Information

Veins collapse when empty


Veins collapse when empty. That's because they have thin and almost inelastic walls. What has inelasticity and thinness of the walls to do with the collapsing of the veins?


Your body exists at a certain pressure, determined by your surroundings; usually, this is about 1 atmosphere of pressure, but it can go up or down (e.g. when you fly on an airplane, or when you go diving). The pressure that your surroundings put on your skin is transmitted throughout your body, and your body "pushed back" against it.

However, this means that all your blood vessels have that pressure weighing down on them along their length. Normally, when they're full of blood, the pressure of that blood will press the blood vessel outwards to counter-act this. Without the blood, however, that pressure within the blood vessel is no longer sufficient to withstand the pressure being exerted on it from the outside.

Since the walls of the blood vessels aren't thick enough to have enough structural integrity to withstand that pressure differential, they then proceed to collapse.


Researchers find reason why many vein grafts fail

NIH intramural-led study uncovers biology behind improper graft remodeling, points to treatment strategies.

Endothelial cells not only form the inner lining of a blood vessel, but also contribute to blood vessel narrowing as shown in this mouse vein graft model. Endothelial cells (green) lose their typical morphology and become more like smooth muscle cells (red). This change in cellular properties indicates that endothelial-to-mesenchymal transition (EndMT) is operative in vein graft stenosis. Manfred Boehm/NHLBI

National Institutes of Health researchers have identified a biological pathway that contributes to the high rate of vein graft failure following bypass surgery. Using mouse models of bypass surgery, they showed that excess signaling via the Transforming Growth Factor Beta (TGF-Beta) family causes the inner walls of the vein become too thick, slowing down or sometimes even blocking the blood flow that the graft was intended to restore. Inhibition of the TGF-B signaling pathway reduced overgrowth in the grafted veins.

The team, led by Manfred Boehm, M.D., chief of the Laboratory of Cardiovascular Regenerative Medicine at NIH's National Heart, Lung, and Blood Institute, identified similar properties in samples of clogged human vein grafts, suggesting that select drugs might be used in reducing vein graft failure in humans.

This study will be published March 12 in Science Translational Medicine.

Bypass surgery to restore blood flow hindered by clogged arteries is a common procedure in the United States. The great saphenous vein, which is the large vein running up the length of the leg, often is used as the bypass conduit due to its size and the ease of removing a small segment. After grafting, the implanted vein remodels to become more arterial, as veins have thinner walls than arteries and can handle less blood pressure. However, the remodeling can go awry and the vein can become too thick, resulting in a recurrence of clogged blood flow. About 40 percent of vein grafts experience such a failure within 18 months of the operation.

Boehm and his colleagues examined veins from mouse models of bypass surgery, and discovered that a process known as an endothelial-to-mesenchymal transition, or EndoMT, causes the inside of the vein to over-thicken. During EndoMT, many of the endothelial cells that line the inner surface of the vein proliferate and convert into more fibrous and muscle-like cells. These mesenchymal cells begin to accumulate on the inner wall, narrowing the vessel.

This process was triggered by TGF-Beta, a secreted protein that controls the proliferation and maturation of a host of cell types the researchers found that TGF-Beta becomes highly expressed just a few hours after graft surgery, indicating the remodeling starts fairly quickly.

Boehm’s team also looked at human veins taken from failed bypass operations, and found corroborating evidence for a role for EndoMT in human graft failure. In short term grafts (less than one year), many of the cells inside the human veins displayed both endothelial and mesenchymal cell characteristics, while in long-term grafts (more than six years) the cells on the inner wall were primarily mesenchymal in nature.

“This study shows for the first time that endothelial cells in the vein directly contribute to blood vessel narrowing following a vein graft,” Boehm said. “Now that we better understand the mechanism that causes the abnormal thickening, we can look for therapeutic strategies to attenuate it, and reduce the number bypass reoperations we need to perform each year.”

Boehm cited the high-blood pressure drug Losartan, which can inhibit TGF-Beta, as one possible treatment strategy, though more proof of concept studies are needed before any clinical studies can commence.


What Is a Collapsed Vein? (with pictures)

A collapsed vein occurs when the exterior walls of the vein cave inward. This may be due to traumatic injury from repeated needle sticks or natural disease processes. Symptoms may include bruising, pain, or itching. Treatment is not usually necessary, as the vein will normally repair itself quite easily. If the collapse occurs due to medical problems such as vascular disease, the underlying medical condition must be addressed. Any specific questions or concerns about a collapsed vein in an individual situation should be discussed with a doctor or other medical professional.

Repeated needle sticks in the same general area of the body are among the leading causes of a collapsed vein. This symptom primarily occurs among those who must receive injections on a regular basis and is particularly common among the elderly due to thinning skin and weakened blood vessels. A long stay in the hospital that requires the use of intravenous medications or repeated blood draws may also increase the risks of having a collapsed vein. Poor technique by the health care provider or the injection of medications that can irritate the blood vessels may also lead to vein collapse.

A disease known as peripheral vascular disease is sometimes the cause of venous collapse. This disease causes reduced blood flow and increased pressure in the blood vessels, occasionally leading to collapse. Varicose veins, which can be highly noticeable and uncomfortable, are particularly vulnerable to collapse.

In most cases, there are no noticeable symptoms associated with a collapsed vein. Sometimes, there may be a slight burning sensation or mild discomfort at the site of the collapse. A few minutes to a few hours later, mild to moderate bruising may occur, but this is generally of no medical significance. As the bruising begins to heal, the area may begin to itch.

Treatment for a collapsed vein is rarely necessary, especially when it occurs as a result of a needle stick. The blood vessel will usually repair itself quickly, and there is rarely a medical risk resulting from the collapse of a vein. The exception to this would be a major rupture associated with a form of vascular disease. If there is severe pain or extreme bruising, a doctor should be consulted right away for further medical evaluation. In the most severe cases, surgical intervention may become necessary to repair the damaged vein and prevent excessive blood loss and other potential complications.


Definitions and Basic Concepts

Venous Capacity and Compliance

There is some confusion in the literature regarding the relevant terminology. The definitions described in this article are used by the majority of authors and clearly summarized by the authority in the field.1,9

Venous capacity is a blood volume contained in a vein at a specific distending pressure.6,9–11

Venous compliance is a change in volume (ΔV) of blood within a vein (or venous system) associated with a change in intravenous distending pressure (ΔP).

Therefore, capacity is a point of volume at a certain pressure while compliance is a slope of change in volume associated with a change in pressure. A decrease in volume within a vein (or venous system) can be achieved by a decrease in capacity (position of the curve) or by a change in compliance (slope of the curve) or both (fig. 1). Venoconstrictors, α-adrenergic agonists, decrease venous capacity without changing compliance.12

Fig. 1. Venous capacity and compliance, stressed and unstressed volumes. Point A1 represents total volume of blood in veins at transmural pressure p 1 . Points A2 and A3 represent change in volume induced by change in pressure within the veins. Thick black linerepresents baseline compliance. Point A 0 is obtained by extrapolation of the thick black line until it crosses the y-axis this point (A 0 ) represents volume of blood at transmural pressure zero, which is unstressed volume (Vu 1 ). Difference between total volume (Vt) and Vu 1 is stressed volume (Vs). When a certain amount of blood is mobilized from the veins, point A1 moves to point B the veins contain now less blood at the same intramural pressure p 1 . Removal of the volume of blood between points A1 and B may be associated with no change in the slope of the pressure–volume relation ( thin black line parallel to the thick black line) this means that venous compliance did not change, but capacity did. Point B 0 ( thin black line extrapolated to the y-axis) represents decreased unstressed volume (from Vu 1 to Vu 2 ). However, the pressure–volume relation within the veins might look like the gray line. The same amount of blood is mobilized (from point A1 to B), but Vu did not change: The gray line crossed the y-axis at the same point A 0 the mobilized blood was recruited by a decrease in compliance rather than from a decrease in Vu.

Fig. 1. Venous capacity and compliance, stressed and unstressed volumes. Point A1 represents total volume of blood in veins at transmural pressure p 1 . Points A2 and A3 represent change in volume induced by change in pressure within the veins. Thick black linerepresents baseline compliance. Point A 0 is obtained by extrapolation of the thick black line until it crosses the y-axis this point (A 0 ) represents volume of blood at transmural pressure zero, which is unstressed volume (Vu 1 ). Difference between total volume (Vt) and Vu 1 is stressed volume (Vs). When a certain amount of blood is mobilized from the veins, point A1 moves to point B the veins contain now less blood at the same intramural pressure p 1 . Removal of the volume of blood between points A1 and B may be associated with no change in the slope of the pressure–volume relation ( thin black line parallel to the thick black line) this means that venous compliance did not change, but capacity did. Point B 0 ( thin black line extrapolated to the y-axis) represents decreased unstressed volume (from Vu 1 to Vu 2 ). However, the pressure–volume relation within the veins might look like the gray line. The same amount of blood is mobilized (from point A1 to B), but Vu did not change: The gray line crossed the y-axis at the same point A 0 the mobilized blood was recruited by a decrease in compliance rather than from a decrease in Vu.

It is important to distinguish intraluminal (intramural ) venous pressure , which is the pressure within a vessel (which can be measured directly via an inserted catheter), regardless of the pressure surrounding the vessel. Transmural pressure or distending pressure refers to a difference between the pressure within the vessel and outside the vessel.

Stressed and Unstressed Volume

The intersection of the line of compliance with the y-axis reflects an unstressed volume (Vu fig. 1), which is a volume of blood in a vein at transmural pressure equal to zero. Stressed volume is a volume of blood within a vein under transmural pressure above zero (Vs fig. 1). The sum of stressed (approximately 30% of total volume) and unstressed (approximately 70% of total volume) volumes is the total blood volume within the venous system.

An analog with a tub is helpful to understand the relation between Vu and Vs13–15(fig. 2). 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.

Fig. 2. 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.

Fig. 2. 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.

Flow–Pressure–Volume Relation

This relation is an important homeostatic mechanism in the body,8,16(fig. 3). 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. 1, black lines).

Fig. 3. Flow–pressure–volume relation in complaint veins. Line 1depicts a schema of the terminal and venous part of the circulation. AP, PVP, and CVP represent pressure in arteries, small (peripheral) veins (capillary pressure is incorporated into PVP), and right atrium, respectively. 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. Therefore, because F is decreased, the difference between PVP and CVP must have decreased. To maintain flow through the system, PVP must be higher than CVP. 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 compliance (C) by definition is a ratio of ΔV to ΔP ( equation 1in the text), the volume within the small veins (PVV) would be equal to compliance in peripheral veins (Cpv) multiplied by pressure within the veins (PVP, line 4). Because an increase in ArtR unavoidably leads to a decrease in PVP ( line 3) and compliance does not change ( fig. 1, black lines), any decrease in PVP must be associated with a decrease in volume of blood within the small veins (PVV, line 5). In reality, a decrease in F is associated with an immediate and simultaneous decrease in PVP and PVV. A decrease in PVV leads to a shift of blood volume from the veins to the heart increasing venous return (VR, line 6). Therefore, an increase in ArtR, through decreases in PVP and PVV, leads to a temporary increase in 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.

Fig. 3. Flow–pressure–volume relation in complaint veins. Line 1depicts a schema of the terminal and venous part of the circulation. AP, PVP, and CVP represent pressure in arteries, small (peripheral) veins (capillary pressure is incorporated into PVP), and right atrium, respectively. 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. Therefore, because F is decreased, the difference between PVP and CVP must have decreased. To maintain flow through the system, PVP must be higher than CVP. 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 compliance (C) by definition is a ratio of ΔV to ΔP ( equation 1in the text), the volume within the small veins (PVV) would be equal to compliance in peripheral veins (Cpv) multiplied by pressure within the veins (PVP, line 4). Because an increase in ArtR unavoidably leads to a decrease in PVP ( line 3) and compliance does not change ( fig. 1, black lines), any decrease in PVP must be associated with a decrease in volume of blood within the small veins (PVV, line 5). In reality, a decrease in F is associated with an immediate and simultaneous decrease in PVP and PVV. A decrease in PVV leads to a shift of blood volume from the veins to the heart increasing venous return (VR, line 6). Therefore, an increase in ArtR, through decreases in PVP and PVV, leads to a temporary increase in 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). Reduction in CO by 27% was associated with 9.2 ml/kg of blood recruitment from the splanchnic system when reflexes were intact.17Similar reduction in CO in conditions of ganglioblockade with hexamethonium led to recruitment of blood volume of 6.8 ml/kg. In a 75-kg human, this would mean a shift of blood volume of approximately 700 versus 500 ml of blood into systemic circulation with and without reflexes intact, respectively. Therefore, the active constriction of veins would transfer only approximately 25% of total transferred blood.17Thus, passive mechanisms due to change in flow followed by change in pressure and volume are more important in maintaining VR and CO than active venoconstricting mechanisms (fig. 3).8,17

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.9,17–19The distribution of blood flow governs the distribution of blood volume within the body.17,20These flow–pressure–volume relations adequately explain many physiologic and clinical conditions. More than 70 yr ago, an enlargement of cardiac dimensions was observed during cross clamping of the thoracic aorta.21The authors attributed this to an increased afterload. They also observed that the cross clamping increased “systemic flow” (CO). They attributed (but did not prove) this increase to “blood transference” from the lower to the upper part of the body. Many other studies confirmed these observations.22We observed a twofold increase in blood flow through the upper part of the body during aortic cross clamping at the diaphragmatic level.23–25Finally, our experiments using whole body scintigraphy with technetium 99m–labeled plasma albumin have demonstrated that aortic cross clamping at the diaphragmatic level is associated with a significant increase in blood volume in the organs and tissues proximal to the level of occlusion.26This is a direct unequivocal illustration of the shift of blood volume from the organs distal to the aortic cross clamp (from the compliant splanchnic veins) to the proximal, upper part of the body. 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.22

Mean Circulatory Filling Pressure

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 .27,28When the heart starts pumping the blood, pressure within the arterial system is increasing and pushes the blood through the arteries, then through the capillaries into the venous system. 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. According to Guyton, the main driving force for VR is MCFP, and

During cardiac arrest, the pressure within the venulae and small veins is not changing and remains the same as it was before cardiac arrest. Therefore, this pressure is considered the “pivoting pressure” for the whole circulatory system.9

The heart cannot pump more blood into circulation than it receives. Therefore, in physiologic conditions, CO is determined entirely by VR, and VR can be increased only by an increase in MCFP and/or a decrease in CVP because venous resistance is usually not changing much and relatively small. 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. In dogs and presumably in humans, MCFP is approximately between 7 and 12 mmHg, whereas CVP is approximately 2–3 mmHg.15,27–31Thus, the gradient for VR is somewhere between 5 and 10 mmHg, and therefore, the change in CVP just by a few millimeters of mercury can have considerable effect on VR.15,32

An interesting question is why in the normally functioning heart an increase in CVP (e.g. , secondary to an infusion of volume) increases CO despite the increased downstream pressure. 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. The problem is solved by an increase in MCFP secondary to an increase in Vs. Because an increase in MCFP is at least equal or usually larger than an increase in CVP, even larger increases in pressure gradient to VR would be achieved at a higher level of both pressures, MCFP and CVP, with subsequent increases in VR and CO.

Venous Resistance

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 veins1,15,33(fig. 4, inside).

Fig. 4. Two-compartment model. Inside:The two circuitsrepresent two compartments the solid red and blue linesrepresent arterial and noncompliant venous compartments (the main, basic circuit). Dashed red and blue linesrepresent 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 linesreflects the amount of flow within the vessels under normal conditions. The size of the junctionsbetween 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. AP = arterial pressure MCFP = mean circulatory filling pressure VR = venous return. 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).

Fig. 4. Two-compartment model. Inside:The two circuitsrepresent two compartments the solid red and blue linesrepresent arterial and noncompliant venous compartments (the main, basic circuit). Dashed red and blue linesrepresent 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 linesreflects the amount of flow within the vessels under normal conditions. The size of the junctionsbetween 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. AP = arterial pressure MCFP = mean circulatory filling pressure VR = venous return. 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).

Venous return is increased by an increase in MCFP secondary to an increase in Vs, which can be achieved by an infusion of additional volume and/or by a decrease in venous capacity by venoconstrictors. The latter decreases Vu and increases Vs without change in the elastic properties of the venous wall, i.e. , without change in venous compliance (fig. 1). 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. 2).

This understanding of physiology and governing variables explains why patients at the beginning of bleeding, (up to 10–12% of blood volume loss) maintain their systemic hemodynamics well without changes in heart rate, blood pressure, or CVP, yet later, hemodynamics quickly deteriorate. 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. Sympathetic stimulation of only 1 Hz results in a capacity response of almost 50% of maximal response observed during 20-Hz stimulation. On the other hand, the resistance response to 1 Hz stimulation is only 10% of maximum.2,34Clinical implications of this and other observations are that a response to a moderate increase in sympathetic tone (or a small dose of vasoconstrictors) is a constriction of capacitance (splanchnic) vessels which would expel blood from the splanchnic vasculature into the systemic circulation without a significant increase in systemic arterial resistance. 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 veins15,35–37or within the liver itself.37One way or the other, an increase in resistance within the distal part of the splanchnic venous system would impede the outflow of blood from splanchnic organs, sequestering blood within the liver and more proximal parts of the splanchnic veins. 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.38A similar picture was observed in a porcine model of endotoxic shock.39

A decrease in resistance to venous flow within the liver and/or hepatic veins would facilitate the blood flow and volume shift from splanchnic vasculature to the inferior caval vein and right atrium, thereby increasing VR. Resistance within the liver and hepatic veins is mainly regulated by adrenergic receptors: Activation of α-adrenergic receptors increases resistance,15,40whereas activation of β 2 -adrenergic receptors decreases it, resulting in volume shift from the splanchnic vasculature into the systemic circulation.15,35Thus, the administration of pure α-adrenergic agonists could result in a decrease in venous capacity and an increase in Vs and MCFP, thereby increasing VR.40–54However, activation of α-adrenergic receptors also could be associated with an increase in resistance within the liver and hepatic veins, which would impede the blood flow and shift of blood volume from the splanchnic system into systemic circulation.46,53–58In conditions of normovolemia and a relatively small degree of α-adrenergic receptor activation, a decrease in venous capacity probably plays a more prominent role than an increase in resistance to the blood flow and volume shift from splanchnic vasculature. However, in conditions of hypovolemia (when further mobilization of Vu is decreased) and/or a high degree of α-adrenergic receptor activation, sequestration of blood volume within the liver and further decrease in VR and CO may occur.53,54The combination of α- and β 2 -adrenergic agonists may facilitate the shift of blood volume from the splanchnic system into the systemic circulation more effectively than α-adrenergic agonists alone: Such a combination would lead to a decrease in venous capacity, recruitment of Vu into Vs, and a decrease in resistance to venous outflow from the splanchnic system. Obviously, in conditions of severe hypovolemia, such shifts of blood volume would not be possible simply because of absence of Vu to be recruited an increase in arterial pressure, if observed, would result mainly from α receptor–mediated arterial constriction.53An increase in venous capacity by an α-adrenergic agonist may also result from an activation of baroreceptors in the carotid sinuses secondary to an increase in arterial blood pressure.59,60

Two-compartment Model of the Venous System

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 introduced61 one is very compliant and slow (splanchnic vasculature) and another is noncompliant and fast (nonsplanchnic venous vasculature fig. 4, inside). This model has been used to explain many physiologic observations. It has also been periodically challenged.62However, as the reader will see, this theoretical model can logically and convincingly explain many observations regarding the behavior of venous system during one or another insult to cardiovascular function. 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. 3and fig. 4, outside). 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. 4, outside). Such an increase may be attributed to a few different mechanisms, including translocation of arterial blood centrally through the venous system as well as direct or more often indirect (via activation of the sympathetic nervous system and/or angiotensin system) constriction of veins leading to translocation of venous blood toward the heart a simultaneous decrease in venous resistance within the distal part of the splanchnic venous vasculature may also play a role in such observations.63,64Finally and most importantly, a decrease in arterial resistance in the nonsplanchnic compartment, if associated with only a minor decrease in arterial pressure, leads to a significant increase in MCFP resulting from a decrease in the gradient between arterial and peripheral venous pressures increasing the MCFP and VR. This relation can be illustrated by an opening of a large arteriovenous fistula.28However, if a decrease in arterial resistance is associated with a significant decrease in arterial pressure, it could be associated with a decrease in MCFP and VR.

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. During exercise, splanchnic blood flow can reduce from 1,500 ml/min to 350 ml/min. Splanchnic oxygen consumption is preserved by an increase in arteriovenous oxygen difference in this region from 4 to 17 ml of oxygen/100 ml of blood.65On the other hand, total muscle blood flow can increase from approximately 1,000 ml/min at rest to almost 22,000 ml/min with an increase in CO to 25 l/min and oxygen uptake of almost 4 l/min. Arteriovenous oxygen difference in the muscle increases to 18 ml of oxygen/100 ml of blood, which represents approximately 90% oxygen extraction.66The mechanisms responsible for such hemodynamic adjustments involve different responses of the arteries and arteriolae in the muscles versus the splanchnic system. 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. 3and fig. 4, outside). The vasodilation within the exercising muscle, resulting to a minor extent from β 2 -adrenergic receptor activation but mainly from a local accumulation of vasodilating metabolites (lactate, adenosine, and other compounds), leads to a decrease in arteriovenous pressure gradient in the muscle and a significant increase in MCFP, VR, and CO. 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. Additional mechanisms include “muscle pump” (during exercise contraction of muscles squeezes blood out of the muscles towards the heart), increase in heart rate and myocardial contractility, and many others.66

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.67,68Decrease in splanchnic flow should be associated with a decrease in pressure and volume within the splanchnic veins (fig. 3and fig. 4, outside). However, it does not happen69,70: 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.68That is, adenosine triphosphate and, to a lesser extent, sodium nitroprusside dilated nonsplanchnic arterial vasculature, leading to an increase in MCFP (due to a decrease in the pressure gradient between arteries and veins) and in VR. 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. 3and fig. 4, outside). 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.71However, it seems that sodium nitroprusside affects arterial resistance to a greater extent than venous capacity, whereas nitroglycerin increases venous capacity to a greater extent than decreases arterial resistance.71

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.72The authors studied captopril, nifedipine, hydralazine, and prazosin in three doses that decreased arterial blood pressure to similar degrees. 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. This was associated with a decrease in the pressure gradient between arterial and venous pressures within the nonsplanchnic system, and increased MCFP and central blood volume, which in the absence of bypass would increase VR and CO. The differences in the effects of two remaining vasodilators were less drastic than the effects of nifedipine and captopril.72

The direct effects of vasodilators may be modified by indirect effects of mediators released during the administration of a drug in question. For example, isoproterenol administration is associated with an increase in norepinephrine release,73–77and that effect is mediated specifically via β 2 - but not β 1 -adrenergic receptors.78Isoproterenol also increases release of angiotensin.79As a result of such complexity, isoproterenol administration is associated with a drastic decrease in splanchnic and intrahepatic volume despite a significant increase in splanchnic blood flow.80According to the basic concepts of the relation between flow, pressure, and volume within the splanchnic vasculature (fig. 3), an increase in splanchnic flow should be associated with sequestration of blood volume within the splanchnic vasculature. In reality, this does not occur, and splanchnic volume significantly decreases.35,80Therefore, an increase in VR by blood volume shift from the splanchnic system results from a decrease in resistance within the liver and hepatic veins (mediated via β 2 -adrenergic receptors), and venoconstriction, elicited by release of norepinephrine and/or angiotensin. Epinephrine increases VR mainly through activation of β 2 -adrenergic receptors.59The role of an increased myocardial contractility (mediated via β 1 -adrenergic receptors) in an increase in CO in a normal heart is probably minimal.53,59,78

Intrathoracic Pressure

An increase in intrathoracic pressure (ThorP) during controlled positive-pressure ventilation increases intramural CVP. This would decrease the pressure gradient for VR, VR itself, and blood volume in the right heart at diastole. On the other hand, every lung inflation moves the diaphragm downward, increasing intraabdominal pressure. The latter squeezes blood out of the veins within the abdominal cavity, increasing MCFP and VR, thereby helping to maintain the MCFP–CVP gradient and minimizing the effect of an increase in ThorP on VR.81

Reflexes and neurohumoral factors that increase MCFP also minimize the effects of increased ThorP on VR by an increase in arterial resistance within the splanchnic vasculature (leading to an increase in passive elastic recoil of splanchnic veins) and active venoconstriction both result in a shift of blood volume from the splanchnic system into systemic circulation, increasing Vs and maintaining VR and CO. This shift is reinforced by an increase in intravascular volume secondary to antidiuresis (release of antidiuretic hormones).82–88An activation of the renin–angiotensin–aldosterone system during positive-pressure ventilation contributes to both mechanisms, namely an increase in MCFP by venoconstriction and an increase in blood volume by water and sodium retention. An increase in intramural CVP during such a situation might be misinterpreted as hypervolemia and/or cardiac failure.

Finally, right ventricular filling pressure (defined as a gradient between CVP and pericardial pressure81) does not change during changes in ThorP because the right atrium, right ventricle, and pericardium are within the thorax, and an increase in ThorP is associated with equal increases in both right atrial and pericardial pressures. Therefore, absence of change in transmural right ventricular pressure during diastole further minimizes the effects of an increase in ThorP on VR. However, overinflation of the lung, introduction of positive end-expiratory pressure, and/or hypovolemia, present before introduction of controlled ventilation, might have exhausted the compensatory mechanisms and lead to a decrease in VR and CO.89An additional infusion of fluid and/or venoconstrictor might be needed to increase MCFP in order to maintain the necessary pressure gradient for VR.

During spontaneous inspiration, ThorP decreases, leading to a decrease in intramural CVP and a subsequent increase in gradient between MCFP and CVP, facilitating VR. However, an increase in VR secondary to a decrease in CVP works only when CVP is equal to or above atmospheric pressure because negative pressure in intrathoracic veins leads to their collapse, preventing a significant increase in VR. Also, pericardial pressure limits the overdistension of the right ventricle (see Pericardial Pressure section). If these mechanisms did not exist, forceful inspirations could lead to overextension of the right ventricle and its failure.31,81,90–93

Systolic Blood Pressure and Pulse Pressure Variations.

During inspiration of positive-pressure ventilation, left ventricular stroke volume initially increases secondary to (1) temporary increase in left ventricular end-diastolic volume resulting from a compression of pulmonary veins, (2) decrease in afterload resulting from a decrease in left ventricular transmural pressure (i.e. , an increase in lung volume compresses the left ventricle and helps the left ventricular ejection), and (3) diminished right ventricular volume secondary to compression of the heart by inflated lungs. These factors lead to a temporary increase in left ventricular stroke volume, pulse pressure, and systolic blood pressure, compared with end of expiration (baseline). This deflection of blood pressure is called delta-up and usually is around 2–4 mmHg.94–96On the other hand, such inflation of the lung and an increase in ThorP decreases the pressure gradient for VR with subsequent decrease in VR. This in a few beats ends up with a decrease in left heart filling, in stroke volume of left ventricle and systolic pressure. This decrease in systolic pressure is called delta-down 94,95and usually is around 5–6 mmHg. Total variation, delta-up/delta-down, thus is approximately 8–10 mmHg. If this variation is larger than that, it may reflect hypovolemia and predict a positive response (an increase in CO) to additional fluid load. Systolic blood pressure variation not exceeding approximately 10 mmHg would reflect adequacy of ventricular preload15,94–99and may reflect the status of preload better than CVP.98

Intraabdominal Pressure

Every inspiration, spontaneous or during positive-pressure breathing, moves the diaphragm downward, increases intraabdominal pressure, and shifts blood volume from the splanchnic system into the systemic circulation. At the same time, venous flow from the lower extremities along the inferior caval vein decreases. During expiration, the diaphragm shifts upward, decreases blood flow from the splanchnic system, and increases blood flow from the lower extremities. These cyclic events overall do not drastically affect VR and CO. However, a longer-lasting increase in intraabdominal pressure to any level lower than pressure within inferior caval vein may lead to a simultaneous increase in VR due to shift of blood volume from the compliant splanchnic venous system toward the right atrium on the other hand, such an increase in intraabdominal pressure may decrease VR secondary to an increase in venous resistance within the inferior caval vein and to a shift of the diaphragm upward, an increase in ThorP with concomitant increase in intramural CVP.100–105Such an increase in CVP does not reflect the volume status of a patient106and may be associated with a decrease in VR100,101,107resulting from a decrease in the gradient between MCFP and CVP. This effect can be modified by an increase in Vs, which in turn can be achieved by an infusion of additional fluid and/or an administration of a venoconstrictor.108Such intervention is not always needed because of the activation of sympathetic and renin–angiotensin systems this is associated with an increase of MCFP and maintenance of the needed MCFP–CVP gradient to preserve VR and CO.103,109,110Anesthetics, sedatives, and other interventions might minimize such a homeostatic response.105,111–114

Positions (Tilts)

Different positions, e.g. , head up versus head down, affect systemic hemodynamics including function of the venous system. A head-up position (e.g. , standing up) could be associated with a gravity-induced shift of blood volume from the upper to the lower part of the body. In healthy, awake patients, head-up or head-down positions do not affect blood pressure, CO, or CVP105because of immediate activation of sympathically mediated reflexes as well as the renin–angiotensin system and release of other vasoconstricting mediators115prevent such a drastic shift of blood volume. However, during anesthesia, the head-up position is practically always associated with a decrease in CVP, CO, and blood pressure100,105,107,116because the reflexes are blunted as the depth of anesthesia increases.105

The head-down (Trendelenburg) position is always associated with an increase in CVP. However, CO and blood pressure may be maintained37,100,107,115or decreased.105,116Left ventricular end-diastolic area (reflecting volume) and intrathoracic blood volume are increased.37After change from a head-down to a horizontal position in an anesthetized patient, a decrease in blood pressure and CO may occur.37It might be due to a failure to increase afterload or to hypovolemia which may have been misinterpreted as normovolemia or hypervolemia secondary to high CVP with the head-down position.105

Pericardial Pressure

Any significant increase in VR (e.g. , during spontaneous inspiration) could lead to overloading of the right heart.117–121The limited rigid space of pericardium prevents overexpansion of the right heart.121In animals and humans, pericardectomy is associated with higher values of stroke volume and CO during exercise compared with similar exercises before pericardiectomy.122Other mechanisms limiting overloading of the right heart include an increase in ThorP during controlled ventilation and, to a certain extent, during spontaneous expiration, as well as so-called ventricular interdependence121–125: An increase in right ventricular volume shifts the intraventricular septum leftward, leading to a decrease in left ventricular compliance, which decreases left ventricular filling, resulting a few beats later in a decrease in right ventricular preload.81

Role of Reflexes

Many different pathophysiologic insults, e.g. , blood loss, the upright position,126initiation of positive pressure breathing, particularly with positive end-expiratory pressure, are associated with immediate increase in sympathetic discharge, which leads to an increase in arterial resistance, heart rate, and myocardial contractility and a decrease in venous capacity. The latter is particularly important: Capacitance vessels respond to hemorrhage much earlier than resistance vessels both of these responses, arterial and venous, are mediated via the sympathetic nervous system. When the carotid sinus receptors sense low blood pressure, the sympathetic tone increases, splanchnic veins constrict, Vs and MCFP increase, and vice versa .2,10,19,127–133Pretreatment with the α-adrenergic antagonist phentolamine decreased such response by 72%, whereas pretreatment with the β-adrenergic antagonist propranolol decreased such response by 35%. Combination of both decreased response by 73%. Therefore, α-adrenergic mechanisms contribute more significantly to active changes in systemic venous capacity than the β-adrenergic system.134The responses to high or low arterial blood pressure are mediated not only through the carotid sinus but also through the aortic baroreceptors. Their role in maintaining blood pressure is smaller than the role of the carotid sinuses.132

There are other types of reflexes, e.g. , an increase in intravenous volume and associated distension of the vein increases arterial resistance (upstream of the affected veins) via the so-called local sympathetic axon reflex or venoarterial reflex.135Teleologically speaking, this reflex helps to modify the degree of venous distention: Less blood inflow into a vein leads to a decrease in intramural pressure and volume (fig. 3).


Discussion

Dive behavior

In emperor penguins equipped with the intravascular PO2 recorder, dive durations and maximum depths were similar to those in past studies(Kooyman et al., 1992 Ponganis et al., 2001) at the isolated dive hole (Fig. 1). Dives of >100 m in depth were rare, and 47% of dives were >5.6 min, the previously measured ADL (Ponganis et al.,1997b). In 2004, birds often performed long-duration dives of>16 min this included a 23.1 min dive(Fig. 3), which is now the longest reported dive in an emperor penguin. Dive profiles and lack of hunting ascents to the undersurface of the sea ice during these exceptional dives suggested that the birds were foraging at 50–80 m depth.

Air sac, arterial and venous PO2 profiles during shallow (less than 30 m), ∼3-min dives in three different birds. PO2 profiles from the air sac (EP 05)(Stockard et al., 2005) and aorta (EP 02) demonstrate initial compression hyperoxia and then a gradual decline in PO2 secondary to air sac O2 depletion and the decrease in ambient pressure during ascent. Vena caval PO2 slowly increased during the dive of EP 20. The PO2 data were recorded at 15 s intervals. Dives began at 0 time. Prior to the onset of the dive for the arterial profile, the bird had just surfaced for a breath after a prior dive.

Air sac, arterial and venous PO2 profiles during shallow (less than 30 m), ∼3-min dives in three different birds. PO2 profiles from the air sac (EP 05)(Stockard et al., 2005) and aorta (EP 02) demonstrate initial compression hyperoxia and then a gradual decline in PO2 secondary to air sac O2 depletion and the decrease in ambient pressure during ascent. Vena caval PO2 slowly increased during the dive of EP 20. The PO2 data were recorded at 15 s intervals. Dives began at 0 time. Prior to the onset of the dive for the arterial profile, the bird had just surfaced for a breath after a prior dive.

Blood analyses of emperor penguins at rest

In emperor penguins at rest, mean arterial PO2 was 68±7 mmHg, less than two-thirds the mean value in the air sac of birds at rest(Stockard et al., 2005). Large air-sac-to-arterial differences in PO2 in birds at rest are considered primarily due to ventilation–perfusion mismatch(Powell, 2000). It is unknown if this air-sac-to-arterial difference in PO2in emperor penguins at rest is also partially secondary to the thickened parabronchial capillary blood-to-air barrier that has been reported in these birds (Welsch and Aschauer,1986).

Although these arterial PO2 values in emperor penguins are in the lower range of values reported for birds at rest(Powell, 2000), the arterial O2 content of 22.5±1.3 ml O2dl –1 still represented greater than 91% saturation of the previously measured average [Hb] of 18 g dl –1 (Kooyman and Ponganis, 1998). Arterial pH, PCO2 and [lactate] in emperor penguins at rest were characteristic of other avian species(Powell, 2000) and are consistent with a lack of stress during the sampling procedure. Venous PO2, O2 content, pH, PCO2 and [lactate] were consistent with the observed arterial values and resulted in an estimated 70% venous Hb saturation.

Venous PO2 and depth profiles from a 23.1 min dive. This shallow (<60 m maximum depth) dive is currently the longest reported dive of an emperor penguin. The blood O2 store was optimized in this bird (EP 19) with a pre-dive venous PO2 of 63 mmHg, which was equivalent to arterial values of birds at rest. PO2 gradually declined throughout the dive to a final value of 6 mmHg and then returned to pre-dive levels within 3 min. Grey background indicates dive time.

Venous PO2 and depth profiles from a 23.1 min dive. This shallow (<60 m maximum depth) dive is currently the longest reported dive of an emperor penguin. The blood O2 store was optimized in this bird (EP 19) with a pre-dive venous PO2 of 63 mmHg, which was equivalent to arterial values of birds at rest. PO2 gradually declined throughout the dive to a final value of 6 mmHg and then returned to pre-dive levels within 3 min. Grey background indicates dive time.

PO2 profiles and final PO2 values during dives

Arterial PO2 profiles reflected the effects of compression hyperoxia and O2-store depletion previously documented in the air sacs during dives(Stockard et al., 2005). For example, during a 5.3-min, 60-m deep dive, arterial PO2 increased from an initial value of 98 mmHg to a peak value of 257 mmHg and then gradually decreased to a final value of 76 mmHg near the end of the dive. Fig. 2 demonstrates the similarity of arterial and air sac PO2 profiles in two different birds during shallow dives of short duration. Near the ends of some dives, the compression hyperoxia resulted in arterial PO2 values that were greater than the mean value (68±7 mmHg) of birds at rest.

Venous PO2 did not always simply decline during dives but sometimes increased (Fig. 2). This accounts for final dive values(Fig. 4A) that are greater than those of birds at rest. In addition, there was a wide range of pre-dive venous PO2 levels (Figs 2 and 3). Prior to a 23.1 min dive(Fig. 3), the blood O2 store was optimized with an elevated pre-dive venous PO2 of 63 mmHg. This value was not only greater than that of birds at rest but was nearly equivalent to arterial values of birds at rest. These findings support the concept that the blood O2store of emperor penguins can be enhanced by `arterialization' of venous blood.

Although final venous PO2 declined in relation to dive duration, the relationship was variable e.g. at a dive duration of 5.6 min (the ADL), final venous PO2values spanned a range of 40 mmHg. These final venous PO2 data and the previously published final air sac PO2 data provide evidence that the total body O2 store is not depleted at the ADL. In fact, the body O2 store is still not depleted even after many minutes beyond the ADL (Fig. 4). The wide range of final values for a given dive duration was consistent with variations in the rates of decline of PO2 in the individual venous profiles and, presumably, was related to differences in rates of O2 consumption during dives. The minimum rate at which final venous PO2 declined in relation to dive duration of emperor penguins at the isolated dive hole is described by the exponential regression in Fig. 4A.

Final PO2 and dive duration. Final PO2 values were recorded within the last 15 s of each dive. (A) Final venous PO2 and dive duration from nine emperor penguins (key shows individual symbols for each penguin). The variability in final PO2 values in relation to dive duration is presumably secondary to differences in metabolic rates during dives. In addition, the span of PO2 values at the aerobic dive limit (ADL)clearly indicates that the blood O2 store is not depleted at this limit, the dive duration associated with post-dive lactate accumulation. The exponential regression(y=96.416e –0.1216 x ,r 2 =0.94, P<0.001) was constructed from the highest final PO2 during each 1-min interval of dive duration. This represents the minimum rate at which final PO2 declines in relation to dive duration. (B)Comparison of final venous PO2, arterial PO2 and air sac PO2(Stockard et al., 2005)demonstrates that air sac, arterial and venous PO2 values become indistinguishable in longer dives.

Final PO2 and dive duration. Final PO2 values were recorded within the last 15 s of each dive. (A) Final venous PO2 and dive duration from nine emperor penguins (key shows individual symbols for each penguin). The variability in final PO2 values in relation to dive duration is presumably secondary to differences in metabolic rates during dives. In addition, the span of PO2 values at the aerobic dive limit (ADL)clearly indicates that the blood O2 store is not depleted at this limit, the dive duration associated with post-dive lactate accumulation. The exponential regression(y=96.416e –0.1216 x ,r 2 =0.94, P<0.001) was constructed from the highest final PO2 during each 1-min interval of dive duration. This represents the minimum rate at which final PO2 declines in relation to dive duration. (B)Comparison of final venous PO2, arterial PO2 and air sac PO2(Stockard et al., 2005)demonstrates that air sac, arterial and venous PO2 values become indistinguishable in longer dives.

We also propose that venous PO2 profiles and end-of-dive values, especially during the latter portions of long dives,approximate arterial values. Comparison of final air sac(Stockard et al., 2005) and venous PO2 values from dives of emperor penguins reveals that final air sac values become indistinguishable from final venous values during longer dives (Fig. 4B). This is particularly apparent after dives beyond the ADL(Fig. 4B). Arterial PO2 data, available over a limited range of relatively short dive durations, occupy the same range as air sac values and,in some cases, overlap venous values. Given the similar distributions of arterial, air sac and even some venous final PO2 values for short dive durations, and the assumption that air sac PO2 represents maximal arterial PO2, we think that venous final PO2 values approximate arterial final PO2 values for long dives. Similar equilibrations of venous and arterial PO2values have also been reported in seals(Elsner et al., 1964 Stockard et al., 2007). Thus,as indices of the entire blood O2 store, the venous PO2 profiles from the longer dives in this study demonstrate that emperor penguins clearly push the limits of hypoxemia and, indeed, are capable of `returning on empty' to the dive hole. In 29% of dives, final venous PO2 values were less than 20 mmHg in some dives, PO2 reached values as low as 1–6 mmHg. These final PO2 values are well below the arterial and venous thresholds (20–25 mmHg) for cardiovascular collapse in pekin ducks(Hudson and Jones, 1986) and are also less than arterial PO2 (22 mmHg) in bar-headed geese at 11 580 m altitude(Black and Tenney, 1980). In the 23 min dive of an emperor penguin, PO2 was less than 20 mmHg for 8 min and eventually reached 6 mmHg(Fig. 3).

One might question whether the extremely low final venous PO2 data could be secondary to O2consumption by the electrode in blood made stagnant by the bradycardia and low cardiac output of diving. We think this is unlikely for several reasons. First, low PO2 values also occurred in the air sacs, which should not be affected by stagnant blood. Second, given the stroke volume and blood volume of emperor penguins(Kooyman et al., 1992 Ponganis et al., 1997a), even if heart rate were 5 beats min –1 during the last 10 min of the 23 min dive, the entire blood volume would circulate during that time period. Presumably, there would still be some flow past the electrode in that situation. Third, low final venous PO2 values also occurred during short dives, which have higher heart rates(Kooyman et al., 1992) that should be associated with higher blood flows. Fourth, during the initial post-dive portion of the surface interval, venous PO2 often stayed the same(Fig. 3) or even decreased further (P.J.P., unpublished data). This lack of an immediate increase in venous PO2 during the tachycardia(Kooyman et al., 1992) and presumed high blood flows of the initial surface period again support our argument that the low values during dives are not secondary to the localized depletion of O2 in a stagnant layer of blood around the electrode. Fifth, in the test-tube evaluation of the potential effect of the PO2 electrode itself on O2 depletion in saline, there was only a minimal initial decline in PO2 over 4 min, and then no change thereafter. This change in PO2 in saline should be the maximum potential effect of the electrode since localized O2depletion in blood would be buffered by release of O2 from Hb. Therefore, we expect that the localized depletion of O2 by the electrode in blood would be even less and that the low venous PO2 values in this study are not secondary to O2 consumption by the electrode.

These low PO2 values in the blood and respiratory systems of diving emperor penguins are also remarkable in comparison to mammalian indices of hypoxemia, including (a) the typical arterial PO2 criterion of 60 mmHg for treatment of human patients (Nunn,1977), (b) end-tidal PO2 values of 35 mmHg from climbers on ambient air at the top of Mount Everest(West et al., 1983), (c) human thresholds for shallow-water blackout near 25 mmHg(Ferrigno and Lundgren, 1999),(d) mixed venous PO2 values of 27–34 mmHg in terrestrial mammals exercising at maximal O2 consumption(Taylor et al., 1987), (e)femoral venous PO2 values of 20 mmHg in humans exercising at maximal O2 consumption(Roca et al., 1992) and (f)arterial and end-tidal PO2 values of 15–20 mmHg in free-diving Weddell seals (Leptonychotes weddellii) and bottlenose dolphins (Tursiops truncatus)(Ponganis et al., 1993 Qvist et al., 1986 Ridgway et al., 1969). The only PO2 values equivalent to the extremes of hypoxemia found in these free-diving emperor penguins are the arterial and venous PO2 levels (10 and 3 mmHg, respectively)found in harbor seals (Phoca vitulina) forcibly submerged to an electroencephalographic threshold for hypoxemic brain damage(Kerem and Elsner, 1973).

These findings of extreme hypoxemia in emperor penguins also suggest that,in contrast to the Hb of the pekin duck or pigeon(Hudson and Jones, 1986 Weinstein et al., 1985), the Hb of the emperor penguin is not stripped of all its O2 at a PO2 of 20 mmHg. In other words, the P50 (PO2 at 50%O2 saturation of Hb) of whole blood in emperor penguins is probably much lower than the P50 of pekin ducks (42–52 mmHg)(Black and Tenney, 1980 Lutz, 1980 Powell, 2000) and perhaps even lower than the P50 of isolated, reconstituted emperor penguin Hb (36 mmHg) (Tamburrini et al.,1994). Rather, it is probably closer to the lowest whole-blood P50 values (30–34 mmHg) found in Adelie, gentoo and chinstrap penguins (Pygoscelis adeliae, P. papua, P. antarctica) and in high-altitude-adapted birds such as the bar-headed goose(Black and Tenney, 1980 Milsom et al., 1973 Petschow et al., 1977). This suggestion of a relatively low P50 in the emperor penguin is supported by the blood gas and O2 content analyses of these birds at rest. At a mean venous PO2 of 41 mmHg,mean O2 content was 17.4 ml O2 dl –1 ,which represents approximately 70% saturation of an average Hb concentration of 18 g dl –1 (Kooyman and Ponganis, 1998).

In comparison to the P50 of the pekin duck, a lower P50 in the emperor penguin would not only increase blood O2 content during hypoxemia but it would also enhance dive capacity by allowing more complete depletion of the respiratory O2 store. In the pekin duck forcibly submerged to the point of `imminent cardiovascular collapse', 25% of the respiratory O2 store was still unused because the blood contained almost no O2 at an air sac PO2 near 30 mmHg(Hudson and Jones, 1986).

In conclusion, intravascular/air sac PO2profiles in diving emperor penguins have revealed that their dive capacity is at least partially achieved through optimum management of the blood/respiratory O2 stores and extreme hypoxemic tolerance. The blood PO2 profiles provide insight into the nature and magnitude of physiological responses during the dive as well as into biochemical/molecular mechanisms underlying hypoxemic tolerance. In particular, a Hb with high O2 affinity (low P50) in penguins is essential not only to enhance blood O2 content during hypoxemia but also to allow depletion of the respiratory O2 store, which in emperor penguins constitutes 19% of the total body O2 store (Kooyman and Ponganis, 1998). Other mechanisms of such extreme hypoxemic tolerance may include increased capillary densities, modifications in reactive O2 species production and/or scavenging, and changes in the concentration and function of neuroglobin and cytoglobin. In addition to their relevance to the diving capacity and biology of emperor penguins, these potential cellular adaptations may also serve as models for improved understanding and treatment of human hypoxemic/ischemic pathologies.


When To Call a Professional

Call your doctor whenever you have pain, swelling, skin ulcers or an unexplained area of bruising on your legs. New leg swelling, especially in just one leg, can be caused by a blood clot, which requires immediate treatment.

If you have varicose veins, call your doctor immediately if you develop an ulcer or a painful, black and blue area near a varicose vein or if you cut the skin over a varicose vein and you have trouble controlling the bleeding.


Common Reasons People Miss Veins When Starting IVs & Drawing Blood

Most new nurses find that starting IVs and drawing blood can be a difficult task to perform at first. When I was a new nurse I had difficulty finding a vein to draw blood from and to start an IV in, and if I did find a vein I often missed it. This caused frustration and I actually thought I would never figure it out. I thought “Well, I must just be one of those types of nurses who aren’t talented at starting IVs and drawing blood”.

Unfortunately, I gave up on trying for the first year and always asked a more experienced nurse to do it for me. This was a mistake because I should have not given up. Looking back at my experience with veins, I discovered that almost all new nurses have to learn how to acquire this skill (they are not “born” with this skill in nursing school). It is learned over time and with lots of practice.

After my year of not “trying”, I forced myself to learn it (it became a New Year’s Resolution) and I started to have success. I had a lot of trial and error, but once I built confidence I started to have a 95-98% success.

In this article, I am going to share with you the most common reasons why people miss veins when starting an IV or drawing blood and how you can increase your success rate.


Why Do Leaves Have Veins?

The primary purpose of the veins in a leaf is to carry food and water throughout the leaf. The veins also have a secondary purpose, which is to help provide support for the rest of the leaf.

In many types of leaves, the veins form a large pattern that resembles a net. This pattern is made up of much larger, primary veins that connect to the leaf stem as well as smaller, secondary veins. The larger veins' main purpose is to carry water from the stem into the leaf, while the smaller veins spread it throughout every part of the leaf. The smaller network of veins also collects chlorophyll created in the leaf, which the larger veins then transport back to the main part of the plant.

Each species of plant has a unique pattern of veins in its leaves, varying in the density of the network and the distance between the larger veins. Some scientists have begun studying exactly what this pattern says about a plant and have made a number of conclusions. For instance, the density of the veins shows how much energy the plant has put into making the leaves. In addition, the number of loops in the pattern can help determine how long the leaf can live, as more loops allow it to circulate food and water through another path.


What Causes A Collapsed Colon?

Large intestine (Colon) collapse is observed in patients having obstruction in the small intestine. Before the obstruction site, the small intestine becomes dilated. Normally when there is no obstruction, the content of small intestine is passed forward into the large intestine with peristaltic wave like movements.

This repeated contraction and relaxation of intestinal muscles is also carried on in intestinal obstruction. However, due to obstruction the content of small intestine cannot move further, but at the same time the remaining content present in large intestine both stool and gas is passed off. Since nothing comes from small bowel, the colon gets collapsed once the residual stool and gas is evacuated.

Here are some of the reasons for intestinal blockage:

  • Strangulation of hernia.
  • Intestinal adhesions due to previous abdominal surgeries.
  • Volvulus (Intestinal twisting).
  • Intussusception of the intestine (a section of intestine overlapping the other part).
  • Carcinoma of cecum or first part of colon. The malignant tumor may cause obstruction. After the content below the obstruction is evacuated the remaining portion of colon collapses.
  • Obstruction of intestine due to presence of foreign body.
  • Polyps and ulcerative colitis.

Symptoms Of A Collapsed Colon

The symptoms of collapse of colon are frequently associated with those of intestinal obstruction. One of the main symptoms is absolute constipation. Other symptoms may be that of intestinal obstruction and they are

  • Severe cramps in abdomen. The spasms are episodic.
  • Nausea and vomiting
  • Abdomen tenderness
  • Distension of abdomen and this is mainly due to intestinal obstruction and not due to collapse of colon.
  • Loss of appetite
  • Fever

Arteries and arterioles

The arteries, which are strong, flexible, and resilient, carry blood away from the heart and bear the highest blood pressures. Because arteries are elastic, they narrow (recoil) passively when the heart is relaxing between beats and thus help maintain blood pressure. The arteries branch into smaller and smaller vessels, eventually becoming very small vessels called arterioles. Arteries and arterioles have muscular walls that can adjust their diameter to increase or decrease blood flow to a particular part of the body.


Clinical points

Coronary Artery Bypass graft (CABG)- Coronary artery disease is the biggest killer in the Western world. It is a complication of hypertension, diabetes and high cholesterol. The saphenous vein can be removed from the leg, and sutured into the heart to bypass a blockage of the coronary arteries. This procedure is known as a heart bypass, and the patient is put on cardiopulmonary bypass during the procedure.

Thrombophlebitis- This condition is characterised by the formation of a thrombus along with inflammation in the superficial veins and involves great saphenous vein in many cases. There is a wide range of predisposing factors including prolonged immobilisation, trauma, malignancies like pancreatic cancer etc. Patients usually present with tender erythematous area overlying the superficial vein, a distended vein may be visible proximal to the thrombus. The occurrence of associated deep venous thrombosis and pulmonary embolism is variable.

Varicose veins- The great saphenous vein is a superficial vein. The deep veins (posterior tibial, anterior tibial, fibular, popliteal, femoral) are separated from the superficial veins by a series of valves. These valves ensure blood flows from the superficial system to the deep system i.e. prevents backflow. The incompetence of these valves results in varicose veins, which are engorged tortuous veins, that can be tender to the touch. Causes include genetic inheritance, pregnancy, chronic heart disease, obesity and prolonged standing.

Great saphenous vein: want to learn more about it?

Our engaging videos, interactive quizzes, in-depth articles and HD atlas are here to get you top results faster.

What do you prefer to learn with?

“I would honestly say that Kenhub cut my study time in half.” – Read more. Kim Bengochea, Regis University, Denver