Normal Circulation

The cardiovascular system has ten unique characteristics that make it an unusually complicated hydraulic system. Understanding how the cardiovascular system functions requires insight into a larger set of variables than that which governs the function of most pump, pipe, and fluid systems found in the world of man-made machines. The ten unique characteristics peculiar to the cardiovascular system are:

1. The system is a closed circle rather than being open-ended and linear.
   
2. The system is elastic rather than rigid.
   
3. The system is filled with liquid at a positive mean pressure ("mean cardiovascular pressure"), which exists independent of the pumping action of the heart.
   
4. The right and left ventricles, which pump into the same system that they pump out of, are in series with two interposed vascular beds (systemic and pulmonary).
   
5. The heart fills passively, rather than by actively sucking.
   
6. As a consequence of the heart's passive filling, the circulation rate is normally regulated by peripheral-vascular factors, rather than by cardiac variables.
   
7. The flow from the heart is intermittent, while the flow to it is continuous.
   
8. Normally, there is an excess expenditure of energy by the heart needed for the circulation rate imposed by peripheral vascular regulators ("pump energy excess").
   
9. Normally, ventricular capacity is in excess of the diastolic filling volume ("pump capacity excess").
   
10. The slowing effect of any vascular resistance on flow rate depends on its location, with reference to upstream compliance, as well as its magnitude.
    

In order to understand circulatory phenomena in the elastic circular hydraulic system (Fig. 1), where every point is both upstream and downstream from every other point, and where the non-sucking ventricles pump out of the same system they pump into, we need to examine the ten unique factors individually, before we can amalgamate them into a meaningful whole.
VENTRICLES (THE PUMPS)
To clarify and facilitate understanding of the features peculiar to the heart, it is helpful to compare three major types of pumps. The heart?s unique characteristics as a pump are of paramount importance in understanding how the cardiovascular system works.

PUMP TYPE #1: This type of pump both sucks and forcibly ejects fluid. This pump uses energy both to actively fill at its inlet and to empty its contents at its outlet. Two examples of this type of pump are: (1) a piston pump, which expends energy to suck in the stroke volume which is then forcibly ejected; and (2) a roller pump, which sucks at its inlet by the recoil of the resilient tubing that has been compressed by the roller as it moves forward, ejecting the fluid in front of it. With type #1 pumps, the output in a hydraulic system is determined exclusively by two pump variables: the stroke rate and the stroke volume. The reason for discussing this is that the heart is a different type of pump, and those two variables are frequently and erroneously projected onto cardiovascular function, in a way in which they do not apply.
PUMP TYPE #2: This pump sucks and blows but, instead of producing a specific flow rate, creates a specific pressure gradient between its inlet and outlet. Centrifugal pumps fall into this category. With this type, two pump factors (rate and power), as well as two non-pump factors (pressure and resistance in the system), effect output. As the heart is not such a pump, there is danger in borrowing explanations of cardiovascular function from hydraulic systems containing centrifugal pumps.
PUMP TYPE #3: This type of pump is passive filling, and does not suck at its inlet. It expends no energy to fill, it only expends energy to empty. An example of this type of pump is the urinary bladder. It is a flaccid, hollow organ that does not create any negative pressure or suck on the ureters or kidneys to fill. The bladder merely exerts energy to empty. To calculate the flow of urine for any given period, you can obtain the answer by multiplying the stroke rate times the stroke volume. However, it is important to underline here that those two things, stroke rate and volume, are not determinants of bladder output. You cannot increase the output merely by changing the rate of bladder contraction (stroke rate). The urinary bladder cannot expend energy to increase its filling and thus its stroke volume. This type of pump, even though it does the work and thus produces the flow, is totally dependent upon external factors (e.g., renal function) to determine the output. At a given rate of urinary production, stroke rate and stroke volume are reciprocals of one another. If the bladder is emptied twice as often, the stroke volume will be one half as much.

THE RIGHT AND LEFT VENTRICLES ARE TWO TYPE #3 PUMPS:
The heart, like the urinary bladder, is a hollow muscular organ that does not suck to fill, but produces circulation by ejecting whatever fluid enters it at diastole. During normal function, the heart not only doesn't develop a pressure negative to the intrathoracic pressure, but it offers an impediment to filling because of its limited volume-pressure compliance.
The evidence that the heart fills passively, and does not suck to fill, is found in the data from innumerable heart catheterizations, which all show a positive diastolic pressure in the ventricles (Fig. 2, a to c). In fact, as ventricles fill, they not only do not suck, but they offer an increasing impediment to filling, as noted by the progressive increase in pressure toward the end of diastole (Fig. 2, c). Negative ventricular pressure, in relation to intrathoracic pressure, has not been found in physiologic states. The heart, like all other muscles in the body, expends energy and does work by contracting. It cannot expend energy to do mechanical work by forcibly elongating its fibers to suck like the type #1 pump, which uses energy to suck in a stroke volume. Do not confuse the negative pressure created in the chest by inspiration as negative heart pressure (Fig. 2, b). The chest can suck, the heart cannot.
One can calculate cardiac output in the same way as in the urinary bladder example: by multiplying stroke rate times stroke volume. Also, just as in that example, while stroke rate multiplied by stroke volume measures the amount of output, those variables are not determinants of that output. The heart, by filling passively, pumps out blood at a rate determined by the rate of blood coming to it. Given that the heart is a pump that produces the flow but has a flow rate determined by extra-cardiac factors, let us examine those factors that determine circulation rate.

DETERMINATION OF CARDIAC OUTPUT IN A CIRCULAR ELASTIC SYSTEM WITH PASSIVE FILLING PUMPS
With pumps that cannot suck to fill, there must be a positive pressure at the inlets for any blood to run into the ventricles, in order for there to be any pump output. If there is no pressure in the cardiovascular system, no blood can run into the ventricles and there can be no flow. Normally, there is a mean cardiovascular pressure above zero, which the heart distributes. The heart, rather than being responsible for the pressure in the vascular system, is a circulating device. It lowers the pressure at the ventricular inlets and raises it at the ventricular outlets. With a positive pressure in the cardiovascular system, when blood is ejected into the arterial side of the circle, a pressure gradient is created between the arteries and veins. This gradient causes blood to flow around the circle back to the ventricular inlets. Therefore, the output rate varies directly with the magnitude of that mean cardiovascular pressure. The higher the pressure, the higher the gradient, the greater the flow rate. The circular system being elastic, and having resistance and other impediments to flow, the energy from ventricular contraction does not transfer instantaneously around the circle after each heart beat, as would occur in a rigid system. The energy of venous flow is several heart beats behind that of ventricular ejection. The greater the elasticity and impediments to flow, the slower the flow rate.
Therefore, during normal function, cardiac output varies directly with the mean cardiovascular pressure and inversely with the impedance to blood flow to the heart.
I. MEAN CARDIOVASCULAR PRESSURE
Definition: The mean cardiovascular pressure is the pressure in the cardiovascular system with the circulation stopped, after the pressure has equalized between the arteries, capillaries, veins, and cardiac chambers. Do not confuse this pressure with central venous pressure, venous filling pressure, or mean-arterial pressure. Mean cardiovascular pressure is the pressure related to the blood volume and the compliance of the entire elastic cardiovascular compartment.
Measurement: Mean cardiovascular pressure is expressed in centimeters of water above ambient pressure, with zero being at mid-heart level. The mean cardiovascular pressure can be approximated during cardiac arrest. After arrest, a pressure equalization occurs between the various cardiovascular compartments in about thirty seconds. The arterial pressure falls and the venous pressure rises as some of the arterial blood moves into the veins during pressure equalization. Therefore, the mean cardiovascular pressure is always above venous pressure and below arterial pressure. Normally, mean cardiovascular pressure is between 15 and 18 cm. of water above mid-heart level. We have some approximation of its magnitude from fortuitous records of the arterial and venous pressures equalizing, obtained during short periods of cardiac arrest of patients in coronary care settings, in emergency rooms, or in operating rooms during heart surgery. Even in these situations, the resulting pressure can be regarded as only an approximation, as the shift in fluid, from hypoxia caused by lack of circulation, may have altered the vascular compliance. (See Appendix for clinical measurement technique)
Significance: Without mean cardiovascular pressure there would be no circulation. The heart doesn't generate the pressure in the vascular system, it merely distributes the mean cardiovascular pressure. The cardiac ventricles take the mean cardiovascular pressure and distribute it by raising the pressure on the arterial sides while lowering it on the venous sides. The two ventricles, being passively filling pumps, cannot suck, so they lower the inlet pressures toward — but never below — zero, in relation to the ambient pressure in the chest.
The higher the mean cardiovascular pressure, if the ventricles are not failing, the higher the ventricles can elevate the arterial pressure while reducing the venous pressure toward zero, and thus the greater the cardiac output. Conversely, the lower the mean cardiovascular pressure, the less the heart can raise the arterial pressure by lowering the venous pressure, and thus the lower the cardiac output.
Origin of the mean cardiovascular pressure: The mean cardiovascular pressure results from the volume of blood and the compliance of the cardiovascular system. The volume in the cardiovascular system results from an equilibrium between the rate of water, electrolytes, and other blood constituents entering the body by way of the gastrointestinal tract, and leaving the body primarily by the kidneys (Fig. 3). The mean cardiovascular pressure is the result of a continuing dynamic process.

MEAN CARDIOVASCULAR PRESSURE = energy forcing fluid into the body / resistance to fluid loss from the body

Homeostatic maintenance of normal mean cardiovascular pressure:

(1) Slow feedback mechanism:
A slow homeostatic feedback mechanism tends to keep the mean cardiovascular pressure at a constant level: Elevation of the mean cardiovascular pressure above normal —› causes increase in cardiac output —› causes increased renal blood flow —› results in increased renal output —› thereby lowering blood volume and mean cardiovascular pressure back to normal. Conversely, low mean cardiovascular pressure —› low cardiac output —› low renal blood flow —› decreased renal output until the mean cardiovascular pressure is restored to normal by continuing fluid intake. With elevated mean cardiovascular pressure, the rate of return to normal is dependent on renal function, whereas, with low mean cardiovascular pressure the rate of return can vary greatly, depending on the rate of restoration of blood volume.
Clinical evidence of the homeostatic mechanism:

• Response to weightlessness by going into orbit: In the absence of gravity, normal blood volume shifts centrally from the lower part of the body, thereby, increasing the mean cardiovascular pressure at heart level —› resulting in increased cardiac output —› causing greater renal blood flow —› leading to greater urinary output —› causing a decrease in blood volume and, thus, a decrease in mean cardiovascular pressure back to normal. The converse is found when astronauts return to gravity. It takes a few hours to restore normal mean cardiovascular pressure by intake of fluid and electrolytes after returning to earth, during which transition time they conserve the fluid they take in by putting out very little urine.
  
• During any hypovolemic shock state, such as massive hemorrhage or severe dehydration, the urinary output goes abruptly down and remains low until restoration of normal mean cardiovascular pressure.
  

(2) Rapid mean cardiovascular pressure buffer mechanisms:

(a) Elasticity: The elasticity of the vascular system prevents sudden blood volume loss or gain from causing a linear, temporary change in mean cardiovascular pressure. Elasticity has, of course, an instantaneous buffer effect. Evidence of this is found in one's ability to give a pint of blood at the blood bank without going into severe low cardiac output. This buffer effect bolsters circulation while the blood volume — and, thus, mean cardiovascular pressure — is restored by subsequent oral intake of fluid.
(b) Vascular/extravascular equilibrium: There is a pressure equilibrium between the various extravascular compartments of the body and the cardiovascular space (Fig. 3). Changes in mean cardiovascular pressure result in shifts of fluid back and forth which tend to buffer sudden changes. This buffer system is fairly rapid but not instantaneous, as evidenced by the observation that a person going into severe shock from sudden loss of blood would not have had the same severe shock state if the loss had occurred more gradually over a period of an hour or so.

(3) Humeral and neuro-muscular-vascular reflexes:
These responses from stimuli, which alter vascular compliance, act as buffer systems. They prevent sudden changes in mean cardiovascular pressure from sudden position changes, such as going from lying to standing. They also buffer the effect of sudden loss of blood volume from hemorrhage.

II. IMPEDANCE TO THE FLOW OF BLOOD FROM THE OUTLETS AROUND TO THE INLETS OF THE VENTRICLES
Four factors tend to impede the flow of blood in the cardiovascular circle. Therefore, they are inverse determinants of cardiac output: (1) resistance, (2) elasticity, (3) limited compliance of the ventricles to filling, and (4) inertia of intermittent blood flow to the ventricles. The interrelationship of these four factors makes flow determination much more complicated than plain resistance, which is the single impediment in rigid, open ended, linear hydraulic systems.
(1) Resistance and (2) Elasticity

Unlike rigid linear hydraulic systems, where a given resistance may have the same effect on flow, irrespective of its location, the elasticity of the vascular system makes location of the resistance a significant parameter. Because of the elasticity of the circle, the location of any particular resistance determines to what extent that resistance has on impeding blood flow. A given resistance may have little or no effect in determining cardiac output if it is near the outlet of the ventricles, yet the same magnitude of resistance may have tremendous slowing effect on circulation if located near the inlets of the heart. Resistance points that have little compliant vascular bed "upstream" (arteriolar resistance), increase pump work but may not affect cardiac output significantly. The heart, except during failure, exerts enough energy to force the blood past any resistance near its outlet, with no hold up in flow. On the other hand, resistance located with a large compliant bed upstream has a tremendous effect on flow rate by slowing blood return to the ventricles. Venous sided resistance, with the compliance of the whole vascular bed upstream, is a major inhibitor of circulation rate. Thus, venous sided resistance is a major determinant of cardiac output, but arterial resistance is not. Interpolation of the additive effect of all resistance points in the circle on cardiac output must include the amount of compliant bed upstream from each resistance point.
All resistance factors — including blood viscosity, cross-section area of any vascular bed, margination of blood constituents, etc. — play roles in flow rate determination only when linked with their location to compliance upstream. Adding venous sided resistance of a magnitude that results in only a few mm. water pressure gradient may cause a marked reduction of flow. Whereas, increasing arteriolar resistance to the point of severe arterial hypertension may not appreciably change cardiac output.
In human cardiovascular physiology, the significance of resistance can only be understood when coupled with upstream compliance. It is not just the magnitude of resistance but the location of that resistance that determines its effect on circulation rate.

(3) Impediment to Ventricular Filling

The end-diastolic pressure: Ventricles not only do not suck to fill, they offer an impediment to filling. The left ventricle has thicker and stiffer walls than the right, so it tends to retard filling more than the right ventricle. Catheterization data shows end-diastolic pressure of five to ten centimeters of water above intrathoracic pressure. Don't confuse the negative pressure of inspiration, transmitted to the heart, as the heart sucking. The intracardiac pressure is always above that intrathoracic pressure (Fig. 2 at C).

(4) Inertia of Intermittent Blood Flow Offset by "The Atrial Effect"

Atrial function facilitates circulation by preventing the retarding effect that would otherwise occur from the intermittent inflow to the intermittent outflow ventricles. By being partially empty and distensible, atria prevent the interruption of venous flow to the heart that would occur during ventricular systole if the veins ended at the inlet valves of the heart.
Atria have four essential characteristics that cause them to promote continuous venous flow. (1) There are no atrial inlet valves to interrupt blood flow during atrial systole. (2) The atrial systole contractions are incomplete and thus do not contract to the extent that would block flow from the veins through the atria into the ventricles. During atrial systole, blood not only empties from the atria to the ventricles, but blood continues to flow uninterrupted from the veins right through the atria into the ventricles. (3) The atrial contractions must be gentle enough so that the force of contraction does not exert significant back pressure that would impede venous flow. (4) The "let go" of the atria must be timed so that they relax before the start of ventricular contraction, to be able to accept venous flow without interruption.
By preventing the inertia of interrupted venous flow that would otherwise occur at each ventricular systole, atria allow approximately 75% more cardiac output than would otherwise occur. The fact that atrial contraction is 15% of the amount of the succeeding ventricular ejection has led to the false conclusion that atria have their benefit by pumping up the ventricles (the so-called "atrial kick"). The real benefit is in preventing inertia and allowing uninterrupted venous flow.
The 20% to 25% increase in cardiac output from synchronized atrial function over that of atrial fibrillation doesn't belie the 75% contribution of the atrial effect, as atrial fibrillation eliminates only part of that effect. Atrial compliance, elasticity, and gravity help in emptying the atria at ventricular diastole during atrial fibrillation. Also, cardiac output during atrial dysfunction is buffered: the initial fall in circulation rate during atrial fibrillation reduces renal flow, thereby causing retention of water and the subsequent rise in mean cardiovascular pressure, which then partially offsets the slowing effect on circulation.

Thus, four factors impede the flow of blood around the cardiovascular circle: (1) resistance with (2) upstream compliance, (3) ventricular non-compliance, and (4) inertia if there is intermittent venous flow. The combined effect of these factors that impede the flow of blood to the inlet of the ventricles and, therefore, determine cardiac output in a negative way, will be referred to as: inlet impedance.

In summary, during normal physiology: CARDIAC OUTPUT=FUNCTION OF MEAN CARDIOVASCULAR PRESSURE / INLET IMPEDANCE

AUTOMATIC BALANCING OF THE PULMONARY AND SYSTEMIC BLOOD VOLUMES
The passive filling characteristic of the ventricles is the feature that accounts for the automatic maintenance of blood volume equilibrium between the pulmonary and systemic vascular beds. With passively filled pumps, the relative blood volume in the two circuits is determined by their relative size and elasticity. On the other hand, if the ventricles were type #1 pumps, which actively fill, any discrepancy in the output of the two pumps, or flow through normal physiological shunts between the two vascular systems, would very quickly shift all of the blood volume into one circuit at the expense of the other, resulting in disaster.
The right and left ventricles, by filling passively, pump out whatever amount comes to them, determined by extracardiac factors. The blood volume equilibrium, therefore, is determined by the relative size and compliance of the two circuits and, to a minor extent, by the relative impediment of flow to the two pumps. It has been noted that the output of the two sides of the heart is never equal because there are physiological shunts, which connect one vascular bed to the other. The largest of these shunts, in normal physiology, are the bronchial arteries, which go from the systemic circuit to the lungs. The bronchial blood flow is a left-to-right shunt that accounts for the left ventricular output normally being at least 10% larger than the right. Because of the shunt, more blood returns to the left ventricle than the right, the left ventricle passively fills more than the right, thereby causing it to produce a greater output and thus the equilibrium is maintained. With other types of pumps this would not occur.
A dramatic illustration of this volume equilibrium, automatically being maintained during a massive discrepancy in output of the two pumps, is seen in atrial septal defects. In this case, the right ventricular output may be four or five times that of the left. Yet, the volume equilibrium is maintained. A large atrial septal defect virtually results in a single atrium above the two ventricles. The shunt occurs during ventricular diastole, because the right, thin walled ventricle is more distensible than the non-compliant thicker walled left ventricle. The blood in the common atrium goes the way of least resistance. The greater filling into the more compliant right ventricle results in greater right ventricular output. The greater right output goes to the lungs and then directly back to the right ventricle, returning again through the septal defect. Because of the passive filling, this results in no progressive increase in the blood volume in the lungs, and no disturbance in the maintenance of the blood volume equilibrium. After closure of the septal defect, resulting in much smaller right heart output, the volume equilibrium remains. This equilibrium, which persists after such sudden, massive changes in right heart output, occurs automatically because of the passive filling characteristic of the ventricles. It is the physical characteristics of the two vascular beds (e.g., relative size, compliance, and impediment to flow), that determines the volume balance with passive filling ventricles.

The passive filling of the ventricles accounts for the maintenance of blood volume equilibrium between the systemic and pulmonary vascular systems.

HEART RATE AND STROKE VOLUME
Normally, the passively filling ventricles are not maximally filled at diastole. Also, they are exerting excess energy over that needed to eject blood at the flow rate of blood entering the ventricles. With such volume and energy reserve, if blood enters the heart faster, the flow rate can go up without any change in strength of contraction or heart rate, unless the heart is being filled maximally (heart failure). Conversely, if blood enters the ventricles at a slower flow rate, the output will go down irrespective of any lowering of the rate or decrease in strength of cardiac contraction.
Thus, at a given flow rate, with the normal excess pump power, in both strength and rate, the heart rate and stroke volume become reciprocals of one another, as long as the heart doesn?t go into failure. At a given flow rate, decreasing the heart rate increases the stroke volume; while increasing the heart rate decreases the stroke volume. The observation — that cardiac output usually parallels the cardiac rate and strength of contraction — has resulted in the fallacious conclusion, based on post hoc ergo propter hoc reasoning ("following this, therefore because of this"), that they are cause and effect.
Even though these two variables do not normally control cardiac output, their variability has physiological benefit in energy conservation. During low circulation rates, when the heart is not filling to its maximal volume during diastole, the heart down shifts its rate and strength of contraction, thus conserving energy. Also, during high output states, it increases its rate and strength of contraction, thus preventing failure from any limitation of output that might be imposed by ventricular chamber size. If the heart functioned at its maximum strength of contraction and a rate of 150 beats a minute, the cardiac output would go up and down just as it does normally. But what a waste of energy would result! So the variability of rate and strength of contraction have only ecological value: that of conserving world food supply.
Two mechanisms cause the heart to roughly parallel its energy expenditure with cardiac output, preventing failure during high output states and saving energy during low output: (1) The neural and humeral stimuli that increase mean cardiovascular pressure are also those that increase heart rate and strength of contraction. (2) Increased stretching of the ventricles at diastole causes some increased strength of contraction at systole (Starling's law of the heart). While this observation of Starling is true and contributes to the paralleling of cardiac output to strength of contraction, it is probably not a major determinant of energy expenditure, as strong cardiac contractions continue even when the heart is completely empty, as seen during cardiac bypass surgery.
The reciprocal relationship of heart rate and stroke volume can be demonstrated in patients with complete heart block by varying the rate of firing of their pacemakers. Variations in rate, within physiological levels, above that required to prevent complete diastolic ventricular filling, are associated with no change in cardiac output. Therefore, a compromise rate of 78 is a commonly used setting that allows a wide range of activity acceptable to most patients.

Conclusion: During normal physiologic states, there is always pump energy excess over that used in circulation.

EXERCISE AND CARDIAC OUTPUT INCREASE
Two factors cause the increase in cardiac output during exercise: Exercise causes the cardiovascular impedance to be decreased and the mean cardiovascular pressure to be increased. The intermittent skeletal muscle contractions around venous beds, which contain one-way valves, act as a peripheral pump which overcomes significant impedance to flow. Neuro-humeral reflexes speed the heart rate, which slightly lowers the inlet impedance to the heart, by lowering the end-diastolic pressure over what it would otherwise be. The increased heart rate guarantees excess energy expenditure, thus preventing cardiac power failure at the higher circulation rate. The neuro-humeral response to exercise also throws the vascular system into spasm, thereby increasing the mean cardiovascular pressure from the "G-suit" effect of tensing the body in general. These are temporary changes, lasting only during the exercise period, which do not effect the long term homeostatic control of circulation.

DISTRIBUTION OF BLOOD FLOW: PULSATILE BLOOD FLOW AND ARTERIOLAR RESISTANCE
Pulsatile arterial blood flow tends to result in diffuse, fairly equal distribution of blood to all tissues of the body. This phenomenon would not occur with a non-pulsatile steady flow. Arteriolar resistance variability from time to time and from place to place, superimposed on the otherwise diffuse distribution, controls preferential blood flow to specific areas, with physiologic benefit. The diverting of a greater portion of cardiac output to the digestive tract after meals and the increased flow to muscles during exercise are examples of changes in distribution of blood flow controlled by variable arteriolar resistance. Peripheral arteriolar resistance, rather than having a cardiac output control function, has its physiological significance by its determination of distribution of blood flow.

thanks for the info u r sharing with us your info is useful for us .......

Connecticut Locksmith