The Cardiovascular system:

A closed system of the heart and blood vessels and blood.

The heart pumps blood.

General function these provide:

1. Transportation: Everything transported by the bead. E. g: deliver

O2, remove Co2, deliver nutrients and rewove other waste.
2. Regulations of the cardiovascular System Intrinsic (SA) node V
Extrinsic (hormone).
3. Protection: against blood loss (blood clot) production / Synthesis.

Blood vessels allow blood to circulate to all parts of the body.

Taking blood to the tissue and back.

Components of the vascular system (blood vessels):

Arteries → Arterioles →Capillaries →Venules → Veins.

1. Arteries: Carry blood away from heart. Strong thick walls, smooth
muscle (elastic), fibrous Coat, Small
Lumen = ↑ high pressure.
2. Veins: Garry blood back to heart, large lumen, Thin Wall / Muscle,
↓ elastic valves.
3. Capillaries: Connect arteries and veins, No Valves, pores. No
muscle / Not elastic, Extremely Thin (1 Cell thick)= Fast
Exchange.

Right and Left side act as separate pumps. Four Chambers:

1. Atria (Receiving chambers) Right-left atrium.

2. Ventricles (Discharging chambers) Right-left ventricle.

a) Pulmonary circuit:

Oxygen poor.

Low ↓ B. P.

Co2 = rich blood.

b) Systemic Circuit:

Oxygen rich.
High ↑ B. P.

Co₂= Poor blood.

Types of Circulation:

1. Pulmonary Circuit: blood flow between the lungs and heart.

Supplied by the right side of the heart.
2. System Circulation: blood flow between the rest of the body and
heart. Supplied by the left side of the heart.
3. Coronary: blood vessels that supply heart muscle with O₂ and
nutrients / remove waste products.

Valves: allow blood to flow in only one direction. Include:

Four valves:

1. Atrioventricular valves – between atria and ventricles.

2. Bicuspid valve (Left).
3. Tricuspid valve (Right).
4. Semilunar valves between ventricle and atria. Includes:
a) Pulmonary semilunar Valve.
b) Aortic semilunar valve.

Valves open as blood is pumped through held in place by chordae

tendineae (heart string).

Close to prevent back flow.

-Tensioned by the papillary muscle.

-semilunar valves- prevent backflow into ventricles.

- Atrioventricular valves-prevented back flow to the atria.

Cardiac Muscle:

Characteristics:

1. Striated.
2. Short branched Cells.
3. Uninucleate.
4. Intercalated discs.
5. T-tubules larger and over z-discs.
The myocardial physiology Characteristics of pacemaker cells:

Smaller than Contractile cells.

Don't contain many myofibrils.

No organized sarcomere Structure.

Do not contribute to the contractile force of the heart.

Intrinsic Conduction system:

Consists of pacemaker cell and Conduction pathways.

Coordinate the contraction of the atria and ventricles.

Sinoatrial node (pacemaker) = 100-110mV

Atrioventricular node = 60 mV

Bundle of His = 40mV

Purkinje fibers = 35mv

Contractile fiber = 25 mV

Cardiac properties:

Excitability: Ability to respond (SA) node.

Action potential (wall atrium and ventricle) =

Contractile = 0.8 sec.

Systole = 0.3 sec.

Diastele-0.5 sec.

Action potential is longer in duration than normal action potential-

due to Ca+² entry and fasting response.

Phases:

1. Phase (4) = resting: resting membrane potential = -90mv.

2. Phase (o) = depolarization: Upon stimulation, gap Junctions
trigger the opening of numerous Na+ Channels allowing rapid
influx Na+.

This Channels close when membrane potential reaches 20mV.

3. Phase (1) = Temporary repolarization: Open K+ channels allow
some K+ to leave (out or efflux) the cell.
4. Phase (2) = plateau : Voltage-gated Ca+2 channels are fully open,
called long-lasting Ca+2 Channels, allows slow influx Ca+2 from
extracellular fluid and same time K+ channels continue to allow
K+ to efflux the cell.

The amount Ca+2 ↓Influx = K+ ↑efflux. →This is why membrane

prandial remains relatively stable.

5. Please (3) = repolarization: Ca channels close and K +

permeability increases slower activated K+ channels open.
Causing rapid repolarization and returning the cell to it's resting
state (-90mV).

Na+ (inactive state) in = Ca+2 out exchange → repolarization.

Amplitude = depolarization (30mV) -resting (-90mV) = 120mV.

Refractory periods:

Absolute refractory period (ARP): phase (0, 1, 2, ½ upper 3).

-Relative refractory period (RRP): phase (½ lower 3).

Characteristic of Contractive wall:

1. Composed mainly of contractile cell (atrial + ventricle).

2. Generates force for heart Contraction.
3. Has stable nesting membrane potential (-90mV).
4. Contains numerous voltage-gated Na+ channels.
5. Action potential is long.
6. Exhibits plateau phase (2)-due to balance Ca +2 in = K+ out.
7. Does not spontaneously depolarize (need Stimulus).
8. Relies on Ca+² for Contraction (Excitation – Contraction Coupling).
9. Connected via gap Junctions for synchronized contraction.

Why is the significance of the plateau phase?

1. Prevent sustained contraction (Tetanus).

2. Allow Ca+2 entry necessary for Contraction.
3. Maintains Cardiac rhythm.

Increased excitability or contraction in the atrial wall may lead to

Fibrillation.
Plateau phase prevents summation of Contraction due to elongated
refractory period.

No summation capacity means = no tetanus → which is Continuous,

sustained contraction → which would be fatal.

Rhythmicity: Ability to in initiate beat. (SA) node.

Or: is the Ability of the Cardiac muscle to beat regularly.

Autorhythmicity: is the inherent property (myogenic) of the heart

and doesn't depend on nerve supply.

Evidence that rhythmicity is myogenic:

1. Human embryo heart's start to beat before development of

nerve.
2. Transplanted hearts → Continue to beat although their nerve
Supply is cut.

Nature of spontaneous rhythmicity: most of the Cardiac fibers have

the Capacity of self excitation specially nodal and Conducting fibers.

Sinoatrial node (SA): has the point of highest rate (rhythmicity) So

it's the (pacemaker).

(SA) node = 100-110 mV.

(AV) node = 60 mV.

Bundle of his = 40mV.

Purkinje fiber = 35mV.

Contractile fiber=25mV → (slowest – ventricular wall).

Self excitation of (SA) node fiber:

(SA) node has resting membrane potential (-55mV) to (-60mV)

Unstable.

Natural leakiness of membrane to Na entry.

Low RMP (-55mV) to (60mV).

Self excitation of (SA) node

Mechanism of automatic rhythmicity of SA node:

1. Phase (1)=pacemaker potential =pre potential = Phase (4): The

membrane potential gradually rises from an unstable resting
value (-60mV) to threshold level or firing level (-40mV) to (-45
mV). The rise happens during diastole so it's also called diastolic
depolarization.
a) Slow Na+ influx through funny channels.
b) Slow Ca+2 influx through T-type → transient Ca+2 channels.
c) Slow K+ efflux.
2. Phase (2) = depolarization → (Upstroke) = phase (0) :
a) It starts When membrane potential reaches threshold (-40mV)
and Continues up to (10mV).
b) It's due to rapid influx of Ca+2 through L-type → Long-lasting Ca+2
channels. Na+ current is present but minimal.
3. Phase (3) = Repolarization=phase (3) :
a) Ca+2 channels Close, Stopping Ca+² influx.
b) K+ channels open. Starting K+ efflux.
c) This causes the membrane potential to return to (-60mV) and the
cycle repeats for life.

No stable.

No plateau.

1. Pacemaker potential. This slow depolarization is due to both

opening of Na channels and closing of K channels. Notice that the
membrane potential is never a flat line.
2. Depolarization. The action potential begins when the pacemaker
potential reaches threshold. 2. Depolarization is due to Ca influx
through Ca channels.
3. Repolarization is due to Ca channels inactivating and K channels
opening. This allows K' efflux, which brings the membrane
potential back to its most negative voltage.

Factors effecting (SA) node → pacemaker:

1. Temperature:

Increased temperature↑: raises the pacemaker slope → making

depolarization faster.
Increases↑ firing level.

Decreased temperature ↓: flattens the slop → slower depolarization.

Decreases↓ firing level.

2. Autonomic Nervous System (ANS):

Sympathetic stimulation (e. g: Norepinephrine):

Increases↑ Na+ and Ca+2 currents. Increases↑ pacemaker slope →

reaches threshold faster.

Increased↑ firing rate.

Parasympathetic stimulation:

Increases↑ K+ efflux hyperpolarization lower firing level (mere

negatives).

Slow slope → decreases↓ firing level.

3. Hyperkalemia (↑K+ in ECF):

Reduces K+ gradient → less efflux.

Resting potential becomes less negative.

Can inactivate Na+ and Ca+2 channels. Slows depolarization →

decreases ↓firing rate or causes arrhythmia.

4. Hypercalcemia (↑Ca+² in ECF):

Increases↑ Ca+2 influx.

May increase ↑ slope of phase (1) → increases↑ firing level, but can
also shorten action potential duration.

5. Hypocalcemia (↓Ca+2 in ECF):

Reduces Ca+2 influx. Decreases↓ depolarization slope slower to

reach threshold → decreased↓ firing level.

Sympathetic activity Summary:

↑ (Chronotropic) ↑heart rate: via faster (SAN) depolarization.

↑(Draiotropic)↑ conduction velocity: through Cardiae nodes.

↑(Conotropic)↑ Contractility: - improves cardiac output.

Parasympathetic activity summary:

↓(Chronotropic)↑ heart rate: via ↑K permeability in (SA) node.

↓(Drometropic) ↓conduction velocity:

Mainly at AV node.

↓(Inotropic) ↓Contractility: minor effect limited to atria.

SKELETAL MUSCLE:

Membrane potential: Stable at-70 mV.

Events leading to threshold potential: Net Na+ entry through Ach-

operated channels.

Rising phase of action potential: Na+ entry.

Repolarization phase: Rapid; caused by K+ efflux.

Hyperpolarization: Due to excessive K+ efflux at high K+

permeability when K+ channels close; leak of K+ and Na+ restores
potential to resting state.

Duration of action potential: Short: 1-2 msec.

Refractory period: Generally brief.

CONTRACTILE MYOCARDIUM:

Membrane potential: Stable at 90 mV.

Events leading to threshold potential: Depolarization enters via gap

junctions.

Rising phase of action potential: Na+ entry.

Repolarization phase: Extended plateau caused by Ca+² entry;

rapid phase caused by K+ efflux.

Hyperpolarization: None; resting potential is -90 mV, the equilibrium

potential for K+ .

Duration of action potential: Extended: 200+ msec.

Refractory period: Long because resetting of Na+ channel gates

delayed until end of action potential.

AUTORHYTHMIC MYOCARDIUM:
Membrane potential: Unstable pacemaker potential; usually starts at
-60 mV.

Events leading to threshold potential: Net Na+ entry through funny,

channels; reinforced by Ca+² entry.

Rising phase of action potential: Ca+2 entry.

Repolarization phase: Rapid; caused by K+ efflux.

Hyperpolarization: Normally none; when repolarization hits-60 mV,

the funny, channels open again. Ach can hyperpolarize the cell.

Duration of action potential: Variable; generally 150+ msec.

Refractory period: None.

Conductivity: is the ability of the cardiac muscle to conduct the

impulse from one part of the heart to another.

Conduction system of the heart:

1. SA node and AV node or tissue

2. Internodal pathways
3. Purkinje fibers

Conduction of the cardiac impulse through the atria:

The impulse is first initiated in the SA node, which generates about

70–80 action potentials per minute, then spreads as follows:

1. Through the right atrial mass.

2. Through the interatrial band to the left atrium.
3. Through gap junctions and internodal pathways to the AV node.

Beats per minute = 70 – 80 bpm

Conduction velocity = 0.5 m/sec

The fibrous connective tissue matrix of the heart prevents further

spread of action potentials to the ventricles.

Conduction of the cardiac impulse through the AV node:

When the impulse reaches the AV node, a delay in conduction of the

wave occurs because of the slower formation of action potentials
and the slowest conductivity.
Significance of the AV nodal pathway:

1. Allows sufficient time for the atria to empty their blood into the
ventricles.
2. Protects the ventricles from pathological high rhythms of the
atria.

Beats per minute = 40 – 60 bpm

Conduction velocity = 0.3 m/sec

Transmission of the impulse through bundle of His:

The impulse is transmitted from the AV node to the bundle of His,

which splits into left and right bundle branches.

Beats per minute = 20 – 40 bpm

Conduction velocity = 1 m/sec

Transmission of the impulse into ventricles by Purkinje fibers:

Once the impulse reaches the end of Purkinje fibers, it's transmitted
very rapidly through the ventricular mass, causing the ventricles to
contract simultaneously, which is beneficial for efficient ventricular
pumping of blood.

Beats per minute = 15 – 30 bpm

Conduction velocity = 4 m/sec

Excitation-Contraction Coupling:

1. Starts with CICR (Ca²⁺-Induced Ca²⁺ Release):

a) AP spreads along sarcolemma.
b) T-tubules contain voltage gated L-type Ca²⁺ channels which open
upon depolarization.
c) Ca²⁺ enters the myocardial cell and opens RyR (ryanodine
receptor) channels.
d) Release of Ca²⁺ from SR causes a Ca²⁺ “spark”.
e) Multiple sparks form a Ca²⁺ signal.
2. Ca²⁺ signal binds to troponin to initiate myosin head attachment
to actin.
Contraction:

The heart contracts in a similar way to skeletal muscle, but the

strength of contraction can change (it is not always the same).

In skeletal muscle, the contraction is "all or none" → either full

contraction or nothing.

But in cardiac muscle, the contraction is graded → it can be weak or

strong depending on certain factors.

If there is low calcium (Ca²⁺) inside the heart cell, only a few myosin
and actin filaments will interact → weak contraction.

If there is more calcium, more interactions happen → stronger

contraction.

The length-tension relationship also matters:

The heart muscle contracts strongest when it is stretched to about

80–100% of its full capacity.

What stretches the heart muscle?

→ The filling of the heart chambers with blood before contraction.

Relaxation :

After the heart muscle contracts, it needs to relax.

To relax, calcium ions (Ca²⁺) must be removed from the inside of the
cell.

Some calcium is pumped back into the sarcoplasmic reticulum (SR)

(a storage area inside the cell).

The rest of the calcium is pushed out of the cell by a special

transporter called the Na⁺/Ca²⁺ exchanger (NCX).

When the amount of calcium inside the cell (ICF Ca²⁺) goes down:

The myosin and actin filaments stop interacting (so no contraction),

The sarcomere (the contractile unit) goes back to its original length
→ the muscle relaxes.
Contraction (Contractility):

It is the ability of the cardiac muscle to contract,

i.e., to convert the potential energy of the filled blood into

mechanical energy – which means pumping blood.

0.3 sec → Systolic phase (contraction phase)

0.5 sec → Diastolic phase (relaxation/filling phase)