Elevations more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality. Arterial hypertension can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, such as a hypertensive emergency. All levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth atheroma that develops within the walls of arteries.
The higher the pressure, the more stress that is present, the more the atheroma tends to progress, and the more heart muscle may thicken, enlarge, and weaken over time. Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure, and arterial aneurysms, and is the leading cause of chronic renal failure. Even moderate elevation of arterial pressure leads to shortened life expectancy.
In the past, most attention was paid to diastolic pressure, but now we know that both high systolic pressure and high pulse pressure the numerical difference between systolic and diastolic pressures are also risk factors for disease. In some cases, a decrease in excessive diastolic pressure can actually increase risk, probably due to the increased difference between systolic and diastolic pressures.
Venous pressure is the vascular pressure in a vein or the atria of the heart, and is much lower than arterial pressure.
Blood pressure generally refers to the arterial pressure in the systemic circulation. However, measurement of pressures in the human venous system and the pulmonary vessels play an important role in intensive care medicine and are physiologically important in ensuring proper return of blood to the heart, maintaining flow in the closed circulatory system.
The Human Venous System : Veins from the Latin vena are blood vessels that carry blood towards the heart. Veins differ from arteries in structure and function; arteries are more muscular than veins, while veins are often closer to the skin and contain valves to help keep blood flowing toward the heart. Venous pressure is the vascular pressure in a vein or the atria of the heart. It is much lower than arterial pressure, with common values of 5 mmHg in the right atrium and 8 mmHg in the left atrium.
Variants of venous pressure include:. In general, veins function to return deoxygenated blood to the heart, and are essentially tubes that collapse when their lumens are not filled with blood. Compared with arteries, the tunica media of veins, which contains smooth muscle or elastic fibers allowing for contraction, is much thinner, resulting in a compromised ability to deliver pressure.
The actions of the skeletal-muscle pump and the thoracic pump of breathing during respiration aid in the generation of venous pressure and the return of blood to the heart. The pressure within the circulatory circuit as a whole is mean arterial pressure MAP. In the past, hypertension was only diagnosed if secondary signs of high arterial pressure were present along with a prolonged high systolic pressure reading over several visits.
Hypotension is typically diagnosed only if noticeable symptoms are present. Clinical trials demonstrate that people who maintain arterial pressures at the low end of these ranges have much better long-term cardiovascular health. The principal medical debate concerns the aggressiveness and relative value of methods used to lower pressures into this range for those with high blood pressure.
Elevations more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality. Arterial hypertension can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, such as a hypertensive emergency. All levels of arterial pressure put mechanical stress on the arterial walls. Transmural pressure or distending pressure refers to a difference between the pressure within the vessel and outside the vessel.
The intersection of the line of compliance with the y-axis reflects an unstressed volume Vu; fig. Stressed volume is a volume of blood within a vein under transmural pressure above zero Vs; fig.
An analog with a tub is helpful to understand the relation between Vu and Vs 13—15 fig. Both volumes are important: Vs determines mean circulatory filling pressure MCFP; see Mean Circulatory Filling Pressure section and directly affects venous return VR and CO, whereas Vu is a reserve of blood that can be mobilized into circulation when needed.
Stressed and unstressed volumes—tub analogy. Water in a tub represents total blood volume. A hole in the wall of the tub between the surface of the water and the bottom of the tub divides total volume into stressed Vs and unstressed Vu volumes, above and below the hole, respectively. The water leaves the tub through the hole at a certain rate that depends on the diameter of the hole which would reflect venous resistance [VenR] , and on the height of the water above the hole, representing Vs; the larger the Vs, the higher the flow through the hole.
The water between the hole and the bottom of the tub does not affect the flow of water through the hole; this is the Vu, a sequestered volume that does not directly participate in the rate of water flow venous return.
With the same amount of water in the tub total blood volume in the venous system , the relation between Vs and Vu can be changed by moving the hole up or down. Moving the hole down represents venoconstriction and increases Vs and venous return. The distal end of the tube, attached to the hole in the tub wall, represents central venous pressure CVP : the higher the distal end, the higher the CVP and the lower the pressure gradient for venous return, and vice versa.
The inflow tap represents the arterial flow. The hydraulic disconnect between the tap and the tub represents functional disconnection between the two arterial flow and the venous system due to high arterial resistance.
This relation is an important homeostatic mechanism in the body, 8,16 fig. The described relation between flow, pressure, and volume within the veins occurs in very compliant splanchnic veins and represents a passive distribution of volume between veins mainly the splanchnic system and the heart, which is associated with changes in venous capacity without change in compliance fig.
Flow—pressure—volume relation in complaint veins. Line 1 depicts a schema of the terminal and venous part of the circulation. ArtR and VenR represent arterial and venous resistance, respectively. At steady state, the flow F through the system must be the same at every point of the schema.
Flow is equal to pressure gradient divided by resistance line 2. An increase in ArtR decreases F through the whole system line 3. VenR is much smaller than ArtR and does not change the overall situation within the system. Assuming that CVP remains unchanged as is almost always the case in normal cardiac function , decreased flow through the system must be associated with a decrease in PVP.
Because an increase in ArtR unavoidably leads to a decrease in PVP line 3 and compliance does not change fig. A decrease in PVV leads to a shift of blood volume from the veins to the heart increasing venous return VR, line 6. At the moment of decreased arterial flow inflow , the flow from the veins is not decreased immediately; there is a transient increase in the flow from the veins but then, after the volume is expelled from the veins, the venous outflow decreases and becomes equal to the decreased arterial flow.
Therefore, the schema is approximately two steady states, and the transient uncoupling between arterial inflow decreased and venous outflow increased is short lasting. A decrease in flow through the splanchnic arteries, being associated with a decrease in volume in the splanchnic veins and the liver and transfer of this volume into the systemic circulation, plays an important role not only in compensation of hypovolemia but also in compensation of cardiac failure.
If CO is decreasing, a simultaneous decrease in flow through splanchnic arteries is associated with a shift of blood volume from splanchnic veins to the heart recruiting Frank-Starling mechanism an increase in preload leading to an increase in contractility. In a kg human, this would mean a shift of blood volume of approximately versus ml of blood into systemic circulation with and without reflexes intact, respectively.
Passive change in blood volume within the splanchnic system is more important within the intestines, whereas the active constriction of the vasculature is more prominent within the liver. More than 70 yr ago, an enlargement of cardiac dimensions was observed during cross clamping of the thoracic aorta. Many other studies confirmed these observations.
Therefore, aortic cross clamping proximal to celiac artery leads to a drastic decrease in splanchnic flow, followed by a decrease in volume within the splanchnic veins and a shift of the volume to the upper part of the body with an increase in VR and CO.
Let us imagine the heart is stopped for a relatively short period of time. Blood will not be flowing from the heart and toward the heart, and pressure will be the same in all parts of the circulatory system.
Such a pressure is called mean circulatory filling pressure. The pressure in the small veins becomes higher than in the large veins and right atrium—CVP. Blood flow from the veins into the heart is determined by the gradient between peripheral and central venous pressures. During cardiac arrest, the pressure within the venulae and small veins is not changing and remains the same as it was before cardiac arrest.
The heart cannot pump more blood into circulation than it receives. A normal heart itself can increase VR mainly by decreasing CVP, and only to a limited extent by increasing MCFP because of high resistance across arterial resistance vessels: The main pressure gradient within the circulatory system occurs at the level of arterial resistance. The main factor determining the MCFP is Vs; others include venomotor tone, the vascular pump, the effects of ventricular contraction and relaxation, and the function of the venous valves and skeletal muscle.
An interesting question is why in the normally functioning heart an increase in CVP e. The tempting answer to this question is because myocardial contractility is increased. But this would not be enough because an increased contractility can increase the ejection fraction and would solve the problem of the heart but would not solve the problem of the circuit.
Constriction of the veins decreases their capacity and expels blood from them into the systemic circulation. However, venoconstriction may increase venous resistance and subsequently decrease VR and CO.
How is the body recruiting the blood volume without an increase in resistance to VR? The constriction of splanchnic veins is not associated with an increase in resistance to VR because the splanchnic system is outside of the mainstream of blood flow to the heart through the caval veins 1,15,33 fig. Two-compartment model. Inside: The two circuits represent two compartments; the solid red and blue lines represent arterial and noncompliant venous compartments the main, basic circuit.
Dashed red and blue lines represent arterial and compliant splanchnic venous compartments. The compartment with compliant veins is outside of the main circuit. Therefore, changes in arterial or venous resistance in compliant compartment do not directly affect arterial or venous resistance in the main circuit with noncompliant veins.
Thickness of the lines reflects the amount of flow within the vessels under normal conditions. The size of the junctions between arteries and veins reflects the blood volumes contained in the two circuits. Outside: Effects of change in arterial resistance feeding compliant splanchnic and noncompliant muscle veins.
SplArtR and NonSplArtR represent arterial resistance in arteries feeding compliant and noncompliant veins, respectively. F, P, and V represent flow, pressure, and volume within the venous vasculature, respectively. Change in resistance in arteries feeding splanchnic and nonsplanchnic vasculature leads to changes in venous return in opposite directions through changes in flows, pressures, and intravenous volumes see text for explanation.
The latter decreases Vu and increases Vs without change in the elastic properties of the venous wall, i. In the analog with the tub, the outlet hole in the tub is moved down by venoconstriction: increasing the volume above the outlet hole and decreasing the volume below it fig. The period of compensation reflects successful mobilization of Vu into Vs. Then, when the entire Vu has been mobilized, decompensation occurs suddenly. Similarly, when mobilization of Vu is secondary to an increase in sympathetic tone, an intervention associated with venodilation general or regional anesthesia, opioids, sedatives , may cause rapid decompensation without additional blood loss because venodilation would be associated with a shift of volume from Vs back to Vu, resulting in a decrease in MCFP.
There is another interesting mechanism: Venous capacitance vessels are much more sensitive to sympathetic stimulation than arterial resistance vessels. On the other hand, the response to larger doses of vasoconstrictors would be associated with both decrease in venous capacity with recruitment of blood volume from splanchnic vasculature and an increase in arterial tone and blood pressure.
There is another important component in this picture: resistance within the splanchnic venous system. The main place of resistance to the venous flow out of the splanchnic vasculature is located within the hepatic veins 15,35—37 or within the liver itself. Profound arterial hypotension during septic shock in piglets was not associated with a decreased MCFP but rather with a drastic increase in venous resistance within the distal part of the splanchnic vasculature.
Another important mechanism regulating the VR is resistance within the splanchnic arterial vasculature. Almost a century ago, the concept of a two-compartment model within the venous system was introduced 61 ; one is very compliant and slow splanchnic vasculature and another is noncompliant and fast nonsplanchnic venous vasculature; fig.
This model has been used to explain many physiologic observations. It has also been periodically challenged. The model can be described as follows: An increase in resistance in arteries and arterioles feeding compliant splanchnic veins decreases flow, pressure, and volume within splanchnic veins, shifting blood volume from the splanchnic veins into the systemic circulation, and vice versa , a dilation of these arteries leads to blood pooling within the splanchnic veins fig.
Such shift of blood volume is reflected in a rapid increase in flow from the splanchnic vasculature into the systemic circulation. Such an increase in flow is transient and the resulting blood volume redistribution would remain until the altered resistance in these arteries is maintained. When the change in resistance is reversed, the opposite shift of blood volume would occur. Nonsplanchnic, less compliant veins behave differently.
Dilation of small arteries and arteriolae in the nonsplanchnic vasculature, if associated with a relatively minor or no decrease in arterial pressure, would increase VR fig. This relation can be illustrated by an opening of a large arteriovenous fistula. Hemodynamic response to exercise is a beautiful illustration of how the different vascular beds respond in opposite directions to fulfill the changing requirements of the body for blood volume and oxygen delivery redistribution. An increase in sympathetic discharge during exercise leads to splanchnic arterial vasoconstriction leading to a decrease in flow, pressure, and volume within the splanchnic veins and an increase in VR and CO fig.
Simultaneous increase in sympathetic discharge constricts vasculature in nonexercising muscle and other tissues, helping to increase arterial pressure and MCFP, also increasing VR and CO. The effect of different vasodilators on VR and CO can depend on blood flow distribution between the two compartments, splanchnic and nonsplanchnic vasculature.
For example, we and others observed that sodium nitroprusside decreases splanchnic blood flow. However, it does not happen 69,70 : In another study, during similar degrees of arterial hypotension, vascular capacity was increased during sodium nitroprusside and to a greater extent during nitroglycerin-induced hypotension, whereas it was not changed during adenosine triphosphate administration.
On the other hand, nitroglycerin dilated arterial vasculature within the splanchnic system, increasing flow, pressure, and splanchnic vascular volume and decreasing VR and CO fig. Active dilation of the splanchnic veins, in addition to the passive distention due to an increase in transmural pressure and volume, reinforces the accumulation of blood volume within the splanchnic venous system. Clinical observations support the notion that both sodium nitroprusside and nitroglycerin decrease arterial resistance and increase venous capacity.
Experiments using right heart bypass preparation, where blood flow and CVP were independently controlled and blood was drained separately from splanchnic and nonsplanchnic vasculature, demonstrated different effects of four vasodilators on splanchnic and nonsplanchnic arterial resistance. Captopril decreased arterial resistance, increased flow and volume within splanchnic vasculature, and decreased central blood volume; in the absence of bypass, it would lead to a decrease in VR and CO.
Nifedipine did not affect arterial resistance within the splanchnic system but did significantly decrease it within the nonsplanchnic system. Variants of venous pressure include central venous pressure, which is a good approximation of right atrial pressure, which can then be used to calculate right ventricular end diastolic volume.
Neurogenic and hypovolemic shock can cause fainting. When the smooth muscles surrounding the veins become slack, the veins fill with the majority of the blood in the body, keeping blood away from the brain and causing unconsciousness. Key Terms central venous pressure : The pressure of blood in the thoracic vena cava, near the right atrium of the heart, reflecting the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system.
Systemic Venous Pressure Venous pressure is the vascular pressure in a vein or the atria of the heart. Variants of venous pressure include: Central venous pressure, a good approximation of right atrial pressure, which is a major determinant of right ventricular end diastolic volume. Jugular venous pressure JVP , the indirectly observed pressure over the venous system.
It can be useful in differentiating different forms of heart and lung disease. Portal venous pressure or the blood pressure in the portal vein. It is normally 5—10 mmHg. Vein Structure and Function In general, veins function to return deoxygenated blood to the heart, and are essentially tubes that collapse when their lumens are not filled with blood.
Pooling and Fainting Standing or sitting for a prolonged period of time can cause low venous return in the absence of the muscle pump, resulting in venous pooling vascular and shock.
0コメント