I. Heart Wall
A. Epicardium – outer layer; a.k.a. visceral pericardium (SSE w/ C.T.)
B. Myocardium – bulk of heart
1. cardiac muscle
a. striated, involuntary
b. intercalated discs – propagate action potentials, support
2. connective tissue
a. collagen and elastic fibers
b. support, strength, elasticity after contraction
3. fibrous skeleton
a. dense bands of fibroelastic tissue
b. isolate atria from ventricles
C. Endocardium – inner lining
1. endothelium cont. w/ vessels
II. Four Chambers
A. 2 Atria and 2 Ventricles
B. Pulmonary Circuit
1. Right Atrium
2. Right Ventricle
C. Systemic Circuit
1. Left Atrium
2. Left Ventricle
III. Vessels
A. Aorta
B. Superior / Inferior Vena Cava, Coronary sinus
C. Pulmonary trunk (splits into R/L pulmonary arteries)
D. Pulmonary veins
IV. Valves – two types
A. Atrioventricular Valves (AV valves)
1. Tricuspid valve – separates RA/RV
2. Biscuspid (Mitral) valve – separates LA/LV
*chordae tendineae – attach to AV flaps and papillary muscles in
ventricles
B. Semilunar valves (SL valves)
1. Pulmonary Semilunar valve – beginning of pulmonary trunk
2. Aortic Semilunar valve – beginning of aorta
V. Cardiac cells
A. Two types of cardiac cells
1. Contractile cells – powerful contracting cells
2. Conducting system (Nodal system) – coordinate contractile cells
B. Contractile cells
1. 99% of cardiac cells
2. Resting potential is –90mV for ventricular contractile cells
3. Threshold is –75mV
C. 3 steps of Action Potential
1. Rapid depolarization
a. Voltage-regulated Na+ channels open at threshold
b. Depolarization occurs
c. Fast Channels – open quickly and close quickly
2. Plateau
a. at +30mV Na+ channels close
b. Slow Calcium Channels open
c. These channels open slowly and stay open for an
extended period of time leading to the Plateau
3. Repolarization
a. Slow Ca2+ channels close and Slow K+ channels open
b. Restores resting potential
D. Refractory Period – membrane will not respond to further stimuli
1. Na+ channels are open or inactivated
2. Long refractory period prevents tetany
E. Action potential causes Ca2+ increases around myofibrils (Contraction)
1. 20% of Ca2+ enters during plateau phase
2. Ca2+ entering triggers Ca2+ release form sarcoplasmic reticulum
3. The heart is sensitive to changing levels of extracellular Ca2+
F. Conducting System
1. Automaticity – cardiac muscle contracts on its own
2. Conducting or Nodal system – specialized cardiac cells that
initiate and distribute impulses to contractile cells
a. Sinoatrial node (SA node or pacemaker)
1) right atrial wall
b. Atrioventricular node (AV node)
2) short delay allows atria to contract before ventricles
c. Bundle of His
d. Bundle branches
e. Purkinje fibers
3. Prepotential – gradual depolarization of cells in the SA (80-
100/min) and AV (40-60/min) node
a. Nodal cells have inherent leakiness to sodium
4. Entire process, from depolarization of SA node to ventricular
depolarization, takes 225 msec.
VI. Cardiac cycle – period between start of one heartbeat and beginning of next
A. Systole – contraction, increase pressure
B. Diastole – relaxation, decrease pressure
C. Pressures are lower in right side, but equal volumes of blood are
ejected
D. 3 Phases of Cardiac Cycle
1. Atrial systole – begins cardiac cycle
a. Atria contract, push last 30% of blood into ventricles past
AV valves
b.70% of blood flowed passively into ventricles during
previous cycle
c. End-diastolic volume (EDV) – ventricles contain max
amount of blood at end of atrial systole (130ml)
2. Ventricular systole – begins as atrial systole ends
a. Ventricles contract – ventricular pressure exceeds atrial
pressure and AV valves close, prevents back flow of blood into atria
*chordae tendineae prevent AV valves from opening into
atria
b. Ventricular ejection – pressure in ventricles exceed
pressure in pulmonary and aortic arteries and SL valves open; blood enters vessels
c. Pressure in pulmonary and aortic arteries will soon
exceed ventricular pressure and blood wants to flow
back from vessels into ventricles, but SL valves close
d. Stroke volume – amount of blood ejected by each
ventricle per contraction (80 ml); this is about 60% of end-diastolic volume
e. End-systolic volume (ESV) – amount of blood in ventricles
when SL valves close (50ml) –about 40% of EDV
3. Ventricular Diastole
a. Ventricles relax and when pressure falls below atrial
pressure – AV valves open and ventricles fill
passively 70% before next cardiac cycle
b. During atrial systole the atria play minor role in ventricular
filling (30%)
E. Listening to Heart sounds (auscultation)
1st sound “Lubb” – AV valves close
2nd sound “Dupp” – SL valves close
*Mitral valve prolapse
-improper closing of bicuspid valve, blood leaks
-produces regurgitation sound (heart murmur)
VII. Electrocardiogram (EKG) – recording of electrical events in the heart
A. Deflection waves
1. P wave – depolarization of SA node and atria
a. Atria contract 100ms after start of P wave
2. QRS Complex – Ventricular depolarization
a. Ventricles contract around R wave
3. T wave – ventricular repolarization
B. 800ms from beginning of P wave to beginning of next P wave
VIII. Cardiodynamics – movements and forces generated by contractions
A. EDV – amount of blood in ventricle at end of ventricular diastole
(130ml)
B. ESV – amount of blood in ventricle at end of ventricular systole (50ml)
C. SV – amount of blood pumped out of ventricle/beat (80ml / 60% of
EDV)
D. Cardiac Output (CO) – amount of blood pumped out of ventricle/min
(ml/min)
E. CO (ml/min) = SV (ml/beat) x HR (beats/min)
F. Regulation of CO by adjusting Stroke Volume and Heart Rate
G. Adjust SV by changing EDV and ESV
1. EDV is affected by:
a. Filling time – duration of ventricular diastole
b. Venous return – rate of blood flow during filling time
2. ESV is affected by:
a. Preload – degree of stretching during ventricular diastole
1) the larger the EDV — the larger the preload –
– the larger the SV
2) Affects cardiac muscle tension
** Frank-Starling Principle –“more in=more out”
b. Contractility – amount of force produced by a
contraction
1) Altered by autonomic innervation or hormones
2) Positive Inotropic action – increases contractility
-examples – SNS (NE & Epi, Glucagon, Thyroid
hormone) and increase Ca2+ entry
3) Negative Inotropic action – decrease contractility
-examples – PNS (ACh) and block Ca2+
c. Afterload – amount of tension the ventricles must produce
to open SL valves
***the greater the afterload – the greater the time of
isovolumetric contraction – the shorter the duration of ventricular ejection – the greater the ESV
-i.e. greater the afterload, the less the SV
-elevated arterial BP will increase afterload
*****Stroke Volume peaks when EDV is high and ESV is low
H. Factors affecting Heart Rate
**Autonomic innervation – (Dual innervation)
1. EFFECT ON SA NODE
a) ACh released by PNS opens K+ gated channels
-slows spontaneous depolarization, slows heart rate
b) NE released by SNS binds to Beta-1 receptors causing
Ca2+ channels to open
-increases rate of spontaneous depolarization,
increases HR
2. Cardiac centers in medulla oblongata
a) cardioacceleratory center – SNS
b) cardioinhibitory center – PNS
3. Cardiac centers monitor baroreceptors and chemoreceptors
innervated by glossopharyngeal CN IX and Vagus CN X
4. Adjust cardiac performance to maintain circulation to vital organs
** Atrial reflex (Bainbridge reflex)
1. Increase HR in response to increase venous return
2. Stimulation of stretch receptors in atrial wall increases SNS
** Hormones
1. NE, Epi, Thyroid Hormone increase HR
