Biomechanics of Circulation with fetal circulation

1. BIOMECHANICS OF CIRCULATION
Poonam N. Banthia 1st MPTh

2. Cardiac Pump Dynamics
• Overview on Anatomy of the heart.
• Electrophysiology of the heart
• Cardiac Cycle
• Pressure

3. Anatomy Review

4. Cardiac muscle cells:
• Two specialized types of cardiac muscle cells
• Contractile cells
• 99% of cardiac muscle cells
• Do mechanical work of pumping
• Normally do not initiate own action potentials
• Autorhythmic cells
• Do not contract
• Specialized for initiating and conducting action potentials responsible for
contraction of working
• Approximately 1% of cardiac muscle cells are autorhythmic rather than
contractile

5. Properties of Cardiac Muscle
• AUTOMACITY: Capability of stimulated by nerves as well as self-excitable
• AUTORHYTHMICITY: Heart beats rhythmically as result of action
potentials it generates by itself
• CONTRACTIBILITY: Cardiac muscle contracts in response to stimulus
• EXCITABILITY: Ability of cardiac muscles to respond to different stimuli
• CONDUCTIVITY: Impulses produced in the SA nodes are conducted by
specialized conducting pathway
• DISTENSIBILITY: Occurs due to compliance of cardiac muscle
• FUNCTIONAL SYNCYTIUM: allows the atria to contract for shorter
duration & before ventricular contraction

6. Atrioventricular and Semilunar Valves
• Atria and ventricles are separated into 2 functional units by a sheet of connective tissue
by AV (atrioventricular) valves.
▫ Left AV valve i.e. Mitral valve is bicuspid
▫ Right AV valve i.e. Tricuspid
• At the origin of the pulmonary artery and aorta are semilunar valves.
▫ Aortic valve lies between the left ventricle and the aorta
▫ Pulmonary valve lies between the right ventricle and pulmonary trunk.
• Opening and closing of valves occur as a result of pressure differences.
Unidirectional
flow

7. Vessels that supply/drain the heart
Coronary Arteries: 2 Main
• Rt. Coronary Artery- branches into marginal
arteries; supplies RV and posterior of heart.
• Lt. Coronary Artery- branches into Lt. Anterior
Descending and circumflex artery; supplies LV
Coronary Veins :
• Small cardiac & Great cardiac veins, Anterior
cardiac, Posterior cardiac & Middle cardiac veins
• Transport deoxygenated blood to coronary sinus
• Coronary Sinus drains into RA.

8. Nerve supply to the heart
• The fibrous pericardium and the parietal layer of serous
pericardium are innervated by Visceral sensory fibers
(the branches of Phrenic nerve). These fibers carries
the sensation of pain.
• Parasympathetic fibers (branch of the Vagus
nerve) that are responsible for slowing down of the heart
rate, innervate the visceral layer of serous pericardium.
• Sympathetic fibers that increase the rate and force of
contraction

9. Circulatory System
• Pulmonary circulation – Path of blood from
right ventricle through the lungs and back to
the heart
• Systemic circulation – Circuit of vessels
carrying blood between heart and other body
system and organs.
• Rate of blood flow through systemic
circulation = flow rate through pulmonary
circulation.

10. Functions of the Circulatory System
A. Transportation:
a. Respiratory: Transport 02 and C02.
b. Nutritive: Carry absorbed digestion products to liver and to tissues.
c. Excretory: Carry metabolic wastes to kidneys to be excreted.
B. Regulation:
a. Hormonal: Carry hormones to target tissues to produce their effects.
b. Temperature: Divert blood to cool or warm the body.
c. Protection: Blood clotting.
d. Immune: Leukocytes, cytokines and complement act against pathogens.

11. ELECTROPHYSIOLOGY OF THE HEART:
• SA node - 75 bpm
– Sets the pace of the heartbeat
• AV node - 50 bpm
– Delays the transmission of action potentials
• Purkinje fibers - 30 bpm
– Can act as pacemakers under some conditions

12. Intrinsic Conduction System
• Autorhythmic cells:
– Initiate action potentials
– Have “drifting” resting potentials called
pacemaker potentials
– Pacemaker potential - membrane slowly
depolarizes “drifts” to threshold, initiates action
potential, membrane repolarizes to -60 mV.
– Use calcium influx (rather than sodium) for
rising phase of the action potential

13. h
• f

14. ACTION POTENTIAL IN HEART :
• In cardiac muscle, the action potential is caused by
opening of two types of channels:
(1) the fast sodium channels and
(2) the slow calcium channels (also k/a calcium-
sodium channels)
• Calcium channels are slower to open and remain
open for several tenths of a second.
• During this time, a large quantity of both calcium
and sodium ions flows through the cardiac muscle
fiber and maintains a prolonged period of
depolarization, causing the plateau in the action
potential

15. • The calcium ions that enter during this plateau phase activates the muscle
contractile process.
• After the onset of the action potential, the permeability of potassium ions decreases
about fivefold due to excess calcium influx
• The decreased potassium permeability decreases the out flux of positively charged
potassium ions during the action potential plateau and thereby prevents early return
of the action potential voltage to its resting level
• When the slow calciumsodium channels closes at the end of 0.2 to 0.3 second and
the influx of calcium and sodium ions stops, the membrane permeability for
potassium ions increases rapidly; this rapid loss of potassium from the fiber
immediately returns the membrane potential to its resting level, thus ending the
action potential.

16. What happens during exchange of ions ?
• In ventricular muscle fiber, during each beat the intracellular potential rises from -
85 millivolts towards a positive value of about +20 millivolts to averages about 105
millivolts. This causes initial spike.
• Plateau causes ventricular contraction to last for longer duration.
• After which the membrane remains depolarized for about 0.2 second leading to a
plateau followed by an abrupt repolarization at the end.

17. Why a Longer AP In Cardiac Contractile Fibers?
• We don’t want Summation and tetanus in our myocardium.
• Because long refractory period occurs in conjunction with prolonged plateau phase,
summation and tetanus of cardiac muscle is impossible
• Ensures alternate periods of contraction and relaxation which are essential for
pumping blood

18. Refractory period of Cardiac Muscle:
• Refractory period is the time period during which a normal cardiac impulse
cannot re-excite an already excited area of cardiac muscle.
• The normal refractory period of the ventricle is 0.25 to 0.30 sec (=plateau period in
action potential.)
• There is an additional relative refractory period of about 0.05 sec during
which the muscle is more difficult than normal to excite but nevertheless can be
excited by a very strong excitatory signal.

20. Membrane Potentials in SA Node and Ventricle
• g

21. Action Potentials
• c

22. SEQUENCE OF EXCITATION :
• Sinoatrial (SA) node generates impulses of
about 75 times/minute.
• Atrioventricular (AV) node delays the
impulse approximately 0.1 second.
• Impulse passes from atria to ventricles via AV
bundle(bundle of His)
• AV bundle splits into two pathways i.e. Rt. &
Lt. bundle branch in the interventricular
septum & carries the impulse toward the apex
of the heart.
• Purkinje fibers carry the impulse to the
heart apex and ventricular walls.

23. • Due to this special arrangement
of the conducting system, there
is a delay of >0.1sec during
passage of the cardiac impulse
from the atria to the ventricles.
• This allows atria to contract
before ventricular contraction
begins.
• Thus, the atria act as Primer
Pumps for the Ventricles, &
the ventricles in turn provide
the major source of power for
moving blood to the body’s
vascular system.

24. Heart Excitation Related to ECG
• s

25. CARDIAC CYCLE
• The cardiac events that occur from the beginning of one heartbeat to the beginning
of the next are called the Cardiac Cycle.
• Each cycle is initiated by spontaneous generation of an action potential in the sinus
node
• The cardiac cycle consists of:
• Diastole- period of relaxation during which the heart fills with blood
• Systole- period of contraction

27. Wiggers Diagram
• v

28. Influences of the Cardiac Cycle
Master controller : The medulla
• Incoming input :
a. Chemoreceptors- Sense changes in pH, PaCO2 and PaO2
b. Baroreceptors- Sense changes in arterial pressure
• Response of the medulla
-Stimulate the autonomic nervous system

29. Autonomic Nervous System
• Sympathetic Nervous System– Extensively innervates the SA node
and ventricular cells
Increase in heart rate
Increase in conduction and contractility in the ventricles
• Parasympathetic Nervous System– Innervates the SA and AV
nodes
Decreases heart rate
Decreases conduction times through the AV node

30. Atria as a primer pump
• Normally about 80% of the blood directly flows through the atria into the
ventricles even before the atria contract.
• Then, atria contracts causing an additional 20% filling of the ventricles.
Therefore, atria function as primer pumps that increase the ventricular
pumping effectiveness by 20%.
• Without this extra 20%the heart can work effectively because ventricles has the
capability of pumping 300 to 400% of more blood than is required by the resting
body.
• Therefore, when the atria fail to function, there is less/no symptoms until unless a
person exercises; then shortness of breath develops

31. Functions of valve
• Atrioventricular Valves (tricuspid and mitral valves) prevent backflow of
blood from the ventricles to the atria during systole
• Semilunar valves (aortic and pulmonary valves) prevent backflow from the
aorta and pulmonary arteries into the ventricles during diastole.
• Valves get closed when a backward pressure gradient pushes blood backward, and
they open when a forward pressure gradient forces blood in the forward direction.
• For anatomical reasons, the thin, filmy A-V valves require almost no backflow to
cause closure, whereas the much heavier semilunar valves require rather rapid
backflow for a few milliseconds.

32. • The semilunar valves function differently from the A-V valves in two manner:
1. The high pressures in the arteries at the end of systole cause the semilunar valves
to snap to the closed position, as compared to the much softer closure of the A-V
valves.
2. Due to smaller openings, the velocity of blood ejection through the aortic
and pulmonary valves is far greater than that through the much larger A-V valves.
• Also, because of the rapid closure and rapid ejection, the edges of the aortic and
pulmonary valves are subjected to much greater mechanical abrasion than are
the A-V valves. Finally, the A-V valves are supported by the chordae
tendineae, which is not true for the semilunar valves

33. Functions of papillary muscles
• The papillary muscles contract when the ventricular walls contract but they do
not help the valves to close
• They pull the valves inward toward the ventricles to prevent their bulging too
far backward toward the atria during ventricular contraction.
• If a chorda tendinea becomes ruptured or if one of the papillary muscles
becomes paralyzed, the valve bulges far backward during ventricular
contraction, causing severe leakage which may result in lethal cardiac
incapacity.

34. Pressure and Volume changes in Heart
• b

35. Cardiac output
Cardiac Output = Heart Rate X Stroke Volume
• CO is the amount of blood pumped by each ventricle in one minute
• CO is the product of heart rate (HR) and stroke volume (SV)
• HR is the number of heart beats per minute
• SV is the amount of blood pumped out by a ventricle with each beat
• Cardiac reserve is the difference between resting and maximal CO

36. Factors Affecting Cardiac Output
• Cardiac Output = Heart Rate X Stroke Volume
• Heart rate
– Autonomic innervation
– Hormones - Epinephrine (E), norepinephrine(NE), and thyroid hormone (T3)
– Cardiac reflexes
• Stroke volume
– Starlings law
– Venous return
– Cardiac reflexes

37. Stroke Volume (SV) :
• SV is the amount of blood pumped out by a ventricle with each beat
• Determined by extent of venous return and by sympathetic activity
– Influenced by two types of controls
• Intrinsic control
• Extrinsic control
– Both controls increase stroke volume by increasing strength of heart
contraction

38. Frank starling mechanism of heart
• The amount of blood pumped by the heart each minute is determined venous
return. The heart, in turn, automatically pumps this incoming blood into the
arteries, so that it can flow around the circuit again.
• This intrinsic ability of the heart to adapt to increasing volumes of inflowing
blood is called the Frank- Starling mechanism of the heart.
• The Frank-Starling mechanism means that the greater the heart muscle is
stretched during filling, the greater is the force of contraction and the greater
the quantity of blood pumped into the aorta

40. Determination of Stroke Volume
• Preload
• Amount of blood delivered to the chamber
• Depend upon venous return to the heart
• Also dependent upon the amount of blood delivered to the ventricle by the
atrium
• Contractility
• The efficiency and strength of contraction
• Frank Starling’s Law
• Afterload
• Resistance to forward blood flow by the vessel walls

41. Preload and Afterload
• Preload: Wall tension at EDV (analogous to EDV or EDP
– As Preload increases, so does Stroke Volume.
This is a regulatory mechanism.
– Factors that increase venous return, or preload: The muscular pump
(muscular action during exercise compresses veins and returns blood to
the heart), an increased venous tone, and increased total blood volume.
• Afterload: A sum of all forces opposing ventricular ejection. Roughly
measured as Aortic Pressure.
– As Afterload increases, stroke volume decreases.

43. Heart sounds :
• When the valves close, the vanes of the valves and the surrounding fluids
vibrate under the influence of sudden pressure changes, giving off sound
that travels in all directions through the chest.
• When the ventricles contract, one first hears a sound caused by closure of
the A-V valves. The vibration is low in pitch and relatively long-lasting and
is known as the first heart sound.
• When the aortic and pulmonary valves close, a rapid snap can be heard
because these valves close rapidly, and the surroundings vibrate for a short
period. This sound is called the second heart sound.

44. FETAL CIRCULATION

45. Anatomy and physiology of fetal circulation
• Umbilical cord
-2 umbilical arteries: return de-
oxygenated blood, fecal waste, CO2 to
placenta
- 1 umbilical vein: brings oxygenated
blood and nutrient to the fetus

46. Special structure in fetal circulation
• Placenta: where gas exchange takes place during fetal life
• Umbilical arteries : carry deoxygenated blood from the fetus to placenta
• Umbilical vein : brings oxygenated blood coming from the placenta to the fetus
• Foramen ovale : connects the left atrium & right atrium. It pushes blood from
the right atrium to the left atrium.
• Ductus venosus – carry oxygenated blood from the umbilical vein to IVC,
bypassing the liver
• Ductus arteriosus : carry oxygenated blood from the pulmonary artery to aorta,
bypassing the fetal lungs

49. Why more blood flow directly to the left atrium ?
• Due to the higher pressure of the blood in the IVC, mor blood flows from it
directly into the left atrium via foramen ovale
• Foramen ovale opens like a valve and can direct the blood stream that comes from
below directly into the left atrium
• The diameters of the IVC & SVC are larger than that of the foramen ovale and
therefore a small portion of the blood seeps into the right ventricle via the
tricuspid valve
• The heart is filled only with the mixed blood

50. What happens to these special structures after birth ?
• Umbilical arteries atrophy
• Umbilical vein becomes part of the fibrous support ligament for the liver
• The foramen ovale, ductus arteriosus, ductus venosus atrophy & become
fibrous ligaments

51. Loss of placenta also leads to :
• First breath
• Lungs expand & fluid is expelled
• Decreased pulmonary resistance
• Increased pressure in left atrium
• Closure of foramen ovale
• Increased systemic resistance
• Pressure in right atrium decreased
• Change from right to left shunting to right to left blood flow
• Increased O2 levels in pulmonary circulation
• Closure of the ductus arteriosus

52. Pediatric Vs Adult ECGs
• Pediatric ECGs findings that may be normal:
• HR >100BPM
• Shorter PR, QT Int and QRS Duration
• Inferior and Lateral small Q waves
• RV Larger than LV in neonates, so:
-Large Precordial R Waves
-Upright T Waves