cardiac reserve - heart efficiency decreases with age

4. fibrosis and conduction problems - nodes and conduction fibers become scarred
over time; may lead to arrhythmias