Mammalian Circulatory system

Topic: Mammalian Circulatory System

Class Reporter: Elino, M. M. H.

Class Instructor: Geonyzl Lepiten-Alviola, MSBio

REPORT OUTLINE:

I- Brief Introduction of the Mammalian Heart

II- Pumps: Mechanical Events of the Mammalian Cardiac Cycle

III- Pumps: Cardiac Output and Its Control

IV-Pumps: Nourishing the Vertebrate Heart Muscle (Coronary Circulation)

VI- Circulatory Pathways and Vessels

VII- Vessels: Flow Regulation and Hemodynamics

VIII-Pathways: Open Circulation

IX- Pathways: Closed Circulation

Animal Physiology: Mammalian Circulatory System Class Reporter: Elino, M. M. H.

The Mammalian Heart has four chambers:

Right Atrium, Left Atrium, Right Ventricle, Left Ventricle

1) The Right Atrium and Left Atrium are reservoirs for blood (to be sent to Right Ventricle and Left Ventricle)

2) The Right Ventricle and Left Ventricle are the main pumping chambers of the heart


Brief Introduction on Mammalian Heart and Circulation



Right Atrium Left Atrium

Right Ventricle

Left Ventricle


The Mammalian Heart has four valves:

two Atrioventricular Valves (AV) and two Semilunar Valves (SV)

1) Tricuspid Valve – an AV valve between Right Atrium - Right Ventricle

2) Bicuspid Valve – an AV valve, also called “Mitral Valve” between Left

Atrium and Left Ventricle

3) Pulmonary Valve – a SV valve between the Right Ventricle and Pulmonary artery

4) Aortic Valve – a SV valve between Left Ventricle and Aorta

Valves act as one-way doors to keep blood moving forward





Pulmonary Valve Aortic Valve

Tricuspid Valve Bicuspid Valve




Sinoatrial Node

Aorta

Atrioventricular Node

Pulmonary Artery

Other Parts

Superior Vena Cava

Inferior Vena Cava

Pulmonary Vein

Bundle of His

Septum

Purkinjie Fibers

Myocardium

The Circulation (Brief Diagram):

Deoxygenated blood from the body returns to the heart via:

Superior and Inferior Vena Cava Right Atrium Tricuspid Valve Right Ventricle Pulmonary Valve Pulmonary Artery Lungs

(the blood now comes oxygenated)

Oxygenated blood from the lungs returns to the heart via:

Pulmonary Vein Left Atrium Bicuspid Valve Left Ventricle

Aortic Valve Aorta Body (the blood now comes deoxygenated)









The cardiac cycle consists of alternate periods of

Systole – the contraction and emptying

Diastole – relaxation and filling

In vertebrates, the atria and ventricles go through separate cycles of systole and diastole.


Pumps: Mechanical Events of the Mammalian Cardiac Cycle

Hearts alternately contract to empty and relax to fill.

Contraction – occurs as a result of the spread of excitation across the heart; depolarization of the muscles of the heart follows the contraction.

Relaxation – follows the subsequent repolarization of the cardiac musculature.



ECG – Electrocardiogram

The electrical currents generated by cardiac muscle during polarization and repolarization spread into tissues surrounding the heart and are conducted through body fluids.

A small portion of this electrical activity reaches the body surface, where it can be detected using recording electrodes on skin. The record produce is an electrocardiogram.



Electrocardiogram

- it is a recording of that portion of the electrical activity induced by the body fluids by the cardiac impulse that reaches the surface of the body.

- is a complex recording representing the over-all spread of activity throughout the heart during depolarization and repolarization.



Electrocardiogram



Electrocardiogram



P wave represents atrial depolarization

QRS complex represents ventricular depolarization.

T wave represents ventricular repolarization

Depolarization – a change in a cell's membrane potential, making it more positive, or less negative.

Repolarization – reestablishment of polarity, especially the return of cell membrane potential to resting potential

Action Potential – is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and fall, following a consistent trajectory; whenever there’s large depolarization among cells

Resting Potential – resting event, opposite to action potential, comes after action potential, whenever there’s a large repolarization among cells



Excitation/Activation of heart by Sino-Atrial Node (especialized auto-rhythmic cells).

(animation / presentation)File name: conduction_ct.swf

Download my file at:

http://www.4shared.com/rar/13zOoh6I/animal_physio_reports_ppt.html



The Full Cardiac Cycle:

1) Early Ventricular Diastole

2) Late Ventricular Diastole3) End of Ventricular Diastole4) Ventricular Excitation and Onset of Ventricular Systole5) Isovolumetric Ventricular Contraction6) Ventricular Ejection7)End of Ventricular Systole8) Ventricular Repolarization and Onset of Ventricular Diastole9) Isovolumetric Ventricular Relaxation10) Ventricular Filling



1st : Early Ventricular Diastole

During early ventricular diastole, the atrium is still also in diastole. This stage corresponds to the TP interval (on the ECG) – the resting stage.

The AV valve is open.



2nd : Late Ventricular Diastole

SA node reaches threshold and fires.

Impulse spreads through out the atria and is recorded on the ECG as P wave.

Atrial depolarization brings about atrial contraction which squeezes more blood into the ventricle, causing a rise in the atrial pressure curve.



3rd : End Ventricular Diastole

Ventricular Diastole ends at the onset of ventricular contraction. By this time, atrial contraction and ventricular filling are completed.

The volume of the blood in the ventricle at the end of diastole is known as “end-diastolic volume” (EDV), which averages about 135mL in humans.

No more blood is added to the ventricle during this cycle.



4th: Ventricular Excitation and Onset of Ventricular Systole

Following atrial excitation, the impulse passes through the AV node and specialized conduction system to excite the ventricle.

QRS complex represents this ventricular excitation which induce ventricular contraction.



5th: Isovolumetric Ventricular Contraction

After ventricular pressure exceeds atrial pressure and AV valve has closed, the ventricular pressure must continue to increase before it can open the aortic valve.

Between closure of the AV valve and opening of Aortic valve, there is a brief period of time when the ventricle remains a closed chamber. During this time, no blood can enter or leave the ventricles.



6th: Ventricular Ejection

It is when ventricular pressure exceeds aortic pressure. The aortic valve is forced open and ejection of the blood begins.

The ventricular volume decreases substantially as blood rapidly pumped out.

Ventricular systole includes both the period of isovolumetric contraction and the ventricular ejection phase.



7th : End of Ventricular Systole

After ventricular pressure exceeds atrial pressure and AV valve has closed, the ventricular pressure must continue to increase before it can open the aortic valve.

Between closure of the AV valve and opening of Aortic valve, there is a brief period of time when the ventricle remains a closed chamber. During this time, no blood can enter or leave the ventricles.



8th : Ventricular Repolarization and Onset of Ventricular Diastole

It is signified by T wave, occurring at the end of ventricular systole. As the ventricles starts to relax on repolarization, ventricular pressure falls below aortic pressure and the aortic valves closes.

Closure of the aortic valve produces a disturbance as notch on the aortic pressure curve known as the “discrotic notch”.

No more blood leaves the ventricle during this cycle/phase, because the aortic valve has closed.



9th : Isovolumetric Ventricular Relaxation

When the aortic valve closes, the AV valve is not yet open, because ventricular pressure still exceeds atrial pressure, so no blood can enter the ventricle from the atrium. Therefore, all valves are once again closed for a brief period of time.

The muscle fiber length and chamber volume remain constant. No blood moves as the ventricle continues to relax; pressure steadily falls.



10th : Ventricular Filling

When the ventricular pressure falls below the atrial pressure, the AV valve opens and ventricular filling occurs once again.

Ventricular Diastole includes both the period of isovolumetric ventricular relaxation and the ventricular filling phase.



(Points to Ponder)

Atrial repolarization and Ventricular depolarization occur simultaneously, so the atria are in diastole throughout ventricular systole.

Blood continues to flow from the pulmonary veins into the left atrium. As this incoming blood pools in the atrium, atrial pressure rises continuously.

When the AV Valve opens at the end of ventricular systole, the blood that accumulated in the atrium during ventricular systole pours rapidly in the ventricle.



(Points to Ponder)

Ventricular filling thus occurs rapidly at first because of the increased atrial pressure resulting from the accumulation of blood in the atria. Then ventricular filling slows down and atrial pressure starts to fall.

During the period of ventricular filling, the blood continues to flow from the pulmonary veins into the left atrium and through the open AV valve into the left ventricle.

During late ventricular diastole, when ventricular filling is proceeding slowly, the SA node fires again and the cardiac cycle starts over.



Cardiac Output

It is the volume of blood per minute pumped by a heart to the body, and is the most important physiological parameter of a circulatory pump.

It depends on the heart rate and the stroke volume. Thus, the key formula is:

Cardiac Output = Heart Rate x Stroke Volume (volume per minute) (beats per minute) (volume per pumped

per beat of stroke)


Pumps: Cardiac Output and Its Control

Cardiac Output depends on the heart rate and the stroke volume.

Heart rates vary tremendously with activity state of an individual and across the animal kingdom.

Larger animals tend to have slower heart rates. Ex: 6 beats/min for whales and 300 beats/min in a rat.

During any period of time, the volume of blood flowing through pulmonary circulation is equivalent to the volume flowing through systemic circulation.

Cardiac output from each ventricle is normally identical, minor variations may occur.






CARDIAC OUTPUT = Heart Rate x Stroke

Volume

Horse 13, 500 mL/min = 30 beats/min x 450 mL/beat

Human 4, 900 mL/min = 70 beats/min x 70 mL/beat

Pigeon 195.5 mL/min = 115 beats/min x 1.7 mL/beat

Trout 17.4 mL/min = 37.8 beats/min x 0.46 mL/beat


Cardiac Output changes with development. In young broiler chicks, stroke volume almost doubles in a two-week period:



CARDIAC OUTPUT = Heart Rate x Stroke Volume

4 weeks old 253 mL/min = 362 beats/min x 0.70 mL/beat

6 weeks old 434 mL/min = 328 beats/min x 1.33 mL/beat




Thorough Bred Horse 300, 000 mL/min

Human (untrained) 25, 000 mL/min

Human (athlete) 40, 000 mL/min

Pigeon 1, 072 mL/min

Trout 53 mL/min

Cardiac Output also changes with activity, often by large amounts.

The following are some values that have been measured at high activity levels ( running, flying, swimming)

Heart rate is determined primarily by antagonistic regulation of autonomic influences on the SA node.

The vertebrate heart is innervated by both division of the ANS, which is the sympathetic and parasympathetic Nervous System, which can modify the rate ( as well as strength) of contraction, even though nervous stimulation is not required to initiate contraction.

The parasympathetic nerve to the mammalian heart, the vagus nerve, primarily supplies the atrium especially the SA and AV nodes. Parasympathetic innervation of the ventricles is sparse.

The cardiac sympathetic nerves also supply the atria, including SA and AV nodes, and richly innervates the ventricles as well.




Both parasympathetic and sympathetic nervous system affect the heart by altering the activity of the cyclic AMP (second messenger system in the innervated cells.




Both parasympathetic and sympathetic affect the heart through the release of:

1) Acetylcholine (Ach) – released from the vagus nerve binds to muscarinic receptors that are coupled to an inhibitory G protein, which reduces the cyclic AMP pathway. cAMP in turn increases the permeability of the SA node to K+ by slowing the closure of EAG K+ channel.





2) Norepinephrine (NE) – sympathetic neurotransmitter binds with a B-adrenergic receptor that is coupled to a stimulatory G protein, which accelerates cAMP pathway. In turn, cAMP appears to decrease K+ permeability by accelerating inactivation of EAG channels.





3) Ach and NE that both affects Ca++ conduction.



Effect of Parasympathetic Stimulation on the Mammalian Heart

Parasympathetic stimulation reduces cardiac output through these effects:

1)It decreases heart rate.

2)It decreases excitability of the AV node.

3)It shortens the action potential of the atrial contractile cells.



Effect of Sympathetic Stimulation on the Mammalian Heart

Sympathetic stimulation increases cardiac output through these effects:

1)It increases heart rate through its effect on pacemaker tissue.

2)It reduces AV nodal delay at the node by increasing conduction velocity.

3)It speeds up the spread of the action potential throughout the specialized conduction pathway.

4)It increases contractile strength of the atrial and ventricular contractile cells.



Control of the Heart Rate

Thus, as typical of the ANS, parasympathetic and sympathetic effects on heart rate are example of antagonistic relation. At any given moment, the heart rate is determined largely by the existing balance between the inhibitory effects of vagus nerve and the stimulatory effects of the cardiac sympathetic nerves.

The relative level of activity in these two branches in turn is primarily coordinated by the cardiovascular control center located at the brain stem.



Control of the Heart Rate

Although autonomic innervation is the primary means by which heart rate is regulated, other factors affect it as well. The most important is epinephrine, a hormone that is secreted into the blood from the adrenal medulla on sympathetic stimulation and the acts in a manner similar to norepinephrine to increase the heart rate.



Stroke Volume is determined by the extent of venous return and by sympathetic activity.

The other component that determines the cardiac output is stroke volume, the amount of blood pumped out by each ventricle during each beat. Two types of controls influence stroke volume:

1)Intrinsic Control – related to the extent of venous return

2)Extrinsic Control – related to the extent of sympathetic stimulation of the heart.



Increased end-diastolic volume results in increased stroke volume

As more blood is returned to the vertebrate heart, the heart pumps out more blood, but the heart does not eject all the blood it contains. The direct correlation between end-diastolic volume and stroke volume constitutes the intrinsic control of stoke volume, which refers to the heart’s inherent ability to vary the stroke volume.



Frank-Starling Law of the Heart

states that:

“ Heart normally pumps all the blood returned to it”

This effect is not unique to invertebrates; for example, mollusk hearts also respond in this way to increased filling (they also beat faster in response)



Frank-Starling Law of the Heart

The built-in relationship matching stroke volume with venous return has two important advantages:

1)It is for equalization of output between the right and left sides of the avian and mammalian hearts, so that the blood pumped out by the heart is equally distributed between pulmonary and systemic circulation.

2)When larger cardiac output is needed in any vertebrate, venous return is increased through action of the sympathetic nervous system.



The contractility of the heart and venous return are increased by sympathetic stimulation.

In addition to intrinsic control, stroke volume is also subject to extrinsic control by factors originating outside the heart, the most important of which are actions of the cardiac sympathetic nerves and epinephrine. Sympathetic stimulation and epinephrine act into two ways:

1)The heart contracts more forcefully and squeezes out a greater percentage of the blood it contains on sympathetic stimulation.

2)Sympathetic stimulation increases stroke volume also by enhancing venous return.



The contractility of the heart and venous return are increased by sympathetic stimulation.

The strength of cardiac muscle contraction and accordingly, the stroke volume can thus be graded by

1)Varying the initial length of the muscle fibers, which turn depends on the degree of ventricular filling before contraction and;

2)Varying the extentof sympathetic stimulation (extrinsic control).



The heart receives most of its own blood supply through the coronary circulation.

Coronary circulation is the circulation of blood in the blood vessels of the heart muscle (the myocardium). The vessels that deliver oxygen-rich blood to the myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins.


Pumps: Nourishing the Vertebrate Heart Muscle

The heart receives most of its own blood supply through the coronary circulation.

Although the blood passes though the heart, the heart muscle cannot extract O2 or nutrients from the blood within its chamber, in part because the walls are too thick to permit diffusion of O2 and other supplies from the blood in the chamber to all the cardiac cells.

Therefore, like other tissues of the body, heart muscle must receive blood through blood vessels, specifically by means of the coronary circulation (which first evolved in fishes). The coronary arteries branch in fishes from the branchial arteries leaving the gills, and in mammals from the aorta just beyond the aortic valve.



Coronary Circulation













During locomotory activity, the rate of coronary blood flow increases several-fold above its resting state. Increased delivery of blood to the cardiac cells is accomplished primarily by vasodilation, or enlargement, of the coronary vessels, which allows more blood to flow through them.

Coronary blood flow is adjusted primarily in response to changes in the heart’s O2 requirements.

The major link that coordinates coronary blood flow with myocardial O2 needs is adenosine (which is formed from ATP).




Increased formation and release of adenosine from cardiac cells occur:

1)When there is cardiac O2 deficit or

2)When cardiac activity is increased and the heart accordingly requires more O2 for ATP production.

The heart primarily uses free fatty acids, glucose, lactate as fuel sources. Note: depending on their availability and it can shift metabolic pathways to use whatever nutrient is available.

The primary danger of insufficient coronary blood flow is not fuel shortage but O2 deficiency.




Reduced O2 in cardiac adenosine release

vasodilation of coronary vessels

increased blood flow and O2 delivery to myocytes



Circulatory fluids transport materials in a parallel manner, especially in closed systems.

Most animals have either open (hemolymph) or a closed (blood) system.

Blood moves through closed vessels.Hemolymph moves more randomly through open spaces “lacunae” among organs.


Circulatory Pathways and Vessels

Circulatory fluids transport materials in a parallel manner, especially in closed systems.

There are two important design features in closed ( and often in open system)

1)Closed systems always have initial parallel branching in arteries, and many open system do as well. Parallel plumbing allows individual organs or body regions to obtain fresh blood (or hemolymph).

2)There can be muscular valves on some of the branching parallel vessels. These appear universally in closed system and occur in some open ones.



Circulatory fluids are driven by pressure and can transmit useful force.

Directing fluid flow in parallel manner can serve another purpose – force of transmission to specific organs. To move from one point to another it needs pressure ( is created by a pump, and is the driving force for fluid movement).

But it can be used to exert a force for other functions:

1)Movement

2)Ultrafiltration

3)Erection




1)Movement – hemolymph pressure (rather then skeletal muscle) is used to extend the legs in arachnids such as spiders. Arteries branch to the legs and flow to them controlled. Hemolymph entering into bent leg at high pressure (from an open artery) makes the leg straighten out.

2)Ultrafiltration – Blood pressure can force water and small, dissolved solutes out of pores in capillary linings. This is usedin the initial process of urine formation in the kidney and for interactions with the ECF in many tissues.




3) Erection – Blood can enter a flaccid organ under high pressure, and if exiting blood is restricted, the force of the pressure will inflate that organ. This occurs during arousal of erectile genitalia (penis, clitoris) Scientist also think it inflates the sensitive snout of the echidna ( a monotreme) which pokes its snout into termite and ant nests to feed.



Blood flow through vessels depends on the pressure gradient and vascular resistance.

Flow of fluid obeys certain physical law called the hemodynamic law. The Flow rate of blood (volume of blood passing through per unit of time) is directly proportional to the pressure gradient and inversely proportional to vascular resistance. Expressed in Hemodynamic Flow Law.

F = P/R or F = (P1 - P2) / R

where F = flow rate of fluid through a vessel

P = (P1 - P2) , P1 =pressure at the inflow end of a vessel P2 =pressure at the end flow end of a vessel

R = resistance of blood vessels


Vessels: Flow Regulation and Hemodynamics


Factors affecting flow rate:

1)Pressure Gradient

2)Resistance




1) Pressure Gradient – the difference in pressure between the beginning and end of a vessel – is the main driving force for flow through the vessel; that is,

The blood flows from an area of higher pressure to an area of lower pressure down a pressure gradient.

The greater the pressure gradient for forcing of blood through a vessel, the greater the rate of flow through that vessel.

Gravity is another major factor in establishing the pressure gradient. This is particularly important in terrestrial animals such as human and giraffe.




2)Resistance – is a measure of the hindrance to blood flow through a vessel caused by friction between the moving fluid and the stationary vascular walls.

As resistance to flow increases, it is more difficult for blood to pass through the vessel, so flow decreases ( as long as the pressure

gradient remains unchanged).

When resistance increases, the pressure gradient must increase correspondingly to maintain the same flow rate.




2)Resistance – is a measure of the hindrance to blood flow through a vessel caused by friction between the moving fluid and the stationary vascular walls.

Resistance to blood flow depends on several factors. (Laminar flow is the term for smooth flow). Three key factors are:

- Viscosity of the blood (the greater the viscosity , the greater the R)

- Vessel Length (the longer the vessel, the greater the R)

- Vessel Radius ( the smaller the radius, the greater the R)



In an open circulatory system, blood is pumped from the heart through blood vessels but then it leaves the blood vessels and enters body cavities (hemocoel), where the organs are bathed in blood, or sinuses (spaces) within the organs.

Blood flows slowly in an open circulatory system because there is no blood pressure after the blood leaves the blood vessels. The animal must move its muscles to move the blood within the spaces.

The most widely studied animals with open circulations are dominated by a single hemolymph space. Wide group of animals that have open circulatory system are: Mollusks (decapods except snails and octopuses) Insects, Crustaceans


Pathways: Open Circulation





Mollusks



Insects



Crustaceans

The heart is a muscular sac, situated dorsally, beneath the carapace, and it gives origin to six arterial trunks, which convey the aerated blood to all parts of the body. The terminations of the arteries open into a series of irregular venous sinuses, whence the blood is collected into a principal ventral sinus, and distributed to the branchiae, where it undergoes aeration.

From the gills the now aerated blood is carried by a series of branchial vessels to a large sac, which is badly termed the "pericardium," and which envelops and surrounds the heart. The arterial blood gains access to the cavity of the heart by means of six pairs of valvular fissures, which allow of the ingress of the blood, but prevent regurgitation. A portion of the venous blood, however, is not sent to the branchiae, but is returned directly, without aeration, to the pericardium; so that the heart finally distributes to the body a mixture of venous and arterial blood.



Diagram of the circulation of the Lobster. The systemic arteries are shaded longitudinally, the veins are dotted, and the branchial vessels are black. h Heart; a a Systemic arteries; b b Branchial vessels; c c Venous sinuses; g g Branchiae; p Pericardium.

In a closed circulatory system, blood is not free in a cavity; it is contained within blood vessels. Valves prevent the backflow of blood within the blood vessels.

Wide group of animals that have closed circulatory system are Nemerteans, Annelids, Fish, Reptiles, Amphibians, Birds, Mammals.


Pathways: Closed Circulation

Fish



Fish have a two-chambered heart with one atrium (A) and one ventricle (V).

The gills contain many capillaries for gas exchange, so the blood pressure is low after going through the gills. Low-pressure blood from the gills then goes directly to the body, which also has a large number of capillaries. The activity level of fish is limited due to the low rate of blood flow to the body.

Amphibians



Amphibians have a 3-chambered heart with two atria and one ventricle.

Blood from the lungs (pulmonary flow) goes to the left atrium. Blood from the body (systemic flow) goes to the right atrium. Both atria empty into the ventricle where some mixing occurs.

The advantage of this system is that there is high pressure in vessels that lead to both the lungs and body.

Reptiles



In most reptiles, the ventricle is partially divided.

This reduces mixing of oxygenated and unoxygenated blood in the ventricle. The partial division of the ventricle is represented by a dashed line.

Birds, Mammals, Crocodilians



Birds and mammals (also crocodilians) have a four-chambered heart which acts as two separate pumps.

After passing through the body, blood is pumped under high pressure to the lungs. Upon returning from the lungs, it is pumped under high pressure to the body. The high rate of oxygen-rich blood flow through the body enables birds and mammals to maintain high activity levels.




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Health & Medicine

Mammalian Circulatory system