Cardiovascular system is composed of:
The heart and blood vessels
Functions in transportation of blood
delivers oxygen and nutrients to tissues
removes carbon dioxide and waste products from tissues
Cardiac muscle
is striated, short, fat, branched, and interconnected
Intercalated discs
anchor cardiac cells together and allow free passage of ions through gap junction
contractile cardiac muscle cells
99% of the heart is made of contractile cardiac muscle cells,
Generates the force of contraction produced by the heart
autorhythmic cells
Generate action potentials spontaneously without neural stimuli
1% self-excitable
Intrinsic conduction system of the heart
Autorhythmic cells coordinates the rhythmic excitation and contraction of the cardiac muscle to ensure efficient pumping
Intrinsic conduction system of the heart
The action potential generated by autorhythmic cells travel through the conduction system and to surrounding myocardial tissue by gap junction
Sinoatrial (SA) node
-pacemaker, generates impulse (70 times/minute)
Atrioventricular (AV) node
(40-60 times/minute), delays the impulse about 0.1 second. Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
Bundle branches
carry the impulse toward the apex of the heart (35 times/minute)
Purkinje fibers
carry the impulse from the heart apex to the ventricular walls (30 times/minute)
Ectopic focus -
Abnormal overly excitable area begins to depolarizes faster than the SA node
Can lead to a premature heartbeat (extrasystole) and/or accelerated heart rate
Can be caused by heart disease, anxiety, lack of sleep, to much caffeine, nicotine
What gives autorhythmic cells the unique ability to spontaneously generate action potentials?
They have an unstable membrane potentials called pacemaker potentials
Their membrane gradually depolarizes and drifts towards threshold due to slow Na+ entry
What gives autorhythmic cells the unique ability to spontaneously generate action potentials? #2
When threshold is reached they fire an action potential
Calcium influx (rather than sodium) causes the depolarization phase of the action potential
Repolarization is cause by K+ efflux
P wave -
atrial depolarization
QRS complex
- ventricles depolarization
T wave -
ventricles repolarization
Cardiac Abnormalities
Bradycardia - <60 BPM
Tachycardia - >100 BPM
Arrhythmias - uncoordinated atrial and ventricular contractions
Damaged SA node - pace set by AV node ~ 50 BPM
Heart block - damage to the AV node, ventricles contract at ~30 BPM
Fibrillation - irregular chaoti
Contraction of cardiac muscle cells:
Must be stimulated by autorhythmic cells to contract
Have a long absolute refractory period
Prevents summation and tetany
Ensures filling of the chambers
Contractile myocardial cells
Have a stable resting membrane potential
Depolarization wave travels through the gap junctions and opens fast voltage gated Na+ channels in the contractile cell
Triggers an action potential
Na+ channels close and slow Ca2+ channels open causing Ca2+ influ
Plateau phase -
Ca2+ influx prolongs the action potential and prevents rapid repolarization
Ca2+ close and K+ channels open causing repolarization
Cardiac muscle contraction
The action potential traveling down the T-tubules triggers the influx of Ca2+ from the ECF.
The Ca2+ influx induces the release of additional Ca2+ from the SR
Ca2+ binds to troponin allowing sliding of the myofilaments
Cardiac muscle contraction
Cardiac cycle
refers to all events associated with one complete heart beat
Systole -
contraction of heart muscle
Diastole -
relaxation of heart muscle
Mid-to-late diastole
Ventricular filling.
Blood passively flows into ventricles from atria
Atria contract (atrial systole)
AV valves open, SL valves closed
Ventricular systole
Atrial diastole
Rising ventricular pressure results in closing of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves
early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary trunk closes semilunar valves
Atria re-filling
Atria pressure increases, AV valves open and cycle repeats
Heart sounds (lub-dup)
associated with closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole
Second sound occurs when SL valves close at the beginning of ventricular diastole
Cardiac Output
the amount of blood pumped by each ventricle in one minute
Cardiac Output
(heart rate [HR]) x (stroke volume [SV])
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)
Regulation of Heart Rate
Heart rate is modulated by the autonomic nervous system
Parasympathetic activity
Slows HR down via ACh
Increases K+ permeability, hyperpolarization - slows depolarization
Sympathetic activity
Increases HR via NE/E
Increases Na+, and Ca2+ channels, speeds up depolarization
Chronotropic agents -
Affect heart rate
Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate
Regulation of Heart Rate-Hormones
Epinephrine and Thyroxine increase HR
Ions
Elevated K+ and Na+ levels in the ECF- decrease HR
Elevated Ca2+ levels in the ECF - increases HR
Physical factors
Age - decreases HR
Exercise - increases HR
Temperature - increases HR
Regulation of Stroke Volume
Stroke volume = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV =
amount of blood collected in a ventricle during diastole
ESV =
amount of blood remaining in a ventricle after contraction
Ejection factor =
SV/EDV
Factors Affecting Stroke Volume
Preload and After load
Preload
amount ventricles are stretched by contained blood, dependent on EDV
Affected by volume of venous return and ventricular filling time
Factors that would increase preload
Exercise
Slower heart beat
Factors that would decrease preload
Blood loss
Rapid heart beat
Frank-Starling's Law:
increased stretch = increased contraction strength
After load
back pressure exerted by blood in the large arteries leaving the heart
Increase in after load decreases stroke volume
Contractility -
Force of the muscle contraction due to factors independent of stretch and EDV
Increase in contractility comes from:
Increased sympathetic stimuli
Hormones - thyroxine, epinephrine
Increased ECF Ca2+
Inotropic agents
effect contractility
Factors Affecting Cardiac Output
Factors Involved in Regulation of Cardiac Output